TY - JOUR T1 - Enhanced DNA repair and resistance to cisplatin in human ovarian cancer. AN - 78584626; 3144285 JF - Biochemical pharmacology AU - Lai, G M AU - Ozols, R F AU - Smyth, J F AU - Young, R C AU - Hamilton, T C AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12/15/ PY - 1988 DA - 1988 Dec 15 SP - 4597 EP - 4600 VL - 37 IS - 24 SN - 0006-2952, 0006-2952 KW - Diterpenes KW - 0 KW - Aphidicolin KW - 38966-21-1 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Diterpenes -- pharmacology KW - Tumor Cells, Cultured KW - Dose-Response Relationship, Drug KW - Humans KW - Female KW - Ovarian Neoplasms -- genetics KW - Cisplatin -- toxicity KW - Drug Resistance KW - DNA Repair -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78584626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhanced+DNA+repair+and+resistance+to+cisplatin+in+human+ovarian+cancer.&rft.au=Lai%2C+G+M%3BOzols%2C+R+F%3BSmyth%2C+J+F%3BYoung%2C+R+C%3BHamilton%2C+T+C&rft.aulast=Lai&rft.aufirst=G&rft.date=1988-12-15&rft.volume=37&rft.issue=24&rft.spage=4597&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 - 1989-01-26 N1 - Date created - 1989-01-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human ethanol-inducible P450IIE1: complete gene sequence, promoter characterization, chromosome mapping, and cDNA-directed expression. AN - 78709506; 3233219 AB - The human P450IIE1 gene, coding for an ethanol-inducible nitrosamine-metabolizing P-450, was isolated from a lambda EMBL3 genomic library and completely sequenced. The human gene spanned 11,413 base pairs and contained nine exons and a typical TATA box. Upstream and downstream DNAs of 2788 and 559 base pairs were also sequenced and compared to the rat gene. Significant areas of sequence similarity were observed within 140 base pairs upstream of the transcription start site in the rat and human genes. Human DNA 539 base pairs upstream of the transcription start site was inserted into the expression vector pSVOAL delta 5', and luciferase activity was detected when the constructs were introduced into a rat hepatoma cell line. The activity was over 100-fold lower than that of pRSVL, a Rous sarcoma virus LTR-driven luciferase gene. By use of panels of rodent-human cell hybrids, the gene was mapped to chromosome 10 (CYP2E locus). A full-length cDNA, constructed with the first exon of the genomic clone and a partial cDNA clone, was expressed in COS cells and found to code for N-nitrosodimethylamine demethylase activity. JF - Biochemistry AU - Umeno, M AU - McBride, O W AU - Yang, C S AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12/13/ PY - 1988 DA - 1988 Dec 13 SP - 9006 EP - 9013 VL - 27 IS - 25 SN - 0006-2960, 0006-2960 KW - Nitrosamines KW - 0 KW - Ethanol KW - 3K9958V90M KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Luciferases KW - EC 1.13.12.- KW - Index Medicus KW - Animals KW - Exons KW - Sequence Homology, Nucleic Acid KW - Humans KW - Nitrosamines -- metabolism KW - Transcription, Genetic KW - Cloning, Molecular KW - Rats KW - Base Sequence KW - Enzyme Induction -- drug effects KW - Transfection KW - Molecular Sequence Data KW - Luciferases -- genetics KW - Promoter Regions, Genetic KW - Ethanol -- pharmacology KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA -- genetics KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Gene Expression Regulation KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78709506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+ethanol-inducible+P450IIE1%3A+complete+gene+sequence%2C+promoter+characterization%2C+chromosome+mapping%2C+and+cDNA-directed+expression.&rft.au=Umeno%2C+M%3BMcBride%2C+O+W%3BYang%2C+C+S%3BGelboin%2C+H+V%3BGonzalez%2C+F+J&rft.aulast=Umeno&rft.aufirst=M&rft.date=1988-12-13&rft.volume=27&rft.issue=25&rft.spage=9006&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-01 N1 - Date created - 1989-05-01 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J02843; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of fluorinated pyrimidine-induced cytotoxicity by leucovorin in human colorectal carcinoma cell lines. AN - 78540062; 2973527 AB - Reduced folates have been shown to increase the cytotoxicity of 5-fluorouracil (5-FU) by stabilizing the 5-fluoro-2'-deoxyuridine-5'-monophosphate-thymidylate synthase complex, thus increasing the block in the DNA synthetic pathway. Using an in vitro colorimetric [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] cytotoxicity assay, we tested the effects of 5-FU and 5-fluoro-2'-deoxyuridine (FdUrd) with and without leucovorin (LV) on a panel of 11 human colorectal carcinoma cell lines. The effect of LV on 5-FU and FdUrd was quantitatively similar. A clinically achievable level of LV (20 microM) increased the cytotoxicity in all three replicate experiments in 10 of the 11 cell lines (P less than .05, binomial test). LV alone at a concentration of 20 microM had no effect on cell survival. In three cell lines, 50% inhibition of growth occurred at a clinically achievable area under the curve of 5-FU alone. With the addition of LV, one additional cell line showed 50% growth inhibition at a clinically achievable level of 5-FU. Hence large clinical trials may be necessary to detect a significant improvement in survival as a result of adding LV to the fluorinated pyrimidines. JF - Journal of the National Cancer Institute AU - Park, J G AU - Collins, J M AU - Gazdar, A F AU - Allegra, C J AU - Steinberg, S M AU - Greene, R F AU - Kramer, B S AD - NCI-Navy Medical Oncology Branch, Bethesda, MD. Y1 - 1988/12/07/ PY - 1988 DA - 1988 Dec 07 SP - 1560 EP - 1564 VL - 80 IS - 19 SN - 0027-8874, 0027-8874 KW - Floxuridine KW - 039LU44I5M KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Cell Survival -- drug effects KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Drug Synergism KW - Fluorouracil -- administration & dosage KW - Floxuridine -- administration & dosage KW - Floxuridine -- pharmacology KW - Carcinoma -- pathology KW - Colorectal Neoplasms -- pathology KW - Leucovorin -- administration & dosage KW - Floxuridine -- pharmacokinetics KW - Fluorouracil -- pharmacology KW - Leucovorin -- pharmacology KW - Fluorouracil -- pharmacokinetics KW - Colorectal Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78540062?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhancement+of+fluorinated+pyrimidine-induced+cytotoxicity+by+leucovorin+in+human+colorectal+carcinoma+cell+lines.&rft.au=Park%2C+J+G%3BCollins%2C+J+M%3BGazdar%2C+A+F%3BAllegra%2C+C+J%3BSteinberg%2C+S+M%3BGreene%2C+R+F%3BKramer%2C+B+S&rft.aulast=Park&rft.aufirst=J&rft.date=1988-12-07&rft.volume=80&rft.issue=19&rft.spage=1560&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 - 1988-12-28 N1 - Date created - 1988-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene conversion and differential regulation in the rat P-450 IIA gene subfamily. Purification, catalytic activity, cDNA and deduced amino acid sequence, and regulation of an adult male-specific hepatic testosterone 15 alpha-hydroxylase. AN - 78536636; 3192524 AB - Previous studies on regulation of the rat hepatic P-450 IIA1 cDNA have provided evidence for a second gene closely related to but regulated in a manner quite distinct from P-450 IIA1. Experiments were carried out to isolate the cDNA for this second P-450 gene, designated IIA2, in order to study more directly its regulation and relationship to IIA1. A full length cDNA to IIA2 was isolated from an adult male rat liver lambda gt11 library and sequenced completely. The IIA2 cDNA shared 93% nucleotide and 88% deduced amino acid similarities with the previously characterized IIA1 cDNA (Nagata, K., Matsunaga, T., Gillette, J., Gelboin, H. V., and Gonzalez, F. J. (1987) J. Biol. Chem. 262, 2787-2793). The protein, deduced from the cDNA, contained 492 amino acids and a calculated Mr of 56,352. Comparison of the IIA1 and IIA2 cDNAs revealed areas of low nucleotide similarity interspersed with areas of absolute identity, suggesting that gene conversions have played a role in the evolution of the IIA subfamily. Expression of IIA1 and IIA2 mRNAs in rat liver during development was studied with use of specific oligonucleotide probes. IIA1 mRNA was increased within 1 week after birth in both male and female rats; however, its postpubertal expression was decreased in males yet remained elevated in females. In contrast, IIA2 mRNA was markedly induced in male rat liver at puberty but was not detectable in females at any age examined. Furthermore, only IIA1 mRNA was induced by treatment of rats with 3-methylcholanthrene. Although IIA1 and IIA2 mRNAs were actively expressed in hepatic tissue, no evidence for their expression was found in lung, kidney, or intestine, suggesting that the IIA genes have tissue-specific promoters. Reconstituted enzyme assays on the purified protein products P-450 IIA1 and P-450 IIA2 showed that, although both enzymes share considerable sequence similarity, their positional specificities toward the prototype substrate testosterone are strikingly different. JF - The Journal of biological chemistry AU - Matsunaga, T AU - Nagata, K AU - Holsztynska, E J AU - Lapenson, D P AU - Smith, A AU - Kato, R AU - Gelboin, H V AU - Waxman, D J AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12/05/ PY - 1988 DA - 1988 Dec 05 SP - 17995 EP - 18002 VL - 263 IS - 34 SN - 0021-9258, 0021-9258 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Steroid Hydroxylases KW - EC 1.14.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - steroid 15-alpha-hydroxylase KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Base Sequence KW - Sex Factors KW - Sequence Homology, Nucleic Acid KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Species Specificity KW - Male KW - Gene Conversion KW - Genes KW - Cytochrome P-450 Enzyme System -- genetics KW - Microsomes, Liver -- enzymology KW - Cytochrome P-450 Enzyme System -- isolation & purification KW - Steroid Hydroxylases -- metabolism KW - Steroid Hydroxylases -- isolation & purification KW - Cytochrome P-450 Enzyme System -- metabolism KW - Steroid Hydroxylases -- genetics KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78536636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Gene+conversion+and+differential+regulation+in+the+rat+P-450+IIA+gene+subfamily.+Purification%2C+catalytic+activity%2C+cDNA+and+deduced+amino+acid+sequence%2C+and+regulation+of+an+adult+male-specific+hepatic+testosterone+15+alpha-hydroxylase.&rft.au=Matsunaga%2C+T%3BNagata%2C+K%3BHolsztynska%2C+E+J%3BLapenson%2C+D+P%3BSmith%2C+A%3BKato%2C+R%3BGelboin%2C+H+V%3BWaxman%2C+D+J%3BGonzalez%2C+F+J&rft.aulast=Matsunaga&rft.aufirst=T&rft.date=1988-12-05&rft.volume=255&rft.issue=5+Pt+1&rft.spage=C661&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 - 1989-01-03 N1 - Date created - 1989-01-03 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J04187; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The molecular biology of cytochrome P450s. AN - 78747186; 3072575 JF - Pharmacological reviews AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 243 EP - 288 VL - 40 IS - 4 SN - 0031-6997, 0031-6997 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Multigene Family KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Chromosome Mapping KW - Cytochrome P-450 Enzyme System -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78747186?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacological+reviews&rft.atitle=The+molecular+biology+of+cytochrome+P450s.&rft.au=Gonzalez%2C+F+J&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1988-12-01&rft.volume=40&rft.issue=4&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Pharmacological+reviews&rft.issn=00316997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Pharmacol Rev 1989 Mar;41(1):91-2 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Species correlation of chemical carcinogens. AN - 78742640; 3244862 JF - Risk analysis : an official publication of the Society for Risk Analysis AU - Portier, C J AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 551 EP - 553 VL - 8 IS - 4 SN - 0272-4332, 0272-4332 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Carcinogenicity Tests KW - Data Interpretation, Statistical KW - Predictive Value of Tests KW - Species Specificity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78742640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+MPTP+analogs+induced+cell+death+in+cultured+rat+hepatocytes+involving+the+formation+of+pyridinium+metabolites.&rft.au=Singh%2C+Y%3BSwanson%2C+E%3BSokoloski%2C+E%3BKutty%2C+R+K%3BKrishna%2C+G&rft.aulast=Singh&rft.aufirst=Y&rft.date=1988-11-01&rft.volume=96&rft.issue=2&rft.spage=347&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 - 1989-06-01 N1 - Date created - 1989-06-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intravenous cocaine: psychiatric effects, biological mechanisms. AN - 78707704; 3233231 AB - Volunteer addicts were administered iv loading doses of cocaine, followed by 4-hr cocaine infusions that maintained steady-state conditions. The loading doses were followed by the "rush" and "high" subjective effects that users typically experience; cocaine infusions maintained the experience of drug "high", but not "rush". In a subsequent experiment, haloperidol pretreatment did not alter cocaine "rush" but partially attenuated cocaine "high." During cocaine infusions, we also noted suspicious and paranoid behavior, which were blindly rated by nurses. During one of the infusion conditions, the degree of suspiciousness observed was related to the amount of cocaine previously administered. Although cardiovascular responses to cocaine were marked, we found no alterations in plasma catecholamines following cocaine administrations. Baseline homovanillic acid (HVA) levels, however, were related to the degree of suspiciousness observed following cocaine dosing. The potential contributions of dopaminergic systems and physiological sensitization to the development of the psychiatric toxicity of cocaine are discussed. JF - Biological psychiatry AU - Sherer, M A AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 865 EP - 885 VL - 24 IS - 8 SN - 0006-3223, 0006-3223 KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Cocaine KW - I5Y540LHVR KW - Haloperidol KW - J6292F8L3D KW - Norepinephrine KW - X4W3ENH1CV KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Euphoria -- drug effects KW - Haloperidol -- adverse effects KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Humans KW - Methoxyhydroxyphenylglycol -- blood KW - Norepinephrine -- blood KW - Chromatography, High Pressure Liquid KW - Homovanillic Acid -- blood KW - Arousal -- drug effects KW - Premedication KW - Adult KW - Male KW - Brain -- drug effects KW - Substance-Related Disorders -- complications KW - Psychoses, Substance-Induced -- blood KW - Cocaine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78707704?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intravenous+cocaine%3A+psychiatric+effects%2C+biological+mechanisms.&rft.au=Sherer%2C+M+A&rft.aulast=Sherer&rft.aufirst=M&rft.date=1988-12-01&rft.volume=24&rft.issue=8&rft.spage=865&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 - 1989-04-28 N1 - Date created - 1989-04-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: NIH Guide Grants Contracts. 1993 Jun 25;22(23):1-4 [8390275] Biol Psychiatry. 1989 Dec;26(8):847-8 [2590695] Erratum In: Biol Psychiatry 1992 Aug 15;32(4):381 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human hepatocyte and kidney cell metabolism of 2-acetylaminofluorene and comparison to the respective rat cells. AN - 78677623; 3228713 AB - The metabolism and mutagenic activation of 2-acetylaminofluorene by human and rat hepatocytes and kidney cells were measured. High performance liquid chromatography was used to separate the 2-acetylaminofluorene metabolites, and a cell-mediated Salmonella typhimurium mutagenesis assay was used to detect mutagenic intermediates. Rat and human differences were observed with cells from both organs and levels of metabolism and mutagenesis were higher in human cells. Within a species, liver and kidney cell differences were also evident, with levels of hepatocyte-mediated metabolism and mutagenesis being greater than kidney cells. Human inter-individual variation was apparent with cells from both organs, but the variation observed was significantly greater in hepatocytes than kidney cells. A knowledge of such differences, including an understanding that they may vary with the chemical being studied, should be useful in the extrapolation of rodent carcinogenesis data to humans. JF - Cell biology and toxicology AU - Langenbach, R AU - Rudo, K AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 453 EP - 465 VL - 4 IS - 4 SN - 0742-2091, 0742-2091 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Index Medicus KW - Rats KW - Animals KW - Mutagenicity Tests KW - Biotransformation KW - Humans KW - Carcinogenicity Tests KW - Species Specificity KW - Male KW - Female KW - Kidney -- metabolism KW - 2-Acetylaminofluorene -- toxicity KW - Liver -- drug effects KW - Kidney -- drug effects KW - Liver -- metabolism KW - 2-Acetylaminofluorene -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78677623?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+hepatocyte+and+kidney+cell+metabolism+of+2-acetylaminofluorene+and+comparison+to+the+respective+rat+cells.&rft.au=Langenbach%2C+R%3BRudo%2C+K&rft.aulast=Langenbach&rft.aufirst=R&rft.date=1988-12-01&rft.volume=4&rft.issue=4&rft.spage=453&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 - 1989-04-17 N1 - Date created - 1989-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protein kinase C-dependent and -independent mechanisms regulating the parotid substance P receptor as revealed by differential effects of protein kinase C inhibitors. AN - 78668707; 2464997 AB - Substance P-induced inositol trisphosphate (InsP3) formation was inhibited by 1 microM-4 beta-phorbol 12,13-dibutyrate (PDBu) in rat parotid acinar cells. The inhibitory effect of PDBu was reversed by the protein kinase C inhibitors H-7 or K252a. Substance P also elicits a persistent desensitization of subsequent substance P-stimulated InsP3 formation. However, this desensitization was not inhibited by H-7. In addition, H-7 had no effect on the time course of substance P-induced InsP3 formation. These results suggest that, although activation of protein kinase C by phorbol esters can inhibit the substance P receptor-linked phospholipase C pathway, this mechanism apparently plays little, if any, role in regulating this system after activation by substance P. JF - The Biochemical journal AU - Sugiya, H AU - Putney, J W AD - Calcium Regulation Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 677 EP - 680 VL - 256 IS - 2 SN - 0264-6021, 0264-6021 KW - Carbazoles KW - 0 KW - Indole Alkaloids KW - Inositol Phosphates KW - Isoquinolines KW - Piperazines KW - Receptors, Neurokinin-1 KW - Receptors, Neurotransmitter KW - Sugar Phosphates KW - Substance P KW - 33507-63-0 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - staurosporine aglycone KW - 97161-97-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Isoquinolines -- pharmacology KW - Animals KW - Carbazoles -- pharmacology KW - Receptors, Neurotransmitter -- drug effects KW - Piperazines -- pharmacology KW - Male KW - Sugar Phosphates -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Substance P -- pharmacology KW - Inositol Phosphates -- metabolism KW - Parotid Gland -- metabolism KW - Phorbol 12,13-Dibutyrate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78668707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Protein+kinase+C-dependent+and+-independent+mechanisms+regulating+the+parotid+substance+P+receptor+as+revealed+by+differential+effects+of+protein+kinase+C+inhibitors.&rft.au=Sugiya%2C+H%3BPutney%2C+J+W&rft.aulast=Sugiya&rft.aufirst=H&rft.date=1988-12-01&rft.volume=256&rft.issue=2&rft.spage=677&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 - 1989-03-16 N1 - Date created - 1989-03-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1985 Sep 12-18;317(6033):124-9 [2993919] J Biol Chem. 1985 Mar 25;260(6):3281-8 [3919020] J Biol Chem. 1986 Apr 25;261(12):5307-13 [3082882] Proc Natl Acad Sci U S A. 1986 Apr;83(7):2032-6 [3083411] Biochem Biophys Res Commun. 1986 May 29;137(1):50-60 [3013192] J Biol Chem. 1987 Feb 5;262(4):1638-43 [3543007] J Cell Physiol. 1987 Jan;130(1):29-36 [3492499] J Pharmacol Exp Ther. 1987 Feb;240(2):617-22 [2879910] Eur J Biochem. 1987 Mar 2;163(2):417-21 [3028803] J Biol Chem. 1987 May 5;262(13):6121-7 [3032956] J Biol Chem. 1987 May 15;262(14):6766-70 [3471761] Biochem Biophys Res Commun. 1987 Apr 14;144(1):35-40 [3579911] J Biol Chem. 1987 Nov 5;262(31):14912-6 [2444592] Mol Pharmacol. 1987 Dec;32(6):737-42 [2892124] Biochem J. 1987 Jun 15;244(3):647-53 [2451500] Biochem J. 1988 Jul 15;253(2):459-66 [2460079] J Physiol. 1977 Jun;268(1):139-49 [195043] Mol Pharmacol. 1980 Jul;18(1):78-83 [6157980] Biochem J. 1982 Sep 15;206(3):555-60 [6184051] Biochem J. 1983 May 15;212(2):473-82 [6309146] Life Sci. 1984 Apr 2;34(14):1347-55 [6323902] Biochem J. 1984 Jun 1;220(2):345-60 [6146314] Mol Pharmacol. 1984 Sep;26(2):261-6 [6237255] Biochem Biophys Res Commun. 1984 Sep 17;123(2):703-9 [6593069] Biochemistry. 1984 Oct 9;23(21):5036-41 [6238627] Biochem Biophys Res Commun. 1984 Nov 30;125(1):258-64 [6239622] Biochem Biophys Res Commun. 1986 Jan 29;134(2):868-75 [3004469] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemotherapy/radiation therapy plus/minus lonidamine in the treatment of non-small cell lung cancer (limited disease): preliminary results. AN - 78641031; 2851173 AB - One hundred sixteen patients with unresectable locally advanced non-small cell lung cancer (NSCLC) were accrued in a prospective randomized trial comparing (A), chemotherapy (cisplatin and etoposide [VP-16]) for two courses plus radiation therapy (30 + 20 Gy split course), followed by an additional two courses to (B), the same regimen plus the addition of lonidamine (LND). There were 93 patients evaluable for response (46 in the chemotherapy/radiation arm and 47 in the chemotherapy/radiation/LND arm). One hundred fifteen patients were evaluable for toxicity. The overall response rates, median time to progression, and median survival time were similar in both arms. For the group of patients with squamous cell histology, time to progression was 27 weeks on arm A and 38 weeks on arm B (P = 0.01). Two-year survival in the squamous cell group in arm A was 9%, in arm B, 39%. LND does not give rise to additional toxicity, although myalgia and testicular pain are characteristic side effects. JF - Seminars in oncology AU - Gallo-Curcio, C AU - Verturo, I AU - Rinaldi, M AU - Ambesi Impiombato, F AU - Del Vecchio, M R AU - Tonachella, R AU - Tropea, F AU - Antilli, A AU - Ciottoli, G B AU - De Gregorio, M AD - National Cancer Institute, Regina Elena, C. Forlanini Hospital, Rome, Italy. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 26 EP - 31 VL - 15 IS - 6 Suppl 7 SN - 0093-7754, 0093-7754 KW - Indazoles KW - 0 KW - Pyrazoles KW - lonidamine KW - U78804BIDR KW - Index Medicus KW - Prospective Studies KW - Random Allocation KW - Combined Modality Therapy KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Time Factors KW - Male KW - Female KW - Pyrazoles -- administration & dosage KW - Indazoles -- administration & dosage KW - Lung Neoplasms -- therapy KW - Carcinoma, Non-Small-Cell Lung -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78641031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chemotherapy%2Fradiation+therapy+plus%2Fminus+lonidamine+in+the+treatment+of+non-small+cell+lung+cancer+%28limited+disease%29%3A+preliminary+results.&rft.au=Gallo-Curcio%2C+C%3BVerturo%2C+I%3BRinaldi%2C+M%3BAmbesi+Impiombato%2C+F%3BDel+Vecchio%2C+M+R%3BTonachella%2C+R%3BTropea%2C+F%3BAntilli%2C+A%3BCiottoli%2C+G+B%3BDe+Gregorio%2C+M&rft.aulast=Gallo-Curcio&rft.aufirst=C&rft.date=1988-12-01&rft.volume=15&rft.issue=6+Suppl+7&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=00937754&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-28 N1 - Date created - 1989-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prenatal exposure of male mice to diethylstilbestrol alter the expression of the lactotransferrin gene in seminal vesicles. AN - 78638766; 3216864 AB - We have previously isolated an estrogen-inducible secretory protein, lactotransferrin (LTF), and a cDNA to its messenger RNA from the uterus of mice. In this report we determined that the level of LTF mRNA is minimal in the seminal vesicles of normal mice. In contrast, expression of LTF mRNA in the seminal vesicles of developmentally estrogenized males was both constitutive and estrogen inducible. The results suggested that this alteration may be an example of atypical gene expression after hormonal manipulation early in development. JF - Molecular endocrinology (Baltimore, Md.) AU - Pentecost, B T AU - Newbold, R R AU - Teng, C T AU - McLachlan, J A AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1243 EP - 1248 VL - 2 IS - 12 SN - 0888-8809, 0888-8809 KW - Androgens KW - 0 KW - Estrogens KW - Genetic Markers KW - Lactoglobulins KW - Prostatic Secretory Proteins KW - Proteins KW - Seminal Plasma Proteins KW - beta-microseminoprotein KW - Diethylstilbestrol KW - 731DCA35BT KW - Lactoferrin KW - EC 3.4.21.- KW - Index Medicus KW - Animals KW - Genetic Markers -- genetics KW - Estrogens -- pharmacology KW - Estrogens -- metabolism KW - Mice KW - Androgens -- pharmacology KW - Proteins -- genetics KW - Male KW - Female KW - Androgens -- metabolism KW - Pregnancy KW - Seminal Vesicles -- metabolism KW - Lactoferrin -- genetics KW - Diethylstilbestrol -- pharmacology KW - Lactoglobulins -- genetics KW - Gene Expression Regulation -- drug effects KW - Seminal Vesicles -- drug effects KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78638766?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prenatal+exposure+of+male+mice+to+diethylstilbestrol+alter+the+expression+of+the+lactotransferrin+gene+in+seminal+vesicles.&rft.au=Pentecost%2C+B+T%3BNewbold%2C+R+R%3BTeng%2C+C+T%3BMcLachlan%2C+J+A&rft.aulast=Pentecost&rft.aufirst=B&rft.date=1988-12-01&rft.volume=2&rft.issue=12&rft.spage=1243&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 - 1989-03-03 N1 - Date created - 1989-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Proteolytic degradation of protein kinase C in the phorbol ester-induced interleukin-2 secreting thymoma cells. AN - 78628299; 3265048 AB - Effects of phorbol 12-myristate 13-acetate (PMA) on the fate of protein kinase C in two mouse thymoma cell lines, which are either responsive (EL4) or unresponsive (IEL4) to PMA-induced interleukin-2 (IL-2) production, were investigated with polyclonal antibodies raised against rat brain enzyme. These antibodies immunoprecipitated completely the protein kinase C from both cell lines and detected mainly an 82-kDa protein by immunoblot analysis of the crude homogenates as well as the partially purified kinase preparations. PMA elicited a time- and dose-dependent redistribution of protein kinase C from cytosol to the particulate fraction and proteolytic degradation of the kinase from both cell lines. The dose of PMA required for half-maximum protein kinase C translocation and degradation was at least five times lower for EL4 than for IEL4. In the presence of 16 nM PMA the rates of protein kinase C translocation and degradation were faster in EL4 than in IEL4, and the half-lives of protein kinase C in EL4 and IEL4 were less than 5 min and greater than 2 h, respectively. Analysis of the tryptic fragments of the immunoprecipitated enzyme, previously phosphorylated in the presence of [gamma-32P]ATP, revealed minor structural differences between the protein kinase C from these two cell lines. In neither cell line did the PMA-induced degradation of protein kinase C result in an accumulation of the Ca2+/phospholipid-independent kinase (catalytic unit) as analyzed by immunoblotting and gel filtration chromatography. Thus, activation of protein kinase C through the proteolytic conversion to the effector-independent catalytic unit plays little role in IL-2 production. The role of protein kinase C translocation and degradation in the PMA-induced responses in EL4 cells is unknown. However, IL-2 production in EL4 cells was reduced when PMA-induced degradation of protein kinase C was retarded by exogenously added protease inhibitors. JF - Archives of biochemistry and biophysics AU - Huang, F L AU - Arora, P K AU - Hanna, E E AU - Huang, K P AD - Section on Metabolic Regulation, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 503 EP - 514 VL - 267 IS - 2 SN - 0003-9861, 0003-9861 KW - Interleukin-2 KW - 0 KW - Peptide Fragments KW - Protease Inhibitors KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Protease Inhibitors -- pharmacology KW - Immunoblotting KW - Animals KW - Phosphorylation KW - Peptide Mapping KW - Cytosol -- enzymology KW - Cell Line -- drug effects KW - Peptide Fragments -- analysis KW - Mice KW - Precipitin Tests KW - Hydrolysis KW - Protein Kinase C -- metabolism KW - Thymoma -- secretion KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Protein Kinase C -- isolation & purification KW - Interleukin-2 -- secretion KW - Thymoma -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78628299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Proteolytic+degradation+of+protein+kinase+C+in+the+phorbol+ester-induced+interleukin-2+secreting+thymoma+cells.&rft.au=Huang%2C+F+L%3BArora%2C+P+K%3BHanna%2C+E+E%3BHuang%2C+K+P&rft.aulast=Huang&rft.aufirst=F&rft.date=1988-12-01&rft.volume=267&rft.issue=2&rft.spage=503&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 - 1989-02-16 N1 - Date created - 1989-02-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The chronic hepatic or renal toxicity of di(2-ethylhexyl) phthalate, acetaminophen, sodium barbital, and phenobarbital in male B6C3F1 mice: autoradiographic, immunohistochemical, and biochemical evidence for levels of DNA synthesis not associated with carcinogenesis or tumor promotion. AN - 78599205; 3206528 AB - Male B6C3F1 mice, 6 weeks of age, were fed diets or water containing di(2-ethylhexyl) phthalate (DEHP) at 12,000 or 6000 ppm, acetaminophen (ACT) at 10,000 or 5000 ppm, sodium barbital (BBS) at 1000 ppm, or phenobarbital (PB) at 500 ppm for 40 weeks. Groups of six mice were terminated at 2, 8, 24, and 40 weeks for evaluation of liver and kidney weights, histopathology, and thymidine kinase (TK) activity in liver and kidney and levels of DNA synthesis, measured by tritiated thymidine [( 3H]T) autoradiography or bromodeoxyuridine (BrdU) immunohistochemistry. Liver weights, as percentage of body weight, were significantly elevated at most time intervals for mice exposed to all chemicals at each dose. The hepatocyte labeling indices (LI) with [3H]T autoradiography or BrdU immunocytochemistry were significantly elevated in mice fed DEHP at 12,000 ppm at 24 and 40 weeks or BBS and ACT at 2 weeks. LI were not elevated in mice fed PB. Hepatic TK activity was significantly elevated in mice fed DEHP, BBS, or ACT at Weeks 2 and 8. Histopathologic hepatic lesions were associated with these elevations, while hepatic lesions were not associated with changes in TK activity in PB-treated mice. In contrast, only DEHP and BBS induced toxic renal lesions. Persistent or transient elevation of the renal LI and TK activity accompanied renal toxicity. Thus, the hepatic toxin DEHP induced chronic renal hyperplasia without evidence of renal carcinogenicity or tumor promotion in previous studies at the doses used. ACT, a hepatotoxin, produced transient chronic hepatic hyperplasia without evidence of carcinogenicity in B6C3F1 mice in earlier studies at the same doses used. Thus, persistent or transient hepatic or renal hyperplasia was associated with carcinogenic or tumor promoting activity of these chemicals in some cases but not in others. JF - Toxicology and applied pharmacology AU - Ward, J M AU - Hagiwara, A AU - Anderson, L M AU - Lindsey, K AU - Diwan, B A AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 494 EP - 506 VL - 96 IS - 3 SN - 0041-008X, 0041-008X KW - Barbiturates KW - 0 KW - Phthalic Acids KW - Acetaminophen KW - 362O9ITL9D KW - Barbital KW - 5WZ53ENE2P KW - DNA KW - 9007-49-2 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - Thymidine Kinase -- analysis KW - Mice, Inbred C3H KW - Mice KW - Autoradiography KW - Immunohistochemistry KW - Male KW - Liver -- pathology KW - Kidney -- pathology KW - Kidney Neoplasms -- chemically induced KW - Diethylhexyl Phthalate -- toxicity KW - Kidney -- drug effects KW - Liver Neoplasms, Experimental -- chemically induced KW - Barbiturates -- toxicity KW - Barbital -- toxicity KW - DNA -- biosynthesis KW - Phthalic Acids -- toxicity KW - Liver -- drug effects KW - Phenobarbital -- toxicity KW - Acetaminophen -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78599205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+chronic+hepatic+or+renal+toxicity+of+di%282-ethylhexyl%29+phthalate%2C+acetaminophen%2C+sodium+barbital%2C+and+phenobarbital+in+male+B6C3F1+mice%3A+autoradiographic%2C+immunohistochemical%2C+and+biochemical+evidence+for+levels+of+DNA+synthesis+not+associated+with+carcinogenesis+or+tumor+promotion.&rft.au=Ward%2C+J+M%3BHagiwara%2C+A%3BAnderson%2C+L+M%3BLindsey%2C+K%3BDiwan%2C+B+A&rft.aulast=Ward&rft.aufirst=J&rft.date=1988-12-01&rft.volume=96&rft.issue=3&rft.spage=494&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 - 1989-02-03 N1 - Date created - 1989-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Concomitant infection of HTLV-I and HIV-1: prevalence of IgG and IgM antibodies in Washington, D.C. area. AN - 78582697; 2904886 AB - Serum samples collected from four groups of individuals in the Washington, D.C. area were examined for the presence of IgG and IgM classes of antibody reacting against HTLV-I and HIV-1. These four groups were: (1) healthy adults with negative premarital VDRL test for syphilis (n = 113), (2) miscellaneous common disease patients (n = 155), (3) drug abusers (n = 130), and (4) homosexual men (n = 187). The former two groups are considered to be low-risk groups, and the latter two, high-risk groups. The prevalence of IgG antibody on ELISA/Western blot tests for these groups were respectively: (1) 5.3%/1.8%, (2) 5.2%/1.9%, (3) 13.9%/4.6%, and (4) 4.3%/1.6% for HTLV-I, and (1) 2.7%/0.9%, (2) 4.5%/0%, (3) 12.3%/5.4%, and (4) 8.0%/5.9% for HIV-1. Instances of possible concomitant infection as shown by the presence of antibodies against both HTLV-I and HIV-1 were found only in the latter two high-risk groups, i.e. two (1.5%) in group (3), and three (1.6%) in group (4) as confirmed by both Western blot and immunofluorescence tests. Out of 97 sera collected from drug abusers in 1985-86 which had IgG antibody by Western blot test against HIV-1, 23 (23.7%) were HTLV-I antibody positive by ELISA test (Group 5), and 8 of these were confirmed by Western blot test. Among these 8 persons, IgM antibody against HTLV-I was found in 2, while that against HIV-1 was positive in 7 persons.(ABSTRACT TRUNCATED AT 250 WORDS) JF - European journal of epidemiology AU - Chang, K S AU - Wang, L C AU - Gao, C L AU - Alexander, S AU - Ting, R C AU - Bodner, A AU - Log, T AU - Kuo, A F AU - Strickland, P AD - Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 426 EP - 434 VL - 4 IS - 4 SN - 0393-2990, 0393-2990 KW - HIV Antibodies KW - 0 KW - HTLV-I Antibodies KW - Immunoglobulin G KW - Immunoglobulin M KW - Index Medicus KW - AIDS/HIV KW - Deltaretrovirus Infections -- immunology KW - Acquired Immunodeficiency Syndrome -- complications KW - Deltaretrovirus Infections -- epidemiology KW - Injections, Intravenous KW - Random Allocation KW - Humans KW - Retrospective Studies KW - Aged KW - Blotting, Western -- methods KW - Homosexuality KW - Deltaretrovirus Infections -- complications KW - District of Columbia KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Acquired Immunodeficiency Syndrome -- immunology KW - Adult KW - Enzyme-Linked Immunosorbent Assay KW - Middle Aged KW - Substance-Related Disorders -- immunology KW - Fluorescent Antibody Technique KW - Male KW - Female KW - HTLV-I Antibodies -- analysis KW - Immunoglobulin G -- analysis KW - HIV -- immunology KW - Immunoglobulin M -- analysis KW - HIV Antibodies -- analysis KW - Human T-lymphotropic virus 1 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78582697?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology&rft.atitle=Concomitant+infection+of+HTLV-I+and+HIV-1%3A+prevalence+of+IgG+and+IgM+antibodies+in+Washington%2C+D.C.+area.&rft.au=Chang%2C+K+S%3BWang%2C+L+C%3BGao%2C+C+L%3BAlexander%2C+S%3BTing%2C+R+C%3BBodner%2C+A%3BLog%2C+T%3BKuo%2C+A+F%3BStrickland%2C+P&rft.aulast=Chang&rft.aufirst=K&rft.date=1988-12-01&rft.volume=4&rft.issue=4&rft.spage=426&rft.isbn=&rft.btitle=&rft.title=European+journal+of+epidemiology&rft.issn=03932990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-07 N1 - Date created - 1989-02-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Eur J Epidemiol 1989 Mar;5(1):128-9 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Caffeinated beverages and decreased fertility. AN - 78576350; 2904572 AB - 104 healthy women who had been attempting to become pregnant for three months were interviewed about their use of caffeinated beverages, alcohol, and cigarettes. In their subsequent cycles, women who consumed more than the equivalent of one cup of coffee per day were half as likely to become pregnant, per cycle, as women who drank less. A dose-response effect was present. JF - Lancet (London, England) AU - Wilcox, A AU - Weinberg, C AU - Baird, D AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1988 SP - 1453 EP - 1456 VL - 2 IS - 8626-8627 SN - 0140-6736, 0140-6736 KW - Coffee KW - 0 KW - Caffeine KW - 3G6A5W338E KW - Abridged Index Medicus KW - Index Medicus KW - Population KW - United States KW - Infertility KW - Fertility KW - Organic Chemicals KW - Population Dynamics KW - Health KW - Treatment KW - Nutrition KW - Developed Countries KW - Ingredients And Chemicals KW - Alkaloids KW - Demographic Factors KW - Drugs KW - North America KW - Americas KW - Maternal Nutrition KW - Fecundability KW - Differential Fertility KW - Northern America KW - Fecundity KW - North Carolina KW - Reproduction KW - Developing Countries KW - Smoking KW - Risk Factors KW - Humans KW - Adult KW - Alcohol Drinking KW - Female KW - Pregnancy KW - Beverages KW - Caffeine -- adverse effects KW - Coffee -- adverse effects KW - Infertility, Female -- chemically induced KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78576350?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Caffeinated+beverages+and+decreased+fertility.&rft.au=Wilcox%2C+A%3BWeinberg%2C+C%3BBaird%2C+D&rft.aulast=Wilcox&rft.aufirst=A&rft.date=1988-12-01&rft.volume=2&rft.issue=8626-8627&rft.spage=1453&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 - 1989-01-26 N1 - Date created - 1989-01-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Lancet. 1989 Feb 18;1(8634):378 [2563522] Lancet. 1990 Mar 31;335(8692):792-3 [1969535] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lineage-specific regulation of the vasoactive intestinal peptide gene in neuroblastoma cells is conferred by 5.2 kilobases of 5'-flanking sequence. AN - 78575001; 3200839 AB - The expression of a transfected plasmid containing 5.2 kilobases (kb) of 5' regulatory DNA sequence of the human vasoactive intestinal peptide (VIP) gene attached to coding sequences of the reporter gene chloramphenicol acetyltransferase (CAT) was compared with endogenous VIP expression in subclones of the human neuroblastoma cell line SK-N-SH. These subclones vary widely in basal and inducible quantities of VIP and its precursor mRNA and can be interconverted under specified culture conditions. Endogenous VIP immunoreactivity, detectable in all subclones, was lowest in the neuronal subclone SH-SY-5Y, whereas 15- to 25-fold higher levels were observed in the epithelial-appearing SH-EP and intermediate SH-IN subclones. Treatment with 10 nM phorbol 12-myristate 13-acetate (PMA) stimulated VIP peptide levels approximately 5-fold in SH-SY-5Y cells but did not increase appreciably VIP levels in the other subclones. Treatment with 2.5 microM forskolin resulted in less than 50% stimulation of VIP expression in all subclones. Levels of mRNA encoding the VIP precursor generally paralleled these differences in VIP immunoreactivity. In cells transfected with the VIP/CAT fusion gene, CAT activity reflected closely these differences in basal VIP expression and the changes in response to PMA and forskolin. Deletion of 2.7 kb of the most upstream sequences resulted in an 80-90% reduction in basal CAT activity in SH-IN, but not SH-SY-5Y cells, and resulted in an 80% reduction in PMA stimulation in SH-SY-5Y cells. Deletion to within 74 nucleotides of the transcription start site resulted in CAT expression in SH-IN cells that was only 3% of that seen with the full 5.2-kb flanking sequences and further diminished the remaining PMA responsiveness in SH-SY-5Y cells. The data indicate that important cell-type-specific transcription regulatory sequences reside greater than 2.5 kb upstream from the VIP transcription start site. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Waschek, J A AU - Hsu, C M AU - Eiden, L E AD - Unit on Molecular and Cellular Neurobiology, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 9547 EP - 9551 VL - 85 IS - 24 SN - 0027-8424, 0027-8424 KW - Colforsin KW - 1F7A44V6OU KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Colforsin -- pharmacology KW - Chromosome Deletion KW - Base Sequence KW - Transfection KW - Humans KW - Enhancer Elements, Genetic KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Plasmids KW - Molecular Weight KW - Cell Line KW - Neuroblastoma -- genetics KW - Vasoactive Intestinal Peptide -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78575001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Lineage-specific+regulation+of+the+vasoactive+intestinal+peptide+gene+in+neuroblastoma+cells+is+conferred+by+5.2+kilobases+of+5%27-flanking+sequence.&rft.au=Waschek%2C+J+A%3BHsu%2C+C+M%3BEiden%2C+L+E&rft.aulast=Waschek&rft.aufirst=J&rft.date=1988-12-01&rft.volume=85&rft.issue=24&rft.spage=9547&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 - 1989-01-26 N1 - Date created - 1989-01-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1978 Dec;15(4):1157-74 [728996] Mol Cell Biol. 1988 Feb;8(2):605-14 [2895420] Brain Res. 1982 Jan 14;231(2):472-7 [7055688] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nature. 1983 Aug 11-17;304(5926):547-9 [6571696] Life Sci. 1983 Aug 22;33(8):687-93 [6888186] J Natl Cancer Inst. 1983 Oct;71(4):741-7 [6137586] Lancet. 1983 Nov 19;2(8360):1163-5 [6139527] Proc Natl Acad Sci U S A. 1984 Jul;81(13):3949-53 [6330725] Endocrinology. 1985 Sep;117(3):1020-6 [3839453] DNA. 1985 Aug;4(4):293-300 [3899557] Biochem Biophys Res Commun. 1985 Nov 15;132(3):885-91 [2416313] Cell. 1986 Aug 29;46(5):705-16 [3091258] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7653-7 [2429314] J Biol Chem. 1986 Nov 5;261(31):14373-6 [3464596] Nature. 1986 Oct 23-29;323(6090):731-4 [3022151] Mol Cell Biol. 1986 Dec;6(12):4305-16 [3025651] Proc Natl Acad Sci U S A. 1987 Jan;84(2):605-9 [3025882] Cell. 1987 Jan 30;48(2):331-42 [3643061] Nature. 1987 Jan 22-28;325(6102):368-72 [3027570] Cancer Res. 1987 Mar 1;47(5):1383-9 [3028608] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] Science. 1987 Jun 5;236(4806):1237-45 [3296191] J Biol Chem. 1987 Jun 25;262(18):8743-7 [3036825] Nature. 1987 Jul 9-15;328(6126):175-8 [2885756] Cell. 1987 Oct 23;51(2):251-60 [2822255] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] Mol Cell Biol. 1987 Nov;7(11):3994-4002 [2828923] Mol Cell Biol. 1987 Nov;7(11):4058-64 [3431549] Science. 1988 Mar 18;239(4846):1400-5 [2831625] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetics of subcutaneous methotrexate. AN - 78570070; 3199171 AB - The pharmacokinetics of subcutaneously administered methotrexate was studied as a parenteral alternative to oral administration. An initial feasibility study was performed in Rhesus monkeys comparing the subcutaneous route to intravenous (IV) injection and oral administration. The subcutaneous dose was completely absorbed and a sustained-release effect was observed when compared with the IV dose. No local or systemic toxicities resulted from subcutaneous methotrexate in the animals. Twelve children with acute lymphoblastic leukemia on maintenance therapy protocols prescribing either 7.5 mg/m2 biweekly or 40 mg/m2 weekly were also monitored after both a subcutaneous and an oral dose of methotrexate. Four children at the higher dosage level were also studied after an equal IV dose. The subcutaneous dose was again completely absorbed in these children at both dose levels, whereas the oral dose, which produced comparable plasma drug concentrations at the lower dosage level, resulted in a total drug exposure (area under the plasma concentration-time curve) that was one third that of the equal subcutaneous dose at the higher dosage level. No local or systemic toxicity was attributed to the subcutaneous methotrexate. Subcutaneous administration of methotrexate is well tolerated and well absorbed and appears to overcome the problems associated with oral administration, including variable absorption and saturation of the absorption mechanism with increasing doses. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Balis, F M AU - Mirro, J AU - Reaman, G H AU - Evans, W E AU - McCully, C AU - Doherty, K M AU - Murphy, R F AU - Jeffries, S AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1882 EP - 1886 VL - 6 IS - 12 SN - 0732-183X, 0732-183X KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Administration, Oral KW - Animals KW - Humans KW - Child KW - Child, Preschool KW - Adult KW - Absorption KW - Injections, Subcutaneous KW - Macaca mulatta KW - Adolescent KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Female KW - Male KW - Methotrexate -- pharmacokinetics KW - Methotrexate -- blood KW - Methotrexate -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78570070?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pharmacokinetics+of+subcutaneous+methotrexate.&rft.au=Balis%2C+F+M%3BMirro%2C+J%3BReaman%2C+G+H%3BEvans%2C+W+E%3BMcCully%2C+C%3BDoherty%2C+K+M%3BMurphy%2C+R+F%3BJeffries%2C+S%3BPoplack%2C+D+G&rft.aulast=Balis&rft.aufirst=F&rft.date=1988-12-01&rft.volume=6&rft.issue=12&rft.spage=1882&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 - 1989-01-18 N1 - Date created - 1989-01-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Binding region for human immunodeficiency virus (HIV) and epitopes for HIV-blocking monoclonal antibodies of the CD4 molecule defined by site-directed mutagenesis. AN - 78560726; 2461565 AB - The binding region for human immunodeficiency virus (HIV) and epitopes for a panel of HIV-blocking anti-CD4 monoclonal antibodies of the CD4 molecule were defined by using in vitro site-directed mutagenesis. Codons for two amino acid residues (Ser-Arg) were inserted at selected positions within the region encoding the first and second immunoglobulin-like domains of CD4. A vaccinia virus-based expression system was used to produce soluble full-length extracellular CD4 fragments containing the insertions. The mutant proteins were tested for direct binding to soluble gp120 (the CD4-binding subunit of the viral envelope glycoprotein) and to a series of HIV-blocking anti-CD4 monoclonal antibodies. Impaired gp120 binding activity resulted from insertions after amino acid residues 31, 44, 48, 52, 55, and 57 in the first immunoglobulin-like domain. The epitopes for two HIV-blocking monoclonal antibodies, OKT4A and OKT4D, were also mapped in the gp120-binding region in the first domain. Insertions after amino acid residues 21 and 91 in the first domain had no effect on gp120 binding but impaired the binding of OKT4E, suggesting that this antibody recognizes a discontinuous epitope not directly involved in gp120 binding. Moderate impairment of gp120 binding resulted from the insertion after amino acid residues 164 in the second immunoglobulin-like domain, where the epitopes for monoclonal antibodies MT151 and OKT4B were also mapped. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Mizukami, T AU - Fuerst, T R AU - Berger, E A AU - Moss, B AD - Laboratory of Viral Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 9273 EP - 9277 VL - 85 IS - 23 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Epitopes KW - HIV Antibodies KW - Immunoglobulins KW - Receptors, HIV KW - Receptors, Virus KW - Index Medicus KW - AIDS/HIV KW - Vaccinia virus -- genetics KW - Animals KW - Base Sequence KW - Molecular Sequence Data KW - Immunoglobulins -- immunology KW - Mice KW - Amino Acid Sequence KW - Antigens, Differentiation, T-Lymphocyte -- genetics KW - HIV Antibodies -- immunology KW - Receptors, Virus -- immunology KW - Receptors, Virus -- genetics KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Epitopes -- immunology KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78560726?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Binding+region+for+human+immunodeficiency+virus+%28HIV%29+and+epitopes+for+HIV-blocking+monoclonal+antibodies+of+the+CD4+molecule+defined+by+site-directed+mutagenesis.&rft.au=Mizukami%2C+T%3BFuerst%2C+T+R%3BBerger%2C+E+A%3BMoss%2C+B&rft.aulast=Mizukami&rft.aufirst=T&rft.date=1988-12-01&rft.volume=85&rft.issue=23&rft.spage=9273&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 - 1988-12-30 N1 - Date created - 1988-12-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1970 Aug 15;227(5259):680-5 [5432063] Nature. 1988 Sep 22;335(6188):363-6 [2843773] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3824-8 [6167991] Cell Immunol. 1983 Sep;80(2):310-9 [6192938] Hum Immunol. 1984 Feb;9(2):89-102 [6199335] Science. 1984 Jul 6;225(4657):59-63 [6328660] Nature. 1984 Dec 20-1985 Jan 2;312(5996):763-7 [6096719] Nature. 1984 Dec 20-1985 Jan 2;312(5996):767-8 [6083454] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Cell. 1985 Aug;42(1):93-104 [2990730] J Immunol. 1985 Nov;135(5):3151-62 [2995487] J Immunol. 1986 Jan;136(2):361-3 [2416802] Science. 1986 Jan 24;231(4736):382-5 [3001934] Nature. 1986 Jul 31-Aug 6;322(6078):470-4 [3016552] J Immunol. 1986 Nov 1;137(9):2937-44 [2428879] Cell. 1986 Nov 7;47(3):333-48 [3094962] Nature. 1986 Oct 23-29;323(6090):725-8 [3095663] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8122-6 [3095828] Science. 1986 Nov 28;234(4780):1120-3 [2430333] J Immunol Methods. 1987 Feb 26;97(1):93-100 [3029227] Proc Natl Acad Sci U S A. 1987 Mar;84(6):1649-53 [3104900] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3891-5 [3495801] Mol Cell Biol. 1987 Jul;7(7):2538-44 [3112559] Cell. 1987 Sep 11;50(6):975-85 [2441877] Nature. 1987 Dec 3-9;330(6147):487-9 [2446142] Science. 1987 Dec 18;238(4834):1704-7 [3500514] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9155-9 [3501122] Nature. 1988 Jan 7;331(6151):76-8 [2829022] Nature. 1988 Jan 7;331(6151):78-81 [2829023] Nature. 1988 Jan 7;331(6151):82-4 [3257544] Nature. 1988 Jan 7;331(6151):84-6 [2829024] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2357-61 [2451247] Science. 1988 Jun 3;240(4857):1335-9 [2453925] AIDS. 1988 Apr;2(2):101-5 [2454642] Annu Rev Immunol. 1988;6:381-405 [3289571] Annu Rev Immunol. 1988;6:555-80 [2454644] Cell. 1988 Jul 1;54(1):65-72 [2454749] Nature. 1988 Jul 14;334(6178):159-62 [3260352] J Mol Biol. 1978 Mar 25;120(1):97-120 [642007] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mood changes associated with reproductive life events: an overview of research and treatment strategies. AN - 78559651; 3198579 JF - The Journal of clinical psychiatry AU - Blumenthal, S J AU - Nadelson, C C AD - Health and Behavior Research Branch, National Institute of Mental Health, Rockville, MD 20857. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 466 EP - 468 VL - 49 IS - 12 SN - 0160-6689, 0160-6689 KW - Contraceptives, Oral KW - 0 KW - Index Medicus KW - Contraceptives, Oral -- adverse effects KW - Humans KW - Menstrual Cycle KW - Aging KW - Male KW - Female KW - Pregnancy KW - Premenstrual Syndrome -- psychology KW - Reproduction KW - Affect UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78559651?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+psychiatry&rft.atitle=Mood+changes+associated+with+reproductive+life+events%3A+an+overview+of+research+and+treatment+strategies.&rft.au=Blumenthal%2C+S+J%3BNadelson%2C+C+C&rft.aulast=Blumenthal&rft.aufirst=S&rft.date=1988-12-01&rft.volume=49&rft.issue=12&rft.spage=466&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+psychiatry&rft.issn=01606689&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-17 N1 - Date created - 1989-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA damage-inducible transcripts in mammalian cells. AN - 78557692; 3194391 AB - Hybridization subtraction at low ratios of RNA to cDNA was used to enrich for the cDNA of transcripts increased in Chinese hamster cells after UV irradiation. Forty-nine different cDNA clones were isolated. Most coded for nonabundant transcripts rapidly induced 2- to 10-fold after UV irradiation. Only 2 of the 20 cDNA clones sequenced matched known sequences (metallothionein I and II). The predicted amino acid sequence of one cDNA had two localized areas of homology with the rat helix-destabilizing protein. These areas of homology were at the two DNA-binding sites of this nucleic acid single-strand-binding protein. The induced transcripts were separated into two general classes. Class I transcripts were induced by UV radiation and not by the alkylating agent methyl methanesulfonate. Class II transcripts were induced by UV radiation and by methyl methanesulfonate. Many class II transcripts were induced also by H2O2 and various alkylating agents but not by heat shock, phorbol 12-tetradecanoate 13-acetate, or DNA-damaging agents which do not produce high levels of base damage. Since many of the cDNA clones coded for transcripts which were induced rapidly and only by certain types of DNA-damaging agents, their induction is likely a specific response to such damage rather than a general response to cell injury. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Fornace, A J AU - Alamo, I AU - Hollander, M C AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 8800 EP - 8804 VL - 85 IS - 23 SN - 0027-8424, 0027-8424 KW - DNA, Single-Stranded KW - 0 KW - Acetoxyacetylaminofluorene KW - 6098-44-8 KW - Index Medicus KW - Xeroderma Pigmentosum KW - Ultraviolet Rays KW - DNA, Single-Stranded -- genetics KW - Humans KW - Acetoxyacetylaminofluorene -- pharmacology KW - Dose-Response Relationship, Radiation KW - Cell Line KW - Cloning, Molecular KW - Transcription, Genetic -- drug effects KW - Transcription, Genetic -- radiation effects KW - DNA Damage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78557692?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+damage-inducible+transcripts+in+mammalian+cells.&rft.au=Fornace%2C+A+J%3BAlamo%2C+I%3BHollander%2C+M+C&rft.aulast=Fornace&rft.aufirst=A&rft.date=1988-12-01&rft.volume=85&rft.issue=23&rft.spage=8800&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 - 1988-12-30 N1 - Date created - 1988-12-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1974 Dec;34(12):3318-25 [4371955] Mol Cell Biol. 1988 Nov;8(11):4716-20 [2463464] Proc Natl Acad Sci U S A. 1977 Apr;74(4):1553-7 [266196] Mutat Res. 1982 Jun;94(2):263-76 [7110177] J Mol Biol. 1983 Jun 5;166(4):557-80 [6345791] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] Nucleic Acids Res. 1984 Jan 11;12(1 Pt 1):417-28 [6546426] Microbiol Rev. 1984 Mar;48(1):60-93 [6371470] Cell. 1985 Feb;40(2):359-69 [3838150] Mol Cell Biol. 1985 Feb;5(2):320-9 [2983189] Mol Cell Biol. 1985 Jan;5(1):75-84 [3920512] J Biol Chem. 1986 Mar 15;261(8):3536-43 [3005291] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1842-6 [3081903] Anal Biochem. 1986 Feb 1;152(2):232-8 [3516005] Nucleic Acids Res. 1986 Jul 25;14(14):5793-811 [2426659] Mol Cell Biol. 1986 May;6(5):1760-6 [3785178] Mol Cell Biol. 1987 Feb;7(2):622-31 [3102944] Int J Radiat Biol Relat Stud Phys Chem Med. 1987 Mar;51(3):493-503 [3553051] Nucleic Acids Res. 1987 Aug 11;15(15):5945-62 [2442723] J Biol Chem. 1988 Mar 5;263(7):3307-13 [2830282] J Biol Chem. 1976 Apr 10;251(7):2133-41 [1270426] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Localization of alpha-casein gene transcription in sections of epoxy resin-embedded mouse mammary tissues by in situ hybridization. AN - 78556720; 3057071 AB - The objective of our study was to evaluate the suitability of aldehyde-fixed, epoxy resin-embedded tissue for efficient and reproducible detection of casein mRNA in mouse mammary tissue by in situ hybridization. We used mouse alpha-casein-specific, 35S-labeled riboprobes generated from a Gemini-3 vector. Both complementary (anti-sense) and homologous (sense) RNA probes were utilized in our study (specific activity ranged from 5-7 x 10(8) cpm/micrograms). We tested the stability of newly synthesized [3H]-uridine-labeled RNA in tissue sections subjected to epoxy plastic solvents and found that no detectable loss of label occurred during preparation of semi-thin (1-2 micron) plastic sections for situ hybridization. In addition, it was possible to detect alpha-casein mRNA in deplasticized sections of mammary gland tissue taken from normal, pregnant, or lactating mice, pre-neoplastic mammary alveolar hyperplasias, explant cultures, and mammary tumors. A positive hybridization signal was consistently obtained in sections of mammary tissues where the estimated average copy number for total casein mRNA was greater than or equal to 250/cell. In mammary tumors, where the estimated casein mRNA content was much lower (less than 5/cell), our positive hybridization signal occurred in regions of the tumor that, in consecutive sections, stained positive for casein by immunoperoxidase. After formaldehyde-glutaraldehyde fixation, loss of hybridizable RNA from epoxy-embedded tissues and sections appears to be minimal. Image resolution was greatly enhanced over frozen or paraffin sections of mammary tissue. Non-specific binding of the radioactive probes was very low. Protease treatment of the sections was not necessary for detection of hybridizable signal. JF - The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society AU - Liscia, D S AU - Doherty, P J AU - Smith, G H AD - Oncogenetics Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1503 EP - 1510 VL - 36 IS - 12 SN - 0022-1554, 0022-1554 KW - Caseins KW - 0 KW - Epoxy Resins KW - RNA Probes KW - RNA, Messenger KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Mammary Neoplasms, Experimental -- analysis KW - Histological Techniques KW - Animals KW - Lactation -- metabolism KW - Mice, Inbred C3H KW - Diethylstilbestrol -- pharmacology KW - Transcription, Genetic KW - Mice KW - Male KW - Female KW - Pregnancy KW - Mammary Glands, Animal -- analysis KW - Mammary Glands, Animal -- drug effects KW - Caseins -- genetics KW - RNA, Messenger -- analysis KW - Nucleic Acid Hybridization UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78556720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Localization+of+alpha-casein+gene+transcription+in+sections+of+epoxy+resin-embedded+mouse+mammary+tissues+by+in+situ+hybridization.&rft.au=Liscia%2C+D+S%3BDoherty%2C+P+J%3BSmith%2C+G+H&rft.aulast=Liscia&rft.aufirst=D&rft.date=1988-12-01&rft.volume=36&rft.issue=12&rft.spage=1503&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 - 1989-01-03 N1 - Date created - 1989-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development after exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene transplacentally and through human milk. AN - 78548636; 3142988 AB - To determine whether exposure to polychlorinated biphenyls (PCBs) or dichlorodiphenyl dichloroethene (DDE), either transplacentally or through breast feeding, affected scores on the Bayley Scales of Infant Development at 6 or 12 months of age. Cohort followed from birth to 1 year of age. General community. Volunteer sample of 858 infants, of whom 802 had Bayley scores available at either 6 months or 12 months or both. None. Bayley scales and chemical measurements were done independently. Higher transplacental exposure to PCBs was associated with lower psychomotor scores at both 6 and 12 months of age; the difference between the mean scores in the lowest and highest PCB groups was 7 points at 6 months and 8 points at 12 months. Higher transplacental exposure to DDE was associated with higher mental scores at 6 months of age (the difference between the mean scores in the lowest and highest DDE groups was 6 points), but no relationship was seen at 12 months. Exposure to either chemical through breast feeding was apparently unrelated to Bayley scores. Transplacental exposure to PCBs was associated with lower psychomotor scores. No deleterious effects were associated with breast feeding. JF - The Journal of pediatrics AU - Gladen, B C AU - Rogan, W J AU - Hardy, P AU - Thullen, J AU - Tingelstad, J AU - Tully, M AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 991 EP - 995 VL - 113 IS - 6 SN - 0022-3476, 0022-3476 KW - Dichlorodiphenyl Dichloroethylene KW - 4M7FS82U08 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Abridged Index Medicus KW - Index Medicus KW - Infant KW - Intelligence -- drug effects KW - Psychomotor Performance -- drug effects KW - Humans KW - Brain -- drug effects KW - Infant, Newborn KW - Follow-Up Studies KW - Neuropsychological Tests KW - Female KW - Pregnancy KW - Child, Preschool KW - Milk, Human -- analysis KW - Dichlorodiphenyl Dichloroethylene -- analysis KW - Breast Feeding KW - Child Development -- drug effects KW - Polychlorinated Biphenyls -- analysis KW - Dichlorodiphenyl Dichloroethylene -- adverse effects KW - Prenatal Exposure Delayed Effects KW - Polychlorinated Biphenyls -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78548636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pediatrics&rft.atitle=Development+after+exposure+to+polychlorinated+biphenyls+and+dichlorodiphenyl+dichloroethene+transplacentally+and+through+human+milk.&rft.au=Gladen%2C+B+C%3BRogan%2C+W+J%3BHardy%2C+P%3BThullen%2C+J%3BTingelstad%2C+J%3BTully%2C+M&rft.aulast=Gladen&rft.aufirst=B&rft.date=1988-12-01&rft.volume=113&rft.issue=6&rft.spage=991&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pediatrics&rft.issn=00223476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-10 N1 - Date created - 1989-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Return of symptoms after discontinuation of clomipramine in patients with obsessive-compulsive disorder. AN - 78546968; 3057923 AB - To evaluate the need for maintenance drug therapy in patients with obsessive-compulsive disorder, the authors assessed 21 patients with obsessive-compulsive disorder who manifested sustained improvement during 5 to 27 months of clomipramine treatment and who agreed to participate in a double-blind discontinuation study. Of 18 patients who completed the study, 16 had substantial recurrence of obsessive-compulsive symptoms by the end of the 7-week placebo period. In addition, 11 had a significant increase in depressive symptoms. Treatment duration before discontinuation of clomipramine was not related to the frequency or severity of obsessive-compulsive or depressive symptom appearance. These findings suggest that prolonged drug treatment may be warranted for obsessive-compulsive disorder. JF - The American journal of psychiatry AU - Pato, M T AU - Zohar-Kadouch, R AU - Zohar, J AU - Murphy, D L AD - Laboratory of Clinical Science, NIMH, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1521 EP - 1525 VL - 145 IS - 12 SN - 0002-953X, 0002-953X KW - Clomipramine KW - NUV44L116D KW - Abridged Index Medicus KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Double-Blind Method KW - Psychotherapy KW - Combined Modality Therapy KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Substance Withdrawal Syndrome -- psychology KW - Middle Aged KW - Recurrence KW - Male KW - Female KW - Obsessive-Compulsive Disorder -- psychology KW - Obsessive-Compulsive Disorder -- drug therapy KW - Clomipramine -- adverse effects KW - Clomipramine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78546968?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Return+of+symptoms+after+discontinuation+of+clomipramine+in+patients+with+obsessive-compulsive+disorder.&rft.au=Pato%2C+M+T%3BZohar-Kadouch%2C+R%3BZohar%2C+J%3BMurphy%2C+D+L&rft.aulast=Pato&rft.aufirst=M&rft.date=1988-12-01&rft.volume=145&rft.issue=12&rft.spage=1521&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 - 1989-01-10 N1 - Date created - 1989-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enflurane metabolism produces covalently bound liver adducts recognized by antibodies from patients with halothane hepatitis. AN - 78546813; 3195754 AB - The existence of a rare syndrome of "enflurane hepatitis" similar to that described for halothane and of a cross-sensitization between halothane and enflurane has been controversial, largely due to equivocal clinical case reports and a lack of a plausible molecular mechanism for the hepatotoxicity. The present study suggests a possible hypersensitivity basis for enflurane hepatitis and the apparent cross-sensitization between halothane and enflurane involving covalently bound liver microsomal adducts. Immunoblotting studies have revealed that antibodies in the sera of six patients with halothane hepatitis recognize liver microsomal antigens of Mr = 100,000, or both 100,000 and 76,000, formed in rats treated with enflurane or halothane. These antigens were not detected in microsomes from isoflurane- or sesame oil-treated rats. The recognition of these antigens could be abolished by preincubation of the sera with microsomes from halothane-treated rats. These data suggest that the difluoromethoxydifluoroacetyl halide metabolite of enflurane, as well as the trifluoroacetyl halide metabolite of halothane, covalently bind to similar hepatic proteins, and may become immunogens in susceptible patients. This mechanism may also account for the apparent cross-sensitization between halothane and enflurane anesthesia, and the development of hepatic necrosis. JF - Anesthesiology AU - Christ, D D AU - Kenna, J G AU - Kammerer, W AU - Satoh, H AU - Pohl, L R AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 833 EP - 838 VL - 69 IS - 6 SN - 0003-3022, 0003-3022 KW - Isoantigens KW - 0 KW - liver specific F antigen KW - Enflurane KW - 91I69L5AY5 KW - Halothane KW - UQT9G45D1P KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Halothane -- adverse effects KW - Male KW - Enflurane -- metabolism KW - Chemical and Drug Induced Liver Injury -- etiology KW - Enflurane -- adverse effects KW - Isoantigens -- immunology KW - Enflurane -- immunology KW - Chemical and Drug Induced Liver Injury -- metabolism KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78546813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anesthesiology&rft.atitle=Enflurane+metabolism+produces+covalently+bound+liver+adducts+recognized+by+antibodies+from+patients+with+halothane+hepatitis.&rft.au=Christ%2C+D+D%3BKenna%2C+J+G%3BKammerer%2C+W%3BSatoh%2C+H%3BPohl%2C+L+R&rft.aulast=Christ&rft.aufirst=D&rft.date=1988-12-01&rft.volume=69&rft.issue=6&rft.spage=833&rft.isbn=&rft.btitle=&rft.title=Anesthesiology&rft.issn=00033022&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-05 N1 - Date created - 1989-01-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activated neutrophils induce prolonged DNA damage in neighboring cells. AN - 78534852; 2847879 AB - We have measured the capacity of highly-purified, paraffin oil-elicited neutrophils to induce DNA single-strand breaks in a newly established plasmacytoma cell line, RIMPC 2304, which was induced by a retrovirus containing the c-myc and V-Ha-ras oncogenes. This cell line effectively repairs DNA damage induced by gamma-irradiation. DNA damage induced by neutrophils was correlated with the oxidative burst of the neutrophils. The levels of superoxide anion, H2O2, and HOCl produced after stimulation of the neutrophils (6 X 10(5)/cm3) with the tumor promoter phorbol myristate acetate (100 nM) were 33.8 microM, 12.8 microM and 1.7 microM respectively in 15 min, and 98 microM, 20 microM and 8.7 microM respectively in 90 min. The results of alkaline elution experiments revealed that when the same concentration of neutrophils was co-incubated for 15 min in serum-free medium with an equal number of radioactively labeled RIMPC 2304 cells, the latter incurred a level of damage that approximated that caused by 300 rad equivalents of gamma-irradiation or by a 1-min treatment with 20 microM H2O2 at 37 degrees C. Damage from neutrophils was coincident with the oxidative burst; it was induced rapidly (within 5 min) but remained high for more than 90 min. The level of damage achieved was dependent upon the ratio of neutrophils: target cells and was clearly detectable at ratios as low as 0.25:1. Induction of single-strand breaks was completely inhibited by catalase and partially inhibited by superoxide dismutase, mannitol, and reduced glutathione but not by Na azide. Addition of the non-steroidal anti-inflammatory drug indomethacin either enhanced (at 50 microM) or had no effect (at 2 microM) on the damage detected. Finally, repair of strand breaks induced by neutrophils was significantly slower (half-time approximately 10 min) than that observed for repair of similar levels of damage induced by H2O2 or gamma-irradiation (half-times approximately 3 min, each). The results indicate that neutrophils cause prolonged DNA damage in neighboring cells. Moreover, they indicate that although H2O2 produced in the oxidative burst is an essential mediator of the damage observed, additional reactive oxygen intermediates including the superoxide anion are also implicated. The data are discussed in relation to the possible role of neutrophils in chronic inflammation and in pristane-induced plasmacytoma formation in mice. JF - Carcinogenesis AU - Shacter, E AU - Beecham, E J AU - Covey, J M AU - Kohn, K W AU - Potter, M AD - Laboratory of Genetics, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 2297 EP - 2304 VL - 9 IS - 12 SN - 0143-3334, 0143-3334 KW - Terpenes KW - 0 KW - Superoxides KW - 11062-77-4 KW - pristane KW - 26HZV48DT1 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Oxygen KW - S88TT14065 KW - Indomethacin KW - XXE1CET956 KW - Index Medicus KW - Animals KW - Superoxides -- metabolism KW - DNA Repair KW - Tumor Cells, Cultured KW - Oxygen -- metabolism KW - Hydrogen Peroxide -- metabolism KW - Mice KW - Terpenes -- pharmacology KW - Mice, Inbred BALB C KW - Time Factors KW - Indomethacin -- pharmacology KW - Neutrophils -- metabolism KW - DNA Damage KW - Neutrophils -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78534852?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activated+neutrophils+induce+prolonged+DNA+damage+in+neighboring+cells.&rft.au=Shacter%2C+E%3BBeecham%2C+E+J%3BCovey%2C+J+M%3BKohn%2C+K+W%3BPotter%2C+M&rft.aulast=Shacter&rft.aufirst=E&rft.date=1988-12-01&rft.volume=9&rft.issue=12&rft.spage=2297&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-12 N1 - Date created - 1989-01-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Carcinogenesis 1989 Mar;10(3):628 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genomic 5-methyldeoxycytidine decreases associated with the induction of squamous differentiation in cultured normal human bronchial epithelial cells. AN - 78532040; 2461263 AB - The terminal squamous differentiation of epithelial cells involves a number of cellular changes. However, the mechanisms underlying this differentiation process are unknown. The present study demonstrates that 5-azacytidine, 12-O-tetradecanoylphorbol-13-acetate (TPA) and type beta-transforming growth factor (TGF-beta) significantly diminish the genomic 5-methyldeoxycytidine (5mdC) content of normal human bronchial epithelial cells concomitantly with the induction of squamous differentiation. 5-Azacytidine or TPA, but not type beta-transforming growth factor, also initiated decreases in the genomic 5mdC content of differentiation nonresponsive human tumor A549 cells. These effects of TPA or type beta-transforming growth factor occurred at concentrations of 1 nM and 1.2 pM, respectively, which were approximately one tenth of kd values of their specific receptors. Therefore, the decreases in genomic 5mdC induced by these agents were probably mediated, directly or indirectly, by receptor--ligand interactions. JF - Carcinogenesis AU - Wilson, V L AU - Masui, T AU - Smith, R A AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 2155 EP - 2159 VL - 9 IS - 12 SN - 0143-3334, 0143-3334 KW - Deoxycytidine KW - 0W860991D6 KW - Transforming Growth Factors KW - 76057-06-2 KW - DNA KW - 9007-49-2 KW - 5-methyldeoxycytidine KW - B200GV71QM KW - Azacitidine KW - M801H13NRU KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Azacitidine -- pharmacology KW - Cells, Cultured KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Epithelium -- metabolism KW - Transforming Growth Factors -- pharmacology KW - Cell Differentiation -- drug effects KW - Epithelium -- drug effects KW - Deoxycytidine -- metabolism KW - Deoxycytidine -- analogs & derivatives KW - DNA -- metabolism KW - Bronchi -- metabolism KW - Bronchi -- drug effects KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78532040?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genomic+5-methyldeoxycytidine+decreases+associated+with+the+induction+of+squamous+differentiation+in+cultured+normal+human+bronchial+epithelial+cells.&rft.au=Wilson%2C+V+L%3BMasui%2C+T%3BSmith%2C+R+A%3BHarris%2C+C+C&rft.aulast=Wilson&rft.aufirst=V&rft.date=1988-12-01&rft.volume=9&rft.issue=12&rft.spage=2155&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-12 N1 - Date created - 1989-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transformation of rat liver epithelial cells with v-H-ras or v-raf causes expression of MDR-1, glutathione-S-transferase-P and increased resistance to cytotoxic chemicals. AN - 78530743; 2903802 AB - We have examined the relationship between transformation and multidrug resistance by employing the v-H-ras or v-raf oncogenes to transform rat liver epithelial (RLE) cells in vitro. The data indicate that transformation of RLE cells with v-H-ras or v-raf results in increased resistance to the cytotoxins adriamycin, vinblastine and 2-acetylaminofluorene. This multidrug resistance is accompanied by increasing expression of P-glycoprotein (MDR-1) and glutathione-S-transferase P (GST-P). Thus, neoplastic transformation of RLE cells with v-raf or v-H-ras, independently of chemical exposure, results in multidrug resistance. JF - Carcinogenesis AU - Burt, R K AU - Garfield, S AU - Johnson, K AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 2329 EP - 2332 VL - 9 IS - 12 SN - 0143-3334, 0143-3334 KW - Antineoplastic Agents KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Rats KW - Animals KW - Drug Resistance -- genetics KW - Placenta -- enzymology KW - Cell Survival -- drug effects KW - Oncogenes KW - Membrane Glycoproteins -- biosynthesis KW - Liver -- drug effects KW - Cell Transformation, Neoplastic -- metabolism KW - Glutathione Transferase -- biosynthesis KW - Glutathione Transferase -- genetics KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78530743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transformation+of+rat+liver+epithelial+cells+with+v-H-ras+or+v-raf+causes+expression+of+MDR-1%2C+glutathione-S-transferase-P+and+increased+resistance+to+cytotoxic+chemicals.&rft.au=Burt%2C+R+K%3BGarfield%2C+S%3BJohnson%2C+K%3BThorgeirsson%2C+S+S&rft.aulast=Burt&rft.aufirst=R&rft.date=1988-12-01&rft.volume=9&rft.issue=12&rft.spage=2329&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-12 N1 - Date created - 1989-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug abuse discharges from non-federal short-stay hospitals. AN - 78525391; 3189633 AB - An analysis of inpatient drug abuse cases was done using the National Hospital Discharge Survey (NHDS). An estimated two million discharges with a drug abuse diagnosis occurred in non-federal short-stay hospitals during 1979-85, a figure which is believed to be an underestimate. Compared to other hospital inpatients, drug abuse inpatients are more likely to be male, ages 15-44, and other than White race. Increases in hospital use for drug abuse treatment were found to have occurred between 1979 and 1985, with discharge rates per 10,000 population increasing from 3.1 to 6.0 for drug dependence and from 3.8 to 7.7 for nondependent drug abuse. Concurrent increases in availability of hospital-based inpatient drug and alcohol treatment programs and insurance coverage for drug abuse treatment were found to have occurred during the same period. JF - American journal of public health AU - Gfroerer, J C AU - Adams, E H AU - Moien, M AD - Statistical and Epidemiologic Analysis Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1559 EP - 1562 VL - 78 IS - 12 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Patient Admission KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Substance-Related Disorders -- therapy KW - Length of Stay KW - Patient Discharge KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78525391?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Drug+abuse+discharges+from+non-federal+short-stay+hospitals.&rft.au=Gfroerer%2C+J+C%3BAdams%2C+E+H%3BMoien%2C+M&rft.aulast=Gfroerer&rft.aufirst=J&rft.date=1988-12-01&rft.volume=78&rft.issue=12&rft.spage=1559&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 - 1988-12-19 N1 - Date created - 1988-12-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Arch Intern Med. 1987 Feb;147(2):349-52 [3813755] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cyclosporin A in severe, treatment-refractory rheumatoid arthritis. A randomized study. AN - 78521017; 3190040 AB - To assess the efficacy and toxicity of cyclosporin A in patients with severe, treatment-refractory rheumatoid arthritis. Prospective randomized, double-blind 6-month trial. Thirty-one patients who had classic seropositive rheumatoid arthritis with active synovitis unresponsive to conventional therapy. Patients were randomly assigned to high-dose (10 mg/kg body weight.d) or low-dose (1 mg/kg.d) cyclosporin A therapy. A reduction in the dose was permitted for adverse side effects. After 6 months of therapy, patients who showed clinically relevant improvement, defined as a 40% or greater reduction in their total joint activity score, were given the option to continue receiving the therapy for an additional 6 months. At 6 months, clinically relevant improvement occurred in 10 of 15 patients (95% CI, 38 to 88) receiving high-dose therapy and in 4 of 16 patients (CI, 7 to 52) receiving low-dose therapy (P = 0.02). Statistically significant improvements in individual measures were shown only in the high-dose group. Improvements were noted in the number of tender joints (-18.8; CI, -24.5 to -13.1) and swollen joints (-12.1; CI, -15.4 to -8.6), as well as in physician's global scores (-1.5; CI, -2.1 to -0.9) and patient's global scores (-1.1; CI, -1.9 to -0.5). Improvement in disease activity was maintained through 12 months in the high-dose group. The clinical responses to cyclosporin A were most evident in patients with depressed in-vitro proliferative responses of peripheral blood mononuclear lymphocytes to soluble recall antigens. Toxicities, such as fatigue, gastrointestinal and neurologic complaints, and hypertrichosis were frequent but often reversible with a reduction in the dose. Nephrotoxicity, with a 20% increase in the serum creatinine level, was seen in 27 of 31 patients (CI, 71 to 97). Cyclosporin A is an effective therapy for severe, treatment-refractory rheumatoid arthritis. Side effects, particularly nephrotoxicity, are common. JF - Annals of internal medicine AU - Yocum, D E AU - Klippel, J H AU - Wilder, R L AU - Gerber, N L AU - Austin, H A AU - Wahl, S M AU - Lesko, L AU - Minor, J R AU - Preuss, H G AU - Yarboro, C AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 863 EP - 869 VL - 109 IS - 11 SN - 0003-4819, 0003-4819 KW - Cyclosporins KW - 0 KW - C-Reactive Protein KW - 9007-41-4 KW - Creatinine KW - AYI8EX34EU KW - Abridged Index Medicus KW - Index Medicus KW - C-Reactive Protein -- drug effects KW - Double-Blind Method KW - Random Allocation KW - Dose-Response Relationship, Drug KW - Humans KW - Nervous System Diseases -- chemically induced KW - Creatinine -- blood KW - Drug Evaluation KW - Prospective Studies KW - Adult KW - Middle Aged KW - Leukocytes, Mononuclear -- drug effects KW - Female KW - Male KW - Kidney Diseases -- chemically induced KW - Cyclosporins -- adverse effects KW - Arthritis, Rheumatoid -- drug therapy KW - Arthritis, Rheumatoid -- blood KW - Cyclosporins -- therapeutic use KW - Cyclosporins -- administration & dosage KW - Arthritis, Rheumatoid -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78521017?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cyclosporin+A+in+severe%2C+treatment-refractory+rheumatoid+arthritis.+A+randomized+study.&rft.au=Yocum%2C+D+E%3BKlippel%2C+J+H%3BWilder%2C+R+L%3BGerber%2C+N+L%3BAustin%2C+H+A%3BWahl%2C+S+M%3BLesko%2C+L%3BMinor%2C+J+R%3BPreuss%2C+H+G%3BYarboro%2C+C&rft.aulast=Yocum&rft.aufirst=D&rft.date=1988-12-01&rft.volume=109&rft.issue=11&rft.spage=863&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 - 1988-12-16 N1 - Date created - 1988-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Colonic perforation. An unusual complication of therapy with high-dose interleukin-2. AN - 78500988; 3263182 AB - The majority (85%) of patients receiving high dose Interleukin-2 (IL-2) experience gastrointestinal side effects, namely nausea, vomiting and diarrhea. In this article we describe four cancer patients that developed localized necrosis or perforation of the colon during IL-2 treatment. They represent 1.3% of patients (n = 315) or 0.9% of treatment courses (n = 452). All underwent surgical intervention and survived to leave the hospital. No common etiologic factor was apparent. Two patients were subsequently retreated with IL-2 without complication. Localized colonic necrosis or perforation is a rare complication associated with high dose IL-2 treatments. Aggressive surgical intervention is advocated and retreatment following recovery is safe. JF - Cancer AU - Schwartzentruber, D AU - Lotze, M T AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 2350 EP - 2353 VL - 62 IS - 11 SN - 0008-543X, 0008-543X KW - Interleukin-2 KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- administration & dosage KW - Colonic Diseases -- surgery KW - Intestinal Perforation -- chemically induced KW - Colonic Diseases -- chemically induced KW - Intestinal Perforation -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78500988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Colonic+perforation.+An+unusual+complication+of+therapy+with+high-dose+interleukin-2.&rft.au=Schwartzentruber%2C+D%3BLotze%2C+M+T%3BRosenberg%2C+S+A&rft.aulast=Schwartzentruber&rft.aufirst=D&rft.date=1988-12-01&rft.volume=62&rft.issue=11&rft.spage=2350&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-12 N1 - Date created - 1988-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of CD2 in activation and cytotoxic function of CD8/Leu-7-positive T cells. AN - 78499693; 2903195 AB - CD3/CD8-positive, Leu-7-positive cells comprise about 3 to 5% of PBL in normal individuals, but the proportion of these cells is increased in patients with a variety of diseases including chronic viral infection, Crohn's disease, and AIDS. To study further the function of these cells, the proliferative and cytotoxic responses of highly purified CD8/Leu-7-positive cells were studied in vitro. These cells had low proliferative responses when exposed to PHA or mitogenic anti-CD3 mAb compared to CD8/Leu-7-negative cells, and their proliferative responses were significantly lower after addition of IL-2 or autologous adherent cells. However, the proliferative responses of both Leu-7-positive and Leu-7-negative CD8 cells were similar when stimulated with PHA, Ionomycin, or anti-CD3 in combination with phorbol ester. In addition, CD8/Leu-7-positive cells demonstrated high proliferative responses when exposed to a combination of both PHA and SRBC, and these responses could be inhibited by prior addition of non-stimulating anti-CD2.1 mAb. CD8/Leu-7-positive cells, but not CD8/Leu-7-negative cells, mediated lectin- and anti-CD3-induced cytotoxicity against K562 target cells. Cytotoxicity was in part dependent on the CD2 Ag because it was inhibited by anti-CD2.1 mAb. Finally, when small CD8-positive T cells having low cytotoxic potential were activated with PHA plus SRBC, but not PHA alone, there was significant enhancement of their cytotoxic function. Thus, the CD2 receptor may be an important activation pathway for cytotoxic cells. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Rüthlein, J AU - James, S P AU - Strober, W AD - Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 3791 EP - 3797 VL - 141 IS - 11 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD2 KW - Antigens, CD8 KW - Antigens, Differentiation, T-Lymphocyte KW - Ethers KW - Immunosuppressive Agents KW - Lymphokines KW - Phytohemagglutinins KW - Receptors, Immunologic KW - Ionomycin KW - 56092-81-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Sheep KW - Humans KW - Cell Separation KW - Phenotype KW - Immunosuppressive Agents -- physiology KW - Antigen-Presenting Cells -- immunology KW - Antibodies, Monoclonal -- physiology KW - Erythrocytes -- immunology KW - Lymphocyte Activation KW - Cytotoxicity, Immunologic KW - Receptors, Immunologic -- immunology KW - T-Lymphocytes, Cytotoxic -- classification KW - T-Lymphocytes, Cytotoxic -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78499693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+CD2+in+activation+and+cytotoxic+function+of+CD8%2FLeu-7-positive+T+cells.&rft.au=R%C3%BCthlein%2C+J%3BJames%2C+S+P%3BStrober%2C+W&rft.aulast=R%C3%BCthlein&rft.aufirst=J&rft.date=1988-12-01&rft.volume=141&rft.issue=11&rft.spage=3791&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 - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects and mechanism of action of lithium chloride on gastric acid secretion in rats. AN - 78493266; 2846401 AB - Lithium chloride reduce the measured parameters of gastric secretion (gastric volume, hydrogen ion concentration, and gastric acid output) 2 h after intracerebroventricular, intravenous, or subcutaneous administration in pylorus-ligated rats, in a dose-dependent manner. Intracerebroventricular administration of lithium was approximately five times and 10 times more potent than intravenous and subcutaneous injection, respectively. Time-course study demonstrated that the action of lithium (400 micrograms) on gastric secretion reached a peak at 1 h after intracerebroventricular administration; however, the effects on volume and output were still significant after 8 h. Prior intracerebroventricular injection of indomethacin (400 micrograms) reversed the action of centrally administered lithium on gastric secretion. However, central administration of the opiate receptor blocker naltrexone (100 micrograms), as well as subcutaneous administration of indomethacin (5 mg/kg), failed to modify the effect of lithium on gastric acid secretion. Our data suggest that lithium appears to act centrally to modulate gastric acid secretion in rats through a mechanism involving the synthesis of prostaglandinlike material(s) in the brain. Furthermore, the effect of centrally administered lithium is independent of stimulation of opiate receptor(s) in the brain. JF - Gastroenterology AU - Guglietta, A AU - Irons, B J AU - Lazarus, L H AU - Sivam, S P AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1988/12// PY - 1988 DA - December 1988 SP - 1454 EP - 1459 VL - 95 IS - 6 SN - 0016-5085, 0016-5085 KW - Chlorides KW - 0 KW - Naltrexone KW - 5S6W795CQM KW - Lithium KW - 9FN79X2M3F KW - Lithium Chloride KW - G4962QA067 KW - Indomethacin KW - XXE1CET956 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals KW - Drug Interactions KW - Injections, Intravenous KW - Dose-Response Relationship, Drug KW - Brain -- drug effects KW - Naltrexone -- pharmacology KW - Injections, Subcutaneous KW - Time Factors KW - Male KW - Injections, Intraventricular KW - Indomethacin -- pharmacology KW - Depression, Chemical KW - Chlorides -- administration & dosage KW - Lithium -- administration & dosage KW - Lithium -- pharmacology KW - Gastric Acid -- secretion KW - Chlorides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78493266?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+and+mechanism+of+action+of+lithium+chloride+on+gastric+acid+secretion+in+rats.&rft.au=Guglietta%2C+A%3BIrons%2C+B+J%3BLazarus%2C+L+H%3BSivam%2C+S+P&rft.aulast=Guglietta&rft.aufirst=A&rft.date=1988-12-01&rft.volume=95&rft.issue=6&rft.spage=1454&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=00165085&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative carcinogenesis by nitrosomethylalkylamines in Syrian hamsters. AN - 78487706; 3180074 AB - Six homologous nitrosomethyl-n-alkylamines, from n-propyl (C-3) to n-octyl (C-8), were administered by gavage to groups of 12 male and 12 female Syrian golden hamsters as solutions in corn oil:ethyl acetate (2:1). The solutions of C-8 to C-4 were equimolar; nitrosomethyl-n-butylamine (C-4) and nitrosomethyl-n-propylamine (C-3) were given at a lower concentration. Treatment with 0.2 ml of solution lasted 23 to 50 wk, being stopped when several hamsters had died. Additional groups of hamsters were treated similarly with nitrosomethylaniline and nitrosomethylcyclohexylamine. Excepting hamsters given the latter, treated animals had reduced survival compared with controls. The incidence of tumors in hamsters given nitrosomethylaniline and nitrosomethylcyclohexylamine was low and occurred in the liver, lungs, and spleen. Hamsters treated with nitrosomethyl-n-propylamine and nitrosomethyl-n-butylamine suffered the greatest decrease in survival. Potency judged by this criterion decreased as the size of the molecule increased in the homologous series. Virtually all of these treated hamsters died with tumors not seen in controls. These tumors, which were common in hamsters given all of the nitrosomethyl-n-alkylamines, were in the liver, lung, forestomach, and nasal mucosa, but the incidences varied somewhat between the compounds and between sexes. Bladder tumors were seen only in hamsters given nitrosamines containing even numbers of carbon atoms in the chain, namely, nitrosomethyl-n-hexylamine and nitrosomethyl-n-octylamine. JF - Cancer research AU - Lijinsky, W AU - Kovatch, R M AD - National Cancer Institute-Frederick Cancer Research Facility, Bionetics Research, Inc., Maryland 21701. Y1 - 1988/12/01/ PY - 1988 DA - 1988 Dec 01 SP - 6648 EP - 6652 VL - 48 IS - 23 SN - 0008-5472, 0008-5472 KW - Nitrosamines KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - DNA -- metabolism KW - Mesocricetus KW - Methylation KW - Male KW - Female KW - Structure-Activity Relationship KW - Cricetinae KW - Nitrosamines -- toxicity KW - Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78487706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+carcinogenesis+by+nitrosomethylalkylamines+in+Syrian+hamsters.&rft.au=Lijinsky%2C+W%3BKovatch%2C+R+M&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1988-12-01&rft.volume=48&rft.issue=23&rft.spage=6648&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 - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Two-year inhalation carcinogenesis studies of methyl methacrylate in rats and mice: inflammation and degeneration of nasal epithelium. AN - 78530642; 3188037 AB - Methyl methacrylate (MMA), a liquid monomer, is used as a chemical intermediate in the manufacture of plexiglass and other acrylic products and as "bone cement" in orthopedic and dental surgery. Toxicology and carcinogenesis inhalation studies of MMA were conducted because of: (1) widespread human exposure; (2) evidence of mutagenicity; and (3) inadequacy of previously conducted long-term oral, dermal, and inhalation studies. Groups of 50 male F344/N rats were exposed to MMA by inhalation at 0, 500, or 1000 ppm, female F344/N rats at 0, 250, or 500 ppm, and male and female B6C3F1 mice at 0, 500, or 1000 ppm, 6 h a day, 5 days a week for 102 weeks. Survival rates of male and female rats and mice exposed to MMA were similar to those of their respective controls. Body weights were reduced in the low and high dose male (3-6% and 5-10%, respectively) and female (5-7% and 8-10%) rats exposed to MMA for more than 80 weeks and in male (7-19% and 6-17%) and female (0-13% and 0-17%) mice for more than 20 weeks. Inhalation exposure of MMA for 102 weeks did not induce any increased incidences of neoplasms in male or female rats or mice. Non-neoplastic lesions in the nasal cavity of MMA-exposed rats and mice were significantly increased and these included inflammation and degeneration of the olfactory epithelium of MMA-exposed male and female rats and inflammation, hyperplasia, cytoplasmic inclusions in the respiratory epithelium, and degeneration of the olfactory epithelium in male and female mice. JF - Toxicology AU - Chan, P C AU - Eustis, S L AU - Huff, J E AU - Haseman, J K AU - Ragan, H AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11/30/ PY - 1988 DA - 1988 Nov 30 SP - 237 EP - 252 VL - 52 IS - 3 SN - 0300-483X, 0300-483X KW - Carcinogens KW - 0 KW - Methylmethacrylates KW - Methylmethacrylate KW - 196OC77688 KW - Index Medicus KW - Animals KW - Nasal Septum -- drug effects KW - Sex Factors KW - Mice KW - Rats KW - Rats, Inbred F344 KW - Nasal Septum -- pathology KW - Body Weight -- drug effects KW - Lung -- drug effects KW - Administration, Inhalation KW - Species Specificity KW - Female KW - Male KW - Rhinitis -- chemically induced KW - Nasal Mucosa -- pathology KW - Methylmethacrylates -- administration & dosage KW - Nasal Mucosa -- drug effects KW - Methylmethacrylates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78530642?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Two-year+inhalation+carcinogenesis+studies+of+methyl+methacrylate+in+rats+and+mice%3A+inflammation+and+degeneration+of+nasal+epithelium.&rft.au=Chan%2C+P+C%3BEustis%2C+S+L%3BHuff%2C+J+E%3BHaseman%2C+J+K%3BRagan%2C+H&rft.aulast=Chan&rft.aufirst=P&rft.date=1988-11-30&rft.volume=52&rft.issue=3&rft.spage=237&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-22 N1 - Date created - 1988-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of secretory responses to gonadotropin-releasing hormone and phorbol esters in cultured pituitary cells. Participation of protein kinase C and extracellular calcium mobilization. AN - 78494552; 2460461 AB - The role of protein kinase C in luteinizing hormone (LH) release was analyzed in studies on the actions of gonadotropin releasing hormone (GnRH) and phorbol esters in cultured pituitary cells. During incubation in normal medium, GnRH stimulated LH release with an ED50 of 0.35 nM. Incubation in Ca2+-deficient medium (Ca2+-free, 10 microM) substantially decreased but did not abolish the LH responses to GnRH. The extracellular Ca2+-dependent component of GnRH action could be mimicked by high K+ concentrations, consistent with the presence of voltage-sensitive calcium channels (VSCC) in pituitary gonadotrophs. Ca2+ channel agonist (Bay K 8644) and antagonist (nifedipine) analogs, respectively, enhanced or partially inhibited LH responses to GnRH and also to K+, the latter confirming the participation of two types of VSCC (dihydropyridine-sensitive and -insensitive) in K+-induced secretion. Phorbol esters, including 12-O-tetradecanoylphorbol-13-acetate (TPA), 4 beta-phorbol-12,13-dibenzoate, and 4 beta-phorbol-12,13-diacetate, stimulated LH release with ED50s of 5, 10, and 1000 nM, respectively, and with about 70% of the efficacy of GnRH. Phorbol ester-stimulated LH secretion was decreased but not abolished by progressive reduction of [Ca2+]e in the incubation medium, and the residual LH response was identical with that elicited by GnRH in Ca2+-deficient medium. TPA increased [Ca2+]i to a peak after 20 s in normal medium but not in the absence of extracellular Ca2+, indicating that protein kinase C (Ca2+/phospholipid-dependent enzyme) promotes calcium entry but can also mediate secretory responses without changes in calcium influx and [Ca2+]i. The extracellular Ca2+-dependent action of TPA on LH release was blocked by Co2+. However, nifedipine did not alter TPA action on [Ca2+]i and LH release. These observations indicate that protein kinase C can participate in GnRH-induced LH release that is independent of Ca2+ entry, but also promotes the influx of extracellular Ca2+ through dihydropyridine-insensitive Ca2+-channels. JF - The Journal of biological chemistry AU - Stojilković, S S AU - Chang, J P AU - Izumi, S AU - Tasaka, K AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20982. Y1 - 1988/11/25/ PY - 1988 DA - 1988 Nov 25 SP - 17301 EP - 17306 VL - 263 IS - 33 SN - 0021-9258, 0021-9258 KW - Phorbol Esters KW - 0 KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester KW - 71145-03-4 KW - Luteinizing Hormone KW - 9002-67-9 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Reference Values KW - Cells, Cultured KW - Kinetics KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium -- pharmacology KW - Ovariectomy KW - Female KW - Luteinizing Hormone -- secretion KW - Calcium -- metabolism KW - Pituitary Gland, Anterior -- drug effects KW - Phorbol Esters -- pharmacology KW - Pituitary Gland, Anterior -- secretion KW - Pituitary Gland, Anterior -- physiology KW - Calcium -- pharmacology KW - Protein Kinase C -- physiology KW - Gonadotropin-Releasing Hormone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78494552?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanisms+of+secretory+responses+to+gonadotropin-releasing+hormone+and+phorbol+esters+in+cultured+pituitary+cells.+Participation+of+protein+kinase+C+and+extracellular+calcium+mobilization.&rft.au=Stojilkovi%C4%87%2C+S+S%3BChang%2C+J+P%3BIzumi%2C+S%3BTasaka%2C+K%3BCatt%2C+K+J&rft.aulast=Stojilkovi%C4%87&rft.aufirst=S&rft.date=1988-11-25&rft.volume=263&rft.issue=33&rft.spage=17301&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 - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for a role of protein kinase C in luteinizing hormone synthesis and secretion. Impaired responses to gonadotropin-releasing hormone in protein kinase C-depleted pituitary cells. AN - 78494227; 3053708 AB - The role of protein kinase C in luteinizing hormone (LH) release was analyzed in studies on the actions of phorbol esters and gonadotropin-releasing hormone (GnRH) in normal and protein kinase C (Ca2+/phospholipid-dependent enzyme)-depleted pituitary cell cultures. LH secretory responses of normal pituitary cells to GnRH were reduced but not abolished in Ca2+-deficient medium, consistent with the existence of extracellular Ca2+-dependent and -independent components of GnRH action. Both of these components could be elicited by treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA). The LH secretory responses to TPA and GnRH were additive only at low doses and converged to a common maximum at high concentrations of the agonists in the presence or absence of extracellular Ca2+. The release of stored LH by GnRH and TPA was accompanied by secretion of newly synthesized LH from 2 to 5 h during stimulation by either of the agonists. LH synthesis was increased in a progressive and dose-dependent manner by GnRH and TPA, and the ratio between newly synthesized and released hormone was near 1:2. TPA caused rapid and complete translocation of cytosolic protein kinase C to the particulate fraction of pituitary cells, followed by a progressive decrease in total enzyme content to approximately 10% after 6 h. Partial recovery of the cytosolic enzyme (to 20%) occurred after washing and reincubation for 15 h. Such kinase C-depleted cells showed prominent, dose-dependent reductions in the actions of GnRH and TPA on LH release and synthesis in both normal and Ca2+-deficient media. These observations support the hypothesis that protein kinase C participates in LH biosynthesis and secretion in pituitary gonadotrophs and is involved in the actions of GnRH upon these processes. JF - The Journal of biological chemistry AU - Stojilković, S S AU - Chang, J P AU - Ngo, D AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20982. Y1 - 1988/11/25/ PY - 1988 DA - 1988 Nov 25 SP - 17307 EP - 17311 VL - 263 IS - 33 SN - 0021-9258, 0021-9258 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 - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Reference Values KW - Cells, Cultured KW - Kinetics KW - Ovariectomy KW - Female KW - Luteinizing Hormone -- secretion KW - Pituitary Gland, Anterior -- drug effects KW - Pituitary Gland, Anterior -- metabolism KW - Pituitary Gland, Anterior -- secretion KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Luteinizing Hormone -- biosynthesis KW - Protein Kinase C -- physiology KW - Gonadotropin-Releasing Hormone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78494227?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+hepatocyte+and+kidney+cell+metabolism+of+2-acetylaminofluorene+and+comparison+to+the+respective+rat+cells.&rft.au=Langenbach%2C+R%3BRudo%2C+K&rft.aulast=Langenbach&rft.aufirst=R&rft.date=1988-12-01&rft.volume=4&rft.issue=4&rft.spage=453&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 - 1988-12-20 N1 - Date created - 1988-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol ester stimulates the synthesis of sphingomyelin in NIH 3T3 cells. A diminished response in cells transformed with human A-raf carrying retrovirus. AN - 78534606; 3191996 AB - The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulated the synthesis of sphingomyelin (CerPCho) from a [14C]choline-labelled phosphatidylcholine (PtdCho) pool in NIH 3T3 cells. Maximal stimulation (68%) of CerPCho synthesis, accompanied by an increase (38%) in its cellular content, required only 2 nM TPA. Higher concentrations of TPA (2-100 nM) had progressively less effect on CerPCho synthesis which correlated with increased hydrolysis of precursor PtdCho. In cells transformed with human or mouse A-raf carrying retroviruses TPA-stimulated PtdCho hydrolysis, but not CerPCho synthesis, suggesting independent regulation of these processes by the TPA-stimulated signal transduction system. JF - FEBS letters AU - Kiss, Z AU - Rapp, U R AU - Anderson, W B AD - Division of Cancer Biology and Diagnosis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/21/ PY - 1988 DA - 1988 Nov 21 SP - 221 EP - 226 VL - 240 IS - 1-2 SN - 0014-5793, 0014-5793 KW - Sphingomyelins KW - 0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Oncogenes KW - Enzyme Activation -- drug effects KW - Mice KW - Protein Kinase C -- physiology KW - Cell Line KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Transformation, Viral KW - Sphingomyelins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78534606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Phorbol+ester+stimulates+the+synthesis+of+sphingomyelin+in+NIH+3T3+cells.+A+diminished+response+in+cells+transformed+with+human+A-raf+carrying+retrovirus.&rft.au=Kiss%2C+Z%3BRapp%2C+U+R%3BAnderson%2C+W+B&rft.aulast=Kiss&rft.aufirst=Z&rft.date=1988-11-21&rft.volume=240&rft.issue=1-2&rft.spage=221&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-30 N1 - Date created - 1988-12-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - High-dose carboplatin with diethyldithiocarbamate chemoprotection in treatment of women with relapsed ovarian cancer. AN - 78506061; 2846858 AB - Diethyldithiocarbamate (DDTC) has been found to protect the bone marrow, kidneys, and gastrointestinal tract from the toxic effects of cisplatin and carboplatin (CBDCA) in animal models. In an attempt to minimize the toxic effects of high-dose CBDCA (800 mg/m2), a pilot study was undertaken in which women with relapsed or refractory epithelial ovarian cancer were treated with high-dose CBDCA, which was followed 3 hours later with DDTC (4 g/m2). There were four partial responses and no complete response in 21 patients who could be evaluated (overall response rate, 19%). Significant toxic effects, including three treatment-related deaths, were associated with the regimen. This study suggests that while high-dose CBDCA plus DDTC may be active in relapsed or refractory ovarian cancer, it is associated with clinically significant hematologic and autonomic toxic effects. JF - Journal of the National Cancer Institute AU - Rothenberg, M L AU - Ostchega, Y AU - Steinberg, S M AU - Young, R C AU - Hummel, S AU - Ozols, R F AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/16/ PY - 1988 DA - 1988 Nov 16 SP - 1488 EP - 1492 VL - 80 IS - 18 SN - 0027-8874, 0027-8874 KW - Organoplatinum Compounds KW - 0 KW - Ditiocarb KW - 99Z2744345 KW - Carboplatin KW - BG3F62OND5 KW - Index Medicus KW - Drug Evaluation KW - Organoplatinum Compounds -- administration & dosage KW - Neoplasm Recurrence, Local -- drug therapy KW - Humans KW - Autonomic Nervous System -- drug effects KW - Adult KW - Aged KW - Middle Aged KW - Bone Marrow -- drug effects KW - Female KW - Ditiocarb -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78506061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=High-dose+carboplatin+with+diethyldithiocarbamate+chemoprotection+in+treatment+of+women+with+relapsed+ovarian+cancer.&rft.au=Rothenberg%2C+M+L%3BOstchega%2C+Y%3BSteinberg%2C+S+M%3BYoung%2C+R+C%3BHummel%2C+S%3BOzols%2C+R+F&rft.aulast=Rothenberg&rft.aufirst=M&rft.date=1988-11-16&rft.volume=80&rft.issue=18&rft.spage=1488&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 - 1988-11-25 N1 - Date created - 1988-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Whither the modulation of platinum? AN - 78505314; 2846854 JF - Journal of the National Cancer Institute AU - Leyland-Jones, B AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/16/ PY - 1988 DA - 1988 Nov 16 SP - 1432 EP - 1433 VL - 80 IS - 18 SN - 0027-8874, 0027-8874 KW - Antimetabolites KW - 0 KW - Methionine Sulfoximine KW - 1982-67-8 KW - Buthionine Sulfoximine KW - 5072-26-4 KW - Ditiocarb KW - 99Z2744345 KW - Amifostine KW - M487QF2F4V KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Antimetabolites -- pharmacology KW - Amifostine -- pharmacology KW - Ditiocarb -- pharmacology KW - Humans KW - Methionine Sulfoximine -- pharmacology KW - Methionine Sulfoximine -- analogs & derivatives KW - Cisplatin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78505314?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Whither+the+modulation+of+platinum%3F&rft.au=Leyland-Jones%2C+B&rft.aulast=Leyland-Jones&rft.aufirst=B&rft.date=1988-11-16&rft.volume=80&rft.issue=18&rft.spage=1432&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 - 1988-11-25 N1 - Date created - 1988-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Isolation and partial characterization of the low-molecular-mass zinc/cadmium-binding protein from the testes of the patas monkey (Erythrocebus patas). Distinction from metallothionein. AN - 78663660; 3223896 AB - The mammalian testes are generally quite susceptible to cadmium. A deficiency of metallothionein (MT), a metal-binding protein linked to Cd tolerance, has been observed in rat testes and may explain the sensitivity in rats. Little is known about the metal-binding proteins in primate testes. Thus this study examined the nature of these proteins in a non-human primate species, the patas monkey (Erythrocebus patas). In all cases proteins isolated from testes were compared with authentic MT isolated from the liver of a zinc-treated monkey. A low-molecular-mass Zn/Cd-binding protein was seen in testicular and hepatic cytosol after gel filtration. Neither protein had substantial amounts of associated copper. These proteins could be partially purified from both sources by heat treatment and acetone precipitation. When such extracts were further separated by reverse-phase h.p.l.c., four hepatic forms were isolated, all of which proved to be authentic MT by amino acid analysis. However, only two testicular forms were separated by h.p.l.c., both of which had amino acid compositions quite unlike that of MT, having a much lower cysteine content and amino acids which are absent from MT (leucine and phenylalanine). The testicular protein appeared to be uninducible by Zn treatment. These results suggest that the low-molecular-mass Cd/Zn-binding proteins in the patas testes are not MTs and further support the hypothesis that a MT deficiency may be an important determinate of the marked testicular sensitivity to Cd toxicity. JF - The Biochemical journal AU - Waalkes, M P AU - Perantoni, A AU - Palmer, A E AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21701. Y1 - 1988/11/15/ PY - 1988 DA - 1988 Nov 15 SP - 131 EP - 137 VL - 256 IS - 1 SN - 0264-6021, 0264-6021 KW - Amino Acids KW - 0 KW - Carrier Proteins KW - cadmium-binding protein KW - zinc-binding protein KW - Cadmium KW - 00BH33GNGH KW - Metallothionein KW - 9038-94-2 KW - Iron KW - E1UOL152H7 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Animals KW - Cytosol -- analysis KW - Iron -- analysis KW - Chromatography, Gel KW - Amino Acids -- analysis KW - Erythrocebus patas KW - Molecular Weight KW - Male KW - Liver -- analysis KW - Chromatography, High Pressure Liquid KW - Zinc -- analysis KW - Cadmium -- analysis KW - Testis -- analysis KW - Metallothionein -- isolation & purification KW - Carrier Proteins -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78663660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Isolation+and+partial+characterization+of+the+low-molecular-mass+zinc%2Fcadmium-binding+protein+from+the+testes+of+the+patas+monkey+%28Erythrocebus+patas%29.+Distinction+from+metallothionein.&rft.au=Waalkes%2C+M+P%3BPerantoni%2C+A%3BPalmer%2C+A+E&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1988-11-15&rft.volume=256&rft.issue=1&rft.spage=131&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 - 1989-03-17 N1 - Date created - 1989-03-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Reprod Fertil. 1965 Oct;10(2):273-5 [5836275] Biochem J. 1984 Jun 15;220(3):811-8 [6466305] J Nutr. 1974 Mar;104(3):345-78 [4590708] Biochem Soc Trans. 1975;3(5):632-4 [1193255] Environ Physiol Biochem. 1975;5(6):378-88 [1213026] Anal Biochem. 1976 May 7;72:248-54 [942051] Toxicol Appl Pharmacol. 1977 Jan;39(1):51-60 [841573] Acta Eur Fertil. 1976 Dec;7(4):339-48 [829013] Am J Physiol. 1978 Apr;234(4):E399-406 [645856] J Biol Chem. 1979 Dec 25;254(24):12399-403 [500722] Anal Biochem. 1980 Feb;102(1):31-4 [7356160] Toxicology. 1980;16(1):1-37 [6250252] J Biol Chem. 1981 Apr 25;256(8):3931-5 [7217064] J Biol Chem. 1981 Jun 10;256(11):5712-6 [7240167] Toxicology. 1981;22(2):91-101 [7324075] J Chromatogr. 1982 Mar 12;228:285-91 [7076751] Biochem J. 1984 Jun 15;220(3):819-24 [6466306] J Toxicol Environ Health. 1984;14(5-6):803-12 [6520888] Toxicol Appl Pharmacol. 1985 Jul;79(3):511-23 [4035692] Biochem J. 1985 Oct 15;231(2):279-83 [4062897] J Biol Chem. 1986 Oct 5;261(28):13097-103 [3759948] J Biol Chem. 1961 Sep;236:2435-42 [13750714] J Natl Cancer Inst. 1963 Oct;31:745-59 [14069825] C R Seances Soc Biol Fil. 1964;158:297-9 [14188425] C R Seances Soc Biol Fil. 1964;158:2113-5 [14282126] Toxicology. 1982;23(1):11-20 [7089981] Toxicol Appl Pharmacol. 1982 Oct;66(1):134-42 [7157381] Biochem J. 1983 Jan 1;209(1):71-80 [6847618] Toxicol Lett. 1984 Jan;20(1):33-9 [6695394] Toxicology. 1984 Mar;30(2):157-69 [6710540] Arch Toxikol. 1971;28(1):46-55 [5569102] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preliminary applications of cross-axis synchronous flow-through coil planet centrifuge for large-scale preparative counter-current chromatography. AN - 78700866; 3069856 AB - The cross-axis synchronous flow-through coil planet centrifuge with a 20-cm revolutional radius and a total capacity of 1600 ml was successfully applied to preparative counter-current chromatography of various biological samples, which include sea buckthorn extract, steroid reaction mixture, indole plant hormones, and dinitrophenylamino acids. The present system offers advantages of stable balance of the centrifuge, a large column capacity, and high resolution. JF - Journal of chromatography AU - Zhang, T Y AU - Lee, Y W AU - Fang, Q C AU - Xiao, R AU - Ito, Y AD - Laboratory of Technical Development, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1988/11/11/ PY - 1988 DA - 1988 Nov 11 SP - 185 EP - 193 VL - 454 KW - Amino Acids KW - 0 KW - Indoleacetic Acids KW - Steroids KW - Index Medicus KW - Space life sciences KW - Plants, Toxic KW - Centrifugation -- methods KW - Plants, Medicinal KW - Steroids -- analysis KW - Rhamnus -- analysis KW - Amino Acids -- analysis KW - Indoleacetic Acids -- analysis KW - Chromatography -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78700866?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography&rft.atitle=Preliminary+applications+of+cross-axis+synchronous+flow-through+coil+planet+centrifuge+for+large-scale+preparative+counter-current+chromatography.&rft.au=Zhang%2C+T+Y%3BLee%2C+Y+W%3BFang%2C+Q+C%3BXiao%2C+R%3BIto%2C+Y&rft.aulast=Zhang&rft.aufirst=T&rft.date=1988-11-11&rft.volume=454&rft.issue=&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-26 N1 - Date created - 1989-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mouse non-histone chromosomal protein HMG-17 cDNA sequence. AN - 78560034; 3194220 JF - Nucleic acids research AU - Landsman, D AU - Zavou, S AU - Soares, N AU - Goodwin, G H AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/11/ PY - 1988 DA - 1988 Nov 11 SP - 10386 VL - 16 IS - 21 SN - 0305-1048, 0305-1048 KW - High Mobility Group Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Base Sequence KW - Genes KW - L Cells (Cell Line) -- metabolism KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - High Mobility Group Proteins -- genetics KW - DNA -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78560034?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mouse+non-histone+chromosomal+protein+HMG-17+cDNA+sequence.&rft.au=Landsman%2C+D%3BZavou%2C+S%3BSoares%2C+N%3BGoodwin%2C+G+H%3BBustin%2C+M&rft.aulast=Landsman&rft.aufirst=D&rft.date=1988-11-11&rft.volume=16&rft.issue=21&rft.spage=10386&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 - 1989-01-05 N1 - Date created - 1989-01-05 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X12944; GENBANK N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Biol Chem. 1986 Jun 5;261(16):7479-84 [3754870] Mol Cell Biol. 1983 Feb;3(2):280-9 [6300662] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antibody-mediated routing of diphtheria toxin in murine cells results in a highly efficacious immunotoxin. AN - 78500506; 3263366 AB - The chemical coupling of diphtheria toxin to an antimurine Thy1 antibody resulted in the most efficacious immunotoxin to date. At 1 micrograms/ml the immunotoxin inhibited protein synthesis of a Thy+ AKR murine cell at a rate of 1.4 logs/h, within the order of magnitude of the efficacy of native toxins. This is unusual since murine cells are highly resistant to diphtheria toxin. The conjugate is highly specific; Thy- AKR cells display no intoxication at 1 microgram/ml even after 18 h. The effects of ammonia, acid pulsing of external media, and low temperature reveal some similarities and some differences between intoxication of sensitive cells by toxin and of murine cells by the antibody-toxin conjugate. The differences that result in the high efficacy of the antibody-toxin conjugate appear to result from the antibody-mediated routing. These results imply that murine cells possess an acidic compartment which can mediate toxin cytosolic entry. Unlike the Thy antigen, the toxin receptor on murine cells is unable to route the toxin to this cellular site. JF - The Journal of biological chemistry AU - Marsh, J W AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/11/05/ PY - 1988 DA - 1988 Nov 05 SP - 15993 EP - 15999 VL - 263 IS - 31 SN - 0021-9258, 0021-9258 KW - Diphtheria Toxin KW - 0 KW - Immunotoxins KW - Isoantibodies KW - Proteins KW - anti-Thy antibody KW - Ammonia KW - 7664-41-7 KW - Index Medicus KW - Proteins -- pharmacology KW - Ammonia -- pharmacology KW - Animals KW - Thermodynamics KW - Kinetics KW - Cell Line KW - Diphtheria Toxin -- immunology KW - Diphtheria Toxin -- pharmacology KW - Immunotoxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78500506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antibody-mediated+routing+of+diphtheria+toxin+in+murine+cells+results+in+a+highly+efficacious+immunotoxin.&rft.au=Marsh%2C+J+W&rft.aulast=Marsh&rft.aufirst=J&rft.date=1988-11-05&rft.volume=263&rft.issue=31&rft.spage=15993&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 - 1988-12-02 N1 - Date created - 1988-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Coinduction of MDR-1 multidrug-resistance and cytochrome P-450 genes in rat liver by xenobiotics. AN - 78466446; 2845109 AB - The levels of mRNA for multidrug-resistance (MDR-1) and selective cytochrome P-450 genes were determined in adult rat liver following administration of various natural and synthetic xenobiotics. MDR-1 (also known as PGY1) was induced following administration of aflatoxin B1, 2-(acetylamino)fluorene (AAF), N-hydroxy-2-(acetylamino)fluorene, isosafrole, phenothiazine, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but not after phenobarbital or 7-hydroxy-2-(acetylamino)fluorene treatment. Cytochrome P-450 isoform d was induced by TCDD, isosafrole, phenothiazine, and AAF, while cytochrome P-450 isoform b was induced by phenobarbital, and to a lesser extent by isosafrole. These observations suggest that both MDR and cytochrome P-450 gene families are evolutionarily selected by the capacity of various xenobiotics to induce their own detoxification either through metabolism to hydrophilic derivatives by the cytochrome P-450 system or direct excretion from the cell by the MDR gene family. Furthermore, the data indicate that induction of selective members of the MDR and the cytochrome P-450 gene families may depend on overlapping regulatory elements. JF - Journal of the National Cancer Institute AU - Burt, R K AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/02/ PY - 1988 DA - 1988 Nov 02 SP - 1383 EP - 1386 VL - 80 IS - 17 SN - 0027-8874, 0027-8874 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Xenobiotics KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Index Medicus KW - Rats KW - Animals KW - 2-Acetylaminofluorene -- pharmacology KW - Multigene Family KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Liver -- metabolism KW - Mice KW - Receptors, Drug -- physiology KW - Drug Resistance -- genetics KW - Cytochrome P-450 Enzyme System -- genetics KW - Xenobiotics -- pharmacology KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78466446?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Coinduction+of+MDR-1+multidrug-resistance+and+cytochrome+P-450+genes+in+rat+liver+by+xenobiotics.&rft.au=Burt%2C+R+K%3BThorgeirsson%2C+S+S&rft.aulast=Burt&rft.aufirst=R&rft.date=1988-11-02&rft.volume=80&rft.issue=17&rft.spage=1383&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 - 1988-11-18 N1 - Date created - 1988-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synthesis and properties of H-ras DNA sequences containing O6-substituted 2'-deoxyguanosine residues at the first, second, or both positions of codon 12. AN - 78819935; 2979756 AB - Nine 16-base oligodeoxyribonucleotides having the sequence of codons 9 through the first base of codon 14 of the rodent H-ras gene, i.e., 5'-d(GTGGGCGCTG*G*AGGCG)-3', have been synthesized containing either an O6-methyl- (G* = m6G), O6-ethyl- (G* = e6G), or the newly described O6-benzyl-2'-deoxyguanosine residue (G* = b6G) at position 10 and/or 11 from the 5'-end. The conversion of the protected O6-substituted 2'-deoxyguanosine derivatives to the corresponding 3'-[O-(2-cyanoethyl) diisopropylphosphoramidites] and their incorporation into oligodeoxyribonucleotides were conveniently accomplished by using an "in situ" activation approach and automated phosphite triester synthetic methods. These oligomers were characterized by enzymatic digestion to their component nucleosides and were shown to be free of detectable contamination by known nucleoside impurities that can be produced during these syntheses. The melting behavior and circular dichroism spectra are described for duplexes of the nine O6-substituted 2'-deoxyguanosine containing oligomers paired with the complementary strand 5'-d(CGCCTCCAGCGCCCAC)-3', and these data have been compared with those for the "wild-type" unsubstituted duplex. JF - Chemical research in toxicology AU - Pauly, G T AU - Powers, M AU - Pei, G K AU - Moschel, R C AD - Laboratory of Chemical and Physical Carcinogenesis, NCI-Frederick Cancer Research Facility, Maryland 21701. PY - 1988 SP - 391 EP - 397 VL - 1 IS - 6 SN - 0893-228X, 0893-228X KW - Codon KW - 0 KW - Deoxyribonucleosides KW - Oligodeoxyribonucleotides KW - DNA KW - 9007-49-2 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Base Sequence KW - Molecular Sequence Data KW - Deoxyribonucleosides -- analysis KW - Genes, ras KW - DNA -- chemical synthesis KW - DNA -- genetics KW - Oligodeoxyribonucleotides -- chemical synthesis KW - Deoxyguanosine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78819935?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Synthesis+and+properties+of+H-ras+DNA+sequences+containing+O6-substituted+2%27-deoxyguanosine+residues+at+the+first%2C+second%2C+or+both+positions+of+codon+12.&rft.au=Pauly%2C+G+T%3BPowers%2C+M%3BPei%2C+G+K%3BMoschel%2C+R+C&rft.aulast=Pauly&rft.aufirst=G&rft.date=1988-11-01&rft.volume=1&rft.issue=6&rft.spage=391&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-09 N1 - Date created - 1992-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Styrene oxide as a stereochemical probe for the mechanism of aralkylation at different sites on guanosine. AN - 78810429; 2979753 AB - The stereochemistry at the alpha-carbon atom of the styrene moiety in styrene oxide-guanosine products was established, and the stereochemical consequences of reaction of optically active styrene oxide with guanosine were investigated. Inversion of stereochemistry in products at the alpha-carbon of styrene oxide decreased in the sequence 7- much greater than N2- greater than O6-substituted guanosines. These findings show that an extensively ionized substrate is needed for reaction at the exocyclic N2 and O6 sites on guanosine but that the reactive intermediate is not an ideal planar trigonal carbonium ion. This follows because inversion exceeds retention in both of the exocyclic substituted products. JF - Chemical research in toxicology AU - Latif, F AU - Moschel, R C AU - Hemminki, K AU - Dipple, A AD - Laboratory of Chemical and Physical Carcinogenesis, NCI-Frederick Cancer Research Facility, Maryland 21701. PY - 1988 SP - 364 EP - 369 VL - 1 IS - 6 SN - 0893-228X, 0893-228X KW - Epoxy Compounds KW - 0 KW - Guanosine KW - 12133JR80S KW - styrene oxide KW - 9QH06NGT6O KW - Index Medicus KW - Stereoisomerism KW - Structure-Activity Relationship KW - Alkylation KW - Guanosine -- analogs & derivatives KW - Guanosine -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78810429?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Styrene+oxide+as+a+stereochemical+probe+for+the+mechanism+of+aralkylation+at+different+sites+on+guanosine.&rft.au=Latif%2C+F%3BMoschel%2C+R+C%3BHemminki%2C+K%3BDipple%2C+A&rft.aulast=Latif&rft.aufirst=F&rft.date=1988-11-01&rft.volume=1&rft.issue=6&rft.spage=364&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-09 N1 - Date created - 1992-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antagonizing the anticonvulsant effect of ethanol using drugs acting at the benzodiazepine/GABA receptor complex. AN - 78774385; 2855119 AB - The ability of various benzodiazepine receptor ligands to antagonize the anticonvulsant action of ethanol was investigated using intravenous infusion of the GABA antagonist bicuculline. The partial inverse agonists FG 7142, RO 15-4513 and RO 15-3505 produced dose-related reductions in seizure threshold. These compounds also partially reversed the anticonvulsant action of ethanol. However, the magnitude of the effects in each case was only equivalent to the reduction in seizure threshold caused by each compound when administered alone. This is the proconvulsant effect of each compound merely subtracted from the anticonvulsant effect of ethanol. ZK 93426, a benzodiazepine receptor antagonist which alone failed to alter seizure threshold, did not affect the anticonvulsant action of ethanol. Both RO 15-4513 and RO 15-3505 also lowered the seizure threshold of barbiturate-treated mice, again in a subtractive fashion. The ability of RO 15-4513 and other inverse agonists to antagonize the anticonvulsant effect of ethanol appears to result from their intrinsic proconvulsant properties. JF - Pharmacology, biochemistry, and behavior AU - Nutt, D J AU - Lister, R G AD - Laboratory of Clinical Studies, NIAAA, Bethesda, MD 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 751 EP - 755 VL - 31 IS - 3 SN - 0091-3057, 0091-3057 KW - Anticonvulsants KW - 0 KW - Azides KW - Benzodiazepinones KW - Carbolines KW - Convulsants KW - Receptors, GABA-A KW - Benzodiazepines KW - 12794-10-4 KW - Ethanol KW - 3K9958V90M KW - FG 7142 KW - 60PO70N1BP KW - Ro 15-3505 KW - 78756-33-9 KW - Ro 15-4513 KW - 91917-65-6 KW - Pentobarbital KW - I4744080IR KW - Index Medicus KW - Seizures -- chemically induced KW - Animals KW - Dose-Response Relationship, Drug KW - Convulsants -- pharmacology KW - Mice KW - Carbolines -- pharmacology KW - Benzodiazepinones -- pharmacology KW - Male KW - Pentobarbital -- pharmacology KW - Ethanol -- pharmacology KW - Azides -- pharmacology KW - Receptors, GABA-A -- drug effects KW - Benzodiazepines -- pharmacology KW - Anticonvulsants -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78774385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antagonizing+the+anticonvulsant+effect+of+ethanol+using+drugs+acting+at+the+benzodiazepine%2FGABA+receptor+complex.&rft.au=Nutt%2C+D+J%3BLister%2C+R+G&rft.aulast=Nutt&rft.aufirst=D&rft.date=1988-11-01&rft.volume=31&rft.issue=3&rft.spage=751&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 - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interactions of ethanol with benzodiazepine receptor ligands in tests of exploration, locomotion and anxiety. AN - 78761792; 2855120 AB - The ability of benzodiazepine receptor ligands to modify the behavioral effects of ethanol in tests of exploration, locomotion and anxiety are reviewed. Drugs with inverse agonist activity appear capable of consistently antagonizing the reductions in exploration and anxiety caused by ethanol. In contrast, the locomotor stimulant action of ethanol has appeared relatively insensitive to inverse agonists, suggesting that this effect may not be mediated primarily by an action of ethanol at the benzodiazepine/GABA receptor complex. JF - Pharmacology, biochemistry, and behavior AU - Lister, R G AD - Laboratory of Clinical Studies, NIAAA, Bethesda, MD 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 761 EP - 765 VL - 31 IS - 3 SN - 0091-3057, 0091-3057 KW - Receptors, GABA-A KW - 0 KW - Benzodiazepines KW - 12794-10-4 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Animals KW - Drug Interactions KW - Mice KW - Meta-Analysis as Topic KW - Receptors, GABA-A -- physiology KW - Benzodiazepines -- antagonists & inhibitors KW - Ethanol -- pharmacology KW - Anxiety -- chemically induced KW - Exploratory Behavior -- drug effects KW - Receptors, GABA-A -- drug effects KW - Motor Activity -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78761792?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Caffeinated+beverages+and+decreased+fertility.&rft.au=Wilcox%2C+A%3BWeinberg%2C+C%3BBaird%2C+D&rft.aulast=Wilcox&rft.aufirst=A&rft.date=1988-12-01&rft.volume=2&rft.issue=8626-8627&rft.spage=1453&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 - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ethanol and the GABA receptor complex: studies with the partial inverse benzodiazepine receptor agonist Ro 15-4513. AN - 78752682; 2855121 AB - Ethanol potentiates GABA-receptor-mediated Cl- ion flux in vitro and, at similar concentrations, has anxiolytic and intoxicating properties in vivo. The imidazobenzodiazepine, Ro 15-4513 (ethyl-8-azido-5,6-dihydro-5-meth-6-oxo-4H- imidazo(1,5-a)(1,4)benzodiazepine-3-carboxylate), is a potent partial inverse agonist of the benzodiazepine/GABA receptor which can antagonize the in vitro actions of ethanol in potentiating GABA receptor-mediated Cl- ion flux. Moreover, several of the behavioral effects of ethanol are also antagonized by Ro 15-4513, and these effects can be demonstrated in several paradigms at doses of Ro 15-4513 that do not produce opposite behavioral effects. In contrast, in our studies, other benzodiazepine receptor antagonist and inverse agonists, including Ro 15-1788, FG-7142, and beta-CCE were not able to antagonize these biochemical or behavioral effects of ethanol at doses that were without intrinsic effects. However, both Ro 15-1788 and beta-CCE blocked the antagonism of ethanol's effects by Ro 15-4513, suggesting a role for the GABA receptor complex in the actions of ethanol. These studies provide further evidence that GABAergic neurones may mediate at least some of the behavioral and biochemical actions of low-to-moderate doses of ethanol. JF - Pharmacology, biochemistry, and behavior AU - Glowa, J R AU - Crawley, J AU - Suzdak, P D AU - Paul, S M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 767 EP - 772 VL - 31 IS - 3 SN - 0091-3057, 0091-3057 KW - Azides KW - 0 KW - Receptors, GABA-A KW - Benzodiazepines KW - 12794-10-4 KW - Ethanol KW - 3K9958V90M KW - Chlorine KW - 4R7X1O2820 KW - Ro 15-4513 KW - 91917-65-6 KW - Pentobarbital KW - I4744080IR KW - Index Medicus KW - Rats KW - Animals KW - Alcoholic Intoxication -- physiopathology KW - Dose-Response Relationship, Drug KW - Mice KW - Time Factors KW - Meta-Analysis as Topic KW - Chlorine -- metabolism KW - Male KW - Pentobarbital -- pharmacology KW - Behavior, Animal -- drug effects KW - Conflict (Psychology) KW - Receptors, GABA-A -- physiology KW - Ethanol -- pharmacology KW - Azides -- pharmacology KW - Receptors, GABA-A -- drug effects KW - Benzodiazepines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78752682?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ethanol+and+the+GABA+receptor+complex%3A+studies+with+the+partial+inverse+benzodiazepine+receptor+agonist+Ro+15-4513.&rft.au=Glowa%2C+J+R%3BCrawley%2C+J%3BSuzdak%2C+P+D%3BPaul%2C+S+M&rft.aulast=Glowa&rft.aufirst=J&rft.date=1988-11-01&rft.volume=31&rft.issue=3&rft.spage=767&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 - 1989-07-18 N1 - Date created - 1989-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of dimethyl hydrogen phosphite and its stability under simulated physiological conditions. AN - 78752208; 3244273 AB - In a study by the National Toxicology Program, dimethyl hydrogen phosphite (DMHP) was shown to cause dose-related neoplastic lesions in the lungs and forestomachs of Fischer 344 rats. This investigation was carried out to study the stability of this carcinogen under conditions similar to those that the chemical may encounter in the physiological environment. To carry out these studies, capillary gas chromatography was utilized to analyze DMHP. The method was linear over a range of 10 to at least 1000 ng. High-performance liquid chromatography (HPLC) also was used to analyze DMHP and its degradation products. In aqueous solutions, DMHP was stable for a period of time before degradation began. Once the process began, degradation continued until 10-20% of the original concentration was reached and further decomposition was minimal. At 10% concentration in 0.1M phosphate buffer, pH 7.4, DMHP was stable for 3.6 h at 37 degrees C. This stability period increased at lower temperature, at lower DMHP concentration, and in slightly more alkaline buffer (pH 8). After the stability period, DMHP disappeared from the solution and this disappearance followed a first order kinetics with a rate dependent upon temperature, concentration of DHMP, and the pH of the solution. The half-time of disappearance of DMHP under the conditions mentioned above was 2.4 h, which increased at lower temperature, at lower DMHP concentration, and in slightly more alkaline buffer (pH 8). The decomposition products of DMHP were identified by HPLC and proton nuclear magnetic resonance (1H-NMR) spectroscopy as methanol, monomethyl hydrogen phosphite, and orthophosphorous acid. JF - Journal of analytical toxicology AU - Nomeir, A A AU - Burka, L T AU - Matthews, H B AD - Toxicology Research and Testing Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. PY - 1988 SP - 334 EP - 338 VL - 12 IS - 6 SN - 0146-4760, 0146-4760 KW - Organophosphonates KW - 0 KW - Organophosphorus Compounds KW - Phosphites KW - dimethyl hydrogen phosphite KW - ST4TBO000H KW - Index Medicus KW - Drug Stability KW - Chemistry KW - Chemical Phenomena KW - Chromatography, High Pressure Liquid KW - Magnetic Resonance Spectroscopy KW - Organophosphorus Compounds -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78752208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Analysis+of+dimethyl+hydrogen+phosphite+and+its+stability+under+simulated+physiological+conditions.&rft.au=Nomeir%2C+A+A%3BBurka%2C+L+T%3BMatthews%2C+H+B&rft.aulast=Nomeir&rft.aufirst=A&rft.date=1988-11-01&rft.volume=12&rft.issue=6&rft.spage=334&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 - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of acute and chronic electroconvulsive shock on [3H]phorbol-dibutyrate binding to rat brain membranes. AN - 78710628; 2853305 AB - The present study investigated the effect of single and repeated electroconvulsive shock (ECS) on proteinkinase C in rat cerebral cortex, cerebellum, hippocampus and striatum using [3H]Phorbol-12,13-butyrate binding. In the postictal period and 24 hr after a single ECS there was no alteration in any brain region. Twenty four hr after 10 once-daily ECS there was a significant decrease the number of binding sites in cerebral cortex (30%) and in cerebellum (20%) without a change in the affinity constant. These findings are discussed with regard to earlier reports on phosphoinositide turnover following chemically and electrically induced seizures. JF - Neurochemical research AU - Gleiter, C H AU - Deckert, J AU - Nutt, D J AU - Marangos, P J AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1023 EP - 1026 VL - 13 IS - 11 SN - 0364-3190, 0364-3190 KW - Caenorhabditis elegans Proteins KW - 0 KW - Carrier Proteins KW - Phosphatidylinositols KW - Receptors, Drug KW - phorbol ester binding protein KW - phorbol ester receptor 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 - Phosphatidylinositols -- metabolism KW - Animals KW - Cerebral Cortex -- metabolism KW - Corpus Striatum -- metabolism KW - Hippocampus -- metabolism KW - Radioligand Assay KW - Male KW - Cerebellum -- metabolism KW - Protein Kinase C -- metabolism KW - Receptors, Drug -- metabolism KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Brain -- metabolism KW - Electroshock UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78710628?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+effect+of+acute+and+chronic+electroconvulsive+shock+on+%5B3H%5Dphorbol-dibutyrate+binding+to+rat+brain+membranes.&rft.au=Gleiter%2C+C+H%3BDeckert%2C+J%3BNutt%2C+D+J%3BMarangos%2C+P+J&rft.aulast=Gleiter&rft.aufirst=C&rft.date=1988-11-01&rft.volume=13&rft.issue=11&rft.spage=1023&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 - 1989-05-02 N1 - Date created - 1989-05-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of some spontaneous tumors by 4-hexylresorcinol in F344/N rats and B6C3F1 mice. AN - 78703133; 3229592 AB - 4-Hexylresorcinol (4-HR) is used as an anthelmintic and antiseptic in human and veterinary medicine. Toxicology and carcinogenesis studies were conducted by administering 4-HR in corn oil by gavage at 0, 62.5, or 125 mg/kg to F344 rats and B6C3F1 mice of each sex for 2 years. The nonneoplastic lesions associated with 4-HR exposure were nephropathy and osteosclerosis in dosed male and female mice. The only evidence of neoplasia associated with 4-HR was marginally increased incidences of adrenal gland pheochromocytomas and harderian gland tumors in male mice. Decreases were observed in the incidences of mononuclear cell leukemia in dosed male and female rats, hepatocellular adenomas or carcinomas in dosed male mice, and circulatory system tumors in high-dose male and female mice. These negative tumor trends in rats and mice, along with an indication of reduced overall incidences of benign and malignant tumors in treated groups compared to controls, suggest that 4-HR may deserve further study as a possible antineoplastic agent. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Chhabra, R S AU - Huff, J E AU - Haseman, J AU - Hall, A AU - Baskin, G AU - Cowan, M AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 685 EP - 690 VL - 11 IS - 4 SN - 0272-0590, 0272-0590 KW - Hexylresorcinol KW - R9QTB5E82N KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Carcinogenicity Tests KW - Mice KW - Male KW - Female KW - Neoplasms -- pathology KW - Neoplasms -- chemically induced KW - Hexylresorcinol -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78703133?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+some+spontaneous+tumors+by+4-hexylresorcinol+in+F344%2FN+rats+and+B6C3F1+mice.&rft.au=Chhabra%2C+R+S%3BHuff%2C+J+E%3BHaseman%2C+J%3BHall%2C+A%3BBaskin%2C+G%3BCowan%2C+M&rft.aulast=Chhabra&rft.aufirst=R&rft.date=1988-11-01&rft.volume=40&rft.issue=4&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Pharmacological+reviews&rft.issn=00316997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-17 N1 - Date created - 1989-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ontogeny of enkephalin- and VIP-containing neurons in dissociated cultures of embryonic mouse spinal cord and dorsal root ganglia. AN - 78702802; 3069239 AB - The ontogeny of vasoactive intestinal polypeptide (VIP), and Met-enkephalin in primary cultures of spinal cord/dorsal root ganglia from 12-day mouse embryos was examined by radioimmunoassay and immunohistochemistry. Met-enkephalin levels rose from less than 5 to 700 pg/culture over 26 days and were half maximal by day 16-18 in culture. VIP levels rose from less than 1 to 30 pg/culture over the same period, but were already half maximal by day 9. Met-enkephalin immunoreactivity was localized in multipolar medium sized neurons while VIP immunoreactivity was visualized both in neurons with extensively branched processes and in bipolar cells some of which appeared to be dorsal root ganglion cells. Tetrodotoxin (TTX)-sensitive spontaneous release of both peptides developed in parallel with the ability to stimulate peptide release with elevated potassium. Factors affecting the ontogeny of neuropeptide expression in, and release from, spinal cord neurons can now be examined in vitro in a strictly defined neurochemical environment. JF - Brain research. Developmental brain research AU - Eiden, L E AU - Siegel, R E AU - Giraud, P AU - Brenneman, D E AD - Unit on Molecular and Cellular Neurobiology, Laboratory of Cell Biology, NIMH, Bethesda, MD 20892. Y1 - 1988/11/01/ PY - 1988 DA - 1988 Nov 01 SP - 141 EP - 150 VL - 44 IS - 1 SN - 0165-3806, 0165-3806 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Tetrodotoxin KW - 4368-28-9 KW - Enkephalin, Methionine KW - 58569-55-4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Fetus KW - Animals KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Tetrodotoxin -- pharmacology KW - Radioimmunoassay KW - Fluorescent Antibody Technique KW - Ganglia, Spinal -- cytology KW - Enkephalin, Methionine -- analysis KW - Ganglia, Spinal -- secretion KW - Spinal Cord -- secretion KW - Spinal Cord -- drug effects KW - Ganglia, Spinal -- drug effects KW - Ganglia, Spinal -- embryology KW - Vasoactive Intestinal Peptide -- analysis KW - Spinal Cord -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78702802?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research.+Developmental+brain+research&rft.atitle=Ontogeny+of+enkephalin-+and+VIP-containing+neurons+in+dissociated+cultures+of+embryonic+mouse+spinal+cord+and+dorsal+root+ganglia.&rft.au=Eiden%2C+L+E%3BSiegel%2C+R+E%3BGiraud%2C+P%3BBrenneman%2C+D+E&rft.aulast=Eiden&rft.aufirst=L&rft.date=1988-11-01&rft.volume=44&rft.issue=1&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=Brain+research.+Developmental+brain+research&rft.issn=01653806&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-03 N1 - Date created - 1989-05-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicology and pathology of methyl bromide in F344 rats and B6C3F1 mice following repeated inhalation exposure. AN - 78700767; 3229585 AB - The toxicity of methyl bromide was studied in male and female F344 rats and B6C3F1 mice exposed by inhalation to 160 ppm methyl bromide or air 6 hr/day, 5 days/week for up to 6 weeks. The animals were killed after 3, 10, or 30 exposure days, or when 50% mortality was observed in any group. Only female rats survived the entire 30 exposure days at 160 ppm methyl bromide with less than 50% mortality. There were clear species- and sex-related differences in susceptibility of specific organs to methyl bromide. Primary target organs were the brain, kidney, nasal cavity, heart, adrenal gland, liver, and testis. In rats, neuronal necrosis occurred in the cerebral cortex, hippocampus, and thalamus of the brain whereas in mice neuronal necrosis occurred primarily in the internal granular layer of the cerebellum. Nephrosis occurred in all exposed mice, but not rats, and was likely a major cause of moribundity and death. Necrosis of the olfactory epithelium was more severe and extensive in rats than mice. Myocardial degeneration occurred in male and female rats and to a lesser degree in male mice. There was atrophy of the inner zone of the adrenal cortex in female mice and cytoplasmic vacuolation of the adrenal cortex in rats. Testicular degeneration occurred in rats and mice. The target organ specificity of methyl bromide is similar to that of methyl chloride, suggesting that the two monohalomethanes may have a common mechanism of action. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Eustis, S L AU - Haber, S B AU - Drew, R T AU - Yang, R S AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 594 EP - 610 VL - 11 IS - 4 SN - 0272-0590, 0272-0590 KW - Hydrocarbons, Brominated KW - 0 KW - methyl bromide KW - 9V42E1Z7B6 KW - Index Medicus KW - Animals KW - Kidney -- pathology KW - Sex Factors KW - Myocardium -- pathology KW - Testis -- pathology KW - Mice KW - Tissue Distribution KW - Adrenal Glands -- pathology KW - Rats KW - Hematologic Tests KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Brain -- pathology KW - Body Weight -- drug effects KW - Administration, Inhalation KW - Species Specificity KW - Female KW - Male KW - Organ Size -- drug effects KW - Hydrocarbons, Brominated -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78700767?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pathology+of+methyl+bromide+in+F344+rats+and+B6C3F1+mice+following+repeated+inhalation+exposure.&rft.au=Eustis%2C+S+L%3BHaber%2C+S+B%3BDrew%2C+R+T%3BYang%2C+R+S&rft.aulast=Eustis&rft.aufirst=S&rft.date=1988-11-01&rft.volume=11&rft.issue=4&rft.spage=594&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 - 1989-04-17 N1 - Date created - 1989-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alkaloids from a panamanian poison frog, Dendrobates speciosus: identification of pumiliotoxin-A and allopumiliotoxin class alkaloids, 3,5-disubstituted indolizidines, 5-substituted 8-methylindolizidines, and a 2-methyl-6-nonyl-4-hydroxypiperidine. AN - 78689407; 3236011 AB - Dendrobates speciosus is a small red or orange frog that occupies a small geographic range in the highlands of western Panama, where it occurs abundantly in some cloud forest habitats. Gc-ms analysis indicated the presence of at least 30 alkaloids in MeOH skin extracts from population samples at the extreme eastern end of the known geographic range. Eleven alkaloids were isolated by cc in quantities sufficient for 2D-nmr spectral analysis, which in some cases confirmed their identity with alkaloids known from other species and in other cases led to assignment of structures. Pumiliotoxin 251D, pumiliotoxin A [307A], pumiliotoxin B [323A], and allopumiliotoxin 267A were identified as major constituents. N-Oxides of 323A and 267A were also isolated. Indolizidines 195B and 223AB with 3-butyl-5-methyl and 3-butyl-5-propyl substituents, respectively, were identified. The 5-substituents of the 8-methyl-indolizidines 207A and 235B' were assigned as -(CH2)3CH = CH2 and -(CH2)5CH = CH2, respectively; indolizidine 235B' from D. speciosus is, thus, a positional double-bond isomer of indolizidine 235B previously isolated from a closely related poison frog, Dendrobates pumilio. A piperidine 241D was isolated and assigned the structure cis-cis-2-methyl-6-nonyl-4-hydroxypiperidine. JF - Journal of natural products AU - Edwards, M W AU - Daly, J W AU - Myers, C W AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. PY - 1988 SP - 1188 EP - 1197 VL - 51 IS - 6 SN - 0163-3864, 0163-3864 KW - Alkaloids KW - 0 KW - Amphibian Venoms KW - Indoles KW - Indolizines KW - Piperidines KW - pumiliotoxin A KW - 67054-00-6 KW - histrionicotoxin KW - TC29F9M9XW KW - Index Medicus KW - Molecular Structure KW - Animals KW - Indoles -- isolation & purification KW - Piperidines -- isolation & purification KW - Magnetic Resonance Spectroscopy KW - Amphibian Venoms -- isolation & purification KW - Alkaloids -- classification KW - Anura KW - Alkaloids -- isolation & purification KW - Amphibian Venoms -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78689407?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alkaloids+from+a+panamanian+poison+frog%2C+Dendrobates+speciosus%3A+identification+of+pumiliotoxin-A+and+allopumiliotoxin+class+alkaloids%2C+3%2C5-disubstituted+indolizidines%2C+5-substituted+8-methylindolizidines%2C+and+a+2-methyl-6-nonyl-4-hydroxypiperidine.&rft.au=Edwards%2C+M+W%3BDaly%2C+J+W%3BMyers%2C+C+W&rft.aulast=Edwards&rft.aufirst=M&rft.date=1988-11-01&rft.volume=51&rft.issue=6&rft.spage=1188&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 - 1989-04-28 N1 - Date created - 1989-04-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Non-sedating antihistamines. AN - 78667656; 3147222 AB - Antihistamines are effective therapy against histamine-mediated conditions, including seasonal and perennial allergic rhinitis and chronic urticaria. They may also have a therapeutic role to play in asthma. Until recently all antihistamines produced some degree of drowsiness, as well as having anticholinergic side effects. Several non-sedating antihistamines have now been developed. Evidence suggests that their freedom from central nervous system effects is due to their lack of penetration of the blood-brain barrier. They also have no appreciable binding to cholinergic receptors. Two of these non-sedating antihistamines, terfenadine and astemizole, have novel binding characteristics with the histamine H1 receptor, exhibiting irreversible binding at higher concentrations. In humans astemizole has a remarkably long half-life of elimination, on the order of 12 to 18 days for metabolites. Clinical trials have demonstrated that these newer antihistamines are as effective as classical antihistamines and that they have no greater incidence of central nervous system or anticholinergic side effects than placebo. JF - Allergy proceedings : the official journal of regional and state allergy societies AU - Kaliner, M A AU - Check, W A AD - Allergic Diseases Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. PY - 1988 SP - 649 EP - 663 VL - 9 IS - 6 SN - 1046-9354, 1046-9354 KW - Benzhydryl Compounds KW - 0 KW - Benzimidazoles KW - Terfenadine KW - 7BA5G9Y06Q KW - Astemizole KW - 7HU6337315 KW - Index Medicus KW - Hypersensitivity -- drug therapy KW - Animals KW - Humans KW - Benzhydryl Compounds -- pharmacokinetics KW - Benzimidazoles -- adverse effects KW - Benzimidazoles -- pharmacology KW - Benzhydryl Compounds -- pharmacology KW - Benzhydryl Compounds -- adverse effects KW - Benzimidazoles -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78667656?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Allergy+proceedings+%3A+the+official+journal+of+regional+and+state+allergy+societies&rft.atitle=Non-sedating+antihistamines.&rft.au=Kaliner%2C+M+A%3BCheck%2C+W+A&rft.aulast=Kaliner&rft.aufirst=M&rft.date=1988-11-01&rft.volume=9&rft.issue=6&rft.spage=649&rft.isbn=&rft.btitle=&rft.title=Allergy+proceedings+%3A+the+official+journal+of+regional+and+state+allergy+societies&rft.issn=10469354&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-29 N1 - Date created - 1989-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of a transfected c-myc proto-oncogene on cellular differentiation. AN - 78654783; 3221882 JF - Molecular immunology AU - Segal, S AU - Dmitrovsky, E AU - Paez de la Cadena, M AD - NCI-Navy Medical Oncology Branch, National Navy Medical Center, Bethesda, MD 20814. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1129 EP - 1132 VL - 25 IS - 11 SN - 0161-5890, 0161-5890 KW - Acetamides KW - 0 KW - hexamethylene bisacetamide KW - LA133J59VU KW - Index Medicus KW - Animals KW - Acetamides -- pharmacology KW - Tumor Cells, Cultured KW - Humans KW - Cell Differentiation KW - Mice KW - Cell Line KW - Teratoma -- genetics KW - Transfection KW - Teratoma -- pathology KW - Leukemia, Erythroblastic, Acute -- genetics KW - Leukemia, Erythroblastic, Acute -- pathology KW - Proto-Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78654783?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+effect+of+a+transfected+c-myc+proto-oncogene+on+cellular+differentiation.&rft.au=Segal%2C+S%3BDmitrovsky%2C+E%3BPaez+de+la+Cadena%2C+M&rft.aulast=Segal&rft.aufirst=S&rft.date=1988-11-01&rft.volume=25&rft.issue=11&rft.spage=1129&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 - 1989-03-21 N1 - Date created - 1989-03-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Unlinked regulation of the sensitivity of primary glucocorticoid-inducible responses in mouse mammary tumor virus infected Fu5-5 rat hepatoma cells. AN - 78654643; 2906113 AB - The enzyme tyrosine aminotransferase (TAT) is induced by unusually low concentrations of glucocorticoids in Fu5-5 cells. We have isolated clones of Fu5-5 cells infected with mouse mammary tumor virus (MMTV) in order to simultaneously compare the glucocorticoid regulation of the host cell gene, TAT, with that of another primary inducible gene, MMTV. In the two clones that were examined in detail, MMTV RNA induction occurred at 4- to 11-fold higher concentrations of dexamethasone than those needed for induction of TAT mRNA. Furthermore, the amount of agonist activity displayed by the irreversible antiglucocorticoid dexamethasone 21-mesylate was greater for the induction of TAT mRNA than for MMTV RNA. These results extend our previous observations of unequal sensitivity of induction of TAT enzyme activity in two hepatoma cell lines and show that differential glucocorticoid regulation of gene induction within the same cell can occur at a pretranslational step. The present data also indicate that the unusual properties of TAT gene induction are not shared by all primary, glucocorticoid-inducible responses of the same cell and imply that additional factors mediating differential regulation of glucocorticoid-responsive genes are involved. JF - Molecular endocrinology (Baltimore, Md.) AU - Wasner, G AU - Oshima, H AU - Thompson, E B AU - Simons, S S AD - Steroid Hormones Section, National Institute of Diabetes, and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1009 EP - 1017 VL - 2 IS - 11 SN - 0888-8809, 0888-8809 KW - Glucocorticoids KW - 0 KW - RNA, Viral KW - Receptors, Glucocorticoid KW - Dexamethasone KW - 7S5I7G3JQL KW - Tyrosine Transaminase KW - EC 2.6.1.5 KW - dexamethasone 21-methanesulfonate KW - O9S11FMA79 KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Dexamethasone -- pharmacology KW - Tyrosine Transaminase -- genetics KW - Mammary Tumor Virus, Mouse KW - Mammary Neoplasms, Experimental -- genetics KW - Mice KW - Receptors, Glucocorticoid -- metabolism KW - Transcriptional Activation KW - Dexamethasone -- analogs & derivatives KW - Clone Cells -- physiopathology KW - RNA, Viral -- genetics KW - Cell Line KW - Liver Neoplasms, Experimental -- genetics KW - Liver Neoplasms, Experimental -- microbiology KW - Liver Neoplasms, Experimental -- chemically induced KW - Gene Expression Regulation -- drug effects KW - Tumor Cells, Cultured -- physiopathology KW - Glucocorticoids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78654643?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Unlinked+regulation+of+the+sensitivity+of+primary+glucocorticoid-inducible+responses+in+mouse+mammary+tumor+virus+infected+Fu5-5+rat+hepatoma+cells.&rft.au=Wasner%2C+G%3BOshima%2C+H%3BThompson%2C+E+B%3BSimons%2C+S+S&rft.aulast=Wasner&rft.aufirst=G&rft.date=1988-11-01&rft.volume=2&rft.issue=11&rft.spage=1009&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bacteriophage T4 DNA polymerase determines the amount and specificity of ultraviolet mutagenesis. AN - 78642075; 3063950 AB - Ultraviolet mutagenesis in bacteriophage T4 proceeds via error-prone repair (EPR) and requires the functional integrity of the uvsWXY system which mediates genetic recombination, recombinational repair, and mutability by diverse DNA damaging agents. Current opinion holds that mutagens acting through EPR generate DNA damage which blocks the progress of the replication complex and that EPR consists of the facilitated bypass of such inaccurate, damaged templates. This notion predicts that the T4 DNA polymerase (encoded by gene 43) mediates EPR in UV irradiated phage T4. This prediction is verified by the discovery that gene 43 mutations often enhance or reduce UV mutagenesis (which is scored by the induction of r mutants) and sometimes change its specificity. JF - Molecular & general genetics : MGG AU - Drake, J W AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 547 EP - 552 VL - 214 IS - 3 SN - 0026-8925, 0026-8925 KW - DNA, Viral KW - 0 KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Alleles KW - Genetic Complementation Test KW - Escherichia coli -- genetics KW - Genes, Viral KW - Escherichia coli -- enzymology KW - Mutation KW - Chromosome Mapping KW - T-Phages -- enzymology KW - DNA Repair -- radiation effects KW - Ultraviolet Rays KW - T-Phages -- genetics KW - DNA-Directed DNA Polymerase -- genetics KW - DNA, Viral -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78642075?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Bacteriophage+T4+DNA+polymerase+determines+the+amount+and+specificity+of+ultraviolet+mutagenesis.&rft.au=Drake%2C+J+W&rft.aulast=Drake&rft.aufirst=J&rft.date=1988-11-01&rft.volume=214&rft.issue=3&rft.spage=547&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 - 1989-03-06 N1 - Date created - 1989-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The ultrasound appearance of radiation-induced hepatic injury. Correlation with computed tomography and magnetic resonance imaging. AN - 78602748; 3062187 AB - The ultrasound findings in three cases of radiation-induced hepatic injury are described and compared with computed tomography and magnetic resonance imaging findings. Fatty infiltration of the liver was present in two of the cases in which concurrent chemotherapy was being administered. On ultrasound B-scans, the regions of radiation injury were hypoechoic relative to the remainder of the liver. This finding was more obvious in the patients with fatty livers. CT scans on the patients with fatty infiltrated livers showed higher attenuation in the irradiated region than in unexposed liver. In the patient where no fatty infiltration was present, the radiated section of liver had lower attenuation consistent with previous reports. Magnetic resonance imaging showed decreased signal in the exposed areas on T1 weighted images. JF - Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine AU - Garra, B S AU - Shawker, T H AU - Chang, R AU - Kaplan, K AU - White, R D AD - Diagnostic Radiology Department, National Institutes of Health, Bethesda, Maryland. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 605 EP - 609 VL - 7 IS - 11 SN - 0278-4297, 0278-4297 KW - Index Medicus KW - Liver -- pathology KW - Humans KW - Middle Aged KW - Liver -- radiation effects KW - Female KW - Child, Preschool KW - Magnetic Resonance Imaging KW - Hepatitis -- diagnostic imaging KW - Radiation Injuries -- diagnostic imaging KW - Tomography, X-Ray Computed KW - Hepatitis -- diagnosis KW - Ultrasonography KW - Radiation Injuries -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78602748?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+ultrasound+in+medicine+%3A+official+journal+of+the+American+Institute+of+Ultrasound+in+Medicine&rft.atitle=The+ultrasound+appearance+of+radiation-induced+hepatic+injury.+Correlation+with+computed+tomography+and+magnetic+resonance+imaging.&rft.au=Garra%2C+B+S%3BShawker%2C+T+H%3BChang%2C+R%3BKaplan%2C+K%3BWhite%2C+R+D&rft.aulast=Garra&rft.aufirst=B&rft.date=1988-11-01&rft.volume=7&rft.issue=11&rft.spage=605&rft.isbn=&rft.btitle=&rft.title=Journal+of+ultrasound+in+medicine+%3A+official+journal+of+the+American+Institute+of+Ultrasound+in+Medicine&rft.issn=02784297&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-15 N1 - Date created - 1989-02-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metal-binding proteins of the Syrian hamster ovaries: apparent deficiency of metallothionein. AN - 78600188; 3207812 AB - A deficiency of metallothionein, a high-affinity metal-binding protein thought to detoxify cadmium, has been observed in rat and mouse testes, tissues that are highly susceptible to the necrotizing and carcinogenic effects of cadmium. Like the testes, the ovaries undergo a hemorrhagic necrosis when exposed to cadmium, and female Syrian hamsters have recently been shown to be highly susceptible to cadmium. However, the nature of cadmium-binding proteins in the ovary is unknown; thus, this study was undertaken to define the nature of any such proteins in the Syrian hamster ovary. A low molecular weight (Mr) zinc- and cadmium-binding protein was detected in cytosol derived from the ovaries after gel filtration that eluted with a relative elution volume similar to authentic metallothionein. This protein was extractable by heat-treatment and sequential acetone precipitation. When such extracts were further purified with a reverse phase high performance liquid chromatography (HPLC) technique developed for the isolation of metallothionein isoforms, two forms were separated. However, neither of these could be classified as metallothionein on the basis of amino acid composition, since both were particularly low in cysteine, a very common amino acid in metallothionein. The ovarian protein also contained significant amounts of aromatic amino acids, unlike metallothionein--which is devoid of aromatics, and contained much more glutamate than metallothionein. Hamsters were also made resistant to cadmium-induced ovarian necrosis by zinc treatment. Such zinc treatment, however, did not alter levels of this protein, yet caused a marked induction of hepatic metallothionein. Likewise, cadmium treatment did not increase the levels of the ovarian metal-binding protein yet markedly induced hepatic metallothionein.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biology of reproduction AU - Waalkes, M P AU - Rehm, S AU - Perantoni, A AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 953 EP - 961 VL - 39 IS - 4 SN - 0006-3363, 0006-3363 KW - Amino Acids KW - 0 KW - cadmium-binding protein KW - Cadmium KW - 00BH33GNGH KW - Metallothionein KW - 9038-94-2 KW - Index Medicus KW - Cytosol -- metabolism KW - Animals KW - Cytosol -- analysis KW - Chromatography, Gel KW - Amino Acids -- analysis KW - Mesocricetus KW - Female KW - Chromatography, High Pressure Liquid KW - Cricetinae KW - Ovary -- metabolism KW - Cadmium -- metabolism KW - Metallothionein -- deficiency KW - Ovary -- pathology KW - Metallothionein -- analysis KW - Ovary -- drug effects KW - Cadmium -- toxicity KW - Metallothionein -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78600188?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+of+reproduction&rft.atitle=Metal-binding+proteins+of+the+Syrian+hamster+ovaries%3A+apparent+deficiency+of+metallothionein.&rft.au=Waalkes%2C+M+P%3BRehm%2C+S%3BPerantoni%2C+A&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1988-11-01&rft.volume=8&rft.issue=4&rft.spage=551&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 - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cunninghamella bertholletiae infection associated with deferoxamine therapy. AN - 78596245; 3060947 AB - Cunninghamella bertholletiae, an uncommon cause of human infection, has been reported with increasing frequency in recent years. C. bertholletiae belongs to the order Mucorales and produces infections similar to those produced by the other agents of mucormycosis. Infections with this group of organisms have typically been seen either in patients with diabetes mellitus or in those receiving chemotherapy. Recent reports of mucormycosis in dialysis patients receiving deferoxamine for iron or aluminum overload have raised the possibility that deferoxamine therapy is a risk factor for mucormycosis. A case of C. bertholletiae infection in a patient receiving deferoxamine for iron overload unrelated to hemodialysis was investigated in detail, and possible explanations for this patient's infection were assessed. JF - Reviews of infectious diseases AU - Rex, J H AU - Ginsberg, A M AU - Fries, L F AU - Pass, H I AU - Kwon-Chung, K J AD - Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. PY - 1988 SP - 1187 EP - 1194 VL - 10 IS - 6 SN - 0162-0886, 0162-0886 KW - Iron KW - E1UOL152H7 KW - Deferoxamine KW - J06Y7MXW4D KW - Index Medicus KW - Mucorales KW - Risk Factors KW - Humans KW - Middle Aged KW - Iron -- metabolism KW - Female KW - Deferoxamine -- adverse effects KW - Lung Diseases, Fungal -- etiology KW - Mucormycosis -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78596245?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cunninghamella+bertholletiae+infection+associated+with+deferoxamine+therapy.&rft.au=Rex%2C+J+H%3BGinsberg%2C+A+M%3BFries%2C+L+F%3BPass%2C+H+I%3BKwon-Chung%2C+K+J&rft.aulast=Rex&rft.aufirst=J&rft.date=1988-11-01&rft.volume=10&rft.issue=6&rft.spage=1187&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 - 1989-02-02 N1 - Date created - 1989-02-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A short-lived nuclear phosphoprotein encoded by the human ets-2 proto-oncogene is stabilized by activation of protein kinase C. AN - 78594080; 3062367 AB - The human ets-2 gene is a homolog of the v-ets oncogene of the E26 virus and codes for a 56-kilodalton nuclear protein. The ets-2 protein is phosphorylated and has a rapid turnover, with a half-life of 20 min. When human lymphocytic CEM cells were treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), the level of the ets-2 protein was quickly elevated 5- to 20-fold. This effect of TPA was mimicked by a synthetic diacylglycerol, 1-oleoyl-2-acetyl glycerol, and was blocked by the protein kinase C inhibitor H7, indicating that protein kinase C is involved in the induction. The increase in the ets-2 protein was due to stabilization of the protein, because the protein had a half-life of more than 2 h in the presence of TPA and the ets-2 mRNA level did not increase significantly upon TPA treatment. The protein synthesis inhibitor cycloheximide enhanced the effect of TPA on the ets-2 protein and could itself slow turnover of the protein. Properties of the ets-2 protein, such as nuclear localization, phosphorylation, rapid turnover, and response to protein kinase C, indicate that this protein belongs to a group of oncogene proteins which are generally thought to have regulatory functions in the nucleus (e.g., myc, fos, myb, and p53). Our results suggest that protein kinase C, either directly or indirectly, regulates the level of the ets-2 protein by posttranslational mechanisms. JF - Molecular and cellular biology AU - Fujiwara, S AU - Fisher, R J AU - Bhat, N K AU - Diaz de la Espina, S M AU - Papas, T S AD - Laboratory of Molecular Oncology, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 4700 EP - 4706 VL - 8 IS - 11 SN - 0270-7306, 0270-7306 KW - Diglycerides KW - 0 KW - Isoquinolines KW - Piperazines KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-ets KW - RNA, Messenger KW - Transcription Factors KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Cycloheximide KW - 98600C0908 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Enzyme Activation KW - Humans KW - Protein Processing, Post-Translational KW - RNA, Messenger -- genetics KW - Proto-Oncogenes KW - Piperazines -- pharmacology KW - Isoquinolines -- pharmacology KW - Diglycerides -- pharmacology KW - RNA, Messenger -- metabolism KW - Half-Life KW - Phosphorylation KW - Cycloheximide -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Cell Line KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Proto-Oncogene Proteins -- metabolism KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78594080?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+short-lived+nuclear+phosphoprotein+encoded+by+the+human+ets-2+proto-oncogene+is+stabilized+by+activation+of+protein+kinase+C.&rft.au=Fujiwara%2C+S%3BFisher%2C+R+J%3BBhat%2C+N+K%3BDiaz+de+la+Espina%2C+S+M%3BPapas%2C+T+S&rft.aulast=Fujiwara&rft.aufirst=S&rft.date=1988-11-01&rft.volume=8&rft.issue=11&rft.spage=4700&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 - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1987 Jun 19;49(6):835-44 [3555845] J Biol Chem. 1985 Mar 25;260(6):3868-74 [3838316] Cell. 1987 Sep 11;50(6):847-61 [3040262] Cell. 1987 Oct 23;51(2):251-60 [2822255] Science. 1987 Dec 4;238(4832):1386-92 [2825349] Mol Cell Biol. 1981 Feb;1(2):101-10 [6100960] Dev Biol. 1988 Feb;125(2):432-40 [3276571] Science. 1985 Sep 20;229(4719):1265-8 [4035354] Proc Natl Acad Sci U S A. 1985 Nov;82(21):7294-8 [2997781] Nature. 1986 Mar 13-19;320(6058):182-4 [3513022] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1792-6 [3513188] Proc Natl Acad Sci U S A. 1986 May;83(10):3213-7 [3010284] Science. 1986 Jul 18;233(4761):305-12 [3014651] Mol Cell Biol. 1985 Oct;5(10):2874-7 [3915538] Cancer Surv. 1986;5(2):309-27 [3779660] Cell. 1986 Dec 26;47(6):921-8 [3096580] EMBO J. 1986 Sep;5(9):2251-6 [3536486] Mol Cell Biol. 1986 Apr;6(4):1050-7 [2431274] Nature. 1987 Jan 22-28;325(6102):368-72 [3027570] Proc Natl Acad Sci U S A. 1987 May;84(10):3161-5 [3472202] Cell. 1987 Jun 19;49(6):729-39 [3034432] Mol Cell Biol. 1988 Feb;8(2):531-9 [2832726] Dev Biol. 1988 May;127(1):45-53 [2834248] Oncogene. 1988 Feb;2(2):99-103 [3285299] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Cancer Res. 1975 Jul;35(7):1662-70 [48421] Nature. 1976 Mar 11;260(5547):170-3 [176594] Nature. 1979 Mar 15;278(5701):261-3 [218111] Virology. 1979 Oct 30;98(2):308-18 [228475] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] J Biol Chem. 1982 Jul 10;257(13):7847-51 [7085651] Cell Calcium. 1982 Oct;3(4-5):323-35 [6218878] Annu Rev Biochem. 1983;52:301-54 [6351725] J Biol Chem. 1983 Oct 10;258(19):11442-5 [6311812] Nature. 1983 Nov 24-30;306(5941):391-5 [6316155] Nature. 1983 Nov 24-30;306(5941):395-7 [6316156] Cell. 1983 Dec;35(3 Pt 2):603-10 [6606489] Cell. 1984 Feb;36(2):259-68 [6319013] J Virol. 1984 Apr;50(1):280-3 [6199515] Nature. 1984 Mar 8-14;308(5955):199-201 [6366574] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2543-7 [6201860] Cell. 1984 Jun;37(2):537-47 [6327074] EMBO J. 1984 Aug;3(8):1887-90 [6479151] J Biol Chem. 1984 Oct 10;259(19):11706-12 [6237101] Nature. 1984 Oct 4-10;311(5985):433-8 [6090941] Biochemistry. 1984 Oct 9;23(21):5036-41 [6238627] Nature. 1984 Nov 15-21;312(5991):280-2 [6438521] Mol Cell Biol. 1984 Nov;4(11):2486-97 [6513926] Cell. 1985 Jan;40(1):209-17 [3881183] Annu Rev Biochem. 1987;56:159-93 [3304132] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biochemical characterization of retinal protein and phospholipid synthesis in mice exposed transplacentally to N-methyl-N-nitrosourea. AN - 78575110; 3197772 AB - Transplacental exposure to the DNA alkylating agent N-methyl-N-nitrosourea on day 16 of gestation in CD-1 albino mice induces a degeneration of the retina, the severity of which depends upon the dosage level of the drug. A 1 mg kg-1 dose provokes a progressive retinal degeneration in the offspring which begins at about 4-6 weeks of age and is characterized by gradual thinning of the retinal layers. A 15 mg kg-1 dosage of MNU provokes severe retinal dysplasia characterized morphologically by rosettes in the outer nuclear layer and loss of rod outer segments (ROS). In the present biochemical experiments, retinal protein synthesis was examined in mice 2-, 4-, and 6 weeks of age exposed to 1 mg kg-1 MNU and 2- and 5 weeks of age exposed to 15 mg kg-1 MNU. Phospholipid synthesis was examined in mice 2-, 4-, 6- and 12 weeks of age exposed to 1 mg kg-1 MNU and at 2 weeks in mice exposed to 15 mg kg-1 MNU. Retinas were incubated for 2 hr at 37 degrees C in media supplemented with either [3H]leucine for protein synthesis studies or [3H]glycerol for phospholipid synthesis experiments. Aliquots of crude ROS and the retinal debris were taken for protein determination, scintillation counting, SDS-PAGE separation of labeled opsin, phosphorus determination and TLC separation of phospholipids. Results indicated that mice exposed to 1 mg kg-1 MNU did not differ significantly from age-matched controls in these measurements, whereas mice exposed to 15 mg kg-1 MNU were significantly different from controls. These results suggest that even as early as 2 weeks of age protein and lipid metabolism are adversely affected in mice exposed to the higher dose of the alkylating agent at a critical time in retinal development, but general protein and lipid synthesis is not affected in animals exposed to 1 mg kg-1 MNU at least up to 12 weeks of age. These studies suggest further investigation of more subtle derangement in the retinal function in animals exposed to low levels of MNU. JF - Experimental eye research AU - Smith, S B AU - O'Brien, P J AD - Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, Bethesda, Md 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 713 EP - 725 VL - 47 IS - 5 SN - 0014-4835, 0014-4835 KW - Eye Proteins KW - 0 KW - Phospholipids KW - Methylnitrosourea KW - 684-93-5 KW - Leucine KW - GMW67QNF9C KW - Glycerol KW - PDC6A3C0OX KW - Index Medicus KW - Rod Cell Outer Segment -- metabolism KW - Animals KW - Glycerol -- metabolism KW - Leucine -- metabolism KW - Mice KW - Rod Cell Outer Segment -- drug effects KW - Female KW - Retinal Degeneration -- chemically induced KW - Pregnancy KW - Retina -- metabolism KW - Maternal-Fetal Exchange KW - Retina -- drug effects KW - Methylnitrosourea -- administration & dosage KW - Methylnitrosourea -- pharmacology KW - Eye Proteins -- biosynthesis KW - Phospholipids -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78575110?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+eye+research&rft.atitle=Biochemical+characterization+of+retinal+protein+and+phospholipid+synthesis+in+mice+exposed+transplacentally+to+N-methyl-N-nitrosourea.&rft.au=Smith%2C+S+B%3BO%27Brien%2C+P+J&rft.aulast=Smith&rft.aufirst=S&rft.date=1988-11-01&rft.volume=47&rft.issue=5&rft.spage=713&rft.isbn=&rft.btitle=&rft.title=Experimental+eye+research&rft.issn=00144835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-25 N1 - Date created - 1989-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - MPTP and MPTP analogs induced cell death in cultured rat hepatocytes involving the formation of pyridinium metabolites. AN - 78551743; 3143167 AB - MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) which has been shown to produce a Parkinson-like syndrome in humans and monkeys also causes cell death in cultures of rat hepatocytes. Treatment of cells with MPTP or its metabolite MPP+ (1-methyl-4-phenyl pyridinium ion), resulted in leakage of lactic acid dehydrogenase and 14C-labeled adenine nucleotides, as well as marked depletion of ATP and glutathione. Deprenyl, a specific inhibitor of monoamine oxidase-B, the enzyme catalyzing the oxidation of MPTP into MPP+, blocked the lethal effect of MPTP, but gave no protection from MPP+-induced cell death. The 4'-fluoro and 4'-chloro analogs of MPTP evoked toxicities similar to that of the parent compound, while N-butyl-PTP, 4'-amino-MPTP, and 2'-methyl-MPTP were relatively less toxic. N-Acetylamino-MPTP was found virtually nontoxic. The cell death produced by these analogs was also associated with leakage of [14C]adenine nucleotides, which is an indicator of loss of ATP from cells. All these compounds except the N-acetylamino analog were converted to corresponding pyridinium metabolites by liver cells when analyzed by high-pressure liquid chromatography and plasma desorption mass spectrometry. MPTP and its analogs also served as substrates for rat liver mitochondrial monoamine oxidase to varying degrees. Toxicity of various analogs, with the noticeable exception of 2'-methyl-MPTP, was inhibited by deprenyl. These findings indicate that the conversion of MPTP and its analogs to corresponding pyridinium metabolites is essential for the expression of toxicity. JF - Toxicology and applied pharmacology AU - Singh, Y AU - Swanson, E AU - Sokoloski, E AU - Kutty, R K AU - Krishna, G AD - Section on Drug Tissue Interaction, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 347 EP - 359 VL - 96 IS - 2 SN - 0041-008X, 0041-008X KW - Pyridines KW - 0 KW - Pyridinium Compounds KW - Selegiline KW - 2K1V7GP655 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Glutathione KW - GAN16C9B8O KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Selegiline -- pharmacology KW - Cell Survival -- drug effects KW - Glutathione -- metabolism KW - Adenosine Triphosphate -- metabolism KW - Male KW - Pyridinium Compounds -- metabolism KW - Liver -- drug effects KW - Pyridines -- toxicity KW - Liver -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78551743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+MPTP+analogs+induced+cell+death+in+cultured+rat+hepatocytes+involving+the+formation+of+pyridinium+metabolites.&rft.au=Singh%2C+Y%3BSwanson%2C+E%3BSokoloski%2C+E%3BKutty%2C+R+K%3BKrishna%2C+G&rft.aulast=Singh&rft.aufirst=Y&rft.date=1988-11-01&rft.volume=96&rft.issue=2&rft.spage=347&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 - 1989-01-09 N1 - Date created - 1989-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dissimilar peptide growth factors can induce normal human mesothelial cell multiplication. AN - 78536875; 2461356 AB - Quiescent normal human mesothelial (NHM) cells will undergo one round of DNA synthesis when they are incubated in a defined medium consisting of LHC basal medium supplemented with hydrocortisone, insulin, transferrin, and one of the following peptide mitogens: epidermal growth factor; transforming growth factor beta (1 or 2); platelet derived growth factor (a,b heterodimer or b,b homodimer); fibroblast growth factor (acid or basic forms); interleukin 1 (alpha or beta forms); interleukin 2; interferon gamma; interferon beta; or cholera toxin. However, sustained cell multiplication does not occur unless the medium contains hydrocortisone, insulin, transferrin, any one of the above-listed peptide growth factors and high density lipoproteins. Growth can be increased twofold if the medium contains certain combinations of these mitogens and high density lipoproteins. The finding that NHM cells can respond to a broad spectrum of growth factors supports the possibility that an autocrine mechanism may be part of the mechanism that leads to transformation of these cells by asbestos. JF - In vitro cellular & developmental biology : journal of the Tissue Culture Association AU - Laveck, M A AU - Somers, A N AU - Moore, L L AU - Gerwin, B I AU - Lechner, J F AD - Division of Cancer Etiology, NCI, Bethesda, Maryland 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1077 EP - 1084 VL - 24 IS - 11 SN - 0883-8364, 0883-8364 KW - Culture Media KW - 0 KW - Growth Substances KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Keratins -- physiology KW - Cells, Cultured KW - Humans KW - Protein Denaturation KW - Cell Division -- drug effects KW - Drug Synergism KW - Structure-Activity Relationship KW - Cell Adhesion KW - Growth Substances -- pharmacology KW - Mesoderm -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78536875?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dissimilar+peptide+growth+factors+can+induce+normal+human+mesothelial+cell+multiplication.&rft.au=Laveck%2C+M+A%3BSomers%2C+A+N%3BMoore%2C+L+L%3BGerwin%2C+B+I%3BLechner%2C+J+F&rft.aulast=Laveck&rft.aufirst=M&rft.date=1988-11-01&rft.volume=24&rft.issue=11&rft.spage=1077&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 - 1989-01-11 N1 - Date created - 1989-01-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dexamethasone accelerates differentiation of A6 epithelia and increases response to vasopressin. AN - 78534709; 3189533 AB - When seeded heavily on a porous tissue culture dish, A6 cells, derived from the kidney of Xenopus laevis, form a highly differentiated epithelium within 4-6 days. When dexamethasone is added to the culture medium, morphological differentiation is completed by day 2, a time at which the control (untreated) is still a disorganized multilayer of cells. In addition to the morphologically evident monolayer of cuboidal cells, the accelerated differentiation is expressed as high transepithelial electrical resistance, short-circuit current, and adenylate cyclase response to vasopressin. When grown on impermeable plastic tissue culture dishes, A6 epithelia are less differentiated and do not respond to vasopressin. With the addition of dexamethasone at the time of seeding on a plastic tissue culture dish, vasopressin responsive adenylate cyclase activity is expressed, albeit at a slower rate than when grown on a porous surface. In addition, dexamethasone treatment of mature epithelia grown on a porous surface results, in hours, in an increase in the adenylate cyclase response to vasopressin. These results reveal two previously unrecognized interactions between adrenal steroid hormones and vasopressin, namely, accelerated differentiation and increased responsiveness of adenylate cyclase. JF - The American journal of physiology AU - Preston, A S AU - Muller, J AU - Handler, J S AD - Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - C661 EP - C666 VL - 255 IS - 5 Pt 1 SN - 0002-9513, 0002-9513 KW - Vasopressins KW - 11000-17-2 KW - Dexamethasone KW - 7S5I7G3JQL KW - Index Medicus KW - Stimulation, Chemical KW - Xenopus laevis KW - Animals KW - Epithelial Cells KW - In Vitro Techniques KW - Drug Synergism KW - Epithelium -- drug effects KW - Cell Line KW - Dexamethasone -- pharmacology KW - Kidney -- drug effects KW - Kidney -- cytology KW - Vasopressins -- pharmacology KW - Cell Differentiation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78534709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dexamethasone+accelerates+differentiation+of+A6+epithelia+and+increases+response+to+vasopressin.&rft.au=Preston%2C+A+S%3BMuller%2C+J%3BHandler%2C+J+S&rft.aulast=Preston&rft.aufirst=A&rft.date=1988-11-01&rft.volume=255&rft.issue=5+Pt+1&rft.spage=C661&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 - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Demonstration of sub-nanomolar affinity of bryostatin 1 for the phorbol ester receptor in rat brain. AN - 78530982; 3190746 AB - The effect of bryostatin 1 on [26-3H]phorbol 12,13-dibutyrate [( 3H]PDBu) binding to a washed particulate preparation from rat brain was examined. Bryostatin 1 inhibited phorbol ester binding at concentrations considerably lower than previously reported. As would be expected for a ligand of high affinity, the apparent displacing potency of bryostatin 1 was dependent on the concentration of tissue/binding sites included in the assay. Decreasing the concentration of [3H]PDBu binding sites to the picomolar detection limit resulted in apparent bryostatin displacing potencies in the picomolar range with these values representing an upper estimate of the true affinity. When included in saturation studies with [3H]PDBu, bryostatin 1 displayed mixed competitive/non-competitive inhibition. Using either repetitive washing or dialysis of the membrane preparation, it was not possible to reverse the inhibition produced by bryostatin 1. The greater affinity of bryostatin 1 compared to other classes of agents that act directly on protein kinase C and the stability of its association may contribute to the unique biological properties of the bryostatins. JF - Biochemical pharmacology AU - de Vries, D J AU - Herald, C L AU - Pettit, G R AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11/01/ PY - 1988 DA - 1988 Nov 01 SP - 4069 EP - 4073 VL - 37 IS - 21 SN - 0006-2952, 0006-2952 KW - Bryostatins KW - 0 KW - Caenorhabditis elegans Proteins KW - Carrier Proteins KW - Lactones KW - Macrolides KW - Phorbol Esters KW - Receptors, Drug KW - phorbol ester binding protein KW - phorbol ester receptor KW - bryostatin 1 KW - 37O2X55Y9E KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Rats KW - Animals KW - Phorbol Esters -- metabolism KW - Kinetics KW - Binding, Competitive KW - Protein Kinase C -- metabolism KW - Receptors, Drug -- metabolism KW - Brain -- metabolism KW - Lactones -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78530982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+psychiatry&rft.atitle=Mood+changes+associated+with+reproductive+life+events%3A+an+overview+of+research+and+treatment+strategies.&rft.au=Blumenthal%2C+S+J%3BNadelson%2C+C+C&rft.aulast=Blumenthal&rft.aufirst=S&rft.date=1988-12-01&rft.volume=49&rft.issue=12&rft.spage=466&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+psychiatry&rft.issn=01606689&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-15 N1 - Date created - 1988-12-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Racial differences in bladder cancer risk: a case-control study. AN - 78526784; 3189279 AB - To determine why the incidence rate of transitional cell bladder cancer in whites in the United States is approximately twice that in blacks, the authors examined data from a large population-based case-control study of bladder cancer conducted in 1978 involving 2,982 cases and 5,782 controls. The relative risk of transitional cell carcinoma for whites compared with blacks was 1.9 before adjustment for the major bladder cancer risk factors, whereas after adjustment for cigarette smoking and occupation it was 1.6 (95% confidence interval (CI): 1.3-2.1). Further adjustment for other risk factors, including history of a bladder infection and a family history of urinary tract cancer, did not alter this estimate. The elevated risk of white compared with blacks was limited, however, to cases whose disease was confined to the mucosa and submucosa. Among cases whose disease had extended to the bladder musculature or beyond, whites were at slightly reduced risk compared with blacks. This suggests that whites may be diagnosed with conditions that go undetected in blacks but that are unlikely as a group to progress to more extensive disease. Because of the population-based nature of the study, it was possible to determine that if bladder cancer incidence among whites of both sexes was reduced to the level among blacks, total incidence in the United States would fall by 36 per cent. JF - American journal of epidemiology AU - Schairer, C AU - Hartge, P AU - Hoover, R N AU - Silverman, D T AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1027 EP - 1037 VL - 128 IS - 5 SN - 0002-9262, 0002-9262 KW - Index Medicus KW - United States KW - Occupational Diseases -- ethnology KW - Age Factors KW - Carcinoma, Transitional Cell -- diagnosis KW - Sex Factors KW - Epidemiologic Methods KW - Humans KW - Carcinoma, Transitional Cell -- ethnology KW - Smoking -- adverse effects KW - Aged KW - Aged, 80 and over KW - Risk Factors KW - Adult KW - Carcinoma, Transitional Cell -- mortality KW - Middle Aged KW - Female KW - Male KW - Urinary Bladder Neoplasms -- diagnosis KW - Urinary Bladder Neoplasms -- mortality KW - Urinary Bladder Neoplasms -- ethnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78526784?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Racial+differences+in+bladder+cancer+risk%3A+a+case-control+study.&rft.au=Schairer%2C+C%3BHartge%2C+P%3BHoover%2C+R+N%3BSilverman%2C+D+T&rft.aulast=Schairer&rft.aufirst=C&rft.date=1988-11-01&rft.volume=128&rft.issue=5&rft.spage=1027&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 - 1988-11-28 N1 - Date created - 1988-11-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-nitrosocimetidine as a modifier of chemically-initiated tumors in mice. AN - 78525779; 3142678 AB - N-Nitrosocimetidine (NCM) is a nitrosation product of cimetidine, a commonly-prescribed pharmaceutical agent. In spite of its known genotoxicity, NCM has failed to cause tumors in assays with rats and mice, but has given indications of enhancing or suppressive effects on tumor development. This possibility was tested by administering NCM topically to the skin or in the drinking water to mice in which tumors had been initiated by treatment with chemical carcinogens. Sencar mouse skin papillomas initiated by 7,12-dimethylbenzanthracene (DMBA) and promoted by 12-O-decanoylphorbol-13-acetate (TPA), progressed more rapidly to carcinoma on mice given treatment during stage 3 (after TPA) with NCM (1 mg/week) or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG, 120 micrograms/week) [corrected] than on stage 3 acetone controls. Oral NCM (1 g/l drinking water) did not have this effect but rather suppressed development of keratoacanthomas, as did stage 3 MNNG or TPA. Primary lung tumors initiated in BALB/c mice by i.p. injection of urethane; and tumors of forestomach, lung, mammary, lymphoid and skin tissues caused in (C57BL/6 X DBA/2)F1 mice by oral DMBA were not markedly affected by NCM given in drinking water (1000-1800 ppm) until 14-16 months of age. These results confirm NCM's general lack of activity as an in vivo toxicant, but show that under certain circumstances it may enhance or suppress tumor development. JF - Cancer letters AU - Anderson, L M AU - Hagiwara, A AU - Giner-Sorolla, A AU - Kovatch, R M AU - Rehm, S AU - Riggs, C W AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21701. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 159 EP - 167 VL - 42 IS - 3 SN - 0304-3835, 0304-3835 KW - Urethane KW - 3IN71E75Z5 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - nitrosocimetidine KW - 73785-40-7 KW - Cimetidine KW - 80061L1WGD KW - Index Medicus KW - Animals KW - Cocarcinogenesis KW - Skin Neoplasms -- chemically induced KW - Mice KW - Lung Neoplasms -- chemically induced KW - Neoplasms, Experimental -- chemically induced KW - Cimetidine -- pharmacology KW - Cimetidine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78525779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=N-nitrosocimetidine+as+a+modifier+of+chemically-initiated+tumors+in+mice.&rft.au=Anderson%2C+L+M%3BHagiwara%2C+A%3BGiner-Sorolla%2C+A%3BKovatch%2C+R+M%3BRehm%2C+S%3BRiggs%2C+C+W%3BRice%2C+J+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1988-11-01&rft.volume=42&rft.issue=3&rft.spage=159&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 - 1988-12-28 N1 - Date created - 1988-12-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Cancer Lett 1989 Mar;44(3):233 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Assessment of the potential for surveillance of alcohol-related casualties using National Hospital Discharge Survey data. AN - 78522092; 3141953 AB - It is well known that alcohol abuse is significantly involved in the incidence of casualties (that is, accidents and injuries as they are defined for the purpose of coding diagnoses in the International Classification of Diseases). Thus, a study was conducted of the feasibility of using data from the National Hospital Discharge Survey (NHDS) for the surveillance of alcohol-related casualties. Trends were analyzed over 7 years (1979-85), and results were discussed from three aspects: number and rates for comorbidity of injuries and accidents with alcohol-related diagnoses, percent of alcohol involvement for injuries and accidents, and proportionate morbidity for alcohol-related and nonalcohol-related injuries and accidents. The incidence of comorbidity and percent of alcohol involvement were found to be relatively low for both accidents and injuries--underreporting being a likely cause. Comorbidity rates over the 7-year period showed no major trends in the rates for injuries that were associated with alcohol use, but the rates for accidents that were associated with alcohol use increased in all but one of the years. Proportionate morbidity as reflected in hospital discharge records with alcohol-related diagnoses showed only small differences by sex and age group (except the 14 to 25 years group) for either injuries or accidents. Only the 25- to 44-year-old group showed a time-trend increase, and that is only for the accident category. For these reasons, we have concluded that data from the NHDS are not currently adequate for use in the surveillance of alcohol-related injuries and accidents. JF - Public health reports (Washington, D.C. : 1974) AU - Towle, L H AU - Stinson, F S AU - Dufour, M AD - NIAAA, Rockville, MD 20857. PY - 1988 SP - 597 EP - 605 VL - 103 IS - 6 SN - 0033-3549, 0033-3549 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Feasibility Studies KW - Humans KW - Alcoholic Intoxication KW - Adult KW - Aged KW - Middle Aged KW - Data Collection KW - Adolescent KW - Male KW - Female KW - Population Surveillance KW - Accidents -- statistics & numerical data KW - Alcoholism -- epidemiology KW - Wounds and Injuries -- etiology KW - Patient Discharge KW - Wounds and Injuries -- diagnosis KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78522092?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Assessment+of+the+potential+for+surveillance+of+alcohol-related+casualties+using+National+Hospital+Discharge+Survey+data.&rft.au=Towle%2C+L+H%3BStinson%2C+F+S%3BDufour%2C+M&rft.aulast=Towle&rft.aufirst=L&rft.date=1988-11-01&rft.volume=103&rft.issue=6&rft.spage=597&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 - 1988-12-12 N1 - Date created - 1988-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Point mutants of Moloney murine leukemia virus that fail to package viral RNA: evidence for specific RNA recognition by a "zinc finger-like" protein sequence. AN - 78519018; 3141927 AB - All retroviruses encode a nucleic acid-binding or nucleocapsid protein that is believed to be associated with RNA in the virion. Further, all retroviral nucleocapsid proteins contain either one or two copies of the sequence Cys-Xaa2-Cys-Xaa4-His-Xaa4-Cys. The conservation of this sequence suggested that it is important for virus replication, and its resemblance to the "zinc-finger" sequences found in eukaryotic transcription factors raised the possibility that it recognizes specific sequences in viral RNA during retrovirus assembly. We used oligonucleotide-directed mutagenesis to generate a series of mutations in the nucleocapsid protein-coding region of Moloney murine leukemia virus. These mutations changed single amino acids, including each of the cysteines, to serine. The mutant viral genomes direct the synthesis of virus particles; these particles lack detectable viral RNA but do contain significant levels of cellular RNAs. Thus it appears that the mutations have destroyed the ability of the viral proteins to specifically package viral RNA during virus assembly. We propose that the conserved sequence in retroviral nucleocapsid proteins functions in RNA sequence recognition and suggest that it is evolutionarily related to the zinc fingers that recognize specific sequences in double-stranded DNA. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Gorelick, R J AU - Henderson, L E AU - Hanser, J P AU - Rein, A AD - Laboratory of Molecular Virology and Carcinogenesis, National Cancer Institute-Frederick Cancer Research Facility 21701. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 8420 EP - 8424 VL - 85 IS - 22 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - Gene Products, gag KW - Metalloproteins KW - RNA, Viral KW - Retroviridae Proteins KW - Index Medicus KW - Immunoblotting KW - Animals KW - Transfection KW - Retroviridae Proteins -- genetics KW - Molecular Sequence Data KW - Genes, Viral KW - Amino Acid Sequence KW - Nucleic Acid Hybridization KW - Cell Line KW - DNA-Binding Proteins -- genetics KW - Moloney murine leukemia virus -- genetics KW - RNA, Viral -- genetics KW - Metalloproteins -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78519018?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Point+mutants+of+Moloney+murine+leukemia+virus+that+fail+to+package+viral+RNA%3A+evidence+for+specific+RNA+recognition+by+a+%22zinc+finger-like%22+protein+sequence.&rft.au=Gorelick%2C+R+J%3BHenderson%2C+L+E%3BHanser%2C+J+P%3BRein%2C+A&rft.aulast=Gorelick&rft.aufirst=R&rft.date=1988-11-01&rft.volume=85&rft.issue=22&rft.spage=8420&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 - 1988-12-22 N1 - Date created - 1988-12-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochim Biophys Acta. 1987 Jul 8;907(2):93-123 [3036230] J Virol. 1987 May;61(5):1639-46 [3502707] Mol Cell Biol. 1988 Apr;8(4):1684-96 [2837652] J Exp Med. 1954 Feb;99(2):167-82 [13130792] Virology. 1987 Oct;160(2):518-22 [3660592] Cell. 1987 Dec 24;51(6):1079-90 [3319186] J Biol Chem. 1988 Feb 15;263(5):2140-5 [2828360] Methods Enzymol. 1987;153:3-11 [3323803] Mol Cell Biol. 1987 Dec;7(12):4582-4 [3437898] Cell. 1988 Jan 15;52(1):1-3 [3125980] Nature. 1971 Feb 19;229(5286):564-6 [4925356] J Gen Virol. 1971 Nov;13(2):245-52 [4333712] J Virol. 1976 May;18(2):709-18 [58075] Virology. 1976 Jul 15;72(2):523-6 [181914] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Virol. 1978 Apr;26(1):54-60 [650738] Cell. 1978 Dec;15(4):1371-81 [83199] J Virol. 1979 Feb;29(2):494-500 [219244] J Virol. 1979 Sep;31(3):741-51 [92571] J Virol. 1980 Mar;33(3):983-92 [6154154] Virology. 1980 Jul 30;104(2):491-6 [6249039] J Virol. 1980 Nov;36(2):450-6 [6253670] Proc Natl Acad Sci U S A. 1980 Sep;77(9):5201-5 [6159641] Proc Natl Acad Sci U S A. 1981 Jan;78(1):177-81 [7017709] J Biol Chem. 1981 Aug 25;256(16):8400-6 [6267042] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Virology. 1982 Jul 15;120(1):251-7 [6285602] J Virol. 1983 Dec;48(3):667-75 [6313966] J Biol Chem. 1983 Dec 10;258(23):14120-5 [6196359] Cell. 1983 May;33(1):153-9 [6678608] Mol Cell Biol. 1984 Aug;4(8):1577-82 [6092920] Curr Top Microbiol Immunol. 1985;115:221-33 [2983943] EMBO J. 1985 Jun;4(6):1609-14 [4040853] Nucleic Acids Res. 1986 Jan 24;14(2):623-33 [2418414] Science. 1986 Apr 25;232(4749):485-7 [2421409] Proc Natl Acad Sci U S A. 1986 Oct;83(19):7246-50 [3489936] J Virol. 1986 Nov;60(2):450-9 [2430109] Nature. 1987 Jan 1-7;325(6099):75-8 [3025750] J Biol Chem. 1987 Apr 15;262(11):4961-7 [2435721] Nature. 1987 Jul 23-29;328(6128):353-5 [3299106] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcohol-related birth defects: an update. AN - 78518694; 3141958 AB - Historically, mankind has at least suspected that alcohol was somehow connected with undesirable effects on progeny. In the 18th century, physicians became aware that maternal alcohol consumption resulted in excess fetal and neonatal mortality, low birth weight, and many other deleterious effects. Perhaps as a response to the temperance and Prohibition periods, scientists lost sight of or interest in the effects of alcohol in pregnancy. In the late 1960s and early 1970s, the issue surfaced again, and scientists began systematic and in-depth studies of fetal alcohol syndrome (FAS) and alcohol-related birth defects (ARBD). Epidemiologic research now suggests that FAS has outranked Down's syndrome and spina bifida in prevalence and is now the leading known cause of mental retardation. Further, it is the only one of these three that is preventable. Because a safe limit of alcohol consumption in pregnancy is not defined, abstinence during pregnancy is the most prudent preventive measure. Factors such as race, beer drinking, maternal weight gain, and low socioeconomic status are associated with a statistical increase in the incidence of FAS. In families where one child has been diagnosed as having FAS, the incidence rate can be as much as 405-fold higher than the worldwide average. Neurobehavioral deficits can occur in the offspring of drinking mothers in the absence of a diagnosis of full FAS. The deficits differ with age and seem to persist into adulthood. Mental retardation or borderline mental retardation is a nearly ubiquitous neurological deficit in diagnosed FAS. In one study, it occurred in 75 percent of the non-FAS offspring of mothers who continued to drink heavily throughout their pregnancy.From the mid-1970s, having established that alcohol is a teratogen, scientists have been trying to uncover the mechanism by which alcohol exerts its embryotoxic effects. Recent promising neuroanatomical studies have demonstrated that alcohol has a deleterious effect on neuronal migration and hence on the development of the cerebral cortex. Other studies have shown that prenatal alcohol exposure,by adversely affecting hippocampal development,may be responsible for the learning deficits so frequently encountered in FAS children. Other research has implicated prostaglandins in the mechanism of alcohol-related dysmorphology. JF - Public health reports (Washington, D.C. : 1974) AU - Warren, K R AU - Bast, R J AD - Office of Scientific Affairs, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. PY - 1988 SP - 638 EP - 642 VL - 103 IS - 6 SN - 0033-3549, 0033-3549 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Maternal-Fetal Exchange KW - Intelligence KW - Intellectual Disability -- chemically induced KW - Humans KW - Infant, Newborn KW - Infant Mortality KW - Female KW - Pregnancy KW - Fetal Alcohol Spectrum Disorders -- psychology KW - Fetal Alcohol Spectrum Disorders -- prevention & control KW - Abnormalities, Drug-Induced -- etiology KW - Fetal Alcohol Spectrum Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78518694?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alcohol-related+birth+defects%3A+an+update.&rft.au=Warren%2C+K+R%3BBast%2C+R+J&rft.aulast=Warren&rft.aufirst=K&rft.date=1988-11-01&rft.volume=103&rft.issue=6&rft.spage=638&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 - 1988-12-12 N1 - Date created - 1988-12-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Bull Acad Natl Med. 1967 Oct 17;151(25):517-21 [4906705] Alcohol Clin Exp Res. 1988 Jun;12(3):440-9 [3044177] N Engl J Med. 1978 May 11;298(19):1063-7 [347295] Alcohol Clin Exp Res. 1980 Apr;4(2):119-22 [6990814] Brain Res. 1981 Jun;227(3):333-40 [7260643] Science. 1981 Nov 13;214(4522):817-9 [7292015] Neurobehav Toxicol Teratol. 1983 Jan-Feb;5(1):139-50 [6856003] Science. 1984 Jul 6;225(4657):80-2 [6729469] Alcohol Clin Exp Res. 1984 Nov-Dec;8(6):513-5 [6393800] Brain Res. 1985 Jan;349(1-2):280-4 [3986593] Soc Biol. 1983 Winter;30(4):374-87 [6336013] Am J Obstet Gynecol. 1987 Jan;156(1):33-9 [3799767] Ann N Y Acad Sci. 1986;477:87-102 [3468841] Drug Alcohol Depend. 1987 Jan;19(1):51-70 [3545731] CMAJ. 1987 Aug 1;137(3):203-7 [3607663] Pediatrician. 1987;14(1-2):51-6 [3615301] Pediatrician. 1987;14(1-2):57-61 [3615302] Adv Alcohol Subst Abuse. 1987 Summer;6(4):87-104 [3425480] Neurotoxicol Teratol. 1988 Jan-Feb;10(1):1-2 [3352564] J Stud Alcohol. 1975 Nov;36(11):1395-420 [545] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulation of arachidonic acid release and inhibition of mitogenesis by cloned genes for muscarinic receptor subtypes stably expressed in A9 L cells. AN - 78518683; 2847172 AB - A family of genes encoding four distinct muscarinic receptors (designated m1-m4) has been cloned and stably expressed in A9 L cells. When the m1 and m3 receptors were stimulated with carbachol, there was a rapid rise of liberated arachidonic acid, inositol phosphates, and cAMP, while m2 and m4 receptor stimulation had no detectable stimulation of these second messengers. Pretreatment with phorbol 12-myristate 13-acetate (PMA) caused a marked acceleration and amplification of m1 and m3 receptor-mediated arachidonic acid release. In contrast, m1- and m3-mediated inositol phosphate formation was inhibited by the same PMA pretreatment. Arachidonic acid release was unaffected by manipulations of cAMP levels. Arachidonic acid production was inhibited by calcium-free medium and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8; an inhibitor of cytosolic calcium mobilization) yet was unaffected by verapamil, a calcium-channel blocker. These experiments show that arachidonic acid release induced by the m1 and m3 receptors is regulated independently of phospholipase C and cAMP accumulation. Carbachol stimulation of the m1 and m3 cAMP accumulation. Carbachol stimulation of the m1 and m3 receptors also markedly decreased mitogenesis as measured by thymidine incorporation. The m1 receptor-mediated inhibition of mitogenesis could be partially blocked by indomethacin, a cyclooxygenase inhibitor. The inhibition of mitogenesis could be mimicked by cAMP elevation. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Conklin, B R AU - Brann, M R AU - Buckley, N J AU - Ma, A L AU - Bonner, T I AU - Axelrod, J AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 8698 EP - 8702 VL - 85 IS - 22 SN - 0027-8424, 0027-8424 KW - Arachidonic Acids KW - 0 KW - Receptors, Muscarinic KW - Arachidonic Acid KW - 27YG812J1I KW - Atropine KW - 7C0697DR9I KW - Carbachol KW - 8Y164V895Y KW - Cyclic AMP KW - E0399OZS9N KW - Type C Phospholipases KW - EC 3.1.4.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - L Cells (Cell Line) -- drug effects KW - L Cells (Cell Line) -- metabolism KW - Enzyme Activation KW - Mice KW - Calcium -- pharmacology KW - Cyclic AMP -- physiology KW - Type C Phospholipases -- metabolism KW - L Cells (Cell Line) -- cytology KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Atropine -- pharmacology KW - Carbachol -- pharmacology KW - Cell Division KW - Receptors, Muscarinic -- genetics KW - Genes KW - Arachidonic Acids -- metabolism KW - Receptors, Muscarinic -- physiology KW - Cloning, Molecular UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78518683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Stimulation+of+arachidonic+acid+release+and+inhibition+of+mitogenesis+by+cloned+genes+for+muscarinic+receptor+subtypes+stably+expressed+in+A9+L+cells.&rft.au=Conklin%2C+B+R%3BBrann%2C+M+R%3BBuckley%2C+N+J%3BMa%2C+A+L%3BBonner%2C+T+I%3BAxelrod%2C+J&rft.aulast=Conklin&rft.aufirst=B&rft.date=1988-11-01&rft.volume=85&rft.issue=22&rft.spage=8698&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 - 1988-12-22 N1 - Date created - 1988-12-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Pharmacol. 1975 Feb;53(2):279-85 [1148488] FEBS Lett. 1988 Jul 18;234(2):283-6 [3391275] Annu Rev Biochem. 1978;47:997-1029 [209733] Endocrinology. 1979 Oct;105(4):988-95 [383470] Nature. 1980 Jan 3;283(5742):90-2 [7350532] Proc Natl Acad Sci U S A. 1980 Jun;77(6):3292-6 [6158043] Biochem J. 1983 May 15;212(2):473-82 [6309146] Biochem Biophys Res Commun. 1984 Sep 17;123(2):703-9 [6593069] Biochem Biophys Res Commun. 1985 Feb 28;127(1):310-7 [2983712] J Biol Chem. 1985 May 10;260(9):5236-9 [2985584] J Biol Chem. 1986 Mar 5;261(7):3428-33 [3081504] J Biol Chem. 1986 Mar 15;261(8):3501-11 [3081507] Science. 1986 Apr 4;232(4746):97-100 [3006254] J Biol Chem. 1986 Jul 5;261(19):8667-73 [3013859] Prostaglandins. 1986 May;31(5):973-87 [3088679] Science. 1986 Jul 18;233(4761):305-12 [3014651] J Biol Chem. 1986 Aug 25;261(24):11236-41 [2874145] Proc Natl Acad Sci U S A. 1986 Sep;83(18):6785-9 [3462727] Science. 1986 Oct 10;234(4773):161-6 [3018928] Nature. 1986 Oct 2-8;323(6087):411-6 [3762692] Proc Natl Acad Sci U S A. 1986 Oct;83(19):7201-5 [3020540] Mol Pharmacol. 1988 Oct;34(4):421-6 [3173332] Trends Neurosci. 1988 Mar;11(3):117-23 [2465609] Neuron. 1988 Jul;1(5):403-10 [3272174] Pharmacol Rev. 1986 Sep;38(3):227-72 [3022313] FEBS Lett. 1986 Dec 15;209(2):367-72 [3792556] J Biol Chem. 1987 Mar 25;262(9):4200-7 [3031065] Annu Rev Neurosci. 1987;10:195-236 [2436543] Science. 1987 May 1;236(4801):600-5 [3107123] Biochem Biophys Res Commun. 1987 Apr 29;144(2):683-91 [3107559] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3623-7 [3108876] Science. 1987 Jul 31;237(4814):527-32 [3037705] Annu Rev Biochem. 1987;56:159-93 [3304132] Proc Natl Acad Sci U S A. 1987 Sep;84(18):6374-8 [2888113] Mol Pharmacol. 1987 Oct;32(4):450-5 [2444870] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] Science. 1987 Oct 30;238(4827):672-5 [2823384] FEBS Lett. 1988 Mar 28;230(1-2):90-4 [3350153] J Biol Chem. 1988 Apr 5;263(10):4764-7 [3162455] Brain Res. 1988 Jan 26;439(1-2):122-6 [3359178] J Biol Chem. 1988 Jun 5;263(16):7610-9 [2836390] Proc Natl Acad Sci U S A. 1988 Jun;85(11):4056-60 [2453885] Exp Cell Res. 1977 Mar 1;105(1):99-108 [556995] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An overview of prevention research: issues, answers, and new agendas. AN - 78518323; 3141964 AB - Efforts to curtail alcohol abuse and alcoholism can be divided into primary, secondary, and tertiary prevention. Primary prevention attempts to stop a problem or illness from occurring in the first place. Secondary prevention identifies persons in the early stages of problematic or illness behavior and refers them for counseling or treatment, which is considered tertiary prevention. Five research areas concerned with primary and secondary prevention are selected for discussion: youth, the mass media, the worksite, blacks and Hispanics, and alcohol-related behavior that increases the risk of AIDS. Several of these themes have been in the forefront of alcohol prevention research; others such as AIDS are emergent areas of injury. The discussion to follow briefly summarizes research approaches, key findings, methodological shortcomings, and suggested issues for future investigation. Although scientifically solid prevention studies have been conducted, more rigorous, more comprehensive, and more innovative research is needed. Given the dynamic sociocultural and economic systems in which prevention occurs, research techniques that can address this complexity are required. A range of appropriate methodologies is described. JF - Public health reports (Washington, D.C. : 1974) AU - Howard, J AU - Taylor, J A AU - Ganikos, M L AU - Holder, H D AU - Godwin, D F AU - Taylor, E D AD - Prevention Research Branch, National Institute on Alcohol Abuse and Alcoholism, (NIAAA), Rockville, MD 20857. PY - 1988 SP - 674 EP - 683 VL - 103 IS - 6 SN - 0033-3549, 0033-3549 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Primary Prevention KW - Humans KW - Adult KW - Sick Role KW - Adolescent KW - Research Design KW - Mass Media KW - Alcoholic Intoxication -- prevention & control KW - Alcoholism -- ethnology KW - Alcoholism -- psychology KW - Alcoholism -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78518323?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=An+overview+of+prevention+research%3A+issues%2C+answers%2C+and+new+agendas.&rft.au=Howard%2C+J%3BTaylor%2C+J+A%3BGanikos%2C+M+L%3BHolder%2C+H+D%3BGodwin%2C+D+F%3BTaylor%2C+E+D&rft.aulast=Howard&rft.aufirst=J&rft.date=1988-11-01&rft.volume=103&rft.issue=6&rft.spage=674&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 - 1988-12-12 N1 - Date created - 1988-12-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Stud Alcohol. 1976 Mar;37(3):357-64 [4670] Health Educ Q. 1986 Winter;13(4):359-71 [3781860] Psychopharmacology (Berl). 1978 Jun 15;58(1):35-41 [97717] Int J Addict. 1978 May;13(4):605-26 [689785] Addict Behav. 1978;3(2):117-21 [717090] J Appl Behav Anal. 1980 Spring;13(1):149-52 [7364693] J Sch Health. 1980 Apr;50(4):206-8 [6900140] J Appl Behav Sci. 1980 Jul-Sep;16(3):407-22 [10248060] J Stud Alcohol. 1980 Jul;41(7):635-51 [7421253] Int J Rehabil Res. 1980;3(3):395-6 [7451002] J Health Soc Behav. 1981 Dec;22(4):337-56 [7320473] J Stud Alcohol. 1981 Nov;42(11):972-97 [7334808] Addict Behav. 1983;8(2):105-8 [6613708] Int J Addict. 1983 Oct;18(7):937-50 [6642800] J Stud Alcohol. 1983 Nov;44(6):929-37 [6664090] Prev Med. 1984 May;13(3):299-319 [6387698] Alcohol Alcohol. 1984;19(1):31-44 [6497950] J Stud Alcohol. 1984 Sep;45(5):393-404 [6503286] Annu Rev Public Health. 1985;6:147-93 [3873246] Community Ment Health J. 1985 Spring;21(1):42-51 [3995902] J Psychoactive Drugs. 1985 Jul-Sep;17(3):173-8 [4056962] Br J Addict. 1985 Dec;80(4):397-410 [3910073] J Stud Alcohol. 1986 May;47(3):256-8 [3724165] Br J Addict. 1986 Jun;81(3):365-79 [3488753] Ann N Y Acad Sci. 1986;472:46-59 [3026217] J Appl Behav Anal. 1986 Winter;19(4):391-6 [3804872] J Stud Alcohol. 1987 Jan;48(1):52-60 [3821119] Hosp Community Psychiatry. 1987 Feb;38(2):180-3 [3557343] J Stud Alcohol. 1987 Mar;48(2):124-35 [3560948] Br J Addict. 1987 Mar;82(3):219-23 [3471253] Pediatrics. 1987 May;79(5):825-8 [3575041] J Subst Abuse Treat. 1986;3(4):271-4 [3586077] J Consult Clin Psychol. 1987 Jun;55(3):293-300 [3597941] Br J Addict. 1987 Jun;82(6):623-31 [3475101] Adv Alcohol Subst Abuse. 1987 Spring;6(3):1-5 [3661298] Soc Sci Med. 1987;25(8):949-60 [3686122] Am J Public Health. 1988 Apr;78(4):394-410 [3279837] Am J Public Health. 1988 Apr;78(4):460-1 [3348475] Adv Alcohol Subst Abuse. 1987;7(2):73-88 [3448894] Am J Public Health. 1988 Jul;78(7):801-5 [3260081] J Stud Alcohol. 1988 Jul;49(4):299-305 [3050280] South Med J. 1986 Mar;79(3):295-8, 302 [3952539] J Stud Alcohol. 1986 Mar;47(2):156-60 [3713178] J Stud Alcohol. 1986 Jul;47(4):333-40 [3747533] J Adolesc Health Care. 1986 Sep;7(5):320-31 [3759600] Int J Addict. 1986 Apr-May;21(4-5):509-37 [2429935] J Sch Health. 1977 Jan;47(1):38-41 [583783] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Guidelines for clinical protocols for chronic lymphocytic leukemia: recommendations of the National Cancer Institute-sponsored working group. AN - 78518207; 3189311 AB - The National Cancer Institute (NCI)-sponsored Chronic Lymphocytic Leukemia (CLL) Working Group was convened to develop a set of standardized eligibility, response, and toxicity criteria for clinical trials. We recognized the previous efforts in 1967 (published again in 1973 as the report of the Chronic Leukemia-Myeloma Task Force [1] and 1978 of Cancer and Leukemia Group B (CALGB) [2]). We have used these reports for guidance during the current effort. Several noteworthy developments in the past few years have made it necessary to modify the previous guidelines. First, the diagnostic criteria for CLL and its clinical staging have been developed and well defined. Second, although staging systems facilitated entry of comparable and relatively homogeneous groups of patients in clinical trials, the definitions of response (CR) and partial response (PR) were not uniformly adopted from the previous guidelines in the clinical trials (Tables IA, IB); therefore, comparisons of results obtained in different studies became difficult. Third, there has been an improvement in our understanding of the immunology and biology of CLL. Finally, we are witnessing the emergence of several chemotherapy agents that promise impressive activity in CLL (e.g., 2'-deoxycoformycin [3], fludarabine monophosphate [4, 5]), and thereby offer the potential for improving survival time in this disease. To best identify regimens worthy of continued pursuit in large comparative trials, standardized guidelines for evaluation are essential. A number of laboratory investigations are also presented for which scientific interest is high yet relevance remains to be determined; thus, they are presented as companion studies to the clinical trials. This mechanism allows for flexibility in the testing of these questions and for additional ideas in the future without requiring modification of an entire treatment protocol. The following guidelines were developed to be used as a form of standardization for clinical trials, incorporating current technologies, yet remaining relevant to the general hematology/oncology community. Based on the membership of the Working Group, it is expected that these guidelines will serve as the criteria for most clinical trials in the near future. JF - American journal of hematology AU - Cheson, B D AU - Bennett, J M AU - Rai, K R AU - Grever, M R AU - Kay, N E AU - Schiffer, C A AU - Oken, M M AU - Keating, M J AU - Boldt, D H AU - Kempin, S J AD - Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 152 EP - 163 VL - 29 IS - 3 SN - 0361-8609, 0361-8609 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - United States KW - Infection -- etiology KW - Neoplasm Staging KW - Antineoplastic Agents -- standards KW - Humans KW - National Institutes of Health (U.S.) KW - Prognosis KW - Eligibility Determination -- standards KW - Drug Evaluation -- standards KW - Leukemia, B-Cell -- drug therapy KW - Leukemia, B-Cell -- diagnosis KW - Antineoplastic Agents -- adverse effects KW - Leukemia, Lymphocytic, Chronic, B-Cell -- diagnosis KW - Health Planning KW - Leukemia, Lymphocytic, Chronic, B-Cell -- drug therapy KW - Leukemia, Lymphocytic, Chronic, B-Cell -- blood KW - Health Planning Guidelines KW - Clinical Trials as Topic -- standards KW - Leukemia, Lymphocytic, Chronic, B-Cell -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78518207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Guidelines+for+clinical+protocols+for+chronic+lymphocytic+leukemia%3A+recommendations+of+the+National+Cancer+Institute-sponsored+working+group.&rft.au=Cheson%2C+B+D%3BBennett%2C+J+M%3BRai%2C+K+R%3BGrever%2C+M+R%3BKay%2C+N+E%3BSchiffer%2C+C+A%3BOken%2C+M+M%3BKeating%2C+M+J%3BBoldt%2C+D+H%3BKempin%2C+S+J&rft.aulast=Cheson&rft.aufirst=B&rft.date=1988-11-01&rft.volume=29&rft.issue=3&rft.spage=152&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 - 1988-12-12 N1 - Date created - 1988-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of mutagenesis in the Escherichia coli mutator mutD5: role of DNA mismatch repair. AN - 78517700; 3054881 AB - To investigate the mechanisms of spontaneous mutation in the Escherichia coli mutD5 mutator strain, 502 mutations generated in this strain in the N-terminal part of the lacI gene were sequenced (i-d mutations). Since the mutator strength of this strain depends on the medium in which it grows, mutations were analyzed in both minimal medium (moderate mutator activity) and rich medium (high mutator activity). In either case, 95% of all mutations were base substitutions and 5% were single-base deletions. However, the nature and site distribution of the base substitutions differed dramatically for the two conditions. In minimal medium (mutation frequency, 480-fold above background), a majority (62%) were transversions, notably A.T----T.A at three 5'-GTGG-3' sequences. Most (64%) of the transitions under this condition occurred at specific sequences that are suggestive of a "dislocation" type of mutagenesis. In rich medium (mutation frequency, 37,000-fold above background), 90% of the base substitutions were transitions. These observations suggest that different modes of mutagenesis operate under the two conditions. mutD5 cells have been reported to be defective in exonucleolytic proofreading during DNA replication. The present data suggest that mutD cells in rich medium also suffer a defect in mutHLS-encoded mismatch correction. This hypothesis was confirmed by the direct measurement of mismatch repair in mutD5 cells by transfection of M13mp2 heteroduplex DNA. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Schaaper, R M AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 8126 EP - 8130 VL - 85 IS - 21 SN - 0027-8424, 0027-8424 KW - DNA, Bacterial KW - 0 KW - Index Medicus KW - Computer Simulation KW - Transfection KW - Mutation KW - DNA Replication KW - DNA Repair KW - Escherichia coli -- genetics KW - DNA, Bacterial -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78517700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanisms+of+mutagenesis+in+the+Escherichia+coli+mutator+mutD5%3A+role+of+DNA+mismatch+repair.&rft.au=Schaaper%2C+R+M&rft.aulast=Schaaper&rft.aufirst=R&rft.date=1988-11-01&rft.volume=85&rft.issue=21&rft.spage=8126&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 - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Annu Rev Genet. 1976;10:135-56 [797306] J Biomol Struct Dyn. 1983 Oct;1(2):509-21 [6401117] Proc Natl Acad Sci U S A. 1983 Apr;80(8):2189-92 [6340117] J Mol Biol. 1983 Jun 5;166(4):557-80 [6345791] Mol Gen Genet. 1980;178(3):703-8 [6993863] Mol Gen Genet. 1981;181(1):24-8 [7012548] Genetics. 1982 Jan;100(1):7-18 [7047297] J Mol Biol. 1982 Mar 25;156(1):37-51 [6212689] Annu Rev Biochem. 1982;51:429-57 [6214209] Biochimie. 1982 Aug-Sep;64(8-9):571-5 [6814503] Cold Spring Harb Symp Quant Biol. 1966;31:77-84 [5237214] Nature. 1969 Mar 22;221(5186):1132 [4378427] J Bacteriol. 1974 Feb;117(2):477-87 [4590472] Mol Gen Genet. 1974;133(3):179-91 [4614067] J Mol Biol. 1983 Jul 15;167(4):757-71 [6224021] Proc Natl Acad Sci U S A. 1983 Dec;80(23):7085-9 [6359162] Proc Natl Acad Sci U S A. 1984 Mar;81(5):1494-8 [6369329] J Biol Chem. 1984 May 10;259(9):5567-73 [6325441] Proc Natl Acad Sci U S A. 1984 Jun;81(12):3665-9 [6328523] J Biol Chem. 1984 Jun 25;259(12):7990-3 [6376496] Proc Natl Acad Sci U S A. 1984 Dec;81(24):7747-51 [6393125] Cold Spring Harb Symp Quant Biol. 1984;49:589-96 [6397313] J Biol Chem. 1986 Jan 5;261(1):160-6 [3941068] Gene. 1985;39(2-3):181-9 [4092929] Proc Natl Acad Sci U S A. 1986 Feb;83(4):1026-30 [2419896] Mol Gen Genet. 1986 Jan;202(1):162-8 [3515128] J Bacteriol. 1986 Jul;167(1):130-7 [3522541] Microbiol Rev. 1986 Jun;50(2):133-65 [3523187] J Mol Biol. 1986 May 20;189(2):273-84 [3018259] J Mol Biol. 1986 Jul 5;190(1):113-7 [3023634] Annu Rev Genet. 1986;20:523-38 [2949693] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4389-92 [3037519] Mol Gen Genet. 1987 May;207(2-3):267-72 [3302596] Annu Rev Biochem. 1987;56:435-66 [3304141] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6220-4 [3306672] J Biol Chem. 1987 Dec 5;262(34):16267-70 [2824485] J Biol Chem. 1988 Mar 25;263(9):4450-9 [2831231] Proc Natl Acad Sci U S A. 1980 Feb;77(2):1063-7 [6987663] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiosensitive Down syndrome lymphoblastoid lines have normal ionizing-radiation-induced inhibition of DNA synthesis. AN - 78514167; 2972926 AB - The extent of X-ray-induced inhibition of DNA synthesis was determined in radiosensitive lymphoblastoid lines from 3 patients with Down syndrome and 3 patients with ataxia telangiectasia (AT). Compared to 6 normal control lines, the 3 AT lines were abnormally resistant to X-ray-induced inhibition of DNA synthesis, while the 3 Down syndrome lines had normal inhibition. These results demonstrate that radiosensitive human cells can have normal X-ray-induced inhibition of DNA synthesis and provide new evidence for the dissociation of radiosensitivity from radioresistant DNA synthesis. JF - Mutation research AU - Ganges, M B AU - Tarone, R E AU - Jiang, H X AU - Hauser, C AU - Robbins, J H AD - Dermatology Branch National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 251 EP - 256 VL - 194 IS - 3 SN - 0027-5107, 0027-5107 KW - Index Medicus KW - X-Rays KW - DNA Repair KW - Humans KW - Dose-Response Relationship, Radiation KW - Cell Survival -- radiation effects KW - Cell Line KW - Ataxia Telangiectasia -- genetics KW - Down Syndrome -- genetics KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78514167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Radiosensitive+Down+syndrome+lymphoblastoid+lines+have+normal+ionizing-radiation-induced+inhibition+of+DNA+synthesis.&rft.au=Umeno%2C+M%3BMcBride%2C+O+W%3BYang%2C+C+S%3BGelboin%2C+H+V%3BGonzalez%2C+F+J&rft.aulast=Umeno&rft.aufirst=M&rft.date=1988-12-13&rft.volume=27&rft.issue=25&rft.spage=9006&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-14 N1 - Date created - 1988-12-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The systemic administration of intravenous melphalan. AN - 78500925; 3054005 AB - Melphalan (L-phenylalanine mustard) is a bifunctional alkylating agent that is commonly administered orally to treat a wide variety of malignancies, including cancers of the breast and ovary, as well as multiple myeloma. Although commercially available in Europe and Canada, intravenous (IV) melphalan remains investigational in the United States. The role of IV melphalan in cancer chemotherapy is not well defined, despite its manageable toxicity and higher and more predictable blood levels following IV administration compared with oral administration. In addition, unlike oral melphalan, an extensive phase I evaluation of IV melphalan has not been undertaken. At lower doses (eg, 30 to 70 mg/m2), both as a single agent and in combination, the activity of IV melphalan has been evaluated in only a limited number of diseases. However, striking activity has been observed in previously untreated patients with rhabdomyosarcoma, a disease not generally considered responsive to alkylating agents. When administered at high doses (greater than 140 mg/m2) requiring bone marrow reinfusion, melphalan effects a high response rate (but no improvement in survival) in a variety of nonhematologic tumor types, including resistant tumors such as melanoma and colon carcinoma. In contrast, in poor-prognosis patients with non-Hodgkin's lymphoma, Hodgkin's disease, multiple myeloma, or neuroblastoma, high-dose melphalan-containing regimens have yielded both high response rates and improved survival, despite considerable toxicity. Additional clinical trials will be necessary to define the spectrum of activity of lower doses of IV melphalan and to define subgroups of patients most likely to benefit from high-dose melphalan. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Sarosy, G AU - Leyland-Jones, B AU - Soochan, P AU - Cheson, B D AD - Investigational Drug Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1768 EP - 1782 VL - 6 IS - 11 SN - 0732-183X, 0732-183X KW - Melphalan KW - Q41OR9510P KW - Index Medicus KW - Administration, Oral KW - Chemistry KW - Infusions, Intravenous KW - Humans KW - Chemical Phenomena KW - Clinical Trials as Topic KW - Body Water -- metabolism KW - Bone Marrow -- drug effects KW - Neoplasms -- drug therapy KW - Melphalan -- administration & dosage KW - Melphalan -- adverse effects KW - Melphalan -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78500925?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+systemic+administration+of+intravenous+melphalan.&rft.au=Sarosy%2C+G%3BLeyland-Jones%2C+B%3BSoochan%2C+P%3BCheson%2C+B+D&rft.aulast=Sarosy&rft.aufirst=G&rft.date=1988-11-01&rft.volume=6&rft.issue=11&rft.spage=1768&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 - 1988-12-06 N1 - Date created - 1988-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Peroxidase-catalyzed oxidation of (bi)sulfite: reaction of free radical metabolites of (bi)sulfite with (+/-)-7,8-dihydroxy-7, 8-dihydroxy[a]pyrene. AN - 78489855; 3141075 AB - The peroxidase-catalyzed metabolism of (bi)sulfite (hydrated sulfur dioxide) in the presence of (+/-)-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (BP-7,8-diol) was examined. Both horseradish peroxidase and prostaglandin peroxidase catalyze the one-electron oxidation of (bi)sulfite. This results in the formation of a sulfur trioxide radical anion which then reacts with molecular oxygen to form a peroxyl radical. This (bi)sulfite-derived peroxyl radical then reacts with BP-7,8-diol to form BP-7,8-diol-9,10-epoxides, the ultimate carcinogenic form of benzo[a]pyrene (BP). Addition of (bi)sulfite to incubations containing BP-7,8-diol and an active peroxidase resulted in significantly increased levels of BP diol-epoxide formation. This result may, in part, explain the reported co-carcinogenic effect of sulfur dioxide on BP-induced tumors in the respiratory tracts of rats and hamsters. The sulfur trioxide radical anion also reacts directly with BP-7,8-diol to form a sulfonate adduct. This reaction was particularly significant under conditions where molecular oxygen was depleted from the incubations. While the significance of this particular adduct is not known, its formation suggests that the sulfur trioxide radical anion generated during the peroxidase-catalyzed oxidation of (bi)sulfite could react with a wide assortment of compounds to form sulfonate adducts. JF - Carcinogenesis AU - Curtis, J F AU - Hughes, M F AU - Mason, R P AU - Eling, T E AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 2015 EP - 2021 VL - 9 IS - 11 SN - 0143-3334, 0143-3334 KW - Dihydroxydihydrobenzopyrenes KW - 0 KW - Free Radicals KW - Sulfites KW - Sulfonic Acids KW - benzo(a)pyrene 7,8-dihydrodiol KW - 13345-25-0 KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - Horseradish Peroxidase KW - EC 1.11.1.- KW - Peroxidases KW - Index Medicus KW - Oxidation-Reduction KW - Mass Spectrometry KW - Animals KW - Seminal Vesicles -- metabolism KW - Sheep KW - Microsomes -- metabolism KW - Male KW - Chromatography, High Pressure Liquid KW - Peroxidases -- metabolism KW - Horseradish Peroxidase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78489855?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Peroxidase-catalyzed+oxidation+of+%28bi%29sulfite%3A+reaction+of+free+radical+metabolites+of+%28bi%29sulfite+with+%28%2B%2F-%29-7%2C8-dihydroxy-7%2C+8-dihydroxy%5Ba%5Dpyrene.&rft.au=Curtis%2C+J+F%3BHughes%2C+M+F%3BMason%2C+R+P%3BEling%2C+T+E&rft.aulast=Curtis&rft.aufirst=J&rft.date=1988-11-01&rft.volume=9&rft.issue=11&rft.spage=2015&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increases in cytochrome P-450 mediated 17 beta-estradiol 2-hydroxylase activity in rat liver microsomes after both acute administration and subchronic administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin in a two-stage hepatocarcinogenesis model. AN - 78489794; 3141074 AB - Administration of single doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (10 micrograms/kg) increased estradiol 2-hydroxylase (E2OHase) activity approximately 2-fold in liver microsomes of female rats but had no effect on E2OHase activity in hepatic microsomes of male rats. In contrast, TCDD increased P-450d (an enzyme which has a high turnover number for E2OHase in a reconstituted enzyme system) 10- to 20-fold in livers of both male and female rats. The discrepancy between the increases in P-450d and E2OHase activity in liver microsomes of TCDD-induced rats was abolished by the addition of exogenous purified P-450 reductase to the microsomal assays for E2OHase, suggesting that reductase was limiting in the in vitro assays. When E2OHase activity was assayed in the presence of exogenous reductase, TCDD increased E2OHase 2-fold and 4-fold respectively in liver microsomes of male and female rates. Antibody to P-450d completely inhibited the increase in E2OHase activity in liver microsomes of TCDD-treated male and female rats, but had little effect on E2OHase activity in liver microsomes of untreated male or female rats. These data indicate that P-450d is responsible for the increase in E2OHase activity in TCDD-treated rats, but other P-450 isozymes are responsible for constitutive E2OHase activity. Biweekly administration of 1.4 micrograms/kg of TCDD for 30 weeks as a potential promoter of hepatocarcinogenesis increased the volume of the liver occupied by gamma-glutamyl transpeptidase (GGT)-positive foci in livers of female rats given a necrogenic dose of diethylnitrosamine (DEN) (200 mg/kg) as the initiator. Biweekly doses of 0.14-1.4 micrograms/kg TCDD in this model also increased P-450d (7-fold) and E2OHase activity maximally (4-fold) in DEN-initiated rats. Moreover, initiation with DEN substantially enhanced the effects of the low dose of TCDD on both hepatic microsomal P-450d and E2OHase activity. JF - Carcinogenesis AU - Graham, M J AU - Lucier, G W AU - Linko, P AU - Maronpot, R R AU - Goldstein, J A AD - Department of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1935 EP - 1941 VL - 9 IS - 11 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - Dioxins KW - Polychlorinated Dibenzodioxins KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Steroid Hydroxylases KW - EC 1.14.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - estrogen 2-hydroxylase KW - NADPH-Ferrihemoprotein Reductase KW - EC 1.6.2.4 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Administration Schedule KW - NADPH-Ferrihemoprotein Reductase -- metabolism KW - Immunologic Techniques KW - Male KW - Female KW - Polychlorinated Dibenzodioxins -- administration & dosage KW - Microsomes, Liver -- enzymology KW - Liver Neoplasms, Experimental -- enzymology KW - Steroid Hydroxylases -- metabolism KW - Dioxins -- administration & dosage KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78489794?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increases+in+cytochrome+P-450+mediated+17+beta-estradiol+2-hydroxylase+activity+in+rat+liver+microsomes+after+both+acute+administration+and+subchronic+administration+of+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+in+a+two-stage+hepatocarcinogenesis+model.&rft.au=Graham%2C+M+J%3BLucier%2C+G+W%3BLinko%2C+P%3BMaronpot%2C+R+R%3BGoldstein%2C+J+A&rft.aulast=Graham&rft.aufirst=M&rft.date=1988-11-01&rft.volume=9&rft.issue=11&rft.spage=1935&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rearrangement of both immunoglobulin and T-cell receptor genes in a prolymphocytic variant of hairy cell leukemia patient resistant to interferon-alpha. AN - 78487194; 2846090 AB - We describe a patient with the so-called "prolymphocytic variant" form of hairy cell leukemia (HCL) resistant to treatment with interferon-alpha (IFN-alpha). Analysis of immunoglobulin (Ig) and T-cell receptor-beta (TCR beta) gene rearrangements from serial peripheral blood mononuclear cell specimens (MNCs) confirmed not only the B-cell nature of the disease, but also the subsequent emergence of a morphologically indistinguishable population of cells with a clonal TCR beta rearrangement in addition to the original Ig gene rearrangement. With the exception of a transient increase in peripheral blood T cells during treatment with deoxycoformycin (DCF), the MNCs remained essentially constant throughout therapy with no evidence of a co-existing T-cell clone to account for the TCR beta rearrangement. Although MNCs from this patient bound significantly less IFN-alpha than did MNCs from other HCL patients, the binding was of high affinity with a kd similar to that of control cells. The number of IFN-gamma receptors on our patient's MNCs was four times higher than the number of IFN-alpha receptors and was similar to the number of IFN-alpha receptors on MNCs from HCL patients responsive to IFN-alpha. While various treatments including IFN-alpha, DCF, chlorambucil, splenectomy, leukopheresis, and IFN-gamma were not able to change the clinical progression of the disease, they may have provided an opportunity for the divergent TCR beta rearranged clone to expand and displace the initially dominant clone. JF - Blood AU - Giardina, S L AU - Young, H A AU - Faltynek, C R AU - Jaffe, E S AU - Clark, J W AU - Steis, R G AU - Urba, W J AU - Mathieson, B J AU - Gralnick, H AU - Lawrence, J AD - Biological Carcinogenesis Development Program, NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1708 EP - 1716 VL - 72 IS - 5 SN - 0006-4971, 0006-4971 KW - Antigens, Differentiation KW - 0 KW - Interferon Type I KW - Interferon-gamma KW - 82115-62-6 KW - Abridged Index Medicus KW - Index Medicus KW - Antigens, Differentiation -- analysis KW - Humans KW - Interferon-gamma -- metabolism KW - Interferon Type I -- therapeutic use KW - Interferon Type I -- metabolism KW - Aged KW - Flow Cytometry KW - Female KW - Leukemia, Hairy Cell -- pathology KW - Gene Rearrangement, B-Lymphocyte, Heavy Chain KW - Gene Rearrangement, beta-Chain T-Cell Antigen Receptor KW - Leukemia, Hairy Cell -- therapy KW - Leukemia, Hairy Cell -- immunology KW - Leukemia, Hairy Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78487194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Rearrangement+of+both+immunoglobulin+and+T-cell+receptor+genes+in+a+prolymphocytic+variant+of+hairy+cell+leukemia+patient+resistant+to+interferon-alpha.&rft.au=Giardina%2C+S+L%3BYoung%2C+H+A%3BFaltynek%2C+C+R%3BJaffe%2C+E+S%3BClark%2C+J+W%3BSteis%2C+R+G%3BUrba%2C+W+J%3BMathieson%2C+B+J%3BGralnick%2C+H%3BLawrence%2C+J&rft.aulast=Giardina&rft.aufirst=S&rft.date=1988-11-01&rft.volume=72&rft.issue=5&rft.spage=1708&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-08 N1 - Date created - 1988-12-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Blood 1989 Feb;73(2):624 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sunlight and other risk factors for cataracts: an epidemiologic study. AN - 78484952; 3177720 AB - A case control study was conducted in North Carolina to explore the relation between individual exposure to sunlight and the risk of cataracts. One hundred thirteen cases and 161 controls aged 40-69 at diagnosis were studied. Sunlight exposure was inferred from interview data on residency and time spent in the sun, combined with solar radiation data from the National Climatic Data Center. Sunlight exposure was very slightly related to all types of opacities combined. Although the numbers of cases with each type of opacity was small, the risk of cataracts was slightly increased in medium and high exposure categories for persons having cortical or posterior subcapsular opacities only, but not nuclear sclerotic changes. Persons with dark brown or hazel eyes are at increased risk. An unexpected finding was that persons who reported using tranquilizers for six months were at increased risk. JF - American journal of public health AU - Collman, G W AU - Shore, D L AU - Shy, C M AU - Checkoway, H AU - Luria, A S AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 22709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 1459 EP - 1462 VL - 78 IS - 11 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - Epidemiologic Methods KW - Risk Factors KW - Humans KW - North Carolina KW - Environmental Exposure KW - Aged KW - Middle Aged KW - Male KW - Female KW - Sunlight -- adverse effects KW - Cataract -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78484952?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sunlight+and+other+risk+factors+for+cataracts%3A+an+epidemiologic+study.&rft.au=Collman%2C+G+W%3BShore%2C+D+L%3BShy%2C+C+M%3BCheckoway%2C+H%3BLuria%2C+A+S&rft.aulast=Collman&rft.aufirst=G&rft.date=1988-11-01&rft.volume=78&rft.issue=11&rft.spage=1459&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 - 1988-11-17 N1 - Date created - 1988-11-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Ophthalmol. 1980 May;64(5):303-10 [7437389] Am J Ophthalmol. 1981 Mar;91(3):381-95 [7211996] Trans Am Ophthalmol Soc. 1980;78:255-64 [7257059] Lancet. 1981 Dec 5;2(8258):1249-50 [6118668] Invest Ophthalmol Vis Sci. 1979 May;18(5):462-7 [437948] Am J Epidemiol. 1983 Aug;118(2):239-49 [6881129] Am J Epidemiol. 1983 Aug;118(2):250-64 [6603790] Am J Epidemiol. 1986 Dec;124(6):916-25 [3776974] Am J Epidemiol. 1977 May;105(5):450-9 [860707] Am J Epidemiol. 1983 Aug;118(2):152-65 [6349331] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cell specific differences in O6-methylguanine-DNA methyltransferase activity and removal of O6-methylguanine in rat pulmonary cells. AN - 78483591; 3180342 AB - Previous studies have demonstrated that cell specificity exists for the alkylation of DNA from lung cells following treatment of rats with the tobacco specific carcinogen 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The concentration of the promutagenic adduct O6-methylguanine (O6MG) was found to be greatest in Clara cells followed by macrophages, type II cells and alveolar small cells. The purpose of this study was to measure the activity of the repair protein O6-methylguanine-DNA methyltransferase (O6MGMT) and to determine whether differences exist for the removal of O6MG among pulmonary cell types. Constitutive activity of O6MGMT was 2-fold greater in macrophages and type II cells than alveolar small cells and Clara cells. Treatment for 4 days with NNK (10 mg/kg/day) had no effect on O6MGMT activity in macrophages, but decreased activity in alveolar small cells and type II cells by 57 and 84%, respectively. O6MGMT activity was reduced to below limits of detection in Clara cells following treatment with NNK. The effect of NNK on O6MGMT activity was consistent with rates of removal of O6MG in macrophages and Clara cells. The loss of O6MG from DNA of macrophages followed first order kinetics (t1/2 = 48 h) while very little loss of this adduct was observed in Clara cells over an 8 day period following cessation of carcinogen treatment. Even though O6MGMT activity was reduced in alveolar small cells and type II cells, approximately 90% of the O6MG bound to DNA in these cell types was removed within 8 days after treatment was discontinued. The loss of O6MG from pulmonary cells appears to result largely from the removal of this adduct by O6MGMT since rates of cell turnover were very low (0.5-1.5%/day) in the lung and were not affected by treatment with NNK. This study indicates that the activity of O6MGMT and the rate of resynthesis of this repair enzyme differ considerably among pulmonary cells following the methylation of DNA. The high concentration of O6MG in Clara cells and the low rate of repair of this promutagenic adduct may be critical factors in the potent pulmonary carcinogenicity induced by the tobacco specific carcinogen NNK. JF - Carcinogenesis AU - Belinsky, S A AU - Dolan, M E AU - White, C M AU - Maronpot, R R AU - Pegg, A E AU - Anderson, M W AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 2053 EP - 2058 VL - 9 IS - 11 SN - 0143-3334, 0143-3334 KW - Nitrosamines KW - 0 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 - Rats KW - Nitrosamines -- pharmacology KW - Animals KW - Kinetics KW - DNA Repair KW - Lung -- cytology KW - Methyltransferases -- metabolism KW - Lung -- enzymology KW - Guanine -- analogs & derivatives KW - Lung -- metabolism KW - Guanine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78483591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cell+specific+differences+in+O6-methylguanine-DNA+methyltransferase+activity+and+removal+of+O6-methylguanine+in+rat+pulmonary+cells.&rft.au=Belinsky%2C+S+A%3BDolan%2C+M+E%3BWhite%2C+C+M%3BMaronpot%2C+R+R%3BPegg%2C+A+E%3BAnderson%2C+M+W&rft.aulast=Belinsky&rft.aufirst=S&rft.date=1988-11-01&rft.volume=9&rft.issue=11&rft.spage=2053&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The impact of toxicity on carcinogenicity studies: implications for risk assessment. AN - 78482190; 3052903 AB - This paper explores the inter-relationship between toxicity, genotoxicity, and carcinogenicity in laboratory rodents. To our knowledge this is the first attempt to integrate these factors and evaluate their implications for the process of risk assessment. The evaluation is based on information obtained from 2-year laboratory-animal studies involving 99 chemicals. The data suggest that only seven of the 53 positive carcinogenicity studies exhibited the types of target organ toxicity that could have been the cause of all observed carcinogenic effects. Furthermore, no apparent difference in mutagenicity as measured by the Ames Salmonella assay was observed between 'high dose only' carcinogens and the entire set of carcinogens. These findings suggest that the number of chemical carcinogens that we can identify solely through rodent studies as being potential tumor inducers through some indirect mechanism is small. Generally speaking, the identification of histopathological effects is not sufficient in itself for justifying mechanistic assumptions, and supplemental biological information will be necessary to reach definitive conclusions. JF - Carcinogenesis AU - Hoel, D G AU - Haseman, J K AU - Hogan, M D AU - Huff, J AU - McConnell, E E AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 2045 EP - 2052 VL - 9 IS - 11 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - Index Medicus KW - Mutation -- drug effects KW - Animals KW - Mutagenicity Tests KW - Liver -- pathology KW - Hyperplasia KW - Sex Factors KW - Liver -- drug effects KW - Dose-Response Relationship, Drug KW - Risk Factors KW - Precancerous Conditions -- chemically induced KW - Precancerous Conditions -- pathology KW - Neoplasms, Experimental -- chemically induced KW - Carcinogens -- classification KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78482190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=The+impact+of+toxicity+on+carcinogenicity+studies%3A+implications+for+risk+assessment.&rft.au=Hoel%2C+D+G%3BHaseman%2C+J+K%3BHogan%2C+M+D%3BHuff%2C+J%3BMcConnell%2C+E+E&rft.aulast=Hoel&rft.aufirst=D&rft.date=1988-11-01&rft.volume=9&rft.issue=11&rft.spage=2045&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol esters enhance attachment of NIH/3T3 cells to laminin and type IV collagen substrates. AN - 78446105; 3169149 AB - The effect of phorbol esters on the adhesive properties of NIH/3T3 mouse fibroblasts was investigated using plastic substrates precoated with the extracellular matrix proteins fibronectin, collagen, and laminin. Treatment with phorbol 12-myristate 13-acetate (PMA) enhanced NIH/3T3 cell attachment to laminin and type IV collagen substrates but had little or no effect on attachment to fibronectin and type I collagen substrates. The effect of PMA in enhancing cell attachment to laminin and type IV collagen substrates was dose dependent between 10(-9) and 10(-7) M. PMA was effective as early as 30 min; the effect reached a maximum at 2 h and decreased gradually. Phorbol 12, 13-dibenzoate and phorbol 12, 13-diacetate were effective but to a lesser extent and phorbol 12-myristate and phorbol 13-acetate showed little or no effect. These results suggest that PMA may enhance NIH/3T3 cell adhesion through effects on laminin and type IV collagen receptors. Retinoic acid, which itself requires at least 6 h to show an effect on attachment, did not have any effect on cell attachment in 2 h and, if anything, slightly inhibited PMA-enhanced cell attachment to laminin and type IV collagen substrates. JF - Experimental cell research AU - Kato, S AU - Ben, T L AU - De Luca, L M AD - Differentiation Control Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/11// PY - 1988 DA - November 1988 SP - 31 EP - 41 VL - 179 IS - 1 SN - 0014-4827, 0014-4827 KW - Laminin KW - 0 KW - Phorbol Esters KW - Tretinoin KW - 5688UTC01R KW - Collagen KW - 9007-34-5 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Tretinoin -- pharmacology KW - Fibroblasts -- drug effects KW - Animals KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Fibroblasts -- cytology KW - Cell Line KW - Phorbol Esters -- pharmacology KW - Cell Adhesion -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78446105?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phorbol+esters+enhance+attachment+of+NIH%2F3T3+cells+to+laminin+and+type+IV+collagen+substrates.&rft.au=Kato%2C+S%3BBen%2C+T+L%3BDe+Luca%2C+L+M&rft.aulast=Kato&rft.aufirst=S&rft.date=1988-11-01&rft.volume=179&rft.issue=1&rft.spage=31&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 - 1988-11-23 N1 - Date created - 1988-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of mouse pro-1 and pro-2 transfectants for responses to tumor promoters and antipromoters. AN - 78442222; 3139288 AB - A previous report demonstrated that mouse JB6 cells transformed to promotion sensitive (P+) phenotype by transfection with an activated promotion sensitivity (pro) gene showed both evidence for the presence of the transfected gene and sensitivity to phorbol ester induced transformation similar to that observed in parental P+ cells. In addition, pro-1 and pro-2 transfectants were similar to each other in phorbol ester response. The current report extends these findings to ask whether pro-1 or pro-2 transfectants are also sensitive to promotion of transformation by other classes of tumor promoters such as epidermal growth factor (EGF), lanthanides, and phthalate esters and to inhibition of phorbol ester promoted transformation by several classes of antipromoters. The results showed that both pro-1 and pro-2 transfectants resembled parental P+ cells in sensitivity to promotion of anchorage independent transformation by lanthanides and by diethylhexylphthalate. In addition both pro-1 and pro-2 transfectants showed inhibition of phorbol ester induced transformation by antipromoters ganglioside GT1b, ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, and forskolin. Thus the pathways implicated by these inducers and inhibitors of transformation appear similar to those implicated for parental P+ cells and similar when controlled by pro-1 or pro-2. The single differential response was that of EGF-induced transformation. pro-2 transfectants but not pro-1 transfectants were sensitive to EGF-induced neoplastic transformation. The nonresponsiveness could not be attributed to lack of EGF receptors since 125I-EGF binding to pro-1 transfectants was similar to that for pro-2 transfectants and parental P+ cells. Thus pro genes transfer responsiveness to a C-kinase mediated promotion of transformation pathway and to putatively non-C kinase pathways triggered by lanthanides or phthalate esters, but not necessarily to an EGF receptor kinase mediated pathway. JF - Cancer research AU - Colburn, N H AU - Smith, B M AU - Wendel, E J AU - Nakamura, Y AU - Winterstein, D AD - Cell Biology Section, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1988/11/01/ PY - 1988 DA - 1988 Nov 01 SP - 6076 EP - 6080 VL - 48 IS - 21 SN - 0008-5472, 0008-5472 KW - Egtazic Acid KW - 526U7A2651 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Diethylhexyl Phthalate -- toxicity KW - Mice KW - Protein Kinase C -- physiology KW - Epidermal Growth Factor -- pharmacology KW - Mice, Inbred BALB C KW - Epidermal Growth Factor -- metabolism KW - Egtazic Acid -- pharmacology KW - Cell Line KW - Transfection KW - Cell Transformation, Neoplastic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78442222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+mouse+pro-1+and+pro-2+transfectants+for+responses+to+tumor+promoters+and+antipromoters.&rft.au=Colburn%2C+N+H%3BSmith%2C+B+M%3BWendel%2C+E+J%3BNakamura%2C+Y%3BWinterstein%2C+D&rft.aulast=Colburn&rft.aufirst=N&rft.date=1988-11-01&rft.volume=48&rft.issue=21&rft.spage=6076&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 - 1988-11-15 N1 - Date created - 1988-11-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mimicry of bryostatin 1 induced phosphorylation patterns in HL-60 cells by high-phorbol ester concentrations. AN - 78433153; 3167850 AB - The bryostatins are a group of macrocyclic lactones isolated from the marine bryozoan Bugula neritina. Bryostatin 1, like the phorbol esters, activates protein kinase C; however, it partially inhibits the phorbol ester induced differentiation of the human promyelocytic leukemic cell line HL-60. We compared the phosphorylation response in HL-60 cells treated with phorbol 12,13-dibutyrate or bryostatin 1. Bryostatin 1 enhanced the phosphorylation of the same proteins as did typical concentrations (10(-8)-10(-9) M) of phorbol 12,13-dibutyrate. In addition, bryostatin 1 caused the appearance of 2 phosphorylated protein spots with molecular weights of 70,000 and pIs of 6.3-6.4. These latter phosphorylations were evident after a 30-min exposure to bryostatin 1 at 6 nM. Phorbol 12,13-dibutyrate concentrations of at least 600 nM, approximately 100-fold that necessary to induce differentiation, also induced the appearance of these phosphoprotein spots. The Mr 70,000 phosphoproteins were located in the ionic detergent-soluble cellular fraction which would contain the cytoskeletal proteins. Their phosphorylation was almost totally on serine residues. We speculate that phorbol esters at very high concentrations may more closely resemble bryostatin 1. JF - Cancer research AU - Warren, B S AU - Kamano, Y AU - Pettit, G R AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/11/01/ PY - 1988 DA - 1988 Nov 01 SP - 5984 EP - 5988 VL - 48 IS - 21 SN - 0008-5472, 0008-5472 KW - Amino Acids KW - 0 KW - Bryostatins KW - Lactones KW - Macrolides KW - Phosphoproteins KW - Proteins KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - bryostatin 1 KW - 37O2X55Y9E KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Tumor Cells, Cultured KW - Phosphorylation KW - Humans KW - Phosphoproteins -- analysis KW - Amino Acids -- analysis KW - Protein Kinase C -- physiology KW - Molecular Weight KW - Leukemia, Promyelocytic, Acute -- metabolism KW - Proteins -- metabolism KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Lactones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78433153?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mimicry+of+bryostatin+1+induced+phosphorylation+patterns+in+HL-60+cells+by+high-phorbol+ester+concentrations.&rft.au=Warren%2C+B+S%3BKamano%2C+Y%3BPettit%2C+G+R%3BBlumberg%2C+P+M&rft.aulast=Warren&rft.aufirst=B&rft.date=1988-11-01&rft.volume=48&rft.issue=21&rft.spage=5984&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 - 1988-11-15 N1 - Date created - 1988-11-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Novel eukaryotic expression vectors which permit single-stranded replication in Escherichia coli and in vitro translational analysis of cloned genes. AN - 78632954; 2850970 AB - The ability to express cloned genes transiently is an important technique in the study of eukaryotic gene expression. Numerous useful expression vectors have been constructed for this purpose although many of them share several common drawbacks. In this paper I describe the construction and characterization of novel expression vectors pSVKII and pSVKIII which have 13 and 8 unique restriction sites, respectively, suitable for cloning genes. These vectors have phage M13 ori, which permits them to produce and package ss DNA molecules in Escherichia coli host, thus facilitating the sequencing and site directed mutagenesis of a cloned gene. Expression vector pSVKIII has a T7 phage promoter located between the SV40 promoter and the multiple cloning sites, which permits efficient transcription and in vitro translation of the cloned gene prior to in vivo studies. JF - Gene AU - Mongkolsuk, S AD - Laboratory of Biochemistry, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10/30/ PY - 1988 DA - 1988 Oct 30 SP - 313 EP - 319 VL - 70 IS - 2 SN - 0378-1119, 0378-1119 KW - DNA, Single-Stranded KW - 0 KW - Recombinant Fusion Proteins KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Recombinant Fusion Proteins -- biosynthesis KW - Protein Biosynthesis KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Promoter Regions, Genetic KW - Tumor Cells, Cultured KW - Chloramphenicol O-Acetyltransferase -- biosynthesis KW - Simian virus 40 -- genetics KW - Humans KW - T-Phages -- genetics KW - Recombinant Fusion Proteins -- genetics KW - Transcription, Genetic KW - DNA, Single-Stranded -- biosynthesis KW - Eukaryotic Cells -- ultrastructure KW - Genetic Vectors KW - Escherichia coli -- genetics KW - Cloning, Molecular -- methods KW - Cells -- ultrastructure KW - Plasmids UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78632954?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Novel+eukaryotic+expression+vectors+which+permit+single-stranded+replication+in+Escherichia+coli+and+in+vitro+translational+analysis+of+cloned+genes.&rft.au=Mongkolsuk%2C+S&rft.aulast=Mongkolsuk&rft.aufirst=S&rft.date=1988-10-30&rft.volume=70&rft.issue=2&rft.spage=313&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-02 N1 - Date created - 1989-03-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Gene 1990 Oct 30;95(1):163 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Short term increase in risk of breast cancer after full term pregnancy. AN - 78562574; 3143438 AB - To determine whether there is a short term increase in the risk of breast cancer after a full term birth data from two hospital based, case-control studies in Italy were pooled. Analysis was restricted to women aged under 50 with two or more children (573 women with cancer and 570 controls). A relative risk for breast cancer of 2.66 was seen in women who had given birth during the three years preceding the interview compared with women whose last birth had occurred 10 or more years before, after adjustment for age, age at first birth, and parity. The relative risk slowly decreased for women who had last given birth three to 10 years before. Multivariate analyses confirmed the protective effect of an early age at first birth and the age dependent effect of parity on the risk of breast cancer--that is, a direct relation below age 40 and an inverse one in older women. These data provide epidemiological evidence that a full term birth is followed by a transient increase in the risk of breast cancer, which for some time contrasts with and overcomes the long term protection of pregnancy at an early age. They therefore confirm predictions from animal studies and theoretical models that pregnancy prevents the early stages of breast carcinogenesis but promotes the late stages of the process. JF - BMJ (Clinical research ed.) AU - Bruzzi, P AU - Negri, E AU - La Vecchia, C AU - Decarli, A AU - Palli, D AU - Parazzini, F AU - Del Turco, M R AD - Unit of Clinical Epidemiology, National Cancer Institute, Genoa, Italy. Y1 - 1988/10/29/ PY - 1988 DA - 1988 Oct 29 SP - 1096 EP - 1098 VL - 297 IS - 6656 SN - 0959-8138, 0959-8138 KW - Abridged Index Medicus KW - Index Medicus KW - Parity KW - Puerperal Disorders -- epidemiology KW - Risk Factors KW - Maternal Age KW - Humans KW - Puerperal Disorders -- etiology KW - Adult KW - Middle Aged KW - Time Factors KW - Italy KW - Female KW - Breast Neoplasms -- etiology KW - Breast Neoplasms -- epidemiology KW - Pregnancy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78562574?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMJ+%28Clinical+research+ed.%29&rft.atitle=Short+term+increase+in+risk+of+breast+cancer+after+full+term+pregnancy.&rft.au=Bruzzi%2C+P%3BNegri%2C+E%3BLa+Vecchia%2C+C%3BDecarli%2C+A%3BPalli%2C+D%3BParazzini%2C+F%3BDel+Turco%2C+M+R&rft.aulast=Bruzzi&rft.aufirst=P&rft.date=1988-10-29&rft.volume=297&rft.issue=6656&rft.spage=1096&rft.isbn=&rft.btitle=&rft.title=BMJ+%28Clinical+research+ed.%29&rft.issn=09598138&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-25 N1 - Date created - 1989-01-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Epidemiol. 1983 Jan;117(1):35-45 [6823951] Breast Cancer Res Treat. 1982;2(1):5-73 [6216933] Nature. 1983 Jun 30;303(5920):767-70 [6866078] Am J Epidemiol. 1984 Jan;119(1):139-41 [6691331] Int J Cancer. 1986 Jan 15;37(1):21-5 [3941020] Int J Cancer. 1986 Feb 15;37(2):173-7 [3455923] Tumori. 1986 Jun 30;72(3):241-9 [3739004] Cancer Surv. 1986;5(3):649-70 [3107814] Int J Epidemiol. 1987 Sep;16(3):347-55 [3667030] Int J Cancer. 1978 Jun 15;21(6):724-30 [669854] J Natl Cancer Inst. 1980 Apr;64(4):977-89 [6929006] Epidemiol Rev. 1979;1:74-109 [398270] J Natl Cancer Inst. 1980 Sep;65(3):559-69 [6931935] Br Med J. 1980 Aug 9;281(6237):419-21 [7427299] J Natl Cancer Inst. 1982 Feb;68(2):211-7 [6950154] Am J Epidemiol. 1982 Nov;116(5):737-42 [6756128] Int J Cancer. 1983 Jun 15;31(6):701-4 [6862681] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of serotonergic input in the down-regulation of beta-adrenoceptors following long-term clorgyline treatment. AN - 78607606; 2463178 AB - Administration of the selective monoamine oxidase (MAO) type A-inhibiting antidepressant clorgyline (1 mg/kg per day) to rats for 21 days caused a significant decrease in cortical [3H]dihydroalprenolol binding. Selective lesioning of central serotonergic axons by 5,7-dihydroxytryptamine (5,7-DHT; confirmed by the presence of the serotonin syndrome in response to a 40 mg/kg dose of 5-hydroxytryptophan (5-HTP) or inhibition of 5-HT synthesis by parachlorophenylalanine (PCPA) caused significant 5-HT and 5-HIAA depletions in the cortex without much effect on NE and DA concentrations, but did not have any significant effect on beta-adrenoceptor density, and furthermore failed to attenuate clorgyline-induced decreases in beta-adrenoceptor density. Clorgyline treatment partially antagonized 5-HT depletion by the 5,7-DHT lesion or PCPA treatment. These findings suggest that due to their ability to raise 5-HT concentrations, MAO-inhibiting antidepressants may be a better alternative than the tricyclics in treating depressed patients with reduced 5-HT if down-regulation of beta-adrenoceptors is critical for antidepressant efficacy. JF - European journal of pharmacology AU - Aulakh, C S AU - Cohen, R M AU - Dauphin, M M AU - McLellan, C A AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/10/26/ PY - 1988 DA - 1988 Oct 26 SP - 63 EP - 70 VL - 156 IS - 1 SN - 0014-2999, 0014-2999 KW - Dihydroxytryptamines KW - 0 KW - Propylamines KW - Receptors, Adrenergic, beta KW - 5,7-Dihydroxytryptamine KW - 31363-74-3 KW - Serotonin KW - 333DO1RDJY KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Clorgyline KW - LYJ16FZU9Q KW - Fenclonine KW - R5J7E3L9SP KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Receptors, Adrenergic, beta -- metabolism KW - Animals KW - Hydroxyindoleacetic Acid -- analysis KW - Dopamine -- analysis KW - Time Factors KW - Norepinephrine -- analysis KW - Male KW - Injections, Intraventricular KW - Fenclonine -- pharmacology KW - Serotonin -- physiology KW - Dihydroxytryptamines -- toxicity KW - 5,7-Dihydroxytryptamine -- administration & dosage KW - Propylamines -- pharmacology KW - Clorgyline -- pharmacology KW - 5,7-Dihydroxytryptamine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78607606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+serotonergic+input+in+the+down-regulation+of+beta-adrenoceptors+following+long-term+clorgyline+treatment.&rft.au=Aulakh%2C+C+S%3BCohen%2C+R+M%3BDauphin%2C+M+M%3BMcLellan%2C+C+A%3BMurphy%2C+D+L&rft.aulast=Aulakh&rft.aufirst=C&rft.date=1988-10-26&rft.volume=156&rft.issue=1&rft.spage=63&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 - 1989-02-21 N1 - Date created - 1989-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Novel non-templated nucleotide addition reactions catalyzed by procaryotic and eucaryotic DNA polymerases. AN - 19560318; 8737991 AB - DNA polymerases catalyze the addition of deoxyribonucleotides onto DNA primers in a template-directed manner. The requirement for template instruction distinguishes these enzymes from other nucleotidyl transferases, such as terminal deoxynucleotidyl transferase, that do not utilize a template. An oligonucleotide substrate was used to characterize a novel, non-templated nucleotide addition reaction carried out by DNA polymerases from a variety of procaryotic and eucaryotic sources. The products of the reaction, in which a deoxyribonucleotide was added to the 3' hydroxyl terminus of a blunt-ended DNA substrate, were analyzed by electrophoresis on high resolution, denaturing polyacrylamide gels. DNA polymerase from Thermus aquaticus, polymerase alpha from chick embryo, rat polymerase beta, reverse transcriptase from avian myeloblastosis virus, and DNA polymerase I from Saccharomyces cerevisiae all carried out the blunt-end addition reaction. The reaction required a duplex DNA substrate but did not require coding information from the template strand. These results demonstrate that template instruction is not an absolute requirement for the catalysis of nucleotidyl transfer reactions by DNA polymerases. Images JF - Nucleic Acids Research AU - Clark, J M AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/10/25/ PY - 1988 DA - 1988 Oct 25 SP - 9677 EP - 9686 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 16 IS - 20 SN - 0305-1048, 0305-1048 KW - Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; Biochemistry Abstracts 2: Nucleic Acids KW - Coding KW - Electrophoresis KW - Enzymes KW - Avian myeloblastosis KW - Oligonucleotides KW - Avian myeloblastosis virus KW - deoxyribonucleotides KW - Nucleotides KW - Saccharomyces cerevisiae KW - Gels KW - DNA-directed DNA polymerase KW - RNA-directed DNA polymerase KW - Thermus aquaticus KW - Primers KW - DNA nucleotidylexotransferase KW - Catalysis KW - J 02310:Genetics & Taxonomy KW - V 22320:Replication KW - N 14810:Methods KW - K 03310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19560318?accountid=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=Novel+non-templated+nucleotide+addition+reactions+catalyzed+by+procaryotic+and+eucaryotic+DNA+polymerases.&rft.au=Clark%2C+J+M&rft.aulast=Clark&rft.aufirst=J&rft.date=1988-10-25&rft.volume=16&rft.issue=20&rft.spage=9677&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 - Coding; Electrophoresis; Enzymes; Avian myeloblastosis; Oligonucleotides; Nucleotides; deoxyribonucleotides; Gels; DNA-directed DNA polymerase; RNA-directed DNA polymerase; Primers; Catalysis; DNA nucleotidylexotransferase; Thermus aquaticus; Avian myeloblastosis virus; Saccharomyces cerevisiae ER - TY - JOUR T1 - Novel anti-inflammatory peptides from the region of highest similarity between uteroglobin and lipocortin I. AN - 78459917; 2971881 AB - Significant future developments in the effective treatment of inflammatory diseases may arise from non-toxic dual inhibitors of both cyclooxygenase and lipoxygenase pathways in the arachidonate cascade. Inhibition of phospholipase A2(PLA2)(EC3.1.1.4), may provide such a dual action and recent research has concentrated on the role of PLA2-inhibitory proteins as possible anti-inflammatory agents. Blastokinin or uteroglobin is a steroid-induced rabbit secretory protein with PLA2-inhibitory activity. Its biochemical and biological properties have been extensively studied and its crystallographic structure has been resolved at 1.34 A (refs 15, 16). Lipocortins are a family of related proteins, which, it has been suggested, mediate the anti-inflammatory effects of glucocorticoids (for a review, see ref. 23). Some proteins of this group have been purified and the complementary DNA sequences of two human lipocortins are known. Lipocortins inhibit PLA2 in vitro, although their mechanism of action is still unclear. Recombinant lipocortin I inhibits eicosanoid synthesis in isolated perfused lungs from the guinea pig. Here, we report that synthetic oligopeptides corresponding to a region of high amino-acid sequence similarity between uteroglobin and lipocortin I have potent PLA2 inhibitory activity in vitro and striking anti-inflammatory effects in vivo. JF - Nature AU - Miele, L AU - Cordella-Miele, E AU - Facchiano, A AU - Mukherjee, A B AD - Section on Developmental Genetics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/10/20/ PY - 1988 DA - 1988 Oct 20 SP - 726 EP - 730 VL - 335 IS - 6192 SN - 0028-0836, 0028-0836 KW - Annexins KW - 0 KW - Anti-Inflammatory Agents KW - Glycoproteins KW - Peptides KW - Recombinant Proteins KW - Uteroglobin KW - 9060-09-7 KW - Phospholipases KW - EC 3.1.- KW - Index Medicus KW - Rats KW - Software KW - Animals KW - Recombinant Proteins -- pharmacology KW - Dose-Response Relationship, Drug KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Phospholipases -- antagonists & inhibitors KW - Glycoproteins -- pharmacology KW - Uteroglobin -- pharmacology KW - Peptides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78459917?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Novel+anti-inflammatory+peptides+from+the+region+of+highest+similarity+between+uteroglobin+and+lipocortin+I.&rft.au=Miele%2C+L%3BCordella-Miele%2C+E%3BFacchiano%2C+A%3BMukherjee%2C+A+B&rft.aulast=Miele&rft.aufirst=L&rft.date=1988-10-20&rft.volume=335&rft.issue=6192&rft.spage=726&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-18 N1 - Date created - 1988-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Correlates of severe or life-threatening toxic effects from trimetrexate. AN - 78451776; 2971817 AB - Trimetrexate, an investigational antifol, has been associated with marked variability in drug tolerance among patients. The agent is extensively protein bound, and hepatic biotransformation plays a major role in its elimination. In early phase II testing, nine of 15 patients who experienced life-threatening or fatal toxic effects from trimetrexate had albumin levels less than or equal to 3.5 g/dL prior to treatment. This prompted a review of the data base on 272 patients entered in phase I clinical trails. The incidence of severe or life-threatening anemia, leukopenia, neutropenia, thrombocytopenia, mucositis, and hepatic toxic effects during the first course of trimetrexate was analyzed according to dose, schedule, prior treatment, and baseline protein and albumin levels. The schedules using doses given by short infusions of 30-60 minutes daily for 5 days or weekly for 3 weeks were generally associated with higher incidence of toxic effects than the schedules using doses given every other week by short infusions or those using continuous infusion. The occurrence of leukopenia and mucositis was dose related. Patients with baseline albumin levels less than or equal to 3.5 g/dL had higher incidence of all types of severe or life-threatening toxic effects than those with albumin levels greater than or equal to 3.6 g/dL, and the differences were significant for the development of anemia, thrombocytopenia, and mucositis. Similar correlations were noted for pretreatment protein levels less than or equal to 6.0 g/dL. The small cohort of patients with leukemia experienced substantial toxic effects and tended to have low protein and albumin levels. Performance status and prior therapy did not emerge as strong predictors of severe toxic effects in the univariate analysis. Multivariate analysis confirmed that the type of cancer (leukemia vs. solid tumor), dose, schedule, and baseline albumin level were significant and independent predictors of severe and life-threatening toxic effects in the phase I patient population. Multivariate analysis including only patients with solid tumors indicated that albumin level, dose, and schedule remained significant predictors of toxic effects. Since normal liver function as reflected by bilirubin and transaminase values were a requirement for eligibility, the results suggest that albumin and protein levels may provide a more sensitive index of hepatic function. Patients with hypoalbuminemia and hypoproteinemia are at increased risk of experiencing severe or life-threatening toxic effects from trimetrexate and should be treated cautiously. JF - Journal of the National Cancer Institute AU - Grem, J L AU - Ellenberg, S S AU - King, S A AU - Shoemaker, D D AD - Investigational Drug Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10/19/ PY - 1988 DA - 1988 Oct 19 SP - 1313 EP - 1318 VL - 80 IS - 16 SN - 0027-8874, 0027-8874 KW - Antineoplastic Agents KW - 0 KW - Folic Acid Antagonists KW - Quinazolines KW - Serum Albumin KW - Trimetrexate KW - UPN4ITI8T4 KW - Index Medicus KW - Drug Evaluation KW - Serum Albumin -- analysis KW - Humans KW - Adult KW - Thrombocytopenia -- chemically induced KW - Quinazolines -- pharmacokinetics KW - Antineoplastic Agents -- pharmacokinetics KW - Folic Acid Antagonists -- adverse effects KW - Quinazolines -- adverse effects KW - Folic Acid Antagonists -- pharmacokinetics KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78451776?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Correlates+of+severe+or+life-threatening+toxic+effects+from+trimetrexate.&rft.au=Grem%2C+J+L%3BEllenberg%2C+S+S%3BKing%2C+S+A%3BShoemaker%2C+D+D&rft.aulast=Grem&rft.aufirst=J&rft.date=1988-10-19&rft.volume=80&rft.issue=16&rft.spage=1313&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 - 1988-11-08 N1 - Date created - 1988-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of bombesin-induced phosphatidylinositol hydrolysis in a small-cell lung-cancer cell line. AN - 78582702; 2849413 AB - Bombesin is an amphibian tetradecapeptide whose mammalian homologue, gastrin-releasing peptide (GRP), is produced by many small-cell lung-cancer (SCLC) cells, and which can function in an autocrine growth-promoting manner in SCLC. Studies reported here show that [Tyr4]bombesin and its congeners increase inositol 1,4,5-trisphosphate within seconds in NCI-H345, a SCLC cell line that constitutively produces GRP. After 30 min in the presence of 0.01 M-Li+ and [Tyr4]bombesin, there is marked accumulation of inositol monophosphates and inositol tetrakisphosphate. Pretreatment with phorbol 12-myristate 13-acetate (PMA) for 20 min inhibited the ability of [Tyr4]bombesin to induce phosphatidylinositol (PtdIns) turnover and to increase intracellular free Ca2+ ([Ca2+]i). Pretreatment with PMA for 48 h attenuated the ability of subsequently added PMA to decrease the response to [Tyr4]bombesin. Pretreatment with pertussis toxin (PT; 1 microgram/ml for 18-24 h) decreased by less than 30% [Tyr4]bombesin-induced increases in [Ca2+]i and PtdIns metabolites. However, interpretation of this result is complicated by the inability of PT to ADP-ribosylate completely its substrates in intact NCI-H345 cells. In contrast, pretreatment with cholera toxin (1 microgram/ml for 18-24 h) lowered basal [Ca2+]i and basal inositol phosphate concentrations, attenuated the response of NCI-H345 to subsequently added [Tyr4]bombesin, and was not mimicked by treatments that increase cellular cyclic AMP. These data demonstrate the activation of phospholipase C in SCLC by bombesin congeners. In addition, the results suggest a regulatory role for protein kinase C, a cholera-toxin substrate, and perhaps a pertussis-toxin substrate in the response of SCLC to bombesin. JF - The Biochemical journal AU - Trepel, J B AU - Moyer, J D AU - Heikkila, R AU - Sausville, E A AD - National Cancer Institute--Navy Medical Oncology Branch, Bethesda, MD 20814. Y1 - 1988/10/15/ PY - 1988 DA - 1988 Oct 15 SP - 403 EP - 410 VL - 255 IS - 2 SN - 0264-6021, 0264-6021 KW - Inositol Phosphates KW - 0 KW - Phorbol Esters KW - Phosphatidylinositols KW - Virulence Factors, Bordetella KW - Adenosine Diphosphate KW - 61D2G4IYVH KW - Cholera Toxin KW - 9012-63-9 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Bombesin KW - PX9AZU7QPK KW - Index Medicus KW - Virulence Factors, Bordetella -- pharmacology KW - Phorbol Esters -- pharmacology KW - Animals KW - Inositol Phosphates -- isolation & purification KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Dose-Response Relationship, Drug KW - Cholera Toxin -- pharmacology KW - Cell Line KW - Structure-Activity Relationship KW - Adenosine Diphosphate -- metabolism KW - Phosphatidylinositols -- metabolism KW - Carcinoma, Small Cell -- metabolism KW - Bombesin -- pharmacology KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78582702?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modulation+of+bombesin-induced+phosphatidylinositol+hydrolysis+in+a+small-cell+lung-cancer+cell+line.&rft.au=Trepel%2C+J+B%3BMoyer%2C+J+D%3BHeikkila%2C+R%3BSausville%2C+E+A&rft.aulast=Trepel&rft.aufirst=J&rft.date=1988-10-15&rft.volume=255&rft.issue=2&rft.spage=403&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 - 1989-01-23 N1 - Date created - 1989-01-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: N Engl J Med. 1980 Oct 9;303(15):878-80 [7412807] J Biol Chem. 1987 Jun 5;262(16):7744-50 [3034904] Science. 1981 Dec 11;214(4526):1246-8 [6272398] J Cell Biol. 1982 Aug;94(2):325-34 [6980885] Biochem J. 1982 Sep 15;206(3):587-95 [7150264] Proc Natl Acad Sci U S A. 1983 May;80(10):2936-40 [6344074] Exp Cell Res. 1984 Jul;153(1):245-8 [6547391] Biochem Biophys Res Commun. 1985 Mar 15;127(2):450-7 [2983721] Life Sci. 1985 Jul 15;37(2):105-13 [2409423] Nature. 1985 Aug 29-Sep 4;316(6031):823-6 [2993906] J Biol Chem. 1985 Oct 25;260(24):13138-45 [2865257] J Biol Chem. 1985 Dec 5;260(28):15194-9 [3905792] Proc Natl Acad Sci U S A. 1985 Nov;82(22):7616-20 [2999772] J Biol Chem. 1986 Feb 15;261(5):2451-7 [3003116] J Biol Chem. 1986 Feb 25;261(6):2918-27 [3005271] J Cell Biol. 1986 Jun;102(6):2211-22 [3011811] J Cell Biol. 1986 Jun;102(6):2223-33 [2423536] J Biol Chem. 1986 Jul 25;261(21):9587-90 [3015900] Proc Natl Acad Sci U S A. 1986 Aug;83(15):5673-7 [3016713] Cell. 1986 Sep 12;46(6):951-8 [3019558] Exp Cell Res. 1986 Nov;167(1):276-80 [3758207] Science. 1986 Nov 28;234(4780):1117-9 [3465038] Cell. 1986 Dec 5;47(5):703-9 [3536125] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8893-7 [3024154] Science. 1986 Dec 19;234(4783):1519-26 [3024320] J Biol Chem. 1987 Jan 5;262(1):182-8 [3025202] Mol Cell Biol. 1986 Dec;6(12):4641-9 [2432404] Cancer Res. 1987 Feb 1;47(3):821-5 [3026617] Biochem J. 1987 Mar 1;242(2):361-6 [3109388] Life Sci. 1987 Jul 20;41(3):251-8 [2439867] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5768-72 [3039507] Annu Rev Biochem. 1987;56:159-93 [3304132] Annu Rev Biochem. 1987;56:615-49 [3113327] Biochem Biophys Res Commun. 1987 Jul 31;146(2):456-63 [3039979] J Biol Chem. 1987 Oct 15;262(29):14241-9 [2820999] Biochem J. 1987 Aug 1;245(3):631-9 [2822028] Dev Biol. 1987 Dec;124(2):295-308 [2824251] J Biol Chem. 1987 Dec 5;262(34):16456-60 [2824495] Proc Natl Acad Sci U S A. 1987 Nov;84(22):7886-90 [3120178] J Biol Chem. 1988 Jan 25;263(3):1111-4 [2447085] Proc Natl Acad Sci U S A. 1988 Feb;85(3):659-63 [3124109] Biochem J. 1988 Jan 1;249(1):271-82 [3342011] J Biol Chem. 1988 Feb 25;263(6):2808-16 [2830264] J Biol Chem. 1988 Mar 25;263(9):4083-91 [3257963] Am J Physiol. 1988 Mar;254(3 Pt 2):H401-10 [2450476] Biochem J. 1988 Feb 1;249(3):917-20 [2833233] J Biol Chem. 1987 Feb 5;262(4):1442-5 [3492494] J Biol Chem. 1987 Feb 5;262(4):1644-51 [2433285] Biochem J. 1986 Dec 15;240(3):917-20 [3827881] Exp Cell Res. 1987 May;170(1):103-15 [3494622] Proc Natl Acad Sci U S A. 1981 Jul;78(7):4392-6 [6270677] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biochemical characterization of rat brain protein kinase C isozymes. AN - 78464396; 3170568 AB - Biochemical characteristics of three rat brain protein kinase C isozymes, types I, II, and III, were compared with respect to their protein kinase and phorbol ester-binding activities. All three isozymes appeared to be alike in their phorbol ester-binding activities as evidenced by their similar Kd for phorbol 12,13-dibutyrate and requirements for Ca2+ and phospholipids. However, differences with respect to the effector-mediated stimulation of protein kinase activity were detectable among these isozymes. The type I enzyme could be stimulated by cardiolipin to a greater extent than those of the type II and III enzymes. In the presence of cardiolipin, the concentrations of dioleoylglycerol or phorbol 12,13-dibutyrate required for half-maximal activation (A1/2) of the type I enzyme were nearly an order of magnitude lower than those for the type II and III enzymes. In the presence of phosphatidylserine, differences in the A1/2 of dioleoylglycerol and phorbol 12,13-dibutyrate for the three isozymes of protein kinase C were less significant than those measured in the presence of cardiolipin. Nevertheless, the A1/2 of these two activators for the type I enzyme were lower than those for the type II and III enzymes. At high levels of phosphatidylserine (greater than 15 mol %), binding of phorbol 12,13-dibutyrate to the type I enzyme evoked a corresponding stimulation of the kinase activity, whereas binding of this phorbol ester to the type II and III enzymes produced a lesser degree of kinase stimulation. For all three isozymes, the concentrations of phosphatidylserine required for half-maximum [3H]phorbol 12,13-dibutyrate binding were almost an order of magnitude less than those for kinase stimulation. Consequently, neither isozyme exhibited a significant kinase activity at lower levels of phosphatidylserine (less than 5 mol %) and phorbol 12,13-dibutyrate (50 nM), a condition sufficient to promote near maximal phorbol ester binding. In addition to their different responses to the various activators, the three protein kinase C isozymes also have different Km values for protein substrates. The type I enzyme appeared to have lower Km values for histone IIIS, myelin basic protein, poly(lysine, serine) (3:1) polymer, and protamine than those for the type II and III enzymes. These results documented that the three protein kinase C isozymes were distinguishable in their biochemical properties. In particular, the type I enzyme, which is a brain-specific isozyme, is distinct from the type II and III enzymes, both have a widespread distribution among different tissues. JF - The Journal of biological chemistry AU - Huang, K P AU - Huang, F L AU - Nakabayashi, H AU - Yoshida, Y AD - Section on Metabolic Regulation, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/10/15/ PY - 1988 DA - 1988 Oct 15 SP - 14839 EP - 14845 VL - 263 IS - 29 SN - 0021-9258, 0021-9258 KW - Diglycerides KW - 0 KW - Isoenzymes KW - Phorbol Esters KW - Phospholipids KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - diolein KW - Z3MP1W91CW KW - Index Medicus KW - Rats KW - Phorbol Esters -- pharmacology KW - Animals KW - Diglycerides -- pharmacology KW - Phospholipids -- pharmacology KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Kinetics KW - Calcium -- pharmacology KW - Protein Binding KW - Protein Kinase C -- metabolism KW - Brain -- enzymology KW - Isoenzymes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78464396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Biochemical+characterization+of+rat+brain+protein+kinase+C+isozymes.&rft.au=Huang%2C+K+P%3BHuang%2C+F+L%3BNakabayashi%2C+H%3BYoshida%2C+Y&rft.aulast=Huang&rft.aufirst=K&rft.date=1988-10-15&rft.volume=263&rft.issue=29&rft.spage=14839&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 - 1988-11-10 N1 - Date created - 1988-11-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenesis by transient misalignment. AN - 78460194; 3049589 AB - Based upon a consideration of two mutational hot spots produced during DNA synthesis by a eukaryotic DNA repair polymerase, we suggested that certain base substitution errors result not from direct miscoding but from correct coding by a transiently misaligned template-primer (Kunkel, T. A., and Alexander, P. S. (1986) J. Biol. Chem. 261, 160-166). This model, which we called dislocation mutagenesis, has been directly tested. Introducing a single, phenotypically silent G----A base change into the template switches the base substitution specificity at the immediately adjacent hot spot, a T residue, from T----G transversions to T----A transversions. The cumulative change in frequency, represented by the disappearance of the T----G events and the appearance of the T----A events, is greater than 300-fold. These data demonstrate that during DNA synthesis in vitro, a base at one position can code a mutation at another position. This mechanism can operate over greater distances to produce complex mutations as well. We present one example in which a 123-base deletion containing three base changes at one end of the deletion can be precisely explained by transient misalignment. It remains to be established whether mutagenesis by dislocation operates in vivo to produce biologically significant changes in genetic information. JF - The Journal of biological chemistry AU - Kunkel, T A AU - Soni, A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/10/15/ PY - 1988 DA - 1988 Oct 15 SP - 14784 EP - 14789 VL - 263 IS - 29 SN - 0021-9258, 0021-9258 KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Genes, Bacterial KW - Chromosome Deletion KW - Base Sequence KW - Transfection KW - Genetic Engineering -- methods KW - DNA-Directed DNA Polymerase -- metabolism KW - Models, Genetic KW - Escherichia coli -- genetics KW - Coliphages -- genetics KW - Mutation KW - DNA Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78460194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+by+transient+misalignment.&rft.au=Kunkel%2C+T+A%3BSoni%2C+A&rft.aulast=Kunkel&rft.aufirst=T&rft.date=1988-10-15&rft.volume=263&rft.issue=29&rft.spage=14784&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 - 1988-11-10 N1 - Date created - 1988-11-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lupus as a renal disease. AN - 78457265; 3139682 JF - Hospital practice (Office ed.) AU - Balow, J E AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda. Y1 - 1988/10/15/ PY - 1988 DA - 1988 Oct 15 SP - 129 EP - 35, 139-40, 142-6 VL - 23 IS - 10 SN - 8750-2836, 8750-2836 KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Lupus Erythematosus, Systemic -- immunology KW - Cyclophosphamide -- therapeutic use KW - Humans KW - Neoplasms -- chemically induced KW - Prognosis KW - Clinical Trials as Topic KW - Cyclophosphamide -- adverse effects KW - Lupus Nephritis -- drug therapy KW - Lupus Nephritis -- pathology KW - Kidney Glomerulus -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78457265?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Lupus+as+a+renal+disease.&rft.au=Balow%2C+J+E&rft.aulast=Balow&rft.aufirst=J&rft.date=1988-10-15&rft.volume=23&rft.issue=10&rft.spage=129&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 - 1988-11-17 N1 - Date created - 1988-11-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of gamma radiation on resting B lymphocytes. II. Functional characterization of the antigen-presentation defect. AN - 78449956; 2844902 AB - The effect of radiation on three discrete Ag-presentation functions in resting B cells was examined: 1) Ag uptake and processing, 2) expression of processed Ag in the context of functional class II molecules, and 3) provision of necessary co-stimulatory, or "second," signals. Analysis of radiation's effect on B cell presentation of intact vs fragmented Ag or its effect on presentation by Ag-pulsed B cells indicated that damage to Ag uptake and processing could not account for the bulk of the radiation-induced Ag-presentation defect. Experiments with phosphatidylinositol hydrolysis as an indirect measure of TCR occupancy suggested that irradiation caused a fairly rapid (within 1 to 2 h) decrease in the ability of the B cell APC to display a stimulatory combination of Ag and class II molecule. Ag dose-response analyses demonstrated that when presenting a fragment of the Ag pigeon cytochrome c to a T cell clone, 3000 rad-treated B cell APC were able to stimulate approximately 50% as much phosphatidylinositol turnover as unirradiated B cells. It was also found that, in contrast to their inability to initiate T cell proliferation, and similarly to chemically cross-linked splenocytes, heavily irradiated resting B cells plus Ag induced a state of Ag hyporesponsiveness in T cell clones. This effect on T cells had the same Ag- and MHC-specificity as did receptor occupancy required for proliferation, indicating that heavily irradiated resting B cells bear functional class II molecules. Co-culture of T cells with allogeneic B cells and syngeneic heavily irradiated B cells or chemically cross-linked splenic APC plus Ag resulted in T cell proliferation and interfered with the induction of the hyporesponsive state. This co-stimulatory function was radiosensitive in resting allogeneic B cells. Together, these data support the hypothesis that the major functional consequences of radiation to resting B cell APC are a reduction in the effective display of Ag plus class II molecules and, probably what is more important, a loss in the ability to provide APC-derived co-stimulatory signals. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Ashwell, J D AU - Jenkins, M K AU - Schwartz, R H AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10/15/ PY - 1988 DA - 1988 Oct 15 SP - 2536 EP - 2544 VL - 141 IS - 8 SN - 0022-1767, 0022-1767 KW - Cytochrome c Group KW - 0 KW - Receptors, Antigen, T-Cell KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Gamma Rays KW - Immune Tolerance -- radiation effects KW - Cytochrome c Group -- immunology KW - Receptors, Antigen, T-Cell -- metabolism KW - Mice KW - Dose-Response Relationship, Radiation KW - Columbidae KW - Mice, Inbred C57BL KW - T-Lymphocytes -- immunology KW - Female KW - Male KW - Clone Cells -- immunology KW - B-Lymphocytes -- radiation effects KW - B-Lymphocytes -- immunology KW - B-Lymphocytes -- metabolism KW - Antigen-Presenting Cells -- radiation effects KW - Antigen-Presenting Cells -- immunology KW - Interphase -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78449956?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+gamma+radiation+on+resting+B+lymphocytes.+II.+Functional+characterization+of+the+antigen-presentation+defect.&rft.au=Ashwell%2C+J+D%3BJenkins%2C+M+K%3BSchwartz%2C+R+H&rft.aulast=Ashwell&rft.aufirst=J&rft.date=1988-10-15&rft.volume=141&rft.issue=8&rft.spage=2536&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 - 1988-11-09 N1 - Date created - 1988-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergistic antitumor effects of combination immunotherapy with recombinant interleukin-2 and a recombinant hybrid alpha-interferon in the treatment of established murine hepatic metastases. AN - 78445953; 3262413 AB - We investigated the antitumor effects of combined immunotherapy with recombinant human interleukin-2 (rhIL-2) and the recombinant human interferon-alpha (rhIFN-alpha) A/D hybrid in the treatment of established single or multiple murine hepatic metastases. Mice bearing either weakly immunogenic MCA-106 or nonimmunogenic MCA-102 were treated with rhIL-2 alone, rhIFN-alpha alone, or the combination of lymphokines. Therapy was initiated on Day 3 or 10 and continued for 3-4 consecutive days. In the treatment of 3- and 10-day multiple MCA-106 liver metastases, significant reductions in the number of metastases, often more than 90%, were observed with the combination of rhIL-2 and rhIFN-alpha at doses of each lymphokine which had no effect when given alone. This decrease in the number of metastases resulted in a survival benefit that was seen in the combination therapy groups in a dose-dependent manner. Similarly, substantial reductions in tumor weight were seen when the combination of rhIL-2 and rhIFN-alpha was administered to mice with single large hepatic metastases. The decreases in both single and multiple metastatic tumor deposits by the combination of lymphokines were more than that predicted by the additive effect of each treatment alone. With the nonimmunogenic tumor, MCA-102, however, no benefit was derived from the addition of rhIFN-alpha to rhIL-2 therapy. Immunotherapy with recombinant murine interferon-gamma and rhIL-2 was directly compared to therapy with rhIL-2 and rhIFN-alpha. The combination of rhIL-2 and rhIFN-alpha again was found to be effective while recombinant murine interferon-gamma added toxicity but no therapeutic benefit to immunotherapy with rhIL-2 alone. The synergy between rhIL-2 and rhIFN-alpha was shown to be dependent on the host's intact immune system since mice immunosuppressed by sublethal irradiation prior to inoculation of tumor did not respond to the combined treatment. Possible mechanisms of the in vivo synergy between rhIL-2 and rhIFN-alpha are discussed. JF - Cancer research AU - Cameron, R B AU - McIntosh, J K AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10/15/ PY - 1988 DA - 1988 Oct 15 SP - 5810 EP - 5817 VL - 48 IS - 20 SN - 0008-5472, 0008-5472 KW - Interferon Type I KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - Index Medicus KW - Sarcoma, Experimental -- secondary KW - Drug Therapy, Combination KW - Animals KW - Sarcoma, Experimental -- therapy KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Recombinant Proteins -- therapeutic use KW - Liver Neoplasms -- therapy KW - Interleukin-2 -- therapeutic use KW - Immunization, Passive KW - Interferon Type I -- therapeutic use KW - Liver Neoplasms -- secondary UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78445953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+antitumor+effects+of+combination+immunotherapy+with+recombinant+interleukin-2+and+a+recombinant+hybrid+alpha-interferon+in+the+treatment+of+established+murine+hepatic+metastases.&rft.au=Cameron%2C+R+B%3BMcIntosh%2C+J+K%3BRosenberg%2C+S+A&rft.aulast=Cameron&rft.aufirst=R&rft.date=1988-10-15&rft.volume=48&rft.issue=20&rft.spage=5810&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 - 1988-11-10 N1 - Date created - 1988-11-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The National Cancer Institute's intervention trials. AN - 78440791; 3048640 AB - The National Cancer Institute (NCI) has increased its emphasis in cancer prevention by undertaking a number of human intervention trials. Special emphasis is placed on chemoprevention, diet, and smoking and tobacco use. Some 24 clinical trials are ongoing in chemoprevention to assess the role of specific chemicals (natural and synthetic) in preventing, inhibiting, or reversing carcinogenesis. In diet and nutrition, several macronutrient trials are underway. The most significant of these is examining the relationship between dietary fat and breast cancer. In 1982, the NCI initiated a broad intervention research effort in smoking and tobacco use which has resulted in 46 prevention and clinical trials covering 25 states and more than 200 cities. More recently, a North American community-based intervention trial was begun to test cessation strategies for heavy smokers in 22 different sites. All of these intervention research efforts are testing strategies which later can be applied to large target population thereby supporting NCI's ambitious goal to reduce cancer mortality in this nation 50% by the year 2000. JF - Cancer AU - Cullen, J W AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, MD 20892-3100. Y1 - 1988/10/15/ PY - 1988 DA - 1988 Oct 15 SP - 1851 EP - 1864 VL - 62 IS - 8 Suppl SN - 0008-543X, 0008-543X KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Plants, Toxic KW - Humans KW - National Institutes of Health (U.S.) KW - Tobacco KW - Clinical Trials as Topic KW - Smoking -- ethnology KW - Smoking -- prevention & control KW - Nutritional Physiological Phenomena KW - Diet KW - Male KW - Female KW - Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78440791?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+National+Cancer+Institute%27s+intervention+trials.&rft.au=Cullen%2C+J+W&rft.aulast=Cullen&rft.aufirst=J&rft.date=1988-10-15&rft.volume=62&rft.issue=8+Suppl&rft.spage=1851&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-09 N1 - Date created - 1988-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Overview of results of randomized clinical trials in heart disease. I. Treatments following myocardial infarction. AN - 78431180; 2901501 JF - JAMA AU - Yusuf, S AU - Wittes, J AU - Friedman, L AD - Clincal Trials Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1988/10/14/ PY - 1988 DA - 1988 Oct 14 SP - 2088 EP - 2093 VL - 260 IS - 14 SN - 0098-7484, 0098-7484 KW - Adrenergic beta-Antagonists KW - 0 KW - Anti-Arrhythmia Agents KW - Anticoagulants KW - Calcium Channel Blockers KW - Nitrates KW - Platelet Aggregation Inhibitors KW - Streptokinase KW - EC 3.4.- KW - Abridged Index Medicus KW - Index Medicus KW - Hemodynamics -- drug effects KW - Platelet Aggregation Inhibitors -- therapeutic use KW - Random Allocation KW - Anticoagulants -- therapeutic use KW - Humans KW - Calcium Channel Blockers -- adverse effects KW - Streptokinase -- therapeutic use KW - Nitrates -- therapeutic use KW - Research Design KW - Adrenergic beta-Antagonists -- therapeutic use KW - Calcium Channel Blockers -- therapeutic use KW - Anti-Arrhythmia Agents -- therapeutic use KW - Myocardial Infarction -- mortality KW - Myocardial Infarction -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78431180?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Overview+of+results+of+randomized+clinical+trials+in+heart+disease.+I.+Treatments+following+myocardial+infarction.&rft.au=Yusuf%2C+S%3BWittes%2C+J%3BFriedman%2C+L&rft.aulast=Yusuf&rft.aufirst=S&rft.date=1988-10-14&rft.volume=260&rft.issue=14&rft.spage=2088&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-27 N1 - Date created - 1988-10-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The structure of the regulatory region of the rat L1 (L1Rn, long interspersed repeated) DNA family of transposable elements. AN - 19795200; 8730646 AB - Here we report the DNA structure of the left 1.5 kb of two newly isolated full length members of the rat L1 DNA family (L1Rn, long interspersed repeated DNA). In contrast to earlier isolated rat L1 members, both of these contain promoter-like regions that are most likely full length. In addition, the promoter-like region of both members has undergone a partial tandem duplication. A second internal region of the left end of one of the reported members is also tandemly duplicated. The propensity of the left end of rat L1 elements to undergo this form of genetic rearrangement, as well as other structural features revealed by the present work, is discussed in light of the fact that during evolution the otherwise conserved mammalian L1 DNA families have each acquired completely different promoter-like regions. In an accompanying paper [Nur, I., Pascale, E., and Furano, A. V. (1988) Nucleic Acids Res. 16, submitted], we report that one of the rat promoter-like regions can function as a promoter in rat cells when fused to the Escherichia coli chloramphenicol acyltransferase gene. JF - Nucleic Acids Research AU - Furano, A V AU - Robb, S M AU - Robb, F T AD - Section on Genomic Structure and Function, National Institute of Diabetes, and Digestive and Kidney Diseases, Bethesda, MD 20892. Y1 - 1988/10/11/ PY - 1988 DA - 1988 Oct 11 SP - 9215 EP - 9231 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 16 IS - 19 SN - 0305-1048, 0305-1048 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Transposons KW - Promoters KW - Chloramphenicol KW - DNA structure KW - nucleic acids KW - Acyltransferase KW - Regulatory sequences KW - Escherichia coli KW - Repeated DNA sequences KW - Evolution KW - J 02310:Genetics & Taxonomy KW - N 14845:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19795200?accountid=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=The+structure+of+the+regulatory+region+of+the+rat+L1+%28L1Rn%2C+long+interspersed+repeated%29+DNA+family+of+transposable+elements.&rft.au=Furano%2C+A+V%3BRobb%2C+S+M%3BRobb%2C+F+T&rft.aulast=Furano&rft.aufirst=A&rft.date=1988-10-11&rft.volume=16&rft.issue=19&rft.spage=9215&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 - Transposons; Promoters; Chloramphenicol; nucleic acids; DNA structure; Acyltransferase; Regulatory sequences; Evolution; Repeated DNA sequences; Escherichia coli ER - TY - JOUR T1 - Ca2+-dependent K+ channels in neuroblastoma hybrid cells activated by intracellular inositol trisphosphate and extracellular bradykinin. AN - 78439951; 3262538 AB - Bradykinin (BK) activation of phosphatidylinositide breakdown in NG108-15 neuroblastoma x glioma hybrid cells in the generation of an outward K+ current through the release of Ca2+ by the intermediary messenger inositol 1,4,5-trisphosphate (InsP3). Channels mediating this outward current were identified using cell-attached patch electrodes. Intracellular iontophoretic injection of InsP3 or Ca2+, or extracellular application of BK, evoked bursts of K+ channel activity coincident with cell hyperpolarization measured with an intracellular recording micropipette. The most frequent channels had a mean single-channel conductance of about 40 pS in symmetrical K+ solutions; additional openings of lower conductance (18 pS) channels were also detected. Bath application of phorbol dibutyrate (PDBu, 1 microM) increased the number and opening probability of the InsP3-induced channels. JF - FEBS letters AU - Higashida, H AU - Brown, D A AD - Laboratory of Biochemical Genetics, National Heart, Lung and Blood Institute, Bethesda, MD 20892. Y1 - 1988/10/10/ PY - 1988 DA - 1988 Oct 10 SP - 395 EP - 400 VL - 238 IS - 2 SN - 0014-5793, 0014-5793 KW - Inositol Phosphates KW - 0 KW - Potassium Channels KW - Sugar Phosphates KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - Bradykinin KW - S8TIM42R2W KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Tumor Cells, Cultured KW - Electric Conductivity KW - Hybrid Cells KW - Potassium Channels -- physiology KW - Mice KW - Potassium Channels -- drug effects KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Glioma -- physiopathology KW - Neuroblastoma -- physiopathology KW - Sugar Phosphates -- pharmacology KW - Calcium -- pharmacology KW - Bradykinin -- pharmacology KW - Inositol Phosphates -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78439951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Ca2%2B-dependent+K%2B+channels+in+neuroblastoma+hybrid+cells+activated+by+intracellular+inositol+trisphosphate+and+extracellular+bradykinin.&rft.au=Higashida%2C+H%3BBrown%2C+D+A&rft.aulast=Higashida&rft.aufirst=H&rft.date=1988-10-10&rft.volume=238&rft.issue=2&rft.spage=395&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-14 N1 - Date created - 1988-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of continuous intravenous infusion of zidovudine (AZT) in children with symptomatic HIV infection. AN - 78422310; 3166511 AB - To produce concentrations of zidovudine (AZT) in plasma and cerebrospinal fluid that would provide constant inhibition of the replication of human immunodeficiency virus (HIV), we gave AZT by continuous intravenous infusion to 21 children ranging in age from 14 months to 12 years who had acquired HIV infection through transfusions or perinatally. All patients were symptomatic before AZT treatment (Class P2 of the Centers for Disease Control); 13 (62 percent) had evidence of neurodevelopmental abnormalities. The mean CD4/CD8 ratio was 0.18; 11 patients had CD4 counts below 0.2 x 10(9) per liter. We administered AZT at four dose levels: 0.5, 0.9, 1.4, and 1.8 mg per kilogram of body weight per hour. The plasma drug concentrations achieved at the respective dose levels were 1.9 +/- 0.3, 2.8 +/- 1.4, 3.1 +/- 1.1, and 4.5 +/- 1.0 microM. The steady-state cerebrospinal fluid:plasma ratio was 0.24 +/- 0.07. The only evidence of toxicity was bone marrow suppression. Transfusion was required in 14 patients because of low levels of hemoglobin (5 mmol per liter [less than 8 g per deciliter]). Dose-limiting neutropenia (less than 0.5 x 10(9) polymorphonuclear leukocytes per cubic millimeter) occurred in most patients who received doses of 1.4 mg per kilogram per hour or more. Improvement in neurodevelopmental abnormalities occurred in all 13 children who had presented with encephalopathy before treatment. Serial measurements of IQ before therapy and after three and six months of continuous therapy with AZT showed that IQ scores, including those for verbal and performance IQ, rose in these 13 patients and in 5 other children who had no detectable evidence of encephalopathy before treatment. Most patients also had increased appetite and weight, decreased lymphadenopathy and hepatosplenomegaly, decreased immunoglobulin levels, and increased numbers of CD4 cells. In some patients the improvement in the features of encephalopathy occurred despite the absence of immunologic improvement. We conclude that AZT is beneficial in children with symptomatic HIV infection, especially those with encephalopathy (which may be subclinical), and that the optimal continuous intravenous dose of AZT in children is between 0.9 and 1.4 mg per kilogram per hour. JF - The New England journal of medicine AU - Pizzo, P A AU - Eddy, J AU - Falloon, J AU - Balis, F M AU - Murphy, R F AU - Moss, H AU - Wolters, P AU - Brouwers, P AU - Jarosinski, P AU - Rubin, M AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10/06/ PY - 1988 DA - 1988 Oct 06 SP - 889 EP - 896 VL - 319 IS - 14 SN - 0028-4793, 0028-4793 KW - Zidovudine KW - 4B9XT59T7S KW - Glucose KW - IY9XDZ35W2 KW - Thymidine KW - VC2W18DGKR KW - Abridged Index Medicus KW - Index Medicus KW - Population KW - AIDS/HIV KW - United States KW - Laboratory Examinations And Diagnoses KW - Age Factors KW - Research Methodology KW - Physiology KW - Child KW - Treatment KW - Developed Countries KW - Hiv Infections KW - Evaluation KW - Drugs--administraction and dosage KW - Population Characteristics KW - Neurologic Effects--changes KW - Demographic Factors KW - Data Collection KW - Diseases KW - Youth KW - Drugs--beneficial effects KW - North America KW - Americas KW - Northern America KW - Viral Diseases KW - Examinations And Diagnoses KW - Biology KW - Infusions, Intravenous KW - Glucose -- metabolism KW - Humans KW - Tomography, X-Ray Computed KW - Brain -- metabolism KW - Brain -- diagnostic imaging KW - Child, Preschool KW - Infant KW - Opportunistic Infections -- etiology KW - Brain Diseases -- diagnostic imaging KW - Follow-Up Studies KW - Brain Diseases -- etiology KW - Intelligence Tests KW - Thymidine -- administration & dosage KW - Acquired Immunodeficiency Syndrome -- complications KW - Acquired Immunodeficiency Syndrome -- diagnostic imaging KW - Thymidine -- pharmacokinetics KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Thymidine -- therapeutic use KW - Thymidine -- analogs & derivatives KW - Thymidine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78422310?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Effect+of+continuous+intravenous+infusion+of+zidovudine+%28AZT%29+in+children+with+symptomatic+HIV+infection.&rft.au=Pizzo%2C+P+A%3BEddy%2C+J%3BFalloon%2C+J%3BBalis%2C+F+M%3BMurphy%2C+R+F%3BMoss%2C+H%3BWolters%2C+P%3BBrouwers%2C+P%3BJarosinski%2C+P%3BRubin%2C+M&rft.aulast=Pizzo&rft.aufirst=P&rft.date=1988-10-06&rft.volume=319&rft.issue=14&rft.spage=889&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-24 N1 - Date created - 1988-10-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1989 Mar 23;320(12):805-6 [2633749] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Membrane currents activated in acutely dissociated rat pineal cells during the circadian cycle. AN - 78510042; 3185985 AB - Whole-cell patch-clamp recordings were performed in cells acutely dissociated from adult rat pineal glands in order to determine possible long lasting influences of the circadian rhythm upon voltage-activated membrane currents. Cells were dissociated either during the light or dark period. From a holding potential of -50 mV, pineal cells bathed in a normal solution responded to depolarizing potentials positive to -20 mV with a slowly rising sustained outward current. From a holding potential of -100 mV, a transient outward current was activated with command potentials positive to -50 mV. This current reached a peak within 15 ms and had a significant decay over 160 ms. In most of the cells, inward currents were not observed and no significant differences were found between the properties of the outward currents in cells dissociated during the light or dark period. This suggests that the previously reported circadian activity in the rat pineal gland is not associated with inward current or with long lasting changes in the voltage-activated membrane currents. JF - Neuroscience letters AU - Aguayo, L G AU - Weight, F F AD - Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1988/10/05/ PY - 1988 DA - 1988 Oct 05 SP - 155 EP - 160 VL - 92 IS - 2 SN - 0304-3940, 0304-3940 KW - Tetrodotoxin KW - 4368-28-9 KW - Potassium KW - RWP5GA015D KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Potassium -- physiology KW - Animals KW - Membrane Potentials -- drug effects KW - Cell Separation KW - Tetrodotoxin -- pharmacology KW - Electric Stimulation KW - Male KW - Circadian Rhythm KW - Pineal Gland -- cytology KW - Lighting KW - Pineal Gland -- drug effects KW - Pineal Gland -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78510042?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Membrane+currents+activated+in+acutely+dissociated+rat+pineal+cells+during+the+circadian+cycle.&rft.au=Aguayo%2C+L+G%3BWeight%2C+F+F&rft.aulast=Aguayo&rft.aufirst=L&rft.date=1988-10-05&rft.volume=92&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 - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acquired immunodeficiency syndrome: progress and prospects for vaccine development. AN - 78420281; 3047406 JF - Journal of the National Cancer Institute AU - Sarma, P S AU - Cremer, K J AU - Gruber, J AD - Biological Carcinogenesis Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10/05/ PY - 1988 DA - 1988 Oct 05 SP - 1193 EP - 1197 VL - 80 IS - 15 SN - 0027-8874, 0027-8874 KW - Viral Vaccines KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Humans KW - Disease Models, Animal KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - HIV -- immunology KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Viral Vaccines -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78420281?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Acquired+immunodeficiency+syndrome%3A+progress+and+prospects+for+vaccine+development.&rft.au=Sarma%2C+P+S%3BCremer%2C+K+J%3BGruber%2C+J&rft.aulast=Sarma&rft.aufirst=P&rft.date=1988-10-05&rft.volume=80&rft.issue=15&rft.spage=1193&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 - 1988-10-25 N1 - Date created - 1988-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Deletion of 3(p14p23) in secondary erythroleukemia arising in long-term survivors of small cell lung cancer. AN - 78416230; 2843653 AB - Cytogenetic studies were done on the leukemia cells of two patients with small cell lung cancer (SCLC) who developed erythroleukemia (acute nonlymphocytic leukemia, French-American-British M6) after combined modality chemotherapy and radiotherapy for their lung cancer. Surprisingly, both erythroleukemias exhibited the del(3)(p14p23) predominantly found in SCLC. In four other patients who had secondary erythroleukemias associated with other cancers, no deletions of 3p were found. These findings could be accounted for by one of three possible mechanisms: (a) an inherited recessive gene (anti-oncogene or tumor suppressor gene) in this region of 3p was uncovered by the combined modality therapy, (b) an inherited predisposition to damage of both chromosomes at 3p14 leads to SCLC and erythroleukemia after exposure to carcinogens and/or chemotherapy-radiotherapy, or (c) the finding of lineage specificity for the 3p deletion with the presence of the 3p deletion in SCLC and erythroleukemia suggests a common bone marrow precursor. JF - Journal of the National Cancer Institute AU - Whang-Peng, J AU - Lee, E C AU - Minna, J D AU - Abeloff, M D AU - Bradley, E C AU - Young, R C AU - Longo, D L AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10/05/ PY - 1988 DA - 1988 Oct 05 SP - 1253 EP - 1255 VL - 80 IS - 15 SN - 0027-8874, 0027-8874 KW - H-2 Antigens KW - 0 KW - Index Medicus KW - Humans KW - Aged KW - Middle Aged KW - Male KW - H-2 Antigens -- analysis KW - Female KW - Chromosomes, Human, Pair 3 KW - Chromosome Deletion KW - Leukemia, Erythroblastic, Acute -- genetics KW - Lung Neoplasms -- genetics KW - Carcinoma, Small Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78416230?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Deletion+of+3%28p14p23%29+in+secondary+erythroleukemia+arising+in+long-term+survivors+of+small+cell+lung+cancer.&rft.au=Whang-Peng%2C+J%3BLee%2C+E+C%3BMinna%2C+J+D%3BAbeloff%2C+M+D%3BBradley%2C+E+C%3BYoung%2C+R+C%3BLongo%2C+D+L&rft.aulast=Whang-Peng&rft.aufirst=J&rft.date=1988-10-05&rft.volume=80&rft.issue=15&rft.spage=1253&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 - 1988-10-25 N1 - Date created - 1988-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Distinct mechanisms of c-myc and lymphokine gene expression in an antigen specific T cell clone. AN - 78790496; 3152599 AB - Experiments were performed to examine the mechanisms regulating the expression of the c-myc gene and the IL-2 and interferon gamma (IFN-gamma) lymphokine genes in an antigen-specific murine T cell clone. IL-2 and the mitogenic lectin, concanavalin A (Con A), as well as the calcium ionophore ionomycin, in concert with phorbol ester, (PMA) enhanced c-myc gene transcription, but by distinct mechanisms as demonstrated by differential sensitivity to inhibition of protein synthesis and by transcriptional run-off assays using c-myc exon 1 and exon 2 probes. Induction of c-myc expression by IL-2, but not lectin or ionomycin plus phorbol ester, was inhibited in the presence of cycloheximide. IL-2 induced the transcription of both c-myc exons 1 and 2, whereas Con A primarily enhanced exon 1 to exon 2 transcriptional read-through. A direct relationship was observed between the level of early c-myc expression following IL-2 stimulation and the magnitude of the subsequent clonal proliferative response. Lymphokine gene expression was enhanced by Con A, but not by IL-2. Induction of the lymphokine genes in this T cell clone was under predominant post-transcriptional control and was sensitive to protein synthesis inhibition. Therefore, mitogenic lectins induce c-myc and lymphokine gene expression via different pathways. JF - Oncogene AU - Heckford, S E AU - Gelmann, E P AU - Matis, L A AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 415 EP - 421 VL - 3 IS - 4 SN - 0950-9232, 0950-9232 KW - DNA Probes KW - 0 KW - Interleukin-2 KW - Lymphokines KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-myc KW - Concanavalin A KW - 11028-71-0 KW - Interferon-gamma KW - 82115-62-6 KW - Cycloheximide KW - 98600C0908 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Clone Cells KW - Animals KW - Interferon-gamma -- genetics KW - Blotting, Northern KW - Cell Nucleus -- metabolism KW - Exons KW - Transcription, Genetic KW - Interleukin-2 -- genetics KW - Lymphocyte Activation KW - Protein-Tyrosine Kinases -- genetics KW - Genes KW - Cycloheximide -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - T-Lymphocytes -- immunology KW - Proto-Oncogenes -- drug effects KW - Cell Line KW - Concanavalin A -- pharmacology KW - Gene Expression -- drug effects KW - Lymphokines -- genetics KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78790496?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Distinct+mechanisms+of+c-myc+and+lymphokine+gene+expression+in+an+antigen+specific+T+cell+clone.&rft.au=Heckford%2C+S+E%3BGelmann%2C+E+P%3BMatis%2C+L+A&rft.aulast=Heckford&rft.aufirst=S&rft.date=1988-10-01&rft.volume=3&rft.issue=4&rft.spage=415&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-07-12 N1 - Date created - 1990-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Applications of fast atom bombardment and tandem mass spectrometry. AN - 78724896; 3242706 AB - The application of fast atom bombardment combined with tandem mass spectrometry to the structure elucidation of carcinogen-modified oligonucleotides, glutathione, cysteine and N-acetyl cysteine conjugates of exogenous toxins and chemically modified peptides is described. JF - Biomedical & environmental mass spectrometry AU - Tomer, K B AU - Guenat, C AU - Dino, J J AU - Deterding, L J AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 473 EP - 476 VL - 16 IS - 1-12 SN - 0887-6134, 0887-6134 KW - Carcinogens KW - 0 KW - Oligonucleotides KW - Peptides KW - Toxins, Biological KW - Glutathione KW - GAN16C9B8O KW - Cysteine KW - K848JZ4886 KW - Acetylcysteine KW - WYQ7N0BPYC KW - Index Medicus KW - Oligonucleotides -- analysis KW - Glutathione -- analysis KW - Cysteine -- analysis KW - Acetylcysteine -- analysis KW - Peptides -- analysis KW - Carcinogens -- analysis KW - Toxins, Biological -- analysis KW - Mass Spectrometry -- instrumentation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78724896?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+%26+environmental+mass+spectrometry&rft.atitle=Applications+of+fast+atom+bombardment+and+tandem+mass+spectrometry.&rft.au=Tomer%2C+K+B%3BGuenat%2C+C%3BDino%2C+J+J%3BDeterding%2C+L+J&rft.aulast=Tomer&rft.aufirst=K&rft.date=1988-10-01&rft.volume=16&rft.issue=1-12&rft.spage=473&rft.isbn=&rft.btitle=&rft.title=Biomedical+%26+environmental+mass+spectrometry&rft.issn=08876134&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic tools in the study of drug self-administration. AN - 78671578; 3067599 AB - Recent studies have shown that large genetic differences exist in the extent to which orally delivered ethanol will come to serve as a positive reinforcer under operantly defined conditions. In addition, these studies suggest that a significant correlation exists between results from two-bottle choice studies of ethanol drinking and operant self-administration studies of ethanol functioning as a reinforcer. The present paper reports further genetic influences on ethanol self-administration which were found using Long Sleep and Short Sleep mice, bred selectively for high and low duration of loss of the righting reflex in responses to ethanol, respectively. It was possible to establish ethanol as a reinforcer in Long Sleep mice but not in Short Sleep mice. These results indicate that neurosensitivity to ethanol may determine the absolute amount of ethanol consumption but is not highly related to the ability of ethanol to serve as a positive reinforcer. In addition, this paper presents genetic correlations which indicate that (a) ethanol preference and self-administration are highly correlated across genotype; (b) sensitivity to ethanol and self-administration of this drug are not highly genetically correlated; (c) ethanol is not self-administered in operant studies solely for its caloric value; and (d) there exist important genetic determinants of drug reinforced behavior. JF - Alcoholism, clinical and experimental research AU - George, F R AD - Behavior Genetics Laboratory, National Institute on Drug Abuse, Addiction Research Center, Baltimore, Maryland 21224. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 586 EP - 590 VL - 12 IS - 5 SN - 0145-6008, 0145-6008 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Reinforcement Schedule KW - Reflex -- drug effects KW - Motor Skills -- drug effects KW - Ethanol -- administration & dosage KW - Conditioning, Operant KW - Mice KW - Sleep Stages -- drug effects KW - Postural Balance -- drug effects KW - Alcohol Drinking -- psychology KW - Alcoholism -- genetics KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78671578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genetic+tools+in+the+study+of+drug+self-administration.&rft.au=George%2C+F+R&rft.aulast=George&rft.aufirst=F&rft.date=1988-10-01&rft.volume=12&rft.issue=5&rft.spage=586&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 - 1989-03-31 N1 - Date created - 1989-03-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antihypertensive therapy with ketanserin: metabolic and hemodynamic effects. AN - 78667362; 2465437 AB - Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 h), blood pressures measured 12 h after dosing were not significantly different from those obtained during the placebo period. However, 2 h after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (p less than 0.01) and 6 +/- 5 mm Hg (p less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. At the time of peak antihypertensive activity, plasma renin activity, aldosterone, growth hormone, and prolactin levels were unchanged. Prolactin levels decreased slightly (4.1 +/- 3.0 vs. 3.7 +/- 2.9 ng/ml, p less than 0.05) during ketanserin therapy when measured 12 h after dosing. Other pituitary hormones, serum testosterone, plasma catecholamines, and plasma lipids showed no changes. Heart rate was also unchanged. Stroke volume, measured 2 h after dosing, increased (70 +/- 22 vs. 85 +/- 31 ml, p less than 0.05) with ketanserin therapy, but cardiac output did not change significantly. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24-h antihypertensive activity. JF - Journal of cardiovascular pharmacology AU - Levinson, P D AU - Zimlichman, R AU - Goldstein, D S AU - Keiser, H R AD - Hypertension-Endocrine Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 384 EP - 389 VL - 12 IS - 4 SN - 0160-2446, 0160-2446 KW - Hormones KW - 0 KW - Ketanserin KW - 97F9DE4CT4 KW - Index Medicus KW - Heart Rate -- drug effects KW - Double-Blind Method KW - Random Allocation KW - Humans KW - Adult KW - Hormones -- blood KW - Clinical Trials as Topic KW - Middle Aged KW - Blood Pressure -- drug effects KW - Hemodynamics -- drug effects KW - Ketanserin -- therapeutic use KW - Hypertension -- physiopathology KW - Ketanserin -- adverse effects KW - Hypertension -- metabolism KW - Hypertension -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78667362?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antihypertensive+therapy+with+ketanserin%3A+metabolic+and+hemodynamic+effects.&rft.au=Levinson%2C+P+D%3BZimlichman%2C+R%3BGoldstein%2C+D+S%3BKeiser%2C+H+R&rft.aulast=Levinson&rft.aufirst=P&rft.date=1988-10-01&rft.volume=12&rft.issue=4&rft.spage=384&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 - 1989-04-05 N1 - Date created - 1989-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of changes in serum androgen binding protein with germinal epithelial damage and infertility induced by di-n-pentyl phthalate. AN - 78650693; 3220221 AB - Androgen binding protein (ABP), produced by Sertoli cells and released into seminiferous tubules and blood, was measured in the serum of di-n-pentyl phthalate (DPP)-treated rats as a potential index of germinal epithelial damage. A single oral dose of DPP (0, 0.25, 1.0, or 2.0 g/kg body wt in corn oil) was given to four groups of 110 Fischer 344 rats; 10 rats per group were killed weekly for 10 weeks. Effects of treatment on serum ABP were then compared with effects on other reproductive endpoints. Treatment did not produce any significant effect on body weight or weights of liver, kidney, prostate, and seminal vesicles. In high-dose rats, serum ABP values more than doubled 2 days after injection, remained significantly elevated for 3 weeks, then fell and remained significantly below control values from Week 4 through Week 10. Accordingly, 95% of the rats in this group showed greater than 50% of the seminiferous tubules degenerated, decreased epididymal sperm density, reduced testicular and epididymal weights, and up to 97% morphologically abnormal sperm. In medium-dose rats, serum ABP increased up to 48% during the first week, returned to control values by Week 2, and remained at control levels thereafter. Of these rats, 20% showed 20-50% degenerated tubules, decreased sperm density, reduced testicular and epididymal weights (which were not always statistically significant), and up to 23% abnormal sperm morphology. In low-dose rats, serum ABP levels were similar to those of controls, and the other parameters, except sperm density, also remained unchanged. To examine the effects of DPP on fertility, a second group of rats was exposed in an identical manner [gavaged once with DPP in corn oil (0, 0.25, 1.0, and 2.0 g/kg body wt)], then mated to untreated females at 3, 6, and 10 weeks postexposure. DPP at 2 (but not 1.0 or 0.25) g/kg caused a significant reduction in pregnancies and live pups and a significant increase in preimplantation loss. Histopathology of the testis in the first experiment suggested a very slow recovery. Therefore, controls and high-dose rats in the mating trial were killed 14, 18, and 30 weeks after dosing and the germinal epithelium was evaluated histologically. All high-dose animals showed testicular lesions typical of phthalate ester exposure and the epithelium did not recover within 30 weeks.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Lindström, P AU - Harris, M AU - Ross, M AU - Lamb, J C AU - Chapin, R E AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 528 EP - 539 VL - 11 IS - 3 SN - 0272-0590, 0272-0590 KW - Androgen-Binding Protein KW - 0 KW - Phthalic Acids KW - di-n-pentyl phthalate KW - 131-18-0 KW - Index Medicus KW - Sexual Behavior, Animal -- drug effects KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Testis -- drug effects KW - Epithelial Cells KW - Spermatozoa -- drug effects KW - Body Weight -- drug effects KW - Time Factors KW - Male KW - Female KW - Organ Size -- drug effects KW - Androgen-Binding Protein -- blood KW - Phthalic Acids -- toxicity KW - Infertility, Female -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78650693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+changes+in+serum+androgen+binding+protein+with+germinal+epithelial+damage+and+infertility+induced+by+di-n-pentyl+phthalate.&rft.au=Lindstr%C3%B6m%2C+P%3BHarris%2C+M%3BRoss%2C+M%3BLamb%2C+J+C%3BChapin%2C+R+E&rft.aulast=Lindstr%C3%B6m&rft.aufirst=P&rft.date=1988-10-01&rft.volume=11&rft.issue=3&rft.spage=528&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 - 1989-03-22 N1 - Date created - 1989-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Subchronic toxicity of orally administered (gavage and dosed-feed) theophylline in Fischer 344 rats and B6C3F1 mice. AN - 78643732; 3220218 AB - Theophylline, a methylated xanthine closely resembling caffeine and theobromine, is a widely used pharmaceutical agent for the treatment of respiratory disorders and certain acute cardiovascular conditions. The National Toxicology Program has conducted 13-week subchronic toxicity studies in F344 rats and B6C3F1 mice (10 animals/group) following administration of theophylline via the diet or by gavage. Administration of theophylline in the feed (0, 1000, 2000, and 4000 ppm) resulted in no mortality or body weight effects in F344 rats, but did induce periarteritis of the arteries adjacent to mesenteric lymph nodes and the pancreas, particularly arterioles in the latter. Also observed in rats dosed with theophylline via the diet was an increased severity of chronic nephropathy in males, especially at the high dose. Administration of theophylline at the same concentrations in the feed to B6C3F1 mice resulted in no mortality, but terminal body weights were significantly decreased in all dosed groups. An increased incidence of hepatocellular glycogen depletion was observed in male and female mice, and this change is believed to represent a physiological alteration exacerbated by the administration of theophylline. Administration of theophylline by gavage to F344 rats (0, 37.5, 75, and 150 mg/kg) resulted in the early death of one high-dose male and female and significantly decreased or increased terminal body weights of high-dose males and females, respectively. Similar to the results of the dosed-feed study, male and female rats receiving theophylline by gavage demonstrated a dose-related increase in the incidence and severity of perivascular inflammation of mesenteric arteries. Gavage administration of theophylline to B6C3F1 mice (0, 75, 150, and 300 mg/kg) resulted in the early death of all high-dose females and 3/10 high-dose males and significant depression of terminal body weights in high- and mid-dose males and low-dose females. As in the dosed-feed study, the primary histopathologic change in the mouse subchronic gavage study was hepatocellular glycogen depletion, although in this case it was seen only in females. In summary, the major target organs for orally administered theophylline in 13-week subchronic toxicity studies appear to be the mesenteric arteries in F344 rats and the liver in B6C3F1 mice. On the basis of organ weight changes and/or minor histopathologic effects, many other tissues were also affected, particularly the kidneys in dosed-feed male rats and the uterus in gavage-dosed female rats. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Collins, J J AU - Elwell, M R AU - Lamb, J C AU - Manus, A G AU - Heath, J E AU - Makovec, G T AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 472 EP - 484 VL - 11 IS - 3 SN - 0272-0590, 0272-0590 KW - Theophylline KW - C137DTR5RG KW - Index Medicus KW - Rats KW - Pancreas -- pathology KW - Eating -- drug effects KW - Administration, Oral KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Kidney -- pathology KW - Body Weight -- drug effects KW - Mice KW - Mesenteric Arteries -- pathology KW - Species Specificity KW - Male KW - Female KW - Theophylline -- toxicity KW - Theophylline -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78643732?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Subchronic+toxicity+of+orally+administered+%28gavage+and+dosed-feed%29+theophylline+in+Fischer+344+rats+and+B6C3F1+mice.&rft.au=Collins%2C+J+J%3BElwell%2C+M+R%3BLamb%2C+J+C%3BManus%2C+A+G%3BHeath%2C+J+E%3BMakovec%2C+G+T&rft.aulast=Collins&rft.aufirst=J&rft.date=1988-10-01&rft.volume=11&rft.issue=3&rft.spage=472&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 - 1989-03-22 N1 - Date created - 1989-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quantification of quinolinic acid in rat brain, whole blood, and plasma by gas chromatography and negative chemical ionization mass spectrometry: effects of systemic L-tryptophan administration on brain and blood quinolinic acid concentrations. AN - 78639644; 2975477 AB - A gas chromatography/mass spectrometry assay is described to quantify the endogenous neurotoxin quinolinic acid (QUIN) in brain, whole blood, and plasma. High specificity and high sensitivity were obtained by using negative chemical ionization and accuracy was achieved by using [18O]QUIN as internal standard. Neutralized perchloric acid extracts were washed with chloroform, applied to Dowex 1 x 8 (formate form), and eluted with 6 M formic acid. After lyophilization, QUIN and [18O]QUIN were esterified with hexafluoroisopropanol (to mass 467 and 471, respectively) using trifluoroacetylimidazole as catalyst. The esters were extracted into heptane and injected onto a gas chromatograph, DB-5 capillary column. QUIN and [18O]QUIN were quantified by selected ion monitoring of QUIN-specific anion currents from the molecular anions (m/z 467 and 471, respectively) and a specific anion fragment (m/z 316 from QUIN and m/z 320 from [18O]QUIN). Minimum sensitivity was 3 fmol, intraassay variability was 3.2%, and interassay variability was 8.1% QUIN concentrations in frontal cortex from over 200 rats ranged from 20 to 180 fmol/mg wet wt. Two hours after systemic L-tryptophan (L-Trp; 0.370 mmol/kg) administration, QUIN increased in whole blood 134.8-fold and in plasma, 74.3-fold. In frontal cortex, increases in QUIN (22.6-fold, corrected for QUIN in blood) exceeded increases in cortical L-Trp (2.54-fold), 5-HT (1.35-fold), and 5-HIAA (1.74-fold). These studies demonstrate that QUIN is present in brain and is sensitive to the availability of systemic L-Trp. JF - Analytical biochemistry AU - Heyes, M P AU - Markey, S P AD - Laboratory of Neurophysiology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 349 EP - 359 VL - 174 IS - 1 SN - 0003-2697, 0003-2697 KW - Pyridines KW - 0 KW - Quinolinic Acids KW - Tryptophan KW - 8DUH1N11BX KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Tryptophan -- pharmacology KW - Reference Values KW - Brain -- drug effects KW - Reference Standards KW - Brain -- metabolism KW - Male KW - Quinolinic Acids -- blood KW - Pyridines -- analysis KW - Gas Chromatography-Mass Spectrometry -- methods KW - Brain Chemistry KW - Quinolinic Acids -- analysis KW - Quinolinic Acids -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78639644?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Quantification+of+quinolinic+acid+in+rat+brain%2C+whole+blood%2C+and+plasma+by+gas+chromatography+and+negative+chemical+ionization+mass+spectrometry%3A+effects+of+systemic+L-tryptophan+administration+on+brain+and+blood+quinolinic+acid+concentrations.&rft.au=Heyes%2C+M+P%3BMarkey%2C+S+P&rft.aulast=Heyes&rft.aufirst=M&rft.date=1988-10-01&rft.volume=174&rft.issue=1&rft.spage=349&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 - 1989-03-08 N1 - Date created - 1989-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Efficacy of chemoimmunotherapy with cyclophosphamide, interleukin-2 and lymphokine activated killer cells in an intraperitoneal murine tumour model. AN - 78596374; 3264714 AB - We have previously reported on the efficacy of intraperitoneal (i.p.) immunotherapy with interleukin-2 (IL-2) and adoptively transferred lymphokine activated killer (LAK) cells in an i.p. murine tumour model. Because of a dose-limiting toxicity associated with IL-2, cures are seldom observed. The development of treatment strategies that combine components that augment or synergise with the antitumour activity of IL-2 is crucial for the successful use of IL-2 in a clinical setting. Because of the known toxicity of high-dose IL-2 or high dose cyclophosphamide (CY) treatment, the goal of our experiments was to investigate the efficacy of chemoimmunotherapy with low or moderate doses of cyclophosphamide (CY) in combination with low or moderate doses of IL-2 with or without adoptively transferred LAK cells. Assessment of i.p. tumour growth 14 days after tumour inoculation, using the peritoneal cancer index (PCI) scoring system, demonstrated that combination treatment of established (day 3) i.p. tumour was clearly superior to single modality treatment. The effect was further enhanced by a second dose of CY at the end of a course of IL-2. Combination treatment led to a significant survival benefit. About 25% of the mice were cured, even when the dose of tumour cells at inoculation was increased. These experiments demonstrate the efficacy of combined treatment with IL-2, LAK cells and CY. Further research should be directed at the design of treatment schedules based on repetitive courses of chemoimmunotherapy associated with little toxicity. JF - British journal of cancer AU - Eggermont, A M AU - Sugarbaker, P H AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 410 EP - 414 VL - 58 IS - 4 SN - 0007-0920, 0007-0920 KW - Interleukin-2 KW - 0 KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Lymphocyte Activation KW - Animals KW - Dose-Response Relationship, Drug KW - Combined Modality Therapy KW - Mice, Inbred C57BL KW - Mice KW - Time Factors KW - Female KW - Sarcoma, Experimental -- therapy KW - Cyclophosphamide -- therapeutic use KW - Interleukin-2 -- therapeutic use KW - Immunization, Passive KW - Sarcoma, Experimental -- mortality KW - Killer Cells, Natural -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78596374?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Efficacy+of+chemoimmunotherapy+with+cyclophosphamide%2C+interleukin-2+and+lymphokine+activated+killer+cells+in+an+intraperitoneal+murine+tumour+model.&rft.au=Eggermont%2C+A+M%3BSugarbaker%2C+P+H&rft.aulast=Eggermont&rft.aufirst=A&rft.date=1988-10-01&rft.volume=58&rft.issue=4&rft.spage=410&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 - 1989-02-17 N1 - Date created - 1989-02-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1974 Jun 14;249(458):654-6 [4275846] Nat Immun Cell Growth Regul. 1987;6(5):260-8 [3502171] J Natl Cancer Inst. 1977 May;58(5):1303-9 [67211] J Exp Med. 1982 Apr 1;155(4):1063-74 [6460831] J Exp Med. 1982 Jun 1;155(6):1823-41 [6176669] J Immunol. 1983 May;130(5):2203-8 [6601147] Science. 1984 Mar 30;223(4643):1412-4 [6367046] Adv Immunol. 1984;35:89-155 [6235727] Science. 1984 Sep 28;225(4669):1487-9 [6332379] J Exp Med. 1985 May 1;161(5):1122-34 [3921652] J Immunol. 1985 Jul;135(1):646-52 [3889158] J Immunol. 1985 Aug;135(2):1488-97 [3891854] Cancer Res. 1985 Aug;45(8):3735-41 [3893689] J Biol Response Mod. 1985 Aug;4(4):377-90 [3875693] Br J Cancer Suppl. 1986;7:140-60 [3459517] Cancer Immunol Immunother. 1986;22(3):217-20 [2942251] Cancer Res. 1986 Oct;46(10):4973-8 [3489517] Cancer. 1986 Dec 15;58(12):2764-72 [3490903] Cell Immunol. 1987 Feb;104(2):366-76 [3493081] N Engl J Med. 1987 Apr 9;316(15):889-97 [3493432] N Engl J Med. 1987 Apr 9;316(15):898-905 [3493433] Cancer. 1987 Oct 1;60(7):1465-73 [3497705] J Biol Response Mod. 1987 Aug;6(4):430-45 [3498012] Br J Cancer. 1987 Aug;56(2):97-102 [2444243] Cancer Res. 1987 Nov 15;47(22):5894-900 [3664490] J Natl Cancer Inst. 1987 Nov;79(5):983-90 [3500357] Cancer Res. 1988 Jan 1;48(1):122-9 [3257159] Cancer Immunol Immunother. 1988;26(1):23-30 [3257900] Ann N Y Acad Sci. 1976;277(00):60-93 [826208] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recommended safe practices for using the neurotoxin MPTP in animal experiments. AN - 78549924; 3264039 AB - The metabolism and distribution of the parkinsonian syndrome inducing neurotoxin MPTP has been studied in non-human primates and mice housed in controlled environmental chambers. 14C6-MPTP was prepared and injected at concentrations normally employed for lesioning experiments (30 mg/kg in mice, 0.3 mg/kg in monkeys). All interior surfaces of the chambers which could be reached by animals or their excreta were contaminated with radiolabeled metabolites. Vapor born unmetabolized MPTP was negligible, although significant amounts of MPTP were found in the excreta of mice (less than or equal to 15% injected dose) and small amounts from rhesus monkeys (less than 2%). Procedures to minimize contact with animal fur, bedding and excreta should protect investigators working with MPTP over extended periods. Permanganate oxidation effectively detoxifies solutions of MPTP. MPTP, MPP+, common synthetic intermediates, and the products of MPTP's oxidation are not mutagenic as measured by a Salmonella-microsome assay. JF - Laboratory animal science AU - Yang, S C AU - Markey, S P AU - Bankiewicz, K S AU - London, W T AU - Lunn, G AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20982. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 563 EP - 567 VL - 38 IS - 5 SN - 0023-6764, 0023-6764 KW - Pyridines KW - 0 KW - Potassium Permanganate KW - 00OT1QX5U4 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Potassium Permanganate -- metabolism KW - Housing, Animal KW - Mice, Inbred C57BL KW - Mice KW - Macaca mulatta KW - Male KW - Chromatography, High Pressure Liquid KW - Laboratory Animal Science KW - Pyridines -- urine KW - Pyridines -- toxicity KW - Occupational Diseases -- prevention & control KW - Pyridines -- metabolism KW - Occupational Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78549924?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Recommended+safe+practices+for+using+the+neurotoxin+MPTP+in+animal+experiments.&rft.au=Yang%2C+S+C%3BMarkey%2C+S+P%3BBankiewicz%2C+K+S%3BLondon%2C+W+T%3BLunn%2C+G&rft.aulast=Yang&rft.aufirst=S&rft.date=1988-10-01&rft.volume=38&rft.issue=5&rft.spage=563&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 - 1988-12-27 N1 - Date created - 1988-12-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of T-cell associated antigens by porcine natural killer cells. AN - 78538508; 3263943 AB - We have examined the cell surface phenotype of porcine natural killer (NK) cells and compared them with classic porcine cytotoxic T lymphocytes (CTL). NK cells were susceptible to treatment with monoclonal antibodies to CD2 (PT11), CD8 (PT8) and Ia plus complement (C), as well as with antiserum to asialo-GM1 (ASGM1) plus C. In addition, monoclonal antibodies to leucocyte function antigen 1 (LFA-1) but not to CD8 blocked NK-mediated lysis in the absence of C. This is in contrast to porcine CTL, which were eliminated by antibodies to CD2, CD8 and Ia plus C, but not by anti-ASGMI plus C, and which were blocked by anti-CD8 in the absence of C. Therefore, although porcine NK cells are similar to porcine CTL, they are distinguished by several important differences. JF - Immunology AU - Pescovitz, M D AU - Lowman, M A AU - Sachs, D H AD - Transplantation Biology Section, National Cancer Institute, Bethesda, Maryland. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 267 EP - 271 VL - 65 IS - 2 SN - 0019-2805, 0019-2805 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Complement System Proteins KW - 9007-36-7 KW - Index Medicus KW - Swine KW - Animals KW - Cytotoxicity Tests, Immunologic KW - T-Lymphocytes, Cytotoxic -- immunology KW - Complement System Proteins -- immunology KW - Antibodies, Monoclonal -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Killer Cells, Natural -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78538508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Expression+of+T-cell+associated+antigens+by+porcine+natural+killer+cells.&rft.au=Pescovitz%2C+M+D%3BLowman%2C+M+A%3BSachs%2C+D+H&rft.aulast=Pescovitz&rft.aufirst=M&rft.date=1988-10-01&rft.volume=65&rft.issue=2&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Immunology&rft.issn=00192805&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-06 N1 - Date created - 1989-01-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 1974 Dec 1;140(6):1534-46 [4139231] Vet Immunol Immunopathol. 1986 Feb;11(2):107-21 [3962168] Proc Natl Acad Sci U S A. 1978 Oct;75(10):5127-31 [154104] J Exp Med. 1979 Sep 19;150(3):471-81 [479761] J Immunol. 1980 Jan;124(1):199-201 [6985637] J Immunol. 1980 Feb;124(2):533-40 [7188699] J Immunol. 1980 Aug;125(2):755-62 [6446578] J Immunol. 1981 Jan;126(1):359-64 [7451976] J Immunol. 1981 Dec;127(6):2401-9 [6975321] J Immunol. 1981 Dec;127(6):2575-80 [7299137] J Exp Med. 1982 May 1;155(5):1579-84 [6978378] Transplantation. 1983 Apr;35(4):394-400 [6404028] J Immunol. 1983 Jun;130(6):2786-93 [6406596] J Immunol. 1983 Jul;131(1):223-31 [6408172] J Immunol. 1983 Aug;131(2):1024-7 [6863925] J Immunol. 1984 May;132(5):2183-4 [6609190] J Immunol. 1984 Jul;133(1):368-75 [6609988] J Immunol. 1985 Jan;134(1):37-44 [3871107] Res Vet Sci. 1984 Sep;37(2):211-8 [6095387] J Exp Med. 1985 Mar 1;161(3):563-76 [2579185] J Immunol. 1985 May;134(5):3272-80 [2580022] J Immunol. 1986 Mar 1;136(5):1586-91 [2936802] Transplantation. 1976 Dec;22(6):559-67 [137560] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation dose and second cancer risk in patients treated for cancer of the cervix. AN - 78519916; 3186929 AB - The risk of cancer associated with a broad range of organ doses was estimated in an international study of women with cervical cancer. Among 150,000 patients reported to one of 19 population-based cancer registries or treated in any of 20 oncology clinics, 4188 women with second cancers and 6880 matched controls were selected for detailed study. Radiation doses for selected organs were reconstructed for each patient on the basis of her original radiotherapy records. Very high doses, on the order of several hundred gray, were found to increase the risk of cancers of the bladder [relative risk (RR) = 4.0], rectum (RR = 1.8), vagina (RR = 2.7), and possibly bone (RR = 1.3), uterine corpus (RR = 1.3), cecum (RR = 1.5), and non-Hodgkin's lymphoma (RR = 2.5). For all female genital cancers taken together, a sharp dose-response gradient was observed, reaching fivefold for doses more than 150 Gy. Several gray increased the risk of stomach cancer (RR = 2.1) and leukemia (RR = 2.0). Although cancer of the pancreas was elevated, there was no evidence of a dose-dependent risk. Cancer of the kidney was significantly increased among 15-year survivors. A nonsignificant twofold risk of radiogenic thyroid cancer was observed following an average dose of only 0.11 Gy. Breast cancer was not increased overall, despite an average dose of 0.31 Gy and 953 cases available for evaluation (RR = 0.9); there was, however, a weak suggestion of a dose response among women whose ovaries had been surgically removed. Doses greater than 6 Gy to the ovaries reduced breast cancer risk by 44%. A significant deficit of ovarian cancer was observed within 5 years of radiotherapy; in contrast, a dose response was suggested among 10-year survivors. Radiation was not found to increase the overall risk of cancers of the small intestine, colon, ovary, vulva, connective tissue, breast, Hodgkin's disease, multiple myeloma, or chronic lymphocytic leukemia. For most cancers associated with radiation, risks were highest among long-term survivors and appeared concentrated among women irradiated at relatively younger ages. JF - Radiation research AU - Boice, J D AU - Engholm, G AU - Kleinerman, R A AU - Blettner, M AU - Stovall, M AU - Lisco, H AU - Moloney, W C AU - Austin, D F AU - Bosch, A AU - Cookfair, D L AU - Krementz, E T AU - Latourette, H B AU - Merrill, J A AU - Peters, L J AU - Schulz, M D AU - Storm, H H AU - Bjorkholm, E AU - Pettersson, F AU - Janine Bell, C M AU - Coleman, M P AU - Fraser, P AU - Neal, F E AU - Prior, P AU - Choi, N W AU - Hislop, T G AU - Koch, M AU - Kreiger, N AU - Robb, D AU - Robson, D AU - Thomson, D H AU - Lochmuller, H AU - von Fournier, D AU - Frischkorn, R AU - Kjørstad, K E AU - Rimpela, A AU - Pejovic, M H AU - Kirn, V P AU - Stankusova, H AU - Berrino, F AU - Sigurdsson, K AU - Hutchison, G B AU - MacMahon, B AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 3 EP - 55 VL - 116 IS - 1 SN - 0033-7587, 0033-7587 KW - Index Medicus KW - Space life sciences KW - Risk Factors KW - Humans KW - Middle Aged KW - Female KW - Neoplasms, Multiple Primary -- etiology KW - Neoplasms, Radiation-Induced -- etiology KW - Radiotherapy Dosage KW - Uterine Cervical Neoplasms -- radiotherapy KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78519916?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+dose+and+second+cancer+risk+in+patients+treated+for+cancer+of+the+cervix.&rft.au=Boice%2C+J+D%3BEngholm%2C+G%3BKleinerman%2C+R+A%3BBlettner%2C+M%3BStovall%2C+M%3BLisco%2C+H%3BMoloney%2C+W+C%3BAustin%2C+D+F%3BBosch%2C+A%3BCookfair%2C+D+L%3BKrementz%2C+E+T%3BLatourette%2C+H+B%3BMerrill%2C+J+A%3BPeters%2C+L+J%3BSchulz%2C+M+D%3BStorm%2C+H+H%3BBjorkholm%2C+E%3BPettersson%2C+F%3BJanine+Bell%2C+C+M%3BColeman%2C+M+P%3BFraser%2C+P%3BNeal%2C+F+E%3BPrior%2C+P%3BChoi%2C+N+W%3BHislop%2C+T+G%3BKoch%2C+M%3BKreiger%2C+N%3BRobb%2C+D%3BRobson%2C+D%3BThomson%2C+D+H%3BLochmuller%2C+H%3Bvon+Fournier%2C+D%3BFrischkorn%2C+R%3BKj%C3%B8rstad%2C+K+E%3BRimpela%2C+A%3BPejovic%2C+M+H%3BKirn%2C+V+P%3BStankusova%2C+H%3BBerrino%2C+F%3BSigurdsson%2C+K%3BHutchison%2C+G+B%3BMacMahon%2C+B&rft.aulast=Boice&rft.aufirst=J&rft.date=1988-10-01&rft.volume=116&rft.issue=1&rft.spage=3&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 - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sonolysis, radiolysis, and hydrogen peroxide photolysis of pyrimidine derivatives in aqueous solutions: a spin-trapping study. AN - 78512186; 2847222 AB - The sonolysis of aqueous solutions of various dihydropyrimidines and substituted pyrimidines was investigated by ESR and spin trapping with the nonvolatile, water soluble spin trap, 3,5-dibromonitrosobenzene sulfonate (DBNBS) and its deuterated analog to examine the possibility of detecting new radicals specifically generated in the high temperature zones produced by collapsing cavitation bubbles. Similar ESR spectra were obtained from sonolysis of argon-saturated aqueous solutions, from uv photolysis of aqueous solutions containing H2O2, and from gamma radiolysis of nitrous oxide saturated solutions, although sonolysis of aqueous solutions leads to the formation of pyrimidine radicals by H atom as well as OH radical addition to the 5,6 double bond of pyrimidines. No evidence for specific new radicals formed in the high temperature regions induced by cavitation could be found. For the reactions of dihydropyrimidines with hydroxyl radicals additional spin adducts could be detected and identified with the spin trap DBNBS compared to 2-methyl-2-nitrosopropane which was used in previous studies; however, for alkylpyrimidines fewer spin adducts were observed. The use of the deuterated analog of DBNBS is helpful for unambiguous radical structure assignment. JF - Radiation research AU - Kondo, T AU - Murali Krishna, C AU - Riesz, P AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 56 EP - 73 VL - 116 IS - 1 SN - 0033-7587, 0033-7587 KW - Benzenesulfonates KW - 0 KW - Free Radicals KW - Nitroso Compounds KW - Pyrimidines KW - Solutions KW - Spin Labels KW - Water KW - 059QF0KO0R KW - Uracil KW - 56HH86ZVCT KW - Orotic Acid KW - 61H4T033E5 KW - 3,5-dibromo-4-nitrosobenzenesulfonate KW - 83016-63-1 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Thymine KW - QR26YLT7LT KW - Index Medicus KW - Space life sciences KW - Uracil -- radiation effects KW - Thymine -- analogs & derivatives KW - Uracil -- analogs & derivatives KW - Orotic Acid -- analogs & derivatives KW - Thymine -- radiation effects KW - Electron Spin Resonance Spectroscopy KW - Orotic Acid -- radiation effects KW - Pyrimidines -- radiation effects KW - Photolysis KW - Ultrasonics KW - Radiation Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78512186?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sonolysis%2C+radiolysis%2C+and+hydrogen+peroxide+photolysis+of+pyrimidine+derivatives+in+aqueous+solutions%3A+a+spin-trapping+study.&rft.au=Kondo%2C+T%3BMurali+Krishna%2C+C%3BRiesz%2C+P&rft.aulast=Kondo&rft.aufirst=T&rft.date=1988-10-01&rft.volume=116&rft.issue=1&rft.spage=56&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 - 1988-12-09 N1 - Date created - 1988-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alterations of the lymphocyte-specific protein tyrosine kinase (p56lck) during T-cell activation. AN - 78511187; 3141789 AB - The lymphocyte-specific tyrosine protein kinase p56lck is abundantly expressed in L3T4+ (CD4+) and Lyt-2+ (CD8+) T-lymphocytes, where it is predominantly phosphorylated in vivo on the carboxy-terminal tyrosine residue 505 (Y-505). Upon exposure to activating signals (mitogenic lectins, antibodies to the T-cell receptor), the p56lck expressed in normal cloned murine T-cells is modified into a product which migrates at approximately 59 kilodaltons on sodium dodecyl sulfate-polyacrylamide gels and which possesses several amino-terminal serine phosphorylations. The changes in both mobility and amino-terminal phosphorylation can be reproduced by known activators of protein kinase C (4 alpha-phorbol 12 beta-myristate, dioctanoylglycerol), suggesting that this signal transduction pathway (or related pathways) mediates at least part of these events. Interestingly, agents raising intracellular calcium (such as A23187) cause the appearance of several of these amino-terminal phosphorylation changes but do not cause the pronounced shift in electrophoretic mobility. These data suggest that at least two serine kinase systems are implicated in the alterations of p56lck associated with T-cell activation and that the lck gene product plays a critical role in normal T-cell physiology. JF - Molecular and cellular biology AU - Veillette, A AU - Horak, I D AU - Horak, E M AU - Bookman, M A AU - Bolen, J B AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 4353 EP - 4361 VL - 8 IS - 10 SN - 0270-7306, 0270-7306 KW - Phosphoproteins KW - 0 KW - Concanavalin A KW - 11028-71-0 KW - Calcimycin KW - 37H9VM9WZL KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Lymphocyte Specific Protein Tyrosine Kinase p56(lck) KW - EC 2.7.10.2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Phosphorylation KW - Peptide Mapping KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Calcimycin -- pharmacology KW - Concanavalin A -- pharmacology KW - Phosphoproteins -- metabolism KW - T-Lymphocytes -- classification KW - Lymphocyte Activation KW - Protein-Tyrosine Kinases -- metabolism KW - T-Lymphocytes -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78511187?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alterations+of+the+lymphocyte-specific+protein+tyrosine+kinase+%28p56lck%29+during+T-cell+activation.&rft.au=Veillette%2C+A%3BHorak%2C+I+D%3BHorak%2C+E+M%3BBookman%2C+M+A%3BBolen%2C+J+B&rft.aulast=Veillette&rft.aufirst=A&rft.date=1988-10-01&rft.volume=8&rft.issue=10&rft.spage=4353&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 - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1987 Oct 15;139(8):2755-60 [3116093] Oncogene Res. 1988 May;2(4):385-401 [3041347] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Proc Natl Acad Sci U S A. 1980 Mar;77(3):1311-5 [6246487] J Biol Chem. 1983 Sep 10;258(17):10738-42 [6604054] J Exp Med. 1983 Sep 1;158(3):988-93 [6604129] Proc Natl Acad Sci U S A. 1983 Oct;80(19):5842-6 [6310596] J Immunol. 1983 Nov;131(5):2178-83 [6195255] Nature. 1984 Apr 19-25;308(5961):693-8 [6232463] Nature. 1984 Nov 29-Dec 5;312(5993):462-5 [6095105] Cell. 1985 Oct;42(3):849-57 [2996780] Proc Natl Acad Sci U S A. 1985 Dec;82(23):7845-9 [2415973] Cell. 1985 Dec;43(2 Pt 1):393-404 [2416464] Nature. 1986 Feb 20-26;319(6055):682-5 [3081813] Science. 1986 Mar 21;231(4744):1431-4 [2420005] J Biol Chem. 1986 Apr 15;261(11):4921-5 [2420795] Annu Rev Immunol. 1986;4:593-619 [2939858] J Immunol. 1986 Dec 1;137(11):3652-63 [3097128] Mol Cell Biol. 1987 Feb;7(2):650-6 [2434833] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1374-8 [2950524] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1384-8 [3103134] Cell. 1987 Jun 19;49(6):845-53 [3034434] J Biol Chem. 1987 Jul 15;262(20):9859-64 [3496339] EMBO J. 1987 Sep;6(9):2727-34 [3119327] Cancer Res. 1988 Feb 15;48(4):856-9 [3257410] Nature. 1988 Mar 10;332(6160):171-3 [3347254] Mol Cell Biol. 1988 Feb;8(2):540-50 [3352600] J Immunol. 1988 Apr 15;140(8):2853-7 [3128613] Oncogene Res. 1987 Jul;1(2):149-68 [2453014] Oncogene Res. 1987 Sep-Oct;1(4):357-74 [2835736] Cell. 1988 Jun 3;53(5):731-41 [3370672] Proc Natl Acad Sci U S A. 1988 Jun;85(11):3870-4 [3287380] J Immunol. 1987 Nov 1;139(9):3166-70 [2822805] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed cytotoxic antibody against the C-terminal segment of the surface glycoprotein gp90 of avian reticuloendotheliosis virus. AN - 78468531; 2459845 AB - The major mature env-gene products of avian reticuloendotheliosis-associated virus (REV-A) are the surface glycoprotein (gp90) and the transmembrane protein (gp20). We have previously reported that gp90 was detected in the REV-A virus by Western blot analysis as well as in the REV-A-infected cells by radioimmunoprecipitation with antibodies raised in rabbits against the gp90 C-terminal tridecapeptide which was predicted from the nucleotide sequence (Wilhemsen et al., J. Virol., 52, 172, 1984). We have now shown that this antibody detected antigens on the REV-A-infected cells by fluorescence-activated cell sorter (FACS) analysis, and conferred specific cytotoxic effects on the infected cells in the presence of rabbit complement using the chromium release assay. These results clearly indicate that the C-terminal epitope of gp90 is situated on the surface of the REV-A-infected cells and accessible to site-directed antibodies which cause cytotoxicity by activating the complement system. The possible in vivo roles of this antibody are discussed. JF - Virology AU - Tsai, W P AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 608 EP - 611 VL - 166 IS - 2 SN - 0042-6822, 0042-6822 KW - Antibodies, Viral KW - 0 KW - Antigens, Surface KW - Antigens, Viral KW - Epitopes KW - Oligopeptides KW - Viral Envelope Proteins KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Oligopeptides -- immunology KW - Cytotoxicity, Immunologic KW - Viral Envelope Proteins -- immunology KW - Retroviridae -- immunology KW - Antigens, Viral -- immunology KW - Reticuloendotheliosis virus -- immunology KW - Antigens, Surface -- immunology KW - Antibodies, Viral -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78468531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Site-directed+cytotoxic+antibody+against+the+C-terminal+segment+of+the+surface+glycoprotein+gp90+of+avian+reticuloendotheliosis+virus.&rft.au=Tsai%2C+W+P%3BOroszlan%2C+S&rft.aulast=Tsai&rft.aufirst=W&rft.date=1988-10-01&rft.volume=166&rft.issue=2&rft.spage=608&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-14 N1 - Date created - 1988-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of CD 4-, CD 8- thymocytes with IL 4 vs IL 1 + IL 2. AN - 78464775; 3262653 AB - Thymocytes from C57BL/6 mice were highly purified to obtain the CD 4-, CD 8- subpopulation which constitutes only 5% of all thymocytes. Substantial proliferation was induced in vitro with either IL-1 + IL-2 or with IL-4 in the presence of PMA. IL-1 and IL-2 synergized in inducing proliferation of these purified CD 4-, CD 8- thymocytes whereas neither synergized with IL-4. In order to determine whether stimulation with IL-1 + IL-2 acted via IL-4 or vice versa, cultures were treated reciprocally with affinity-purified anti-IL-2 or anti-IL-4 antibodies. Cultures with IL-4 were inhibited by anti-IL-4 but were unaffected by anti-IL-2. The CD 4-, CD 8- thymocytes cultured with IL-1 + IL-2 + anti-IL-2 were inhibited to baseline IL-1 stimulation. At low concentrations of IL-1 (1 U/ml) and IL-2 (100 U/ml), anti-IL-4 had no effect, whereas at higher levels of IL-1 (2 U/ml IL-1), and 100 or 200 U/ml IL-2, anti-IL-4 significantly reduced DNA synthesis. This result suggests that at higher concentrations the combination of IL-1 + IL-2 can induce cells to produce IL-4 which then contributes to overall proliferation. When CD 4-, CD 8- thymocytes were cultured with the low doses of IL-1 + IL-2 for 72 h, 62% expressed cell surface T3 complex (vs 11% at initiation) and 27% were F23.1+ (vs 5% at initiation). In contrast, culture with IL-4 led to no increase in numbers of T3+ cells and none were F23.1+; however, there was coexpression of Thy1 and 6B2 on 20% of cells at the end of culture (vs 4% at initiation). Thus, IL-1 + IL-2 causes expansion of a CD 4-, CD 8- thymocyte population expressing the alpha, beta-T cell receptor, whereas IL-4 induces cells to express a phenotype present in small numbers in the periphery of normal mice and in larger numbers in mice bearing the lpr gene. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Gause, W C AU - Takashi, T AU - Mountz, J D AU - Finkelman, F D AU - Steinberg, A D AD - Cellular Immunology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892. Y1 - 1988/10/01/ PY - 1988 DA - 1988 Oct 01 SP - 2240 EP - 2245 VL - 141 IS - 7 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Drug Combinations KW - Interleukin-1 KW - Interleukin-2 KW - Interleukins KW - Interleukin-4 KW - 207137-56-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-2 -- pharmacology KW - Interleukin-1 -- pharmacology KW - Mice KW - Phenotype KW - Mice, Inbred C57BL KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Interleukin-2 -- immunology KW - Drug Synergism KW - Female KW - T-Lymphocytes -- classification KW - Lymphocyte Activation -- drug effects KW - Interleukins -- pharmacology KW - Interleukins -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78464775?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activation+of+CD+4-%2C+CD+8-+thymocytes+with+IL+4+vs+IL+1+%2B+IL+2.&rft.au=Gause%2C+W+C%3BTakashi%2C+T%3BMountz%2C+J+D%3BFinkelman%2C+F+D%3BSteinberg%2C+A+D&rft.aulast=Gause&rft.aufirst=W&rft.date=1988-10-01&rft.volume=141&rft.issue=7&rft.spage=2240&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 - 1988-11-03 N1 - Date created - 1988-11-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cell-mediated immune response toward viral envelope and core antigens in gibbon apes (Hylobates lar) chronically infected with human immunodeficiency virus-1. AN - 78458673; 3262661 AB - The specific cellular immune response toward envelope and core proteins of human immunodeficiency virus-1 (HIV-1) was investigated in gibbon apes chronically infected with the HTLV-IIIB isolate. After in vitro stimulation of PBMC from infected and control animals with HIV-1 Ag, DNA synthesis, IL-2R expression and IL-2 release were assayed. Cells from infected gibbon apes demonstrated a group-specific response toward whole virus preparations from three divergent HIV-1 isolates (HTLV-IIIB, HTLV-IIIRF, HTLV-IIIMN). Consistent responses were also detected against purified HIV-1 Ag, i.e., native gp120 envelope glycoprotein, recombinant gp160 glycoprotein, a synthetic peptide (peptide 7) representing a highly conserved region of gp120, and purified native core protein p24. In addition, lymphocytes from infected gibbon apes displayed a specific, MHC-restricted, cytotoxic activity against autologous cells expressing HIV-1 envelope or gag proteins. The specific T cell reactivity toward HIV-1 proteins observed in infected gibbons contrasts with findings in HIV-1 infected humans, and may help to explain the apparent discrepancy in the natural history of the infection between the two species. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Lusso, P AU - Markham, P D AU - Ranki, A AU - Earl, P AU - Moss, B AU - Dorner, F AU - Gallo, R C AU - Krohn, K J AD - Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10/01/ PY - 1988 DA - 1988 Oct 01 SP - 2467 EP - 2473 VL - 141 IS - 7 SN - 0022-1767, 0022-1767 KW - HIV Antigens KW - 0 KW - Interleukin-2 KW - Receptors, Interleukin-2 KW - Viral Core Proteins KW - Viral Envelope Proteins KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Animals KW - T-Lymphocytes -- metabolism KW - Interleukin-2 -- metabolism KW - Receptors, Interleukin-2 -- analysis KW - Hylobates KW - Humans KW - Cytotoxicity Tests, Immunologic KW - T-Lymphocytes, Cytotoxic -- immunology KW - Chronic Disease KW - T-Lymphocytes -- immunology KW - Lymphocyte Activation KW - Viral Envelope Proteins -- immunology KW - HIV Antigens -- isolation & purification KW - Viral Core Proteins -- immunology KW - Acquired Immunodeficiency Syndrome -- immunology KW - Viral Envelope Proteins -- isolation & purification KW - Viral Core Proteins -- isolation & purification KW - HIV Antigens -- immunology KW - Acquired Immunodeficiency Syndrome -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78458673?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cell-mediated+immune+response+toward+viral+envelope+and+core+antigens+in+gibbon+apes+%28Hylobates+lar%29+chronically+infected+with+human+immunodeficiency+virus-1.&rft.au=Lusso%2C+P%3BMarkham%2C+P+D%3BRanki%2C+A%3BEarl%2C+P%3BMoss%2C+B%3BDorner%2C+F%3BGallo%2C+R+C%3BKrohn%2C+K+J&rft.aulast=Lusso&rft.aufirst=P&rft.date=1988-10-01&rft.volume=141&rft.issue=7&rft.spage=2467&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 - 1988-11-03 N1 - Date created - 1988-11-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The measurement of cisplatin-DNA adduct levels in testicular cancer patients. AN - 78453567; 2458857 AB - Seventeen patients with 'poor prognosis' non-seminomatous testicular cancer were monitored for formation of intrastrand bidentate N7-d(ApG)- and N7-d(GpG)-diammineplatinum adducts in peripheral blood cell DNA during the course of cisplatin-based chemotherapy. Adduct values from blood cell DNA samples were compared with disease response data from the same individuals. Patients who received a dose of 40 mg/m2 cisplatin for 5 days generally formed more adducts than patients receiving 20 mg/m2 for 5 days, and adduct levels ranged from 0 to approximately 300 amol/micrograms DNA. Among the individuals who achieved a complete response, the median adduct level was 170 amol/micrograms DNA and the mean was 162. Among the individuals who achieved a partial response, the median adduct level was 78 amol/micrograms DNA and the mean was 83. Comparison of adduct levels between response groups using the Mann-Whitney test gave a two-sided P value of 0.072 (one-sided P value 0.036). Of 11 patients forming high levels of adduct (greater than 140 amol/micrograms DNA), 10 achieved a complete response; this compares with two complete responders in the group of six patients forming low levels (less than 100 amol/micrograms DNA) of adduct (P = 0.055, two-sided Fisher exact test). We conclude that cisplatin-DNA adduct formation in peripheral blood cell DNA correlates with the occurrence of complete response in patients with poor prognosis testicular cancer. JF - Carcinogenesis AU - Reed, E AU - Ozols, R F AU - Tarone, R AU - Yuspa, S H AU - Poirier, M C AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 1909 EP - 1911 VL - 9 IS - 10 SN - 0143-3334, 0143-3334 KW - Biomarkers, Tumor KW - 0 KW - DNA Adducts KW - DNA, Neoplasm KW - cisplatin-DNA adduct KW - Bleomycin KW - 11056-06-7 KW - Vinblastine KW - 5V9KLZ54CY KW - Etoposide KW - 6PLQ3CP4P3 KW - DNA KW - 9007-49-2 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Etoposide -- administration & dosage KW - Bleomycin -- administration & dosage KW - Humans KW - Vinblastine -- administration & dosage KW - Prognosis KW - Male KW - Testicular Neoplasms -- drug therapy KW - Testicular Neoplasms -- blood KW - DNA, Neoplasm -- blood KW - DNA -- blood KW - Cisplatin -- blood KW - Biomarkers, Tumor -- blood KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Cisplatin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78453567?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=The+measurement+of+cisplatin-DNA+adduct+levels+in+testicular+cancer+patients.&rft.au=Reed%2C+E%3BOzols%2C+R+F%3BTarone%2C+R%3BYuspa%2C+S+H%3BPoirier%2C+M+C&rft.aulast=Reed&rft.aufirst=E&rft.date=1988-10-01&rft.volume=9&rft.issue=10&rft.spage=1909&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-08 N1 - Date created - 1988-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis--a synopsis of human experience with external exposure in medicine. AN - 78447707; 3049457 AB - Studies in the 1980s of medically irradiated populations have increased our knowledge of radiation carcinogenesis. (1) Investigations of prenatal x-ray exposures, especially in twins, provide evidence that very low doses of ionizing radiation may cause cancer in humans. (2) Fractionated doses appear as effective as single exposures of the same total dose in causing breast cancer, but seem less effective for lung cancer. (3) Excess breast cancers can occur among women exposed under age 10, indicating that the immature breast is susceptible to the carcinogenic action of radiation. (4) Moderate doses on the order of 1 Gy to the brains of children can cause tumors later in life; moderately high doses to the skin can cause cancer when followed by frequent exposure to ultraviolet light. (5) Radiotherapy for cervical cancer can increase the rate of subsequent leukemia with the best fitting dose-response functions including a negative exponential term to account for cell-killing. (6) Low-dose exposures of about 10 cGy may increase the risk of thyroid cancer. (7) Second cancers following radiotherapy for a variety of cancers occur primarily among long-term survivors. (8) Radiotherapy may not significantly increase the risk of leukemia following childhood cancer, whereas chemotherapy with alkylating agents is a major risk factor. (9) Bone cancer occurs after high-dose radiotherapy for childhood cancer, but children with retinoblastoma are not more susceptible to radiation-induced disease than children with other malignancies. (10) High-dose external beam therapy can cause thyroid cancer, whereas high-dose radioactive 131I may not. (11) Studies of cervical cancer patients indicate that the risk of radiation-induced second malignancies follows a time-response model consistent with a constant multiplication of the underlying background incidence, i.e. a relative risk model seems to hold for projecting risks forward in time. JF - Health physics AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 621 EP - 630 VL - 55 IS - 4 SN - 0017-9078, 0017-9078 KW - Index Medicus KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Child KW - Male KW - Female KW - Neoplasms, Radiation-Induced -- etiology KW - Radiography -- adverse effects KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78447707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Carcinogenesis--a+synopsis+of+human+experience+with+external+exposure+in+medicine.&rft.au=Boice%2C+J+D&rft.aulast=Boice&rft.aufirst=J&rft.date=1988-10-01&rft.volume=55&rft.issue=4&rft.spage=621&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 - 1988-11-18 N1 - Date created - 1988-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of the 32P-postlabeling method to detect DNA adducts of 2-amino-3-methylimidazolo[4,5-f]quinoline (IQ) in monkeys fed IQ: identification of the N-(deoxyguanosin-8-yl)-IQ adduct. AN - 78432965; 3168152 AB - Eight DNA adducts of 2-amino-3-methylimidazolo[4,5-f]-quinoline (IQ) were found by the standard 32P-postlabeling method in livers from male Cynomolgus monkeys fed IQ (5 days/week, 3 weeks, 20 mg/kg, nasal-gastric intubation). The IQ-DNA adduct fingerprints observed in monkeys were identical to those observed in rats that received IQ (0.03%) in the diet for 2 weeks. The C8-guanine-IQ adduct was identified by comigration with the synthetic 3',5'-bisphosphate derivative of N(-deoxyguanosin-8-yl)-IQ. DNA modified in vitro with N-hydroxy-IQ showed seven adducts, including the C8-guanine-IQ adduct, that were identical to those found in monkeys and rats. Thus it appears that N-hydroxy-IQ, the reactive metabolite of IQ, was responsible for all adducts found in vivo, except one. In order to detect adducts in other organs that were present at lower levels, the intensification (ATP-deficient) method for 32P-postlabeling was used. Five of the adducts detected under standard conditions, including the C8-guanine-IQ adduct, were also detected under intensification conditions. The total level of DNA-IQ adducts was highest in the liver, followed by the kidney, colon and stomach, and bladder. The adduct patterns were identical in all organs examined. The results indicate that IQ is potentially genotoxic in primates and therefore a likely human carcinogen. JF - Carcinogenesis AU - Snyderwine, E G AU - Yamashita, K AU - Adamson, R H AU - Sato, S AU - Nagao, M AU - Sugimura, T AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 1739 EP - 1743 VL - 9 IS - 10 SN - 0143-3334, 0143-3334 KW - Mutagens KW - 0 KW - Phosphorus Radioisotopes KW - Quinolines KW - N-(deoxyguanosin-8-yl)-2-amino-3-methylimidazolo(4,5-f)quinoline KW - 115747-35-8 KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - DNA KW - 9007-49-2 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Macaca fascicularis KW - Tissue Distribution KW - Autoradiography -- methods KW - Male KW - Quinolines -- metabolism KW - Mutagens -- metabolism KW - DNA -- metabolism KW - Deoxyguanosine -- isolation & purification KW - Quinolines -- isolation & purification KW - Quinolines -- pharmacokinetics KW - Deoxyguanosine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78432965?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Use+of+the+32P-postlabeling+method+to+detect+DNA+adducts+of+2-amino-3-methylimidazolo%5B4%2C5-f%5Dquinoline+%28IQ%29+in+monkeys+fed+IQ%3A+identification+of+the+N-%28deoxyguanosin-8-yl%29-IQ+adduct.&rft.au=Snyderwine%2C+E+G%3BYamashita%2C+K%3BAdamson%2C+R+H%3BSato%2C+S%3BNagao%2C+M%3BSugimura%2C+T%3BThorgeirsson%2C+S+S&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1988-10-01&rft.volume=9&rft.issue=10&rft.spage=1739&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-08 N1 - Date created - 1988-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular distribution of c-myc transcripts during chemical hepatocarcinogenesis in rats. AN - 78414332; 3416306 AB - The expression of cellular myc (c-myc) was studied during early and late stages of chemical hepatocarcinogenesis in the rat using Northern blot analysis and in situ hybridization. Hepatocarcinogenesis was induced according to the resistant hepatocyte model of Solt and Farber. An uninitiated version of this model was also used to examine the expression of c-myc during proliferation and differentiation of oval cells. The expression of c-myc was increased throughout hepatocarcinogenesis starting with early preneoplastic foci and oval cells. Similar levels of c-myc transcripts were detected in oval cells and basophilic hepatocytes generated by the uninitiated version of the protocol as were found in preneoplastic foci and oval cells during hepatocarcinogenesis. Whereas c-myc expression remained elevated in late neoplastic nodules and carcinomas, it gradually declined in both "remodelling" nodules and uninitiated livers. Our data indicate that c-myc expression is elevated during the undifferentiated stages of hepatocyte development. Furthermore, the data support the hypothesis that a critical early step in chemical hepatocarcinogenesis involves a block in the normal differentiation program of the hepatocytes. JF - Cancer research AU - Nagy, P AU - Evarts, R P AU - Marsden, E AU - Roach, J AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10/01/ PY - 1988 DA - 1988 Oct 01 SP - 5522 EP - 5527 VL - 48 IS - 19 SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Nucleic Acid Hybridization KW - Liver Neoplasms, Experimental -- genetics KW - Oncogenes KW - Liver Neoplasms, Experimental -- chemically induced KW - Transcription, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78414332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+distribution+of+c-myc+transcripts+during+chemical+hepatocarcinogenesis+in+rats.&rft.au=Nagy%2C+P%3BEvarts%2C+R+P%3BMarsden%2C+E%3BRoach%2C+J%3BThorgeirsson%2C+S+S&rft.aulast=Nagy&rft.aufirst=P&rft.date=1988-10-01&rft.volume=48&rft.issue=19&rft.spage=5522&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 - 1988-10-25 N1 - Date created - 1988-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acetylcholine and coronary artery spasm: important insight or squeeze play? AN - 78412865; 3262132 JF - Journal of the American College of Cardiology AU - Cannon, R O AD - Cardiology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/10// PY - 1988 DA - October 1988 SP - 889 EP - 891 VL - 12 IS - 4 SN - 0735-1097, 0735-1097 KW - Biological Products KW - 0 KW - Nitric Oxide KW - 31C4KY9ESH KW - Acetylcholine KW - N9YNS0M02X KW - Ergonovine KW - WH41D8433D KW - Abridged Index Medicus KW - Index Medicus KW - Coronary Vessels KW - Humans KW - Biological Products -- physiology KW - Injections KW - Acetylcholine -- administration & dosage KW - Coronary Vasospasm -- chemically induced KW - Angina Pectoris, Variant -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78412865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Acetylcholine+and+coronary+artery+spasm%3A+important+insight+or+squeeze+play%3F&rft.au=Cannon%2C+R+O&rft.aulast=Cannon&rft.aufirst=R&rft.date=1988-10-01&rft.volume=12&rft.issue=4&rft.spage=889&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 - 1988-10-27 N1 - Date created - 1988-10-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer families: human models of susceptibility to neoplasia--the Richard and Hinda Rosenthal Foundation Award lecture. AN - 78401259; 2843281 AB - Members of cancer families are at exceptionally high risk and can be studied as human models of cancer susceptibility. These patients represent rare "experiments of nature" that can reveal new insights into carcinogenic processes. We use clinical observations to identify the high risk patient, epidemiological studies to quantitate the excess risk, and laboratory investigations to examine the biological basis of susceptibility. We have uncovered a series of new family cancer syndromes that are under study for molecular mechanisms involved in the pathogenesis of cancers in general. This presentation describes our investigations of four disorders: the syndrome of sarcomas, breast cancer, and other neoplasms; inheritance of both renal cell carcinoma and a constitutional chromosome translocation in a kindred; familial Wilms' tumor; and the hepatoblastoma-adenomatous polyposis association. JF - Cancer research AU - Li, F P AD - Clinical Studies Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/10/01/ PY - 1988 DA - 1988 Oct 01 SP - 5381 EP - 5386 VL - 48 IS - 19 SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Breast Neoplasms -- genetics KW - Kidney Neoplasms -- genetics KW - Pedigree KW - Adenomatous Polyposis Coli -- genetics KW - Chromosome Banding KW - Humans KW - Wilms Tumor -- genetics KW - Carcinoma, Hepatocellular -- genetics KW - Sarcoma -- genetics KW - Adenoma -- genetics KW - Carcinoma, Renal Cell -- genetics KW - Female KW - Male KW - Liver Neoplasms -- genetics KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78401259?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cancer+families%3A+human+models+of+susceptibility+to+neoplasia--the+Richard+and+Hinda+Rosenthal+Foundation+Award+lecture.&rft.au=Li%2C+F+P&rft.aulast=Li&rft.aufirst=F&rft.date=1988-10-01&rft.volume=48&rft.issue=19&rft.spage=5381&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 - 1988-10-25 N1 - Date created - 1988-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disposition of 1,2,3,7,8-pentachlorodibenzofuran in the rat. AN - 78514411; 3188012 AB - 1,2,3,7,8-Pentachlorodibenzofuran (1PeCDF) is one of several toxic polychlorinated dibenzofurans (PCDFs) which are ubiquitous environmental contaminants. Related in structure and toxicity to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), PCDFs have been detected in municipal and industrial effluents, PCB mixtures, and in a variety of antiseptics and preservative solutions. The objective of this study was to evaluate the distribution and elimination of 1PeCDF in the rat and to compare these parameters with that of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF) and 2,3,7,8-tetrachlorodibenzofuran (TCDF). After iv administration of 0.1 mumol [3H]1PeCDF/kg, 1PeCDF was rapidly cleared from the blood and distributed to the liver, muscle, skin, and adipose tissue in a manner similar to that for other dibenzofurans. The initial pool sizes of 1PeCDF-derived radioactivity in the liver, muscle, skin, and adipose tissue were 43,35,10, and 7% of the administered dose, respectively. In all cases, loss of radioactivity from these tissues could be described by exponential decay and the initial half-lives for these tissues were 1.36, 0.03, 13, and 1 day, respectively. After redistribution from the muscle, skin, and adipose tissues to the liver, 1PeCDF was metabolized to a polar metabolite(s) and excreted from the body via the bile into the feces. No parent compound was detected in the bile and fecal excretion was the major route of elimination. Most of the radioactivity in the urine was excreted within the first day, after which less than 0.5% of the dose/day was detected. More than half of the administered dose was excreted in the urine and feces within 2 days. The whole-body half-life of related compounds is 4PeCDF much greater than 1PeCDF greater than or equal to TCDF. Therefore, persistence appears to be inversely related to the metabolism of these compounds and metabolism is inhibited by chlorine-substituted carbon atoms adjacent to the oxygen atom in the dibenzofuran ring. JF - Toxicology and applied pharmacology AU - Brewster, D W AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/09/30/ PY - 1988 DA - 1988 Sep 30 SP - 490 EP - 498 VL - 95 IS - 3 SN - 0041-008X, 0041-008X KW - Benzofurans KW - 0 KW - Environmental Pollutants KW - 1,2,3,7,8-pentachlorodibenzofuran KW - QNE7ZLB7SS KW - 2,3,4,7,8-pentachlorodibenzofuran KW - U4C2RV3124 KW - 2,3,7,8-tetrachlorodibenzofuran KW - XZJ41GQI5D KW - Index Medicus KW - Rats KW - Feces -- analysis KW - Animals KW - Rats, Inbred F344 KW - Lethal Dose 50 KW - Bile -- metabolism KW - Tissue Distribution KW - Male KW - Structure-Activity Relationship KW - Benzofurans -- pharmacokinetics KW - Environmental Pollutants -- pharmacokinetics KW - Benzofurans -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78514411?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+of+1%2C2%2C3%2C7%2C8-pentachlorodibenzofuran+in+the+rat.&rft.au=Brewster%2C+D+W%3BBirnbaum%2C+L+S&rft.aulast=Brewster&rft.aufirst=D&rft.date=1988-09-30&rft.volume=95&rft.issue=3&rft.spage=490&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 - 1988-12-05 N1 - Date created - 1988-12-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression and amplification in transgenic mice of a polyoma virus mutant regulatory region. AN - 19624922; 8728494 AB - Two hybrid gene constructs consisting of wild-type and mutant polyoma regulatory regions fused to a bacterial reporter gene were inserted in the mouse germline. Both transgenes were expressed in a large number of different organs. However, marker gene expression controlled by the polyoma wild-type regulatory region was not detectable in the early embryo and remained low throughout the life of the animal while expression controlled by the polyoma F9-1 mutation was detectable in blastocysts and was significantly higher at later stages of development. The F9-1 hybrid gene was also amplifiable when large T-antigen was supplied in trans to mice or to kidney cells derived from these transgenic mice. Amplification resulted in the appearance of several hundred copies of episomal transgenes and a marked increase of marker gene RNA and protein. Our results suggest that the F9-1 mutation does not alter the target spectrum of gene expression in vivo but does create a more efficient enhancer element in the polyoma early control region. Transgene amplification based upon use of the polyoma regulatory elements may be a means of increasing expression of genes in transgenic mice. Images JF - Nucleic Acids Research AU - Krippl, B AU - Griep, A E AU - Mahon, K A AU - Boehnlein, E AU - Gruss, P AU - Westphal, H AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/09/26/ PY - 1988 DA - 1988 Sep 26 SP - 8963 EP - 8976 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 16 IS - 18 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Regulatory sequences KW - Transgenes KW - Developmental stages KW - Polyomavirus KW - Transgenic mice KW - Gene expression KW - Enhancers KW - blastocysts KW - RNA KW - Reporter gene KW - Hybrids KW - Kidney KW - Embryos KW - Mutation KW - J 02310:Genetics & Taxonomy KW - W 30925:Genetic Engineering KW - V 22410:Animal Diseases KW - N 14830:RNA KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19624922?accountid=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=Expression+and+amplification+in+transgenic+mice+of+a+polyoma+virus+mutant+regulatory+region.&rft.au=Krippl%2C+B%3BGriep%2C+A+E%3BMahon%2C+K+A%3BBoehnlein%2C+E%3BGruss%2C+P%3BWestphal%2C+H&rft.aulast=Krippl&rft.aufirst=B&rft.date=1988-09-26&rft.volume=16&rft.issue=18&rft.spage=8963&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 - Regulatory sequences; Transgenes; Developmental stages; Transgenic mice; Gene expression; Enhancers; blastocysts; RNA; Reporter gene; Hybrids; Kidney; Embryos; Mutation; Polyomavirus ER - TY - JOUR T1 - Cloning of the chicken chromosomal protein HMG-14 cDNA reveals a unique protein with a conserved DNA binding domain. AN - 78427530; 3417670 AB - The isolation and sequencing of a cDNA clone coding for the entire sequence of chicken chromosomal protein HMG-14 is described. The open reading frame constitutes only 25% of the transcript; the 5'-untranslated region is extremely rich in GC residues; and the 3'-untranslated region is highly enriched in AT residues. Comparison with other cDNAs coding for HMG-14 and HMG-17 reveals that the transcripts of genes coding for this family of chromosomal proteins have a characteristic structure. The deduced amino acid sequence is unique and different from all other known HMG-14 and -17 sequences. Analysis of amino acid position identity between the chicken HMG-14 and other HMG-14/-17 proteins revealed that the protein has 37% similarity to the HMG-17 group and 69% similarity to the HMG-14 group; therefore, the protein is classified as belonging to the HMG-14 group. Additional analysis leads to the conclusion that the chicken cDNA described here codes for the true homolog of calf and human HMG-14 protein. Comparison of all the known HMG-14 sequences reveals the DNA binding domain is conserved and contains the invariant dodecapeptide PKRRSARLSAKP. The HMG-14 proteins have a distinct charge distribution along the polypeptide chain: while the central region is positively charged the C-terminal domain is negatively charged. JF - The Journal of biological chemistry AU - Srikantha, T AU - Landsman, D AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09/25/ PY - 1988 DA - 1988 Sep 25 SP - 13500 EP - 13503 VL - 263 IS - 27 SN - 0021-9258, 0021-9258 KW - High Mobility Group Proteins KW - 0 KW - Nucleosomes KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Protein Biosynthesis KW - Oviducts -- analysis KW - Animals KW - Chickens KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Biological Evolution KW - Humans KW - Nucleosomes -- metabolism KW - Molecular Sequence Data KW - Binding Sites KW - DNA -- isolation & purification KW - High Mobility Group Proteins -- genetics KW - DNA -- metabolism KW - DNA -- genetics KW - High Mobility Group Proteins -- metabolism KW - Cloning, Molecular UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78427530?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cloning+of+the+chicken+chromosomal+protein+HMG-14+cDNA+reveals+a+unique+protein+with+a+conserved+DNA+binding+domain.&rft.au=Srikantha%2C+T%3BLandsman%2C+D%3BBustin%2C+M&rft.aulast=Srikantha&rft.aufirst=T&rft.date=1988-09-25&rft.volume=263&rft.issue=27&rft.spage=13500&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 - 1988-10-19 N1 - Date created - 1988-10-19 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M20817; GENBANK N1 - SuppNotes - Erratum In: J Biol Chem 1989 Jul 25;264(21):12744 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hydroxyl radical production by stimulated neutrophils reappraised. AN - 78414055; 2843536 AB - Release of active oxygen species during the human neutrophil respiratory burst is thought to be mandatory for effective defense against bacterial infections and may play an important role in damage to host tissues. Part of the critical bacterial and host tissue damage has been attributed to hydroxyl radicals produced from superoxide and hydrogen peroxide. Because of the short life time of the very reactive hydroxyl radical, direct study of hydroxyl radical production is not possible; therefore, indirect detection methods such as electron spin resonance (ESR) coupled with appropriate spin-trapping agents such as 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) have been used. Superoxide production during the oxidative burst has been unambiguously demonstrated. Recent reports claim that hydroxyl radicals are not made during neutrophil stimulation and offer as an explanation the presence of granular components that interfere with hydroxyl radical production. When using the spin-trap agent DMPO, absence of the relatively long-lived adducts DMPO-OH and DMPO-CH3 has been assumed to be prima facie evidence for lack of hydroxyl radical participation. We show that high superoxide flux produced during stimulation of human neutrophils rapidly destroys both DMPO-OH and DMPO-CH3. In accord with previous implications, our results provide an alternative explanation for the absence of .OH adduct in spin-trapping studies and corroborate results obtained using other methods that implicate hydroxyl radical production during neutrophil stimulation. JF - The Journal of biological chemistry AU - Samuni, A AU - Black, C D AU - Krishna, C M AU - Malech, H L AU - Bernstein, E F AU - Russo, A AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1988/09/25/ PY - 1988 DA - 1988 Sep 25 SP - 13797 EP - 13801 VL - 263 IS - 27 SN - 0021-9258, 0021-9258 KW - Cyclic N-Oxides KW - 0 KW - Free Radicals KW - Hydroxides KW - Spin Labels KW - Superoxides KW - 11062-77-4 KW - Hydroxyl Radical KW - 3352-57-6 KW - 5,5-dimethyl-1-pyrroline-1-oxide KW - 7170JZ1QF3 KW - Zymosan KW - 9010-72-4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Zymosan -- pharmacology KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Superoxides -- blood KW - Neutrophils -- metabolism KW - Neutrophils -- drug effects KW - Hydroxides -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78414055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hydroxyl+radical+production+by+stimulated+neutrophils+reappraised.&rft.au=Samuni%2C+A%3BBlack%2C+C+D%3BKrishna%2C+C+M%3BMalech%2C+H+L%3BBernstein%2C+E+F%3BRusso%2C+A&rft.aulast=Samuni&rft.aufirst=A&rft.date=1988-09-25&rft.volume=263&rft.issue=27&rft.spage=13797&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 - 1988-10-19 N1 - Date created - 1988-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of cyclosporine A on T cell development and clonal deletion. AN - 78431014; 3262237 AB - Cyclosporine A (CsA) is an important immunosuppressive drug that is widely used in transplantation medicine. Many of its suppressive effects on T cells appear to be related to the inhibition of T cell receptor (TCR)-mediated activation events. Paradoxically, in certain situations CsA is responsible for the induction of a T cell-mediated autoimmunity. The effects of CsA on T cell development in the thymus were investigated to elucidate the physiologic events underlying this phenomenon. Two major effects were revealed: (i) CsA inhibits the development of mature single positive (CD4+8- or CD4-8+) TCR-alpha beta+ thymocytes without discernibly affecting CD4-8- TCR-gamma delta+ thymocytes and (ii) CsA interferes with the deletion of cells bearing self-reactive TCRs in the population of single positive thymocytes that do develop. This suggests a direct mechanism for CsA-induced autoimmunity and may have implications for the relative contribution of TCR-mediated signaling events in the development of the various T cell lineages. JF - Science (New York, N.Y.) AU - Jenkins, M K AU - Schwartz, R H AU - Pardoll, D M AD - Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/09/23/ PY - 1988 DA - 1988 Sep 23 SP - 1655 EP - 1658 VL - 241 IS - 4873 SN - 0036-8075, 0036-8075 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Cyclosporins KW - Receptors, Antigen, T-Cell KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Antigens, Differentiation, T-Lymphocyte -- genetics KW - Autoimmune Diseases -- chemically induced KW - Mice KW - Receptors, Antigen, T-Cell -- drug effects KW - Cell Differentiation -- drug effects KW - Receptors, Antigen, T-Cell -- genetics KW - T-Lymphocytes -- drug effects KW - Cyclosporins -- pharmacology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78431014?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+cyclosporine+A+on+T+cell+development+and+clonal+deletion.&rft.au=Jenkins%2C+M+K%3BSchwartz%2C+R+H%3BPardoll%2C+D+M&rft.aulast=Jenkins&rft.aufirst=M&rft.date=1988-09-23&rft.volume=241&rft.issue=4873&rft.spage=1655&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 - 1988-10-24 N1 - Date created - 1988-10-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective killing of HIV-infected cells by recombinant human CD4-Pseudomonas exotoxin hybrid protein. AN - 78422181; 2843774 AB - It is projected that in the absence of effective therapy, most individuals infected with human immunodeficiency virus (HIV) will develop acquired immune deficiency syndrome (AIDS) and ultimately succumb to a combination of opportunistic microbial infections, malignancies and direct pathogenic effects of the virus. Anti-viral agents, immunomodulators, and inhibitors of specific HIV functions are being tested as potential treatments to alleviate the high morbidity and mortality. An alternative therapeutic concept involves the development of cytotoxic agents that are targeted to kill HIV-infected cells. Here we describe the purification and characterization of a recombinant protein produced in Escherichia coli that contains the HIV-binding portion of the human CD4 molecule linked to active regions of Pseudomonas exotoxin A. This hybrid protein displays selective toxicity toward cells expressing the HIV envelope glycoprotein and thus represents a promising novel therapeutic agent for the treatment of AIDS. JF - Nature AU - Chaudhary, V K AU - Mizukami, T AU - Fuerst, T R AU - FitzGerald, D J AU - Moss, B AU - Pastan, I AU - Berger, E A AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09/22/ PY - 1988 DA - 1988 Sep 22 SP - 369 EP - 372 VL - 335 IS - 6188 SN - 0028-0836, 0028-0836 KW - CD4-Pseudomonas toxin KW - 0 KW - Exotoxins KW - HIV Envelope Protein gp120 KW - Immunotoxins KW - Receptors, HIV KW - Receptors, Virus KW - Recombinant Proteins KW - Retroviridae Proteins KW - Index Medicus KW - AIDS/HIV KW - Cells, Cultured KW - Humans KW - Escherichia coli -- genetics KW - Pseudomonas KW - Cell Survival KW - Acquired Immunodeficiency Syndrome -- therapy KW - Retroviridae Proteins -- metabolism KW - Recombinant Proteins -- pharmacology KW - Recombinant Proteins -- metabolism KW - Exotoxins -- metabolism KW - Receptors, Virus -- metabolism KW - Immunotoxins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78422181?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Selective+killing+of+HIV-infected+cells+by+recombinant+human+CD4-Pseudomonas+exotoxin+hybrid+protein.&rft.au=Chaudhary%2C+V+K%3BMizukami%2C+T%3BFuerst%2C+T+R%3BFitzGerald%2C+D+J%3BMoss%2C+B%3BPastan%2C+I%3BBerger%2C+E+A&rft.aulast=Chaudhary&rft.aufirst=V&rft.date=1988-09-22&rft.volume=335&rft.issue=6188&rft.spage=369&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-17 N1 - Date created - 1988-10-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diethylcarbamazine prophylaxis for human loiasis. Results of a double-blind study. AN - 78391810; 3166107 AB - To determine whether infection with Loa loa could be prevented in temporary residents of endemic areas, we conducted a randomized, double-blind, placebo-controlled trial of diethylcarbamazine as a chemoprophylactic agent. Diethylcarbamazine (300 mg) or placebo was taken orally once a week by Peace Corps volunteers serving in Gabon, Cameroon, and the Central African Republic. The participants were assessed clinically and with serologic and parasitologic testing before and yearly during their two years of service. One hundred one persons satisfactorily completed the study. In Gabon (where exposure to the parasite was heaviest), 6 of 20 volunteers (30 percent) in the placebo group had clinical disease, as compared with none of 16 (0 percent) in the diethylcarbamazine-treated group (P less than 0.02). Of those taking placebo, 10 of 20 (50 percent) became seropositive for antifilarial IgG antibody, as compared with 2 of 16 (12 percent) in the drug-treated group (P less than 0.02). Exposure to the parasite appeared to be much lower among the 65 Peace Corps volunteers in Cameroon and the Central African Republic. No volunteer in either group in these countries had overt loiasis; 2 of 40 (5 percent) in the placebo groups in Cameroon and the Central African Republic seroconverted, as compared with none of 25 (0 percent) of those receiving diethylcarbamazine. Occasional nausea was the only symptom significantly associated with the prophylactic drug regimen. We conclude that diethylcarbamazine given orally once weekly can be an effective, acceptable chemoprophylactic agent to prevent loiasis in temporary residents of regions of Africa where Loa loa is endemic. JF - The New England journal of medicine AU - Nutman, T B AU - Miller, K D AU - Mulligan, M AU - Reinhardt, G N AU - Currie, B J AU - Steel, C AU - Ottesen, E A AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Md 20892. Y1 - 1988/09/22/ PY - 1988 DA - 1988 Sep 22 SP - 752 EP - 756 VL - 319 IS - 12 SN - 0028-4793, 0028-4793 KW - Diethylcarbamazine KW - V867Q8X3ZD KW - Abridged Index Medicus KW - Index Medicus KW - Central African Republic KW - Double-Blind Method KW - Random Allocation KW - Humans KW - Adult KW - Middle Aged KW - Gabon KW - Cameroon KW - Male KW - Female KW - Diethylcarbamazine -- adverse effects KW - Diethylcarbamazine -- administration & dosage KW - Loiasis -- prevention & control KW - Diethylcarbamazine -- therapeutic use KW - Filariasis -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78391810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Diethylcarbamazine+prophylaxis+for+human+loiasis.+Results+of+a+double-blind+study.&rft.au=Nutman%2C+T+B%3BMiller%2C+K+D%3BMulligan%2C+M%3BReinhardt%2C+G+N%3BCurrie%2C+B+J%3BSteel%2C+C%3BOttesen%2C+E+A&rft.aulast=Nutman&rft.aufirst=T&rft.date=1988-09-22&rft.volume=319&rft.issue=12&rft.spage=752&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cephalotaxine esters: antileukemic advance or therapeutic failure? AN - 78387508; 3045335 AB - Clinical trials conducted in the People's Republic of China and the United States of the antileukemic efficacy of the cephalotaxine esters are reviewed. Harrington has been incorporated into combination regimens for the treatment of newly diagnosed acute nonlymphocytic leukemia (ANLL) in China, and activity with cephalotaxine esters has also been noted in chronic myelogenous leukemia. While the investigational agent homoharringtonine has shown some activity in the United States in ANLL, investigator interest in the United States has waned because of toxicity and inconvenient schedules. The Chinese trials have used different schedules than have U.S. studies and have been associated with less toxicity. These trials provide new information that may lead to further investigations of the cephalotaxine esters in the United States. JF - Journal of the National Cancer Institute AU - Grem, J L AU - Cheson, B D AU - King, S A AU - Leyland-Jones, B AU - Suffness, M AD - Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/09/21/ PY - 1988 DA - 1988 Sep 21 SP - 1095 EP - 1103 VL - 80 IS - 14 SN - 0027-8874, 0027-8874 KW - Alkaloids KW - 0 KW - Harringtonines KW - Index Medicus KW - United States KW - Humans KW - Clinical Trials as Topic KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - China KW - Leukemia -- drug therapy KW - Harringtonines -- therapeutic use KW - Harringtonines -- administration & dosage KW - Alkaloids -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78387508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cephalotaxine+esters%3A+antileukemic+advance+or+therapeutic+failure%3F&rft.au=Grem%2C+J+L%3BCheson%2C+B+D%3BKing%2C+S+A%3BLeyland-Jones%2C+B%3BSuffness%2C+M&rft.aulast=Grem&rft.aufirst=J&rft.date=1988-09-21&rft.volume=80&rft.issue=14&rft.spage=1095&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 - 1988-10-13 N1 - Date created - 1988-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational analysis of domain I of Pseudomonas exotoxin. Mutations in domain I of Pseudomonas exotoxin which reduce cell binding and animal toxicity. AN - 78429084; 2901411 AB - Pseudomonas exotoxin (PE) is a single polypeptide chain that contains 613 amino acids and is arranged into three structural domains. Domain I is responsible for cell recognition, II for translocation of PE across membranes and III for ADP ribosylation of elongation factor 2. Treatment of PE with reagents that react with lysine residues has been shown to lead to a reduction in cytotoxic activity apparently due to a modification of domain I (Pirker, R., FitzGerald, D. J. P., Hamilton, T. C., Ozols, R. F., Willingham, M. C., and Pastan, S. (1985) Cancer Res. 45, 751-757). To determine which lysine residues are important in cell recognition, all 12 lysines in domain I were converted to glutamates by site-directed mutagenesis. Also, two deletion mutants encompassing almost all of domain I (amino acids 4-252) or most of domain I (amino acids 4-224) were studied. The mutant proteins were produced in Escherichia coli, purified, and tested for their cytotoxic activity against Swiss 3T3 cells and in mice. The data indicate that conversion of lysine 57 to glutamate reduces cytotoxic activity towards 3T3 cells 50-100-fold and in mice about 5-fold. Deletion of amino acids 4-224 causes a similar reduction in toxicity towards cells and mice. Deletion of most of the rest of domain I (amino acids 4-252) causes a further reduction in toxicity toward cells and mice indicating this second region between amino acids 225 and 252 of domain I is also important in the toxicity of PE. Competition assays indicated that the ability of PEGlu57 to bind to 3T3 cells was greatly diminished, accounting for its diminished cytotoxic activity. JF - The Journal of biological chemistry AU - Jinno, Y AU - Chaudhary, V K AU - Kondo, T AU - Adhya, S AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09/15/ PY - 1988 DA - 1988 Sep 15 SP - 13203 EP - 13207 VL - 263 IS - 26 SN - 0021-9258, 0021-9258 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Glutamates KW - Virulence Factors KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Glutamic Acid KW - 3KX376GY7L KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Lysine KW - K3Z4F929H6 KW - Index Medicus KW - Animals KW - Cell Survival -- drug effects KW - Binding, Competitive KW - Mice KW - Adenosine Diphosphate Ribose -- metabolism KW - Mutation KW - Structure-Activity Relationship KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Bacterial Adhesion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78429084?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Mutational+analysis+of+domain+I+of+Pseudomonas+exotoxin.+Mutations+in+domain+I+of+Pseudomonas+exotoxin+which+reduce+cell+binding+and+animal+toxicity.&rft.au=Jinno%2C+Y%3BChaudhary%2C+V+K%3BKondo%2C+T%3BAdhya%2C+S%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Jinno&rft.aufirst=Y&rft.date=1988-09-15&rft.volume=263&rft.issue=26&rft.spage=13203&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 - 1988-10-19 N1 - Date created - 1988-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA strand breaks produced by etoposide (VP-16,213) in sensitive and resistant human breast tumor cells: implications for the mechanism of action. AN - 78394813; 2842045 AB - Pleotropic resistant human breast cancer cells (MCF-7), selected for resistance to Adriamycin, were used to study the production of DNA strand breaks by etoposide (VP-16) and its relationship to drug cytotoxicity. It was shown that the resistant MCF-7 cell line was cross-resistant to VP-16, and the degree of resistance was found to be 125-200-fold. Alkaline elution studies indicated that the parental cell line was very sensitive to VP-16 which caused extensive DNA strand breakage. In contrast, little DNA strand breakage was detected in the resistant MCF-7 cells, even at very high drug concentrations, indicating a good agreement between strand breaks and cytotoxicity. Further studies indicated that the nuclei isolated from the parental cell line were more resistant to VP-16-induced DNA strand breaks than the intact cells, while the opposite was found in the resistant cell line. In addition, the alkaline elution studies in isolated nuclei showed only a 2-fold reduction of VP-16-induced DNA breaks in nuclei from the resistant cells. In agreement with this result, it was found that nuclear extract from the resistant cells produced 2-3-fold less VP-16-induced DNA breaks than that from the sensitive cells in 32P-end-labeled SV40 DNA. VP-16 uptake and efflux studies indicated that there was a 2-3-fold decrease in net cellular accumulation of VP-16 in the resistant cells. Although the reduced uptake of VP-16 and decreased drug sensitivity of topoisomerase II appear to contribute to the mechanism of action and the development of resistance to VP-16, they do not completely explain the degree of resistance to VP-16 in this multidrug-resistant MCF-7 cell line indicating that other biochemical factors, such as activation of VP-16, are also involved in drug resistance and suggesting that the resistance is multifactorial. JF - Cancer research AU - Sinha, B K AU - Haim, N AU - Dusre, L AU - Kerrigan, D AU - Pommier, Y AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09/15/ PY - 1988 DA - 1988 Sep 15 SP - 5096 EP - 5100 VL - 48 IS - 18 SN - 0008-5472, 0008-5472 KW - DNA, Neoplasm KW - 0 KW - Etoposide KW - 6PLQ3CP4P3 KW - DNA Topoisomerases, Type II KW - EC 5.99.1.3 KW - Index Medicus KW - DNA Damage KW - Humans KW - Cell Line -- drug effects KW - DNA Topoisomerases, Type II -- metabolism KW - Drug Resistance KW - Time Factors KW - Female KW - DNA, Neoplasm -- drug effects KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- pathology KW - Etoposide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78394813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+strand+breaks+produced+by+etoposide+%28VP-16%2C213%29+in+sensitive+and+resistant+human+breast+tumor+cells%3A+implications+for+the+mechanism+of+action.&rft.au=Sinha%2C+B+K%3BHaim%2C+N%3BDusre%2C+L%3BKerrigan%2C+D%3BPommier%2C+Y&rft.aulast=Sinha&rft.aufirst=B&rft.date=1988-09-15&rft.volume=48&rft.issue=18&rft.spage=5096&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 - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mixing studies during hepatic artery infusion in an in vitro model. AN - 78385978; 2970291 AB - A glass model of the hepatic artery network was used to study the effect of infusion rate on the degree of mixing from an end hole catheter placed in the gastroduodenal artery. Red dye solutions were infused at rates ranging from 1 ml/hour to 20 ml/minute. Effluent samples from each of 16 branch arteries were collected and dye concentrations were analyzed by means of a spectrophotometer. Low infusion rates, e.g., up to 5 ml/minute, showed streaming of the dye solutions and a nonhomogeneous dye distribution in the distal branches. At 20 ml/minute, dye distribution was much more uniform. These experiments are designed to simulate intrahepatic infusion of chemotherapeutic drug solutions. Theoretical considerations suggesting a pharmacokinetic advantage of intraarterial delivery implicitly assume uniform distribution of drug solutions to all perfused tissue. The in vitro data in this study suggests that this assumption may not be operative under certain infusion conditions. Slow infusion can lead to streaming and nonuniform distribution of infused drug solutions, which may in part explain the variability in tumor response in different tissue regions and also some observed toxicities, such as bile duct stricturing and fibrosis after intrahepatic infusions. JF - Cancer AU - Lutz, R J AU - Miller, D L AD - Biomedical Engineering and Instrumentation Branch, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/09/15/ PY - 1988 DA - 1988 Sep 15 SP - 1066 EP - 1073 VL - 62 IS - 6 SN - 0008-543X, 0008-543X KW - Antineoplastic Agents KW - 0 KW - Coloring Agents KW - Abridged Index Medicus KW - Index Medicus KW - Rheology KW - Chemistry, Physical KW - Humans KW - Chemical Phenomena KW - Cholangitis -- chemically induced KW - Spectrophotometry KW - Catheters, Indwelling KW - Hepatic Artery KW - Antineoplastic Agents -- pharmacokinetics KW - Models, Biological KW - Infusions, Intra-Arterial -- adverse effects KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78385978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mixing+studies+during+hepatic+artery+infusion+in+an+in+vitro+model.&rft.au=Lutz%2C+R+J%3BMiller%2C+D+L&rft.aulast=Lutz&rft.aufirst=R&rft.date=1988-09-15&rft.volume=62&rft.issue=6&rft.spage=1066&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-03 N1 - Date created - 1988-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retroviral activation of a novel gene encoding a zinc finger protein in IL-3-dependent myeloid leukemia cell lines. AN - 78380207; 2842066 AB - Normal hematopoietic stem cells proliferate and differentiate in the presence of growth factors such as interleukin-3 (IL-3). Transformation can alter their growth factor requirements, the ability of the cells to differentiate, or both. To identify genes that are capable of transforming hematopoietic cells, IL-3-dependent cell lines, isolated from retrovirus induced myeloid leukemias, were examined for viral insertions in proto-oncogenes and in common sites of viral integration. Five of 37 cell lines contained proviruses in a common viral integration site termed the ecotropic virus integration 1 site (Evi-1). The integrations were correlated with the activation of transcription from the locus. Sequencing of cDNA clones and genomic clones demonstrated that the integrations had occurred near or in 5' noncoding exons of a novel gene. The sequence of the cDNA clones predicts that the gene product is a 120 kd protein that contains two domains with seven and three repeats of a DNA binding consensus sequence (zinc finger) initially described in the Xenopus transcription factor III A (TFIIIA). This represents the first demonstration of the retroviral activation of a gene encoding a zinc finger protein and the first implication for a member of this gene family in the transformation of hematopoietic cells. JF - Cell AU - Morishita, K AU - Parker, D S AU - Mucenski, M L AU - Jenkins, N A AU - Copeland, N G AU - Ihle, J N AD - NCI-Frederick Cancer Research Facility, Molecular Mechanisms of Carcinogenesis Laboratory, Maryland 21701. Y1 - 1988/09/09/ PY - 1988 DA - 1988 Sep 09 SP - 831 EP - 840 VL - 54 IS - 6 SN - 0092-8674, 0092-8674 KW - DNA-Binding Proteins KW - 0 KW - Interleukin-3 KW - Metalloproteins KW - Transcription Factors KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Base Sequence KW - Interleukin-3 -- physiology KW - Multigene Family KW - DNA -- genetics KW - Molecular Sequence Data KW - Mice KW - Gene Expression Regulation KW - Amino Acid Sequence KW - Cloning, Molecular KW - Leukemia Virus, Murine -- genetics KW - DNA-Binding Proteins -- genetics KW - Metalloproteins -- genetics KW - Transcription Factors -- genetics KW - Leukemia, Experimental -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78380207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell&rft.atitle=Retroviral+activation+of+a+novel+gene+encoding+a+zinc+finger+protein+in+IL-3-dependent+myeloid+leukemia+cell+lines.&rft.au=Morishita%2C+K%3BParker%2C+D+S%3BMucenski%2C+M+L%3BJenkins%2C+N+A%3BCopeland%2C+N+G%3BIhle%2C+J+N&rft.aulast=Morishita&rft.aufirst=K&rft.date=1988-09-09&rft.volume=54&rft.issue=6&rft.spage=831&rft.isbn=&rft.btitle=&rft.title=Cell&rft.issn=00928674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Response of canine esophagus to intraoperative electron beam radiotherapy. AN - 85277883; pmid-3138218 AB - Tolerance of esophagus to intraoperative radiotherapy (IORT) was investigated in dogs. Thirteen adult foxhounds were subjected to right thoractomy, mobilization of the intrathoracic esophagus, and IORT to a 6 cm full-thickness esophageal segment using 9 MeV electrons at doses of 0, 2,000, or 3,000 cGy. Dogs were followed clinically and were evaluated at regular intervals after treatment with fiberoptic esophagoscopy, barium swallows, and postmortem histologic evaluations. One sham-irradiated control dog showed no abnormalities during follow-up of 24 months. Seven dogs receiving 2,000 cGy IORT showed transient mild dysphagia and mild esophagitis, but no clinically or pathologically significant complications. Five dogs receiving 3,000 cGy demonstrated severe ulcerative esophagitis within 6 weeks of treatment which progressed to chronic ulcerative esophagitis with stricture formation by 9 months following IORT. One 3,000 cGy dog died at 13 months from an esophageal perforation. On the basis of a pilot experience using 13 experimental animals, it was concluded that intact canine esophagus tolerates IORT well to doses of 2,000 cGy, but doses of 3,000 cGy pose serious and potentially lethal risks. The clinical application of IORT to the treatment of human intrathoracic neoplasms requiring esophageal irradiation should be approached with caution, particularly at doses exceeding 2,000 cGy. JF - International Journal of Radiation Oncology, Biology, Physics AU - Sindelar, W F AU - Hoekstra, H J AU - Kinsella, T J AU - Barnes, M AU - DeLuca, A M AU - Tochner, Z AU - Pass, H I AU - Kranda, K C AU - Terrill, R E AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. PY - 1988 SP - 663 EP - 669 VL - 15 IS - 3 SN - 0360-3016, 0360-3016 KW - Deglutition Disorders KW - Esophagus KW - Esophagitis KW - Intraoperative Care KW - Animal KW - Dogs KW - Radiation Tolerance KW - Dose-Response Relationship, Radiation KW - Male KW - Radiotherapy, High-Energy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85277883?accountid=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=International+Journal+of+Radiation+Oncology%2C+Biology%2C+Physics&rft.atitle=Response+of+canine+esophagus+to+intraoperative+electron+beam+radiotherapy.&rft.au=Sindelar%2C+W+F%3BHoekstra%2C+H+J%3BKinsella%2C+T+J%3BBarnes%2C+M%3BDeLuca%2C+A+M%3BTochner%2C+Z%3BPass%2C+H+I%3BKranda%2C+K+C%3BTerrill%2C+R+E&rft.aulast=Sindelar&rft.aufirst=W&rft.date=1988-09-01&rft.volume=15&rft.issue=3&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Radiation+Oncology%2C+Biology%2C+Physics&rft.issn=03603016&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Reye's syndrome-like illness in a patient receiving amiodarone. AN - 85223174; pmid-3414648 AB - A 16-yr-old boy who was receiving amiodarone for ventricular arrhythmias developed a Reye's syndrome-like illness several days after an upper respiratory infection. Liver biopsy revealed microvesicular fat and spotty hepatocellular necrosis, typical of Reye's syndrome. Recovery was complete. This case report suggests that medications other than aspirin may predispose to Reye's syndrome, and that children receiving amiodarone should receive prophylaxis against influenza B and chicken pox. JF - The American Journal of Gastroenterology AU - Jones, D B AU - Mullick, F G AU - Hoofnagle, J H AU - Baranski, B AD - Liver Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. PY - 1988 SP - 967 EP - 969 VL - 83 IS - 9 SN - 0002-9270, 0002-9270 KW - Arrhythmia KW - Human KW - Reye Syndrome KW - Liver KW - Case Report KW - Adolescent KW - Amiodarone KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85223174?accountid=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=Reye%27s+syndrome-like+illness+in+a+patient+receiving+amiodarone.&rft.au=Jones%2C+D+B%3BMullick%2C+F+G%3BHoofnagle%2C+J+H%3BBaranski%2C+B&rft.aulast=Jones&rft.aufirst=D&rft.date=1988-09-01&rft.volume=83&rft.issue=9&rft.spage=967&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 - Corticotrophin-releasing factor, vasopressin and pro-opiomelanocortin mRNA responses to stress and opiates in the rat. AN - 78776768; 3267021 AB - 1. Rats underwent either: (1) acute or chronic morphine or naloxone administration; (2) simple morphine withdrawal or naloxone-precipitated withdrawal in morphine-dependent animals; or (3) stress from I.P. administration of hypertonic saline. 2. Quantitative in situ hybridization histochemistry was performed using synthetic oligonucleotide probes for corticotrophin-releasing factor (CRF), vasopressin, pro-opiomelanocortin (POMC), dynorphin, enkephalin and oxytocin mRNAs. The paraventricular and supraoptic nuclei were examined in all studies and the arcuate nucleus and pituitary gland in the acute withdrawal study. 3. Neither acute nor chronic morphine administration altered either (a) hypothalamic parvocellular or magnocellular CRF mRNA, or (b) anterior pituitary or pars intermedia POMC mRNA. 4. Naloxone-precipitated morphine withdrawal resulted in a marked increase in parvocellular (but not magnocellular) CRF mRNA within 4 h and levels remained elevated through 24 h. There was no change in arcuate nucleus or pars intermedia POMC mRNA, but in the anterior pituitary there was a delayed increase, significant at 24 h. 5. Simple morphine withdrawal without the use of naloxone did not result in any change in CRF mRNA but there were increases in magnocellular vasopressin and dynorphin mRNA, presumably related to decreased water intake. 6. Intraperitoneal hypertonic saline stress also resulted in a marked accumulation of both parvocellular CRF and vasopressin mRNA without any concomitant change in magnocellular vasopressin mRNA. Increased translation of CRF mRNA was also evidenced by increased immunoreactive CRF detected by immunocytochemistry. JF - The Journal of physiology AU - Lightman, S L AU - Young, W S AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 511 EP - 523 VL - 403 SN - 0022-3751, 0022-3751 KW - Narcotics KW - 0 KW - RNA, Messenger KW - Vasopressins KW - 11000-17-2 KW - Pro-Opiomelanocortin KW - 66796-54-1 KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Substance Withdrawal Syndrome -- physiopathology KW - Pituitary Gland -- analysis KW - Narcotics -- pharmacology KW - Paraventricular Hypothalamic Nucleus -- analysis KW - Male KW - Vasopressins -- genetics KW - Pro-Opiomelanocortin -- genetics KW - RNA, Messenger -- analysis KW - Stress, Physiological -- physiopathology KW - Corticotropin-Releasing Hormone -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78776768?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+physiology&rft.atitle=Corticotrophin-releasing+factor%2C+vasopressin+and+pro-opiomelanocortin+mRNA+responses+to+stress+and+opiates+in+the+rat.&rft.au=Lightman%2C+S+L%3BYoung%2C+W+S&rft.aulast=Lightman&rft.aufirst=S&rft.date=1988-09-01&rft.volume=403&rft.issue=&rft.spage=511&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+physiology&rft.issn=00223751&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-08-25 N1 - Date created - 1989-08-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neuroendocrinology. 1969;4(6):326-32 [5394282] Neuroendocrinology. 1983 Dec;37(6):467-9 [6606790] Endocrinology. 1971 Jan;88(1):3-15 [4320769] J Pharmacol Exp Ther. 1976 Feb;196(2):269-79 [943520] Nature. 1979 Mar 29;278(5703):463-4 [313009] Nature. 1982 Sep 23;299(5881):355-7 [6287293] Neuroendocrinology. 1983;36(3):165-86 [6601247] Neuroendocrinology. 1983 Jun;36(6):415-23 [6348576] Endocrinology. 1984 Jan;114(1):164-9 [6317342] Methods Enzymol. 1983;103:565-77 [6321896] Proc Natl Acad Sci U S A. 1984 Mar;81(6):1854-8 [6608732] Proc Natl Acad Sci U S A. 1984 Mar;81(6):1883-7 [6369332] Neuroendocrinology. 1984 May;38(5):411-7 [6328347] Biochem Biophys Res Commun. 1984 Oct 30;124(2):407-15 [6093800] Endocrinology. 1985 Feb;116(2):723-7 [2981677] Fed Proc. 1985 Jan;44(1 Pt 2):145-263 [3871407] Fed Proc. 1985 Jan;44(1 Pt 2):203-6 [2981742] Nature. 1985 May 2-8;315(6014):59-61 [3873012] Endocrinology. 1985 Jul;117(1):323-9 [2988921] Endocrinology. 1985 Oct;117(4):1293-9 [3161722] Endocrinology. 1985 Oct;117(4):1314-20 [2992910] Nature. 1985 Sep 19-25;317(6034):248-50 [3900740] Endocrinology. 1986 Jun;118(6):2534-9 [2938937] Neuroendocrinology. 1986;43(3):277-82 [2942792] Neurosci Lett. 1986 Oct 8;70(2):198-203 [3490635] Endocr Rev. 1986 Nov;7(4):351-78 [3023041] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9827-31 [2432603] Neuroendocrinology. 1987 Mar;45(3):212-8 [3561697] Nature. 1987 Aug 13-19;328(6131):643-5 [3614366] Cell Tissue Res. 1987 Sep;249(3):497-507 [3499227] J Physiol. 1987 Dec;394:23-39 [2895179] J Endocrinol. 1988 Apr;117(1):27-34 [3356957] J Physiol. 1988 Feb;396:297-317 [2900890] Psychopharmacologia. 1970;17(2):137-50 [5462744] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Erythroproliferation in vitro can be induced by abl, fes, src, ras, bas, raf, raf/myc, erb B and cbl oncogenes but not by myc, myb and fos. AN - 78677866; 3226726 AB - To assess the erythroproliferative effects of a variety of retroviruses in vitro, hemopoietic precursors were incubated with the viruses then plated in methylcellulose. Only replication defective transforming viruses were active in this assay and produced colonies of erythroid cells. The effective transforming viruses were: Friend virus and viruses containing the abl, fes, src, Ha-ras, Ki-ras, bas, raf, raf/myc, erb B and cbl oncogenes. Replication competent viruses and those bearing the myc, myb and fos oncogenes were unable to initiate colony formation. Significant differences were observed in the colonies induced by several of the transforming genes based on (i) colony size, (ii) morphology, (iii) time course of development and (iv) sensitivity to erythropoietin. The oncogene-expressing retroviruses appeared to have the same target cell, which may be less differentiated erythroid precursor than the target cell for Friend virus. JF - Oncogene research AU - Klinken, S P AD - Laboratory of Experimental Carcinogenesis and Immunopathology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 187 EP - 192 VL - 3 IS - 2 SN - 0890-6467, 0890-6467 KW - Index Medicus KW - Phenotype KW - Animals KW - Mice KW - Colony-Forming Units Assay KW - Oncogenes KW - Erythropoiesis KW - Hematopoietic Stem Cells -- cytology KW - Retroviridae -- genetics KW - Hematopoietic Stem Cells -- microbiology KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78677866?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+research&rft.atitle=Erythroproliferation+in+vitro+can+be+induced+by+abl%2C+fes%2C+src%2C+ras%2C+bas%2C+raf%2C+raf%2Fmyc%2C+erb+B+and+cbl+oncogenes+but+not+by+myc%2C+myb+and+fos.&rft.au=Klinken%2C+S+P&rft.aulast=Klinken&rft.aufirst=S&rft.date=1988-09-01&rft.volume=3&rft.issue=2&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Oncogene+research&rft.issn=08906467&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-28 N1 - Date created - 1989-03-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hypothesis: a nicotine-dopamine interaction linking smoking with Parkinson's disease and tardive dyskinesia. AN - 78661586; 3066487 AB - 1. Nicotine, an important pharmacological component of cigarette smoke, is known to have significant effects on central nervous system (CNS) dopaminergic function. Although acute doses of nicotine have been shown to facilitate dopamine release, recent data indicate that chronic nicotine treatment may actually decrease CNS dopamine turnover in the striatum. 2. A number of epidemiological investigations have demonstrated that individuals who are or who have been smokers are less likely to develop idiopathic Parkinson's disease (a disorder involving a deficit in nigrostriatal dopaminergic neurotransmission). In addition, there is preliminary evidence that individuals with tardive dyskinesia (a hyperkinetic movement disorder observed in some cases of chronic neuroleptic treatment and thought by some to be associated with striatal dopamine receptor supersensitivity) are more likely to be smokers. 3. A unitary hypothesis is presented, proposing that smoking in early adult life may decrease CNS catecholamine turnover, thereby protecting against free radical formation from catecholamine oxidation that in turn damages striatal neurons. These individuals are thereby "protected" from the later development of Parkinson's disease. In this hypothetical scheme, individuals who are given neuroleptics and who also are smokers may develop a greater degree of dopamine receptor supersensitivity due to combined receptor blockade by neuroleptics and a decrease in CNS dopamine turnover caused by nicotine, resulting in an increased prevalence of tardive dyskinesia in this group. JF - Cellular and molecular neurobiology AU - Kirch, D G AU - Alho, A M AU - Wyatt, R J AD - Neuropsychiatry Branch, National Institute of Mental Health, Washington, D.C. 20032. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 285 EP - 291 VL - 8 IS - 3 SN - 0272-4340, 0272-4340 KW - Nicotine KW - 6M3C89ZY6R KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Drug Interactions KW - Humans KW - Parkinson Disease, Secondary -- metabolism KW - Dyskinesia, Drug-Induced -- metabolism KW - Nicotine -- metabolism KW - Smoking -- metabolism KW - Smoking -- adverse effects KW - Dopamine -- metabolism KW - Dyskinesia, Drug-Induced -- etiology KW - Parkinson Disease, Secondary -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78661586?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+molecular+neurobiology&rft.atitle=Hypothesis%3A+a+nicotine-dopamine+interaction+linking+smoking+with+Parkinson%27s+disease+and+tardive+dyskinesia.&rft.au=Kirch%2C+D+G%3BAlho%2C+A+M%3BWyatt%2C+R+J&rft.aulast=Kirch&rft.aufirst=D&rft.date=1988-09-01&rft.volume=8&rft.issue=3&rft.spage=285&rft.isbn=&rft.btitle=&rft.title=Cellular+and+molecular+neurobiology&rft.issn=02724340&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-29 N1 - Date created - 1989-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of a simian virus 40-based shuttle vector to analyze enhanced mutagenesis in mitomycin C-treated monkey cells. AN - 78652944; 2851732 AB - When monkey cells were treated with mitomycin C 24 h before transfection with UV-irradiated pZ189 (a simian virus 40-based shuttle vector), there was a twofold increase in the frequency of mutations in the supF gene of the vector. These results suggest the existence of an enhancible mutagenesis pathway in mammalian cells. However, DNA sequence analysis of the SupF- mutants suggested no dramatic changes in the mechanisms of mutagenesis due to mitomycin C treatment of the cells. JF - Molecular and cellular biology AU - Roilides, E AU - Munson, P J AU - Levine, A S AU - Dixon, K AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 3943 EP - 3946 VL - 8 IS - 9 SN - 0270-7306, 0270-7306 KW - Mitomycins KW - 0 KW - Mitomycin KW - 50SG953SK6 KW - RNA, Transfer KW - 9014-25-9 KW - Index Medicus KW - RNA, Transfer -- drug effects KW - Animals KW - Ultraviolet Rays KW - Base Sequence KW - Genes KW - Base Composition KW - RNA, Transfer -- genetics KW - Cercopithecus aethiops KW - Molecular Sequence Data KW - Kidney KW - Cell Line KW - Transfection -- drug effects KW - Simian virus 40 -- genetics KW - Genetic Vectors -- radiation effects KW - Mitomycins -- pharmacology KW - Mutation KW - Transfection -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78652944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Use+of+a+simian+virus+40-based+shuttle+vector+to+analyze+enhanced+mutagenesis+in+mitomycin+C-treated+monkey+cells.&rft.au=Roilides%2C+E%3BMunson%2C+P+J%3BLevine%2C+A+S%3BDixon%2C+K&rft.aulast=Roilides&rft.aufirst=E&rft.date=1988-09-01&rft.volume=8&rft.issue=9&rft.spage=3943&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1967 Jun 14;26(2):365-9 [4291934] Somat Cell Mol Genet. 1988 Jul;14(4):351-7 [3135602] Exp Cell Res. 1973 Sep;81(1):120-6 [4357029] Photochem Photobiol. 1980 Dec;32(6):823-30 [6450424] Prog Nucleic Acid Res Mol Biol. 1981;25:53-126 [6784186] Proc Natl Acad Sci U S A. 1981 Jul;78(7):4480-4 [6945596] Cell. 1982 May;29(1):11-22 [7049397] Mutat Res. 1982 Nov;105(5):291-8 [6292708] Cell. 1982 Nov;31(1):5-7 [6760987] Genetics. 1984 Mar;106(3):347-64 [6368314] Microbiol Rev. 1984 Mar;48(1):60-93 [6371470] Mol Cell Biol. 1984 Mar;4(3):435-41 [6325877] Cell. 1984 Jun;37(2):675-82 [6373019] EMBO J. 1984 Dec 20;3(13):3117-21 [6098464] Cancer Invest. 1985;3(2):163-74 [2986797] J Mol Biol. 1985 Mar 5;182(1):45-65 [3923204] Mol Cell Biol. 1985 Jul;5(7):1685-93 [2991746] Gene. 1985;38(1-3):233-7 [2998945] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8606-10 [3001711] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8273-7 [3464953] Mol Cell Biol. 1986 Jan;6(1):277-85 [3537686] Mol Cell Biol. 1986 Apr;6(4):1102-7 [3023869] Mol Cell Biol. 1986 Oct;6(10):3349-56 [3540589] EMBO J. 1987 Jan;6(1):63-7 [3034580] Mutat Res. 1987 Jul;179(1):103-14 [3037362] Environ Mol Mutagen. 1987;10(1):97-116 [2826138] Environ Mol Mutagen. 1988;11(1):119-33 [3276505] Mutat Res. 1988 Mar;198(1):199-206 [3127698] J Natl Cancer Inst. 1968 Aug;41(2):351-7 [4299537] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transposon tagging using Ty elements in yeast. AN - 78650624; 2851484 AB - We have used the ability to induce high levels of Ty transposition to develop a method for transposon mutagenesis in Saccharomyces cerevisiae. To facilitate genetic and molecular analysis, we have constructed GAL1-promoted TyH3 or Ty917 elements that contain unique cloning sites, and marked these elements with selectable genes. These genes include the yeast HIS3 gene, and the plasmid PiAN7 containing the Tn903 NEO gene. The marked Ty elements retain their ability to transpose, to mutate the LYS2, LYS5, or STE2 genes, and to activate the promoterless his3 delta 4 target gene. Ty elements containing selectable genes are also useful in strain construction, in chromosomal mapping, and in gene cloning strategies. JF - Genetics AU - Garfinkel, D J AU - Mastrangelo, M F AU - Sanders, N J AU - Shafer, B K AU - Strathern, J N AD - Bionetics Research, Inc., National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 95 EP - 108 VL - 120 IS - 1 SN - 0016-6731, 0016-6731 KW - DNA Transposable Elements KW - 0 KW - Index Medicus KW - Genotype KW - Genes, Fungal KW - Crosses, Genetic KW - Nucleic Acid Hybridization KW - Plasmids KW - Saccharomyces cerevisiae -- genetics KW - Mutation KW - Cloning, Molecular UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78650624?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genetics&rft.atitle=Transposon+tagging+using+Ty+elements+in+yeast.&rft.au=Garfinkel%2C+D+J%3BMastrangelo%2C+M+F%3BSanders%2C+N+J%3BShafer%2C+B+K%3BStrathern%2C+J+N&rft.aulast=Garfinkel&rft.aufirst=D&rft.date=1988-09-01&rft.volume=120&rft.issue=1&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Genetics&rft.issn=00166731&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-22 N1 - Date created - 1989-03-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1970 Oct 14;53(1):159-62 [4922220] Mol Cell Biol. 1988 Apr;8(4):1432-42 [2837641] Proc Natl Acad Sci U S A. 1978 Apr;75(4):1929-33 [347451] J Cell Biol. 1980 Jun;85(3):811-22 [6993497] Cell. 1980 Aug;21(1):239-49 [6250713] Science. 1980 Sep 19;209(4463):1375-80 [6251544] Cell. 1980 Nov;22(2 Pt 2):427-36 [6256080] J Mol Biol. 1981 Feb 5;145(4):619-32 [7021854] Mol Gen Genet. 1981;182(1):159-63 [6267430] J Mol Biol. 1981 Apr 5;147(2):217-26 [6270337] J Bacteriol. 1983 Jan;153(1):163-8 [6336730] Nucleic Acids Res. 1983 Apr 25;11(8):2427-45 [6856467] Methods Enzymol. 1983;100:468-500 [6225933] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] Cell. 1983 Dec;35(2 Pt 1):521-9 [6360378] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2431-4 [6326126] Gene. 1984 Feb;27(2):183-91 [6327466] J Bacteriol. 1984 May;158(2):636-43 [6233260] Genetics. 1984 Jun;107(2):179-97 [6329902] Mol Gen Genet. 1984;197(2):345-6 [6394957] Cell. 1985 Mar;40(3):491-500 [2982495] Nucleic Acids Res. 1985 Jun 11;13(11):4097-112 [2989787] Proc Natl Acad Sci U S A. 1985 Aug;82(16):5423-7 [2991922] Proc Natl Acad Sci U S A. 1985 Aug;82(16):5428-32 [2991923] Nucleic Acids Res. 1985 Sep 25;13(18):6679-93 [2997719] Nature. 1985 Dec 12-18;318(6046):583-6 [2415827] Cell. 1985 Dec;43(2 Pt 1):483-92 [3907857] Nucleic Acids Res. 1985 Dec 9;13(23):8587-601 [3001645] Proc Natl Acad Sci U S A. 1986 Feb;83(3):735-9 [3003748] Gene. 1986;42(2):169-73 [3015730] Science. 1986 Dec 19;234(4783):1582-5 [3538420] Mol Cell Biol. 1986 Nov;6(11):3575-81 [3025601] Mol Cell Biol. 1987 Jan;7(1):258-65 [3031464] Genetics. 1987 Jun;116(2):191-9 [3038670] J Virol. 1987 Oct;61(10):3004-12 [3041020] Nucleic Acids Res. 1987 Sep 25;15(18):7309-24 [2821507] J Biol Chem. 1988 Jan 25;263(3):1413-23 [2447089] Science. 1988 Jan 15;239(4837):280-2 [2827308] Mol Cell Biol. 1988 Feb;8(2):978-81 [3280976] Curr Genet. 1986;11(3):193-200 [2834090] J Mol Biol. 1977 Oct 15;116(1):125-59 [338917] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Directed drug distribution: adding controlled brain activity to a drug. AN - 78605810; 3061952 AB - Environmental factors can alter the state of an organism so as to influence the response to drugs. This fact is widely recognized even though the responsible mechanisms are difficult to understand and control. The capacity of environmental influences to alter local drug pharmacokinetics is rarely considered. Drug localization and resulting action within the brain are influenced by vascular blood flow factors, local concentration differences in competing neurohumours, and receptor density. These are all frequently asymmetrically represented in the brain and drug effects are correspondingly laterality dependent. Attention to regional brain pharmacokinetics and the influence of environment on regional blood flow, local neurohumor concentration, and receptor density represents an untapped opportunity to enhance the desired effect of a centrally active drug at its site of action without enhancing general systemic toxicity. Combined pharmacotherapy and psychotherapy may result in superior therapeutic responses. Psychotherapy is a potential tool deliberately to manipulate environmental factors that influence physiological and physical chemical parameters that determine drug disposition. JF - The International journal of neuroscience AU - Myslobodsky, M S AU - Weiner, M AD - NIMH/NIH, Neuropsychiatry Branch, St. Elizabeths Hospital, Washington, DC.20032. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 7 EP - 19 VL - 42 IS - 1-2 SN - 0020-7454, 0020-7454 KW - Central Nervous System Agents KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Tissue Distribution KW - Brain -- drug effects KW - Central Nervous System Agents -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78605810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+International+journal+of+neuroscience&rft.atitle=Directed+drug+distribution%3A+adding+controlled+brain+activity+to+a+drug.&rft.au=Myslobodsky%2C+M+S%3BWeiner%2C+M&rft.aulast=Myslobodsky&rft.aufirst=M&rft.date=1988-09-01&rft.volume=42&rft.issue=1-2&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=The+International+journal+of+neuroscience&rft.issn=00207454&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-14 N1 - Date created - 1989-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Improving the use of anticancer drugs: clinical pharmacokinetic approaches. AN - 78590788; 3204004 AB - There are many areas in which clinical oncologists and pharmacologists can work together to improve the chemotherapy of cancer. In new drug development, the conduct of Phase I clinical trials is greatly facilitated by cooperative selection of appropriate schedules and dose escalation procedures. For established anticancer agents, continual surveillance is necessary to assure that new insights regarding a drug's mechanism of action can be translated into rational clinical trends, which are intended to improve response rates and/or reduce toxicity. Specific areas of optimization include alternate schedules or routes of drug delivery and selection of agents that penetrate the CNS. Adjustment of drug dosage for an individual patient and assessment of drug interactions can also be facilitated by collaboration between clinicians and pharmacologists. JF - Israel journal of medical sciences AU - Collins, J M AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD 20892. PY - 1988 SP - 483 EP - 487 VL - 24 IS - 9-10 SN - 0021-2180, 0021-2180 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Drug Evaluation KW - Infusions, Intravenous KW - Humans KW - Chemotherapy, Cancer, Regional Perfusion KW - Injections KW - Neoplasms -- drug therapy KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78590788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Israel+journal+of+medical+sciences&rft.atitle=Improving+the+use+of+anticancer+drugs%3A+clinical+pharmacokinetic+approaches.&rft.au=Collins%2C+J+M&rft.aulast=Collins&rft.aufirst=J&rft.date=1988-09-01&rft.volume=24&rft.issue=9-10&rft.spage=483&rft.isbn=&rft.btitle=&rft.title=Israel+journal+of+medical+sciences&rft.issn=00212180&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-08 N1 - Date created - 1989-02-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Confidence bands for logistic regression with restricted predictor variables. AN - 78589747; 3203128 AB - Confidence bands are constructed for the logistic response function when there is an interval restriction on each of the predictor variables. The construction involves application of a general fitting procedure using Scheffé's S-method, described by Casella and Strawderman (1980, Journal of the American Statistical Association 75, 862-868). Specific details are given for the case of one predictor variable, along with details for a fixed-width alternative to the S-method bands. In the one-predictor case, Monte Carlo results suggest that both bands are conservative for small sample sizes, such as N = 25. By N = 200 the S-method's coverage probabilities are seen to attain their nominal levels while the fixed-width bands remain conservative. The procedures are exemplified with data from a genetic toxicology experiment. JF - Biometrics AU - Piegorsch, W W AU - Casella, G AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 739 EP - 750 VL - 44 IS - 3 SN - 0006-341X, 0006-341X KW - Index Medicus KW - Probability KW - Mutagenicity Tests KW - Dose-Response Relationship, Drug KW - Humans KW - Monte Carlo Method KW - Regression Analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78589747?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Confidence+bands+for+logistic+regression+with+restricted+predictor+variables.&rft.au=Piegorsch%2C+W+W%3BCasella%2C+G&rft.aulast=Piegorsch&rft.aufirst=W&rft.date=1988-09-01&rft.volume=44&rft.issue=3&rft.spage=739&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-02-03 N1 - Date created - 1989-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tamoxifen and fluoxymesterone versus tamoxifen and danazol in metastatic breast cancer--a randomized study. AN - 78556689; 3058238 AB - A prospective randomized trial of tamoxifen and fluoxymesterone versus tamoxifen and danazol in metastatic breast cancer was conducted from December 1980 to September 1985. Patients were eligible regardless of site of disease, estrogen receptor status, or age. Sixty-two of sixty-three randomized patients were evaluable for response. Overall response for tamoxifen and fluoxymesterone was 11% with 61% stabilization of disease, versus 12% response rate for tamoxifen and danazol with 59% stabilization. Toxicities with tamoxifen and fluoxymesterone were greater with an increase in masculinization. We conclude that the response rates to the combinations of tamoxifen and fluoxymesterone or tamoxifen and danazol reported are equivalent in this study but that the increased toxicity with tamoxifen and fluoxymesterone would make tamoxifen and danazol the treatment of choice if a combination were to be used. JF - Breast cancer research and treatment AU - Swain, S M AU - Steinberg, S M AU - Bagley, C AU - Lippman, M E AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 51 EP - 57 VL - 12 IS - 1 SN - 0167-6806, 0167-6806 KW - Tamoxifen KW - 094ZI81Y45 KW - Fluoxymesterone KW - 9JU12S4YFY KW - Danazol KW - N29QWW3BUO KW - Index Medicus KW - Fluoxymesterone -- administration & dosage KW - Random Allocation KW - Humans KW - Adult KW - Danazol -- administration & dosage KW - Clinical Trials as Topic KW - Aged KW - Middle Aged KW - Tamoxifen -- administration & dosage KW - Menopause KW - Female KW - Breast Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78556689?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Breast+cancer+research+and+treatment&rft.atitle=Tamoxifen+and+fluoxymesterone+versus+tamoxifen+and+danazol+in+metastatic+breast+cancer--a+randomized+study.&rft.au=Swain%2C+S+M%3BSteinberg%2C+S+M%3BBagley%2C+C%3BLippman%2C+M+E&rft.aulast=Swain&rft.aufirst=S&rft.date=1988-09-01&rft.volume=12&rft.issue=1&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Breast+cancer+research+and+treatment&rft.issn=01676806&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-01-26 N1 - Date created - 1989-01-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preclinical antitumor activity of batracylin (NSC 320846). AN - 78545718; 3192381 AB - Batracylin (NSC 320846, BAY H 2049), given ip on days 2 and 9 at a dose 400 mg/kg, inhibited tumor growth completely in 80-100% of mice with early-stage colon adenocarcinoma 38. Therapeutic efficacy against this subcutaneously implanted tumor was retained upon oral administration of Batracylin although, compared to ip treatment, larger doses were required. Batracylin also caused regression of advanced (400 mg) colon 38 tumors. Only modest activity was observed for this compound against P388 leukemia, but P388 sublines with acquired resistance to either adriamycin or cisplatin demonstrated collateral sensitivity. Batracylin currently is undergoing toxicological evaluation by NCI prior to clinical trials. JF - Investigational new drugs AU - Plowman, J AU - Paull, K D AU - Atassi, G AU - Harrison, S D AU - Dykes, D J AU - Kabbe, H J AU - Narayanan, V L AU - Yoder, O C AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 147 EP - 153 VL - 6 IS - 3 SN - 0167-6997, 0167-6997 KW - Antineoplastic Agents KW - 0 KW - Quinazolines KW - batracylin KW - 67199-66-0 KW - Index Medicus KW - Injections, Intraperitoneal KW - Administration, Oral KW - Mice, Inbred Strains KW - Animals KW - Tumor Cells, Cultured -- drug effects KW - Colonic Neoplasms -- drug therapy KW - Mice KW - Drug Evaluation, Preclinical KW - Quinazolines -- administration & dosage KW - Leukemia P388 -- drug therapy KW - Leukemia, Experimental -- drug therapy KW - Quinazolines -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Adenocarcinoma -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78545718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preclinical+antitumor+activity+of+batracylin+%28NSC+320846%29.&rft.au=Plowman%2C+J%3BPaull%2C+K+D%3BAtassi%2C+G%3BHarrison%2C+S+D%3BDykes%2C+D+J%3BKabbe%2C+H+J%3BNarayanan%2C+V+L%3BYoder%2C+O+C&rft.aulast=Plowman&rft.aufirst=J&rft.date=1988-09-01&rft.volume=6&rft.issue=3&rft.spage=147&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 - 1989-01-12 N1 - Date created - 1989-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA alkylation by nitrosobis-(2-oxopropyl)amine in rats of different ages. AN - 78542439; 3142834 AB - We have examined the methylation of liver DNA (O6- and N7-methylguanine) by nitrosobis-(2-oxopropyl)amine (BOP) in male and female rats at various ages, following treatment with 2.5 mg of BOP; this dose given twice weekly for 30 weeks induces tumors in all animals. Except in young rats there was more methylation in female rat liver than in male rat liver, when adjusted for different sizes of the animals. There were differences in the extent of methylation between young (4 weeks) and older rats, but not between young adult (20 weeks) and old adult (65 weeks) males; the latter developed liver tumors when treated with BOP, and the former did not. There was no obvious relation between increased susceptibility to liver tumor induction by BOP and the extent of alkylation of liver DNA. Methylation of DNA was lower in the kidney than in the liver and, here, there was little difference between the sexes. In the testis there was N7-methylation of guanine in DNA, but no O6-methylguanine was detected. JF - Japanese journal of cancer research : Gann AU - Thomas, B J AU - Lijinsky, W AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, MD 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1039 EP - 1042 VL - 79 IS - 9 SN - 0910-5050, 0910-5050 KW - Nitrosamines KW - 0 KW - nitrosobis(2-oxopropyl)amine KW - 60599-38-4 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Kidney -- metabolism KW - Liver -- metabolism KW - Methylation KW - Male KW - Female KW - Alkylation KW - Nitrosamines -- pharmacology KW - DNA -- metabolism KW - Aging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78542439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+alkylation+by+nitrosobis-%282-oxopropyl%29amine+in+rats+of+different+ages.&rft.au=Thomas%2C+B+J%3BLijinsky%2C+W&rft.aulast=Thomas&rft.aufirst=B&rft.date=1988-09-01&rft.volume=79&rft.issue=9&rft.spage=1039&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 - 1989-01-10 N1 - Date created - 1989-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Plasma amine metabolites before and after withdrawal from neuroleptic treatment in chronic schizophrenic inpatients. AN - 78522439; 2903509 AB - Plasma catecholamine metabolites were measured in paired blood samples from 22 subjects with chronic schizophrenia. One sample was drawn while patients were on a stable dose of neuroleptic medication; the second was drawn 6 weeks after discontinuation of medication. In comparison with baseline values during neuroleptic treatment, there was a significant increase in the plasma concentration of the norepinephrine metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), and a trend toward an increase in the plasma concentration of the dopamine metabolite, homovanillic acid (HVA), in the medication-free subjects. There were no significant correlations between plasma MHPG or HVA concentrations and the corresponding ratings of psychopathology for these patients. JF - Psychiatry research AU - Kirch, D G AU - Jaskiw, G AU - Linnoila, M AU - Weinberger, D R AU - Wyatt, R J AD - Neuropsychiatry Branch, National Institute of Mental Health, St. Elizabeths Hospital, Washington DC. 20032. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 233 EP - 242 VL - 25 IS - 3 SN - 0165-1781, 0165-1781 KW - Antipsychotic Agents KW - 0 KW - Catecholamines KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Homovanillic Acid -- blood KW - Double-Blind Method KW - Methoxyhydroxyphenylglycol -- blood KW - Humans KW - Brain -- drug effects KW - Dyskinesia, Drug-Induced -- blood KW - Adult KW - Clinical Trials as Topic KW - Schizophrenic Psychology KW - Adolescent KW - Male KW - Female KW - Catecholamines -- blood KW - Antipsychotic Agents -- therapeutic use KW - Schizophrenia -- drug therapy KW - Substance Withdrawal Syndrome -- blood KW - Antipsychotic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78522439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Plasma+amine+metabolites+before+and+after+withdrawal+from+neuroleptic+treatment+in+chronic+schizophrenic+inpatients.&rft.au=Kirch%2C+D+G%3BJaskiw%2C+G%3BLinnoila%2C+M%3BWeinberger%2C+D+R%3BWyatt%2C+R+J&rft.aulast=Kirch&rft.aufirst=D&rft.date=1988-09-01&rft.volume=25&rft.issue=3&rft.spage=233&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 - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic administration of morphine and naltrexone up-regulate[3H][D-Ala2,D-leu5]enkephalin binding sites by different mechanisms. AN - 78510809; 2847072 AB - Previous studies have demonstrated that chronic administration of morphine up-regulated the lower affinity binding site for [3H][D-ala2,D-leu5]enkephalin, without producing a detectable alteration in the higher affinity binding site for [3H][D-ala2,D-leu5]enkephalin (Rothman et al., Eur. J. Pharmac. 124: 113-119, 1986). The experiments reported in this paper tested the hypothesis that chronic administration of morphine and naltrexone up-regulated the binding sites for [3H][D-ala2,D-leu5]enkephalin by different mechanisms. Rats were given either morphine or naltrexone chronically. Chronic administration of morphine up-regulated the lower affinity site, while chronic administration of naltrexone up-regulated both the higher and lower affinity binding sites for [3H][D-ala2,D-leu5]enkephalin. Unlike the lower affinity binding site for [3H][D-ala2,D-leu5]enkephalin present in membranes prepared from rats treated with placebo pellets, the lower affinity binding sites which were up-regulated by naltrexone and morphine were partially (naltrexone) or completely (morphine) labile to preincubation for 60 min at 25 degrees C in 50 mM Tris-HCl, pH 7.4, containing 0.4 M NaCl. These data suggest that chronic administration of morphine and naltrexone up-regulate binding sites for [3H][D-ala2,D-leu5]enkephalin through different mechanisms, and that the lower affinity binding sites for [3H][D-ala2, D-leu5]enkephalin which are up-regulated by chronic administration of morphine and naltrexone might differ biochemically from the lower affinity binding sites present in membranes treated with placebo. JF - Neuropharmacology AU - Danks, J A AU - Tortella, F C AU - Long, J B AU - Bykov, V AU - Jacobson, A E AU - Rice, K C AU - Holaday, J W AU - Rothman, R B AD - Laboratory of Preclinical Pharmacology, NIMH, St. Elizabeths Hospital, Washington, DC 20002. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 965 EP - 974 VL - 27 IS - 9 SN - 0028-3908, 0028-3908 KW - Receptors, Opioid KW - 0 KW - Sodium Chloride KW - 451W47IQ8X KW - Naltrexone KW - 5S6W795CQM KW - Morphine KW - 76I7G6D29C KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Drug Tolerance KW - Animals KW - Morphine Dependence KW - Male KW - Sodium Chloride -- pharmacology KW - Naltrexone -- administration & dosage KW - Receptors, Opioid -- drug effects KW - Naltrexone -- pharmacology KW - Morphine -- administration & dosage KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78510809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chronic+administration+of+morphine+and+naltrexone+up-regulate%5B3H%5D%5BD-Ala2%2CD-leu5%5Denkephalin+binding+sites+by+different+mechanisms.&rft.au=Danks%2C+J+A%3BTortella%2C+F+C%3BLong%2C+J+B%3BBykov%2C+V%3BJacobson%2C+A+E%3BRice%2C+K+C%3BHoladay%2C+J+W%3BRothman%2C+R+B&rft.aulast=Danks&rft.aufirst=J&rft.date=1988-09-01&rft.volume=27&rft.issue=9&rft.spage=965&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=00283908&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-16 N1 - Date created - 1988-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro inhibition of human herpesvirus-6 by phosphonoformate. AN - 78496787; 2972736 AB - HSB-2 cell cultures productively infected with human herpesvirus-6 were treated with the antiviral drugs phosphonoformic acid (PFA), acyclovir (ACV), and gancyclovir (DHPG). ACV and DHPG showed significant toxic effects on uninfected HSB-2 cells, yet only incompletely inhibited viral expression upon infection of the cells. PFA, however, showed little direct toxicity on HSB-2 cells while viral replication was inhibited significantly. JF - Journal of virological methods AU - Streicher, H Z AU - Hung, C L AU - Ablashi, D V AU - Hellman, K AU - Saxinger, C AU - Fullen, J AU - Salahuddin, S Z AD - National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 301 EP - 304 VL - 21 IS - 1-4 SN - 0166-0934, 0166-0934 KW - Antiviral Agents KW - 0 KW - Organophosphorus Compounds KW - Foscarnet KW - 364P9RVW4X KW - Phosphonoacetic Acid KW - N919E46723 KW - Ganciclovir KW - P9G3CKZ4P5 KW - Acyclovir KW - X4HES1O11F KW - Index Medicus KW - Acyclovir -- pharmacology KW - Humans KW - Cell Line KW - Acyclovir -- analogs & derivatives KW - Antiviral Agents -- pharmacology KW - Phosphonoacetic Acid -- analogs & derivatives KW - Phosphonoacetic Acid -- pharmacology KW - Organophosphorus Compounds -- pharmacology KW - Herpesviridae -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78496787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+virological+methods&rft.atitle=In+vitro+inhibition+of+human+herpesvirus-6+by+phosphonoformate.&rft.au=Streicher%2C+H+Z%3BHung%2C+C+L%3BAblashi%2C+D+V%3BHellman%2C+K%3BSaxinger%2C+C%3BFullen%2C+J%3BSalahuddin%2C+S+Z&rft.aulast=Streicher&rft.aufirst=H&rft.date=1988-09-01&rft.volume=21&rft.issue=1-4&rft.spage=301&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 completed - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolic and renal effects of interleukin-2 immunotherapy for metastatic cancer. AN - 78485036; 3263237 AB - The systemic administration of recombinant interleukin-2 (IL-2) either alone or in combination with lymphokine activated killer cells is a new approach to the immunotherapy of metastatic cancer in man. Renal toxicity is often a dose-limiting side effect of IL-2 administration. This prospective study of 17 consecutive patients receiving parenteral high dose IL-2 documents a reversible syndrome of hypotension, oliguria, fluid retention, azotemia and very low urinary excretion of sodium (median FeNa of 0.04%). The median nadir urinary uric acid to urinary creatinine ratio during IL-2 therapy was 0.2. This IL-2 regimen induces a reversible renal hypoperfusion syndrome (pre-renal azotemia) without evidence of acute uric acid nephropathy. Hypophosphatemia [median serum phosphorus of 1.9 mg/dl (0.61 mmol/l)] prompted further study of tubular function. Urinary excretions of phosphorus, calcium and magnesium were very low. Arterial blood gases revealed hyperventilation without alkalemia. The hypophosphatemia probably reflects increased utilization of inorganic phosphorus by rapidly proliferating lymphoid cells. JF - Clinical nephrology AU - Webb, D E AU - Austin, H A AU - Belldegrun, A AU - Vaughan, E AU - Linehan, W M AU - Rosenberg, S A AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 141 EP - 145 VL - 30 IS - 3 SN - 0301-0430, 0301-0430 KW - Interleukin-2 KW - 0 KW - Lymphokines KW - Phosphates KW - Recombinant Proteins KW - Index Medicus KW - Phosphates -- blood KW - Humans KW - Recombinant Proteins -- adverse effects KW - Natriuresis KW - Middle Aged KW - Recombinant Proteins -- therapeutic use KW - Kidney Neoplasms -- therapy KW - Interleukin-2 -- adverse effects KW - Carcinoma, Renal Cell -- therapy KW - Uremia -- etiology KW - Killer Cells, Natural KW - Interleukin-2 -- therapeutic use KW - Hypotension -- etiology KW - Carcinoma, Renal Cell -- secondary KW - Acute Kidney Injury -- etiology KW - Immunotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78485036?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nephrology&rft.atitle=Metabolic+and+renal+effects+of+interleukin-2+immunotherapy+for+metastatic+cancer.&rft.au=Webb%2C+D+E%3BAustin%2C+H+A%3BBelldegrun%2C+A%3BVaughan%2C+E%3BLinehan%2C+W+M%3BRosenberg%2C+S+A&rft.aulast=Webb&rft.aufirst=D&rft.date=1988-09-01&rft.volume=30&rft.issue=3&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=Clinical+nephrology&rft.issn=03010430&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-19 N1 - Date created - 1988-12-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hepatic cholesterol metabolism as a function of carbon disulfide concentration and treatment with phenobarbital. AN - 78473511; 3177220 AB - Male F344 rats were exposed to carbon disulfide (CS2) at 0, 30, 75, 150, 300, or 600 ppm for 6 hr by inhalation in the presence or absence of 0.1% phenobarbital (PB) in the drinking water starting 5 days before exposure to CS2. Exposure to 600 ppm CS2 only resulted in a decrease in hepatic cholesterol synthesis and an increase in the liver-to-body-weight ratio (relative liver weight); however, it caused no histopathological damage and had little or no consistent effect on the concentration of hepatic cholesterol or on hepatic water content. Treatment with PB alone resulted in increases in the concentration of hepatic cholesterol and relative liver weight. Exposure to 300 ppm CS2 + PB or to 600 ppm CS2 + PB resulted in a decrease in hepatic cholesterol synthesis and increases in the concentration of hepatic cholesterol, relative liver weight, hepatic water content, and histopathological damage. A concentration-response relationship was demonstrated between exposure to CS2 only and decreased hepatic cholesterol synthesis. A concentration-response relationship also was demonstrated between exposure to CS2 in rats that had been treated with PB and decreased hepatic cholesterol synthesis, increased hepatic cholesterol concentration, increased relative liver weight, increased hepatic water content, and histopathological damage. Treatment with PB lowered the concentration of CS2 required to alter hepatic cholesterol metabolism. The reported observations are consistent with the theory that oxidative metabolism is involved in the expression of CS2-mediated alterations of hepatic cholesterol metabolism. JF - American Industrial Hygiene Association journal AU - Simmons, J E AU - Sloane, R A AU - Van Stee, E W AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27711. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 427 EP - 433 VL - 49 IS - 9 SN - 0002-8894, 0002-8894 KW - Cholesterol KW - 97C5T2UQ7J KW - Carbon Disulfide KW - S54S8B99E8 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Male KW - Organ Size -- drug effects KW - Phenobarbital -- pharmacology KW - Liver -- pathology KW - Cholesterol -- biosynthesis KW - Liver -- drug effects KW - Carbon Disulfide -- toxicity KW - Liver -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78473511?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Industrial+Hygiene+Association+journal&rft.atitle=Hepatic+cholesterol+metabolism+as+a+function+of+carbon+disulfide+concentration+and+treatment+with+phenobarbital.&rft.au=Simmons%2C+J+E%3BSloane%2C+R+A%3BVan+Stee%2C+E+W&rft.aulast=Simmons&rft.aufirst=J&rft.date=1988-09-01&rft.volume=49&rft.issue=9&rft.spage=427&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 completed - 1988-11-21 N1 - Date created - 1988-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oxidation of cyanide to the cyanyl radical by peroxidase/H2O2 systems as determined by spin trapping. AN - 78428373; 2844117 AB - The cyanyl radical was formed during the oxidation of potassium or sodium cyanide by horseradish peroxidase, lactoperoxidase, chloroperoxidase, NADH peroxidase, or methemoglobin in the presence of hydrogen peroxide. The spin adducts of the cyanyl radical with 5,5-dimethyl-1-pyrroline-N-oxide and N-tert-butyl-alpha-phenylnitrone were quite stable at neutral pH. The identity of these spin adducts could be demonstrated using 13C-labeled cyanide and by comparison with the spin adducts of the formamide radical, a hydrolysis product of the cyanyl radical adduct. The enzymatic conversion of cyanide to cyanyl radical by peroxidases should be considered in addition to its well-known role as a metal ligand. Furthermore, since cyanide is used routinely as an inhibitor of peroxidases, some consideration should be given to the biochemical consequences of this formation of the cyanyl radical by the catalytic activity of these enzymes. JF - Archives of biochemistry and biophysics AU - Moreno, S N AU - Stolze, K AU - Janzen, E G AU - Mason, R P AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 267 EP - 271 VL - 265 IS - 2 SN - 0003-9861, 0003-9861 KW - Cyanides KW - 0 KW - Free Radicals KW - Methemoglobin KW - 9008-37-1 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Peroxidases KW - EC 1.11.1.- KW - Potassium Cyanide KW - MQD255M2ZO KW - Sodium Cyanide KW - O5DDB9Z95G KW - Index Medicus KW - Oxidation-Reduction KW - Electron Spin Resonance Spectroscopy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78428373?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oxidation+of+cyanide+to+the+cyanyl+radical+by+peroxidase%2FH2O2+systems+as+determined+by+spin+trapping.&rft.au=Moreno%2C+S+N%3BStolze%2C+K%3BJanzen%2C+E+G%3BMason%2C+R+P&rft.aulast=Moreno&rft.aufirst=S&rft.date=1988-09-01&rft.volume=265&rft.issue=2&rft.spage=267&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 - 1988-10-21 N1 - Date created - 1988-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Exploring relationships between mutagenic and carcinogenic potencies. AN - 78426402; 3419441 AB - Salmonella mutagenic and rodent carcinogenic potencies are calculated for 112 compounds recently studied by the U.S. National Toxicology Program. 28 of the 112 compounds are seen to exhibit simultaneous non-zero mutagenic and carcinogenic potencies. These are combined with an earlier list of mutagenic and carcinogenic compounds (McCann et al., 1988) in order to study possible trends in the data. A significant positive correlation is exhibited between mutagenic and carcinogenic potencies in the combined data, although the observed scatter is too great for the overall result to be predictive. Classification by chemical class further indicates positive correlations near one for chemicals classified as nitroaromatic and related compounds. Patterns in mutagenic and carcinogenic potency over time are also examined. Mean potencies of recently-studied compounds are seen to trend lower than those of compounds studied 10 or more years ago. JF - Mutation research AU - Piegorsch, W W AU - Hoel, D G AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 161 EP - 175 VL - 196 IS - 2 SN - 0027-5107, 0027-5107 KW - Carcinogens KW - 0 KW - Carcinogens, Environmental KW - Environmental Pollutants KW - Mutagens KW - Index Medicus KW - Salmonella -- drug effects KW - Animals KW - Environmental Pollutants -- toxicity KW - Dose-Response Relationship, Drug KW - Mice KW - Carcinogens, Environmental -- toxicity KW - Time Factors KW - Mutagens -- classification KW - Mutagenicity Tests -- methods KW - Carcinogens -- classification KW - Carcinogens -- toxicity KW - Mutagens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78426402?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Exploring+relationships+between+mutagenic+and+carcinogenic+potencies.&rft.au=Piegorsch%2C+W+W%3BHoel%2C+D+G&rft.aulast=Piegorsch&rft.aufirst=W&rft.date=1988-09-01&rft.volume=196&rft.issue=2&rft.spage=161&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 - 1988-10-24 N1 - Date created - 1988-10-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adjuvant chemotherapy for patients with high-grade soft-tissue sarcomas of the extremity. AN - 78415375; 3047339 AB - We have previously reported the results of a randomized trial that demonstrated the survival benefit of adjuvant chemotherapy in the treatment of patients with high-grade extremity sarcomas compared with no chemotherapy. This regimen included doxorubicin, cyclophosphamide, and methotrexate. This report updates and extends our experience. The median follow-up of this trial is now 7.1 years and reveals a 5-year disease-free survival of 75% and 54% for chemotherapy and no chemotherapy groups, respectively (two-sided P [P2] = .037). The 5-year overall survival for patients in this trial was 83% and 60% for the chemotherapy and no chemotherapy groups, respectively, with a trend towards improved survival in the chemotherapy arm (P2 = .124). Because of doxorubicin-induced cardiomyopathy we performed a subsequent randomized trial comparing this high-dose regimen to reduced cumulative doses of doxorubicin and cyclophosphamide without methotrexate. Eighty-eight patients were entered into this trial which has a median follow-up of 4.4 years. The 5-year disease-free and overall survival for patients treated with the reduced doses of chemotherapy was 72% and 75%, respectively, and was not significantly different from the high-dose regimen. No patients developed congestive heart failure on this study. We conclude that adjuvant chemotherapy improves disease-free survival in patients with extremity soft-tissue sarcomas. The overall survival advantage in patients receiving adjuvant chemotherapy in our initial randomized high-dose chemotherapy trial has diminished though it continues to favor the chemotherapy group. A reduced-dose chemotherapy regimen was found to be comparable to the high-dose regimen. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Chang, A E AU - Kinsella, T AU - Glatstein, E AU - Baker, A R AU - Sindelar, W F AU - Lotze, M T AU - Danforth, D N AU - Sugarbaker, P H AU - Lack, E E AU - Steinberg, S M AD - Surgery Branch, National Institutes of Health, Bethesda, MD. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1491 EP - 1500 VL - 6 IS - 9 SN - 0732-183X, 0732-183X KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Drug Administration Schedule KW - Random Allocation KW - Combined Modality Therapy KW - Humans KW - Clinical Trials as Topic KW - Follow-Up Studies KW - Doxorubicin -- administration & dosage KW - Time Factors KW - Methotrexate -- administration & dosage KW - Extremities KW - Soft Tissue Neoplasms -- mortality KW - Sarcoma -- mortality KW - Soft Tissue Neoplasms -- drug therapy KW - Sarcoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78415375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adjuvant+chemotherapy+for+patients+with+high-grade+soft-tissue+sarcomas+of+the+extremity.&rft.au=Chang%2C+A+E%3BKinsella%2C+T%3BGlatstein%2C+E%3BBaker%2C+A+R%3BSindelar%2C+W+F%3BLotze%2C+M+T%3BDanforth%2C+D+N%3BSugarbaker%2C+P+H%3BLack%2C+E+E%3BSteinberg%2C+S+M&rft.aulast=Chang&rft.aufirst=A&rft.date=1988-09-01&rft.volume=6&rft.issue=9&rft.spage=1491&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 - 1988-10-25 N1 - Date created - 1988-10-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increased angiotensin II receptors in brain nuclei of DOCA-salt hypertensive rats. AN - 78409865; 3414825 AB - We analyzed angiotensin II (ANG II) receptors by in vitro autoradiography in selective brain nuclei of control, salt-treated (1% NaCl in drinking water), deoxycorticosterone acetate (DOCA)-treated (DOCA pivalate, 25 mg/kg sc weekly), and DOCA-salt-treated (DOCA + salt treatments) uninephrectomized male Wistar-Kyoto rats. After 4 wk of treatment, only the DOCA-salt group developed hypertension. ANG II binding increased in median preoptic nucleus and subfornical organ of salt- and DOCA-treated rats. DOCA-treated rats also showed increased ANG II binding in paraventricular nucleus. DOCA-salt-treated rats showed higher ANG II binding in nucleus of the solitary tract and area postrema, as well as in the areas mentioned before. Although salt and/or DOCA treatments alone increased ANG II receptors in some brain nuclei, after combined DOCA-salt treatment there was significantly higher ANG II binding in all areas, except the median preoptic nucleus. These results suggest that increased ANG II receptors in selected brain areas may play a role in the pathophysiology of mineralocorticoid-salt experimental hypertension. JF - The American journal of physiology AU - Gutkind, J S AU - Kurihara, M AU - Saavedra, J M AD - Unit on Preclinical Neuropharmacology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - H646 EP - H650 VL - 255 IS - 3 Pt 2 SN - 0002-9513, 0002-9513 KW - Iodine Radioisotopes KW - 0 KW - Receptors, Angiotensin KW - Sodium, Dietary KW - Angiotensin II KW - 11128-99-7 KW - Desoxycorticosterone KW - 40GP35YQ49 KW - Index Medicus KW - Subfornical Organ -- metabolism KW - Animals KW - Reference Values KW - Brain Stem -- metabolism KW - Rats, Inbred WKY KW - Blood Pressure KW - Organ Specificity KW - Autoradiography KW - Rats KW - Preoptic Area -- metabolism KW - Olfactory Bulb -- metabolism KW - Male KW - Paraventricular Hypothalamic Nucleus -- metabolism KW - Hypertension -- chemically induced KW - Angiotensin II -- metabolism KW - Suprachiasmatic Nucleus -- metabolism KW - Receptors, Angiotensin -- metabolism KW - Brain -- metabolism KW - Hypertension -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78409865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+angiotensin+II+receptors+in+brain+nuclei+of+DOCA-salt+hypertensive+rats.&rft.au=Gutkind%2C+J+S%3BKurihara%2C+M%3BSaavedra%2C+J+M&rft.aulast=Gutkind&rft.aufirst=J&rft.date=1988-09-01&rft.volume=255&rft.issue=3+Pt+2&rft.spage=H646&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 - 1988-10-12 N1 - Date created - 1988-10-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antisense Myc sequences induce differentiation of F9 cells. AN - 78397809; 2842791 AB - Down-regulation of Myc expression is the earliest documented change in gene expression in retinoic acid-induced differentiation of murine F9 teratocarcinoma cells. F9 cells transfected with plasmids expressing antisense Myc sequences under control of the simian virus 40 (SV40) early promoter exhibit a decrease in Myc protein. The result of this decrease is the spontaneous differentiation into cells that resemble retinoic acid-treated F9 cells as judged by plasminogen activator assays. In contrast, when F9 cells are transfected with a plasmid expressing Myc under control of the SV40 early promoter, resulting cell clones are resistant to differentiation by retinoic acid as shown by the lack of induction of plasminogen activator. These results suggest that down-regulation of Myc is sufficient and necessary for F9 cell differentiation. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Griep, A E AU - Westphal, H AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 6806 EP - 6810 VL - 85 IS - 18 SN - 0027-8424, 0027-8424 KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Phenotype KW - Tretinoin -- pharmacology KW - Animals KW - Transfection KW - Simian virus 40 -- genetics KW - Cell Differentiation KW - Plasmids KW - Cell Line KW - Teratoma -- genetics KW - Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78397809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antisense+Myc+sequences+induce+differentiation+of+F9+cells.&rft.au=Griep%2C+A+E%3BWestphal%2C+H&rft.aulast=Griep&rft.aufirst=A&rft.date=1988-09-01&rft.volume=85&rft.issue=18&rft.spage=6806&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 - 1988-10-13 N1 - Date created - 1988-10-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res. 1981 Jul 20;216(2):361-74 [7195765] Cell. 1980 Sep;21(2):347-55 [6250719] Proc Natl Acad Sci U S A. 1982 Apr;79(8):2490-4 [6283530] Exp Cell Res. 1983 Jul;146(2):439-44 [6192006] EMBO J. 1983;2(12):2375-83 [6321164] Cell. 1984 Apr;36(4):1007-15 [6323013] Nature. 1984 Aug 16-22;310(5978):592-4 [6462247] Mol Cell Biol. 1985 May;5(5):1136-42 [3158804] Cell. 1985 Aug;42(1):129-38 [2410135] Cell. 1985 Sep;42(2):519-26 [2992802] EMBO J. 1985 Jun;4(6):1441-7 [2992931] Exp Cell Res. 1986 May;164(1):223-31 [3956593] Nature. 1986 Apr 24-30;320(6064):760-3 [3458027] Proc Natl Acad Sci U S A. 1986 Aug;83(15):5539-43 [3526333] Nature. 1986 Aug 28-Sep 3;322(6082):848-50 [3528863] Mol Cell Biol. 1986 Feb;6(2):518-24 [3785153] Mol Cell Biol. 1987 Feb;7(2):639-49 [3547078] Proc Natl Acad Sci U S A. 1987 Feb;84(4):1040-4 [2434948] J Virol. 1987 May;61(5):1630-8 [3033289] Cell. 1987 Jul 3;50(1):69-78 [3036366] EMBO J. 1987 Aug;6(8):2365-71 [3665880] Nature. 1987 Nov 19-25;330(6145):272-4 [2823151] Nature. 1987 Dec 3-9;330(6147):444-50 [2825025] Nature. 1987 Dec 17-23;330(6149):624-9 [2825036] Proc Natl Acad Sci U S A. 1987 Nov;84(22):7881-5 [2825168] Genes Dev. 1987 Nov;1(9):938-45 [3480843] Mol Cell Biol. 1988 Feb;8(2):963-73 [3280975] Eur J Biochem. 1973 Jul 2;36(1):32-8 [4200179] Cell. 1978 Oct;15(2):393-403 [214238] Dev Biol. 1979 Jun;70(2):515-21 [89977] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Dev Biol. 1982 Feb;89(2):516-20 [7056445] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adriamycin-induced free radical formation in the perfused rat heart: implications for cardiotoxicity. AN - 78394705; 2842038 AB - Adriamycin is an anthracycline drug with a wide spectrum of clinical antineoplastic activity. However, the usefulness of the drug is limited by its dose-dependent cardiotoxicity. Adriamycin-stimulated free radical formation has been suggested as one of the mechanisms for its cardiotoxic effects. In order to evaluate this underlying mechanism, we have perfused rat hearts with Adriamycin, using a modified Langendorf technique, and the free radicals formed were analyzed by electron spin resonance spectroscopy using spin-trapping techniques. Our studies show that Adriamycin stimulated the formation of .OH in the heart, and the maximum .OH was formed with 1 microM of the drug. The addition of superoxide dismutase (600 units/ml) inhibited the hydroxyl radical formation by 2- to 3-fold, while catalase (550 units/ml) abolished it completely, showing the intermediacy of superoxide and H2O2. Furthermore, ICRF-187, an iron chelator and a cytotoxic drug, was also an effective inhibitor of .OH formation in the rat heart. The heart rate was not significantly modified by all the above experiments. This study demonstrates that Adriamycin stimulates the formation of .OH in the isolated rat heart and suggests that this mechanism may be significant in Adriamycin-induced cardiotoxicity. JF - Cancer research AU - Rajagopalan, S AU - Politi, P M AU - Sinha, B K AU - Myers, C E AD - Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1988/09/01/ PY - 1988 DA - 1988 Sep 01 SP - 4766 EP - 4769 VL - 48 IS - 17 SN - 0008-5472, 0008-5472 KW - Free Radicals KW - 0 KW - Hydroxides KW - Hydroxyl Radical KW - 3352-57-6 KW - Razoxane KW - 5AR83PR647 KW - Doxorubicin KW - 80168379AG KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Razoxane -- pharmacology KW - Superoxide Dismutase -- pharmacology KW - Perfusion KW - Myocardium -- metabolism KW - Male KW - Heart -- drug effects KW - Doxorubicin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78394705?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adriamycin-induced+free+radical+formation+in+the+perfused+rat+heart%3A+implications+for+cardiotoxicity.&rft.au=Rajagopalan%2C+S%3BPoliti%2C+P+M%3BSinha%2C+B+K%3BMyers%2C+C+E&rft.aulast=Rajagopalan&rft.aufirst=S&rft.date=1988-09-01&rft.volume=48&rft.issue=17&rft.spage=4766&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Continuous cell lines with altered growth and differentiation properties originate after transfection of human keratinocytes with human papillomavirus type 16 DNA. AN - 78392813; 2457456 AB - Immortalization of human keratinocytes (HKc) by human papillomavirus type 16 (HPV16) is reproducible at a high frequency, is due directly to the presence of the viral sequences in the cells, and occurs independently from the genetic characteristics of the host cells. Ten human keratinocyte strains, each derived from a different individual, were transfected with pMHPV16d and selected with G418. Eight became established lines. Two strains, which failed to grow shortly after successful G418 selection, were negative for HPV16 DNA. No lines were established following transfection of the same HKc strains with vector sequences only. The immortalized lines maintained a constant number of copies of the viral genome integrated into the cellular DNA. Each line showed a unique integration pattern of HPV16 sequences into the cellular genome, but expressed similar patterns of viral messages. Sublines able to grow in the absence of growth factors (epidermal growth factor and bovine pituitary extract), and others which became resistant to differentiation stimuli (serum and calcium) were obtained by selection in growth factor-free medium and serum-supplemented medium, respectively. The establishment of continuous cell lines is a direct consequence of the presence of viral sequences; however, because none of these lines formed tumors in nude mice, additional events must be necessary for progression of malignancy. HPV16-immortalized human keratinocyte lines can be used to investigate and identify the viral factors involved with the modification of growth and differentiation control by HPV16. JF - Carcinogenesis AU - Pirisi, L AU - Creek, K E AU - Doniger, J AU - DiPaolo, J A AD - Laboratory of Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1573 EP - 1579 VL - 9 IS - 9 SN - 0143-3334, 0143-3334 KW - DNA, Viral KW - 0 KW - Growth Substances KW - RNA, Viral KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Aneuploidy KW - DNA, Viral -- analysis KW - Humans KW - Cell Differentiation KW - Genes, Viral KW - Gene Expression Regulation KW - Growth Substances -- physiology KW - Cell Cycle KW - Cell Line KW - RNA, Viral -- analysis KW - Epidermis -- microbiology KW - Epidermis -- cytology KW - Papillomaviridae -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78392813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Continuous+cell+lines+with+altered+growth+and+differentiation+properties+originate+after+transfection+of+human+keratinocytes+with+human+papillomavirus+type+16+DNA.&rft.au=Pirisi%2C+L%3BCreek%2C+K+E%3BDoniger%2C+J%3BDiPaolo%2C+J+A&rft.aulast=Pirisi&rft.aufirst=L&rft.date=1988-09-01&rft.volume=9&rft.issue=9&rft.spage=1573&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relation of changes in amount and type of dietary fat to fecapentaenes in premenopausal women. AN - 78392534; 3412371 AB - Correlation studies suggest that fecal mutagenicity is increased in groups eating high-fat diets, the same groups who are often found to have high colorectal cancer incidence and mortality. The fecapentaenes are the best characterized class of fecal mutagens, but the relationship of dietary fat intake to the excretion of these potent genotoxins is unknown. We studied the effect of changes in amount and type of dietary fat on fecapentaene levels in 31 premenopausal women 20-40 years of age who participated in a controlled feeding study. After a pre-diet free-living period lasting 1 menstrual cycle, women were placed on a high-fat (40% energy from fat) diet for 4 menstrual cycles and then switched to a low-fat (20% energy from fat) diet for an additional 4 menstrual cycles. One-half the subjects were maintained throughout the study at a ratio of polyunsaturated-to-saturated fatty acids (P/S ratio) of 1.0, the other half at 0.3; body weight was constant. All meals during the controlled diet periods were prepared at the Human Study Facility of the Beltsville Human Nutrition Research Center. Fecapentaene and fecapentaene precursor levels were measured in acetone extracts from 3-day pooled stool samples collected during the study. No differences in fecapentaene or precursor levels were observed between the high- and low-fat diets at either P/S ratio. Fecapentaene and precursor levels were higher while on controlled diets than during the pre-diet free-living period, and levels declined again in the post-diet free-living period. We conclude that dietary fat has no significant effect on fecapentaene or precursor levels in acetone extracts of stool in premenopausal women. The effect of other dietary or non-dietary factors on fecapentaenes remains unknown. JF - Mutation research AU - Taylor, P R AU - Schiffman, M H AU - Jones, D Y AU - Judd, J AU - Schatzkin, A AU - Nair, P P AU - Van Tassell, R AU - Block, G AD - Cancer Prevention Studies Branch, NCI, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 3 EP - 9 VL - 206 IS - 1 SN - 0027-5107, 0027-5107 KW - Dietary Fats KW - 0 KW - Fatty Acids, Unsaturated KW - Mutagens KW - Polyenes KW - Index Medicus KW - Fatty Acids, Unsaturated -- metabolism KW - Feces -- metabolism KW - Humans KW - Adult KW - Time Factors KW - Female KW - Dietary Fats -- metabolism KW - Mutagens -- metabolism KW - Polyenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78392534?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Relation+of+changes+in+amount+and+type+of+dietary+fat+to+fecapentaenes+in+premenopausal+women.&rft.au=Taylor%2C+P+R%3BSchiffman%2C+M+H%3BJones%2C+D+Y%3BJudd%2C+J%3BSchatzkin%2C+A%3BNair%2C+P+P%3BVan+Tassell%2C+R%3BBlock%2C+G&rft.aulast=Taylor&rft.aufirst=P&rft.date=1988-09-01&rft.volume=206&rft.issue=1&rft.spage=3&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 - 1988-10-07 N1 - Date created - 1988-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A theoretical study of the effect of methylation or ethylation at O6-guanine in the structure and energy of DNA double strands. AN - 78392167; 3409460 AB - Quantum and molecular mechanical calculations were employed to examine the effect on binding energies and structure of methylation and ethylation at O6-guanine in double-stranded DNA. Ab initio quantum chemical calculations (STO-3G, 3-21G) were initially used to pseudo-optimize the structure of the 9-methyl derivative of O6-methylguanine. The distal orientation for the O6-methyl group was found to be lower in energy than the proximal orientation. The geometry determined for the distal O6-methyl group was in agreement with recent X-ray work. These results were used in supplementary parameterization of the AMBER molecular mechanics force field necessary for the minimization of DNA double strands containing O6-methylguanosine. Resulting calculations with AMBER on two 5-mer DNA sequences containing the promutagenic G(GM)A subsequence showed that the proximal orientation, while higher in energy in the isolated molecule, is both less disruptive to the DNA double helix and more stable than the distal orientation. Binding energies and degree of destabilization upon methylation were found to be functions of the adjacent bases around a GGA subsequence. Sequence-dependent destabilization could play a role in the repair of alkylated bases. Quantum and molecular mechanics calculations indicate that the O6-methyl and O6-ethylguanines behave energetically in a very similar manner. These calculations suggest that the necessity for the different repair mechanisms for methylation and ethylation lesions cannot be simply explained by energy differences or observed structural differences. JF - Carcinogenesis AU - Pedersen, L G AU - Darden, T A AU - Deerfield, D W AU - Anderson, M W AU - Hoel, D G AD - Biometry Branch, NIEHS, Research Triangle Park, NC 27709. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1553 EP - 1562 VL - 9 IS - 9 SN - 0143-3334, 0143-3334 KW - 6-ethylguanine KW - 51866-19-4 KW - Guanine KW - 5Z93L87A1R KW - DNA KW - 9007-49-2 KW - O-(6)-methylguanine KW - 9B710FV2AE KW - Index Medicus KW - Base Sequence KW - Computer Simulation KW - Thermodynamics KW - Chemistry, Physical KW - Chemical Phenomena KW - Molecular Conformation KW - Methylation KW - Hydrogen Bonding KW - Structure-Activity Relationship KW - Alkylation KW - Guanine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78392167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+theoretical+study+of+the+effect+of+methylation+or+ethylation+at+O6-guanine+in+the+structure+and+energy+of+DNA+double+strands.&rft.au=Pedersen%2C+L+G%3BDarden%2C+T+A%3BDeerfield%2C+D+W%3BAnderson%2C+M+W%3BHoel%2C+D+G&rft.aulast=Pedersen&rft.aufirst=L&rft.date=1988-09-01&rft.volume=9&rft.issue=9&rft.spage=1553&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of cytokines on polymorphonuclear neutrophil infiltration in the mouse. Prostaglandin- and leukotriene-independent induction of infiltration by IL-1 and tumor necrosis factor. AN - 78391646; 3261759 AB - The i.p. injection of mice with highly purified recombinant human rIL-1 alpha or beta resulted in the rapid influx of a large number of polymorphonuclear neutrophils (PMN) into the peritoneal cavity. Significant increases in the number of PMN were induced by doses of IL-1 which ranged from 0.005 to 5 ng/injection. Interestingly the dose response for PMN influx was bell-shaped because 50 ng of IL-1 did not result in a significant increase in peritoneal PMN. IL-1 induced PMN infiltration was detectable by 1 h with peak levels of PMN obtained by about 2 h, followed by a subsequent decline by 24 h. Other cytokines, IL-2, IFN-gamma, IFN alpha beta, granulocyte-CSF, granulocyte-macrophage-CSF, IL-3, TNF-alpha, and TNF-beta were compared to IL-1 for their ability to induce a PMN influx into the peritoneum. Only TNF-alpha or TNF-beta (lymphotoxin) were able to induce a significant influx of PMN within 2 h. However, based on total protein administered, about 100 times more TNF than IL-1 was required to produce a comparable PMN infiltration. Intraperitoneal injection of inhibitors of the cyclooxygenase or lipoxygenase pathways did not inhibit the IL-1-induced influx of PMN. Also, neither IL-1 nor TNF triggered an increase in PG or leukotriene release from peritoneal cells in vitro. Furthermore, direct peritoneal injection of leukotriene B4, a potent PMN chemoattractant in vitro, did not induce any significant increase in PMN in the peritoneal cavity indicating that chemotactic activity alone is insufficient for inducing peritoneal infiltration. These results suggest that the local production of very low levels of IL-1 in vivo would be sufficient to initiate a sequence of events that results in a rapid accumulation of PMN. Because IL-1 was not chemotactic for PMN in vitro, our data suggest that IL-1 induces production of factors that are chemotactic for PMN. Alternatively, IL-1 may act on other stages of the complex sequence of events that regulates the emigration of PMN into tissue sites in vivo. The synergy apparent in PMN influx when suboptimal concentrations of IL-1 and TNF were injected suggests that the local production of very low concentrations of these cytokines in situ could play a critical role in the emigration of PMN during infection. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Sayers, T J AU - Wiltrout, T A AU - Bull, C A AU - Denn, A C AU - Pilaro, A M AU - Lokesh, B AD - Biological Carcinogenesis Development Program, NCI-FCRF, Frederick, MD 21701-1013. Y1 - 1988/09/01/ PY - 1988 DA - 1988 Sep 01 SP - 1670 EP - 1677 VL - 141 IS - 5 SN - 0022-1767, 0022-1767 KW - Interleukin-1 KW - 0 KW - Prostaglandins KW - Recombinant Proteins KW - SRS-A KW - Tumor Necrosis Factor-alpha KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Recombinant Proteins -- pharmacology KW - Peritoneal Cavity -- pathology KW - Kinetics KW - Dose-Response Relationship, Immunologic KW - Mice KW - Mice, Inbred BALB C KW - Drug Synergism KW - Male KW - Prostaglandins -- physiology KW - Neutrophils -- pathology KW - Interleukin-1 -- pharmacology KW - Chemotaxis, Leukocyte -- drug effects KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Neutrophils -- physiology KW - SRS-A -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78391646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+cytokines+on+polymorphonuclear+neutrophil+infiltration+in+the+mouse.+Prostaglandin-+and+leukotriene-independent+induction+of+infiltration+by+IL-1+and+tumor+necrosis+factor.&rft.au=Sayers%2C+T+J%3BWiltrout%2C+T+A%3BBull%2C+C+A%3BDenn%2C+A+C%3BPilaro%2C+A+M%3BLokesh%2C+B&rft.aulast=Sayers&rft.aufirst=T&rft.date=1988-09-01&rft.volume=141&rft.issue=5&rft.spage=1670&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-1 as a co-factor for lymphokine-secreting CD8+ murine T cells. AN - 78389340; 2970506 AB - Immunologically important among the known biologic activities of IL-1 is its ability to function as a co-factor for responses mediated by lymphokine secreting CD4+ Th cells. In contrast to its known effects in CD4+ T cell responses, IL-1 is not known to play a role in CD8+ T cell responses. In the present study, we have assessed the ability of murine recombinant IL-1 to function as a co-factor for stimulating CD8+ T cells to secrete lymphokines such as IL-2. We found that, in conjunction with either Ag or mitogen, IL-1 is able to stimulate lymphokine-secreting CD8+ T cells. Furthermore, we found that, as a consequence of its stimulation of lymphokine-secreting CD8+ T cells, IL-1 is able to reconstitute MHC class I allospecific cytolytic T lymphocyte responses by cell populations depleted of both accessory cells and CD4+ T cells. These results demonstrate that the biologic activity of IL-1 is not restricted to CD4+ cell responses, and suggests that IL-1 can function as a co-factor for the stimulation of lymphokine-secreting Th cells regardless of their CD4/CD8 phenotype. If IL1 acts directly on lymphokine-secreting T cells or on the APC with which they interact is not yet certain. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Mizuochi, T AU - McKean, D J AU - Singer, A AD - Experimental Immunology Branch, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/09/01/ PY - 1988 DA - 1988 Sep 01 SP - 1571 EP - 1575 VL - 141 IS - 5 SN - 0022-1767, 0022-1767 KW - Antigens, Differentiation, T-Lymphocyte KW - 0 KW - Interleukin-1 KW - Lymphokines KW - Recombinant Proteins KW - Concanavalin A KW - 11028-71-0 KW - Abridged Index Medicus KW - Index Medicus KW - Phenotype KW - Cytotoxicity, Immunologic KW - Animals KW - Recombinant Proteins -- pharmacology KW - Mice, Inbred C57BL KW - T-Lymphocytes, Cytotoxic -- immunology KW - Mice KW - T-Lymphocytes, Helper-Inducer -- metabolism KW - Drug Synergism KW - Concanavalin A -- pharmacology KW - T-Lymphocytes -- classification KW - Lymphokines -- metabolism KW - T-Lymphocytes -- metabolism KW - Interleukin-1 -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78389340?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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-1+as+a+co-factor+for+lymphokine-secreting+CD8%2B+murine+T+cells.&rft.au=Mizuochi%2C+T%3BMcKean%2C+D+J%3BSinger%2C+A&rft.aulast=Mizuochi&rft.aufirst=T&rft.date=1988-09-01&rft.volume=141&rft.issue=5&rft.spage=1571&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of Hermissenda K+ channels by cytoplasmic and membrane-associated C-kinase. AN - 78382004; 2457656 AB - Pharmacologic activation of endogenous protein kinase C (PKC) together with elevation of the intracellular Ca2+ level was previously shown to cause reduction of two voltage-dependent K+ currents (IA and ICa2+-K+) across the soma membrane of the type B photoreceptor within the eye of the mollusc Hermissenda crassicornis. Similar effects were also found to persist for days after acquisition of a classically conditioned response. Also, the state of phosphorylation of a low-molecular-weight protein was changed only within the eyes of conditioned Hermissenda. To examine the role of PKC in causing K+ current changes as well as changes of phosphorylation during conditioning (and possibly other physiologic contexts), we studied here the effects of endogenous PKC activation and exogenous PKC injection on phosphorylation and K+ channel function. Several phosphoproteins (20, 25, 56, and 165 kilodaltons) showed differences in phosphorylation in response to PKC activators applied to intact nervous systems or to isolated eyes. Specific differences were observed for membrane and cytosolic fractions in response to both the phorbol ester 12-deoxyphorbol 13-isobutyrate 20-acetate (DPBA) or exogenous PKC in the presence of Ca2+ and phosphatidylserine/diacylglycerol. Type B cells pretreated with DPBA responded to PKC injection with a persistent reduction of K+ currents. In the absence of DPBA, PKC injection also caused K+ current reduction only following Ca2+ loading conditions. However, the direct effect of PKC injection in the absence of DPBA was only to increase ICa2+-K+. According to a proposed model, the amplitude of the K+ currents would depend on the steady-state balance of effects mediated by PKC within the cytoplasm and membrane-associated PKC. The model further specifies that the effects on K+ currents of cytoplasmic PKC require an intervening proteolytic step. Such a model predicts that increasing the concentration of cytoplasmic protease, e.g., with trypsin, will increase K+ currents, whereas blocking endogenous protease, e.g., with leupeptin, will decrease K+ currents. These effects should be opposed by preexposure of the cells to DPBA. Furthermore, prior injection of leupeptin should block or reverse the effects of subsequent injection of PKC into the type B cell. All of these predictions were confirmed by results reported here. Taken together, the results of this and previous studies suggest that PKC regulation of membrane excitability critically depends on its cellular locus. The implications of such function for long-term physiologic transformations are discussed. JF - Journal of neurochemistry AU - Alkon, D L AU - Naito, S AU - Kubota, M AU - Chen, C AU - Bank, B AU - Smallwood, J AU - Gallant, P AU - Rasmussen, H AD - Section on Neural Systems, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 903 EP - 917 VL - 51 IS - 3 SN - 0022-3042, 0022-3042 KW - Ion Channels KW - 0 KW - Leupeptins KW - Nerve Tissue Proteins KW - Phorbol Esters KW - 12-deoxyphorbol-13-isobutyrate-20-acetate KW - 25090-71-5 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Trypsin KW - EC 3.4.21.4 KW - leupeptin KW - J97339NR3V KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Cell Membrane -- enzymology KW - Electric Conductivity KW - Models, Biological KW - Calcium -- metabolism KW - Leupeptins -- pharmacology KW - Phorbol Esters -- pharmacology KW - Phosphorylation KW - Central Nervous System -- enzymology KW - Nerve Tissue Proteins -- metabolism KW - Mollusca KW - Trypsin -- pharmacology KW - Photoreceptor Cells -- ultrastructure KW - Photoreceptor Cells -- enzymology KW - Protein Kinase C -- isolation & purification KW - Protein Kinase C -- physiology KW - Ion Channels -- physiology KW - Cytoplasm -- enzymology KW - Protein Kinase C -- pharmacology KW - Potassium -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78382004?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Regulation+of+Hermissenda+K%2B+channels+by+cytoplasmic+and+membrane-associated+C-kinase.&rft.au=Alkon%2C+D+L%3BNaito%2C+S%3BKubota%2C+M%3BChen%2C+C%3BBank%2C+B%3BSmallwood%2C+J%3BGallant%2C+P%3BRasmussen%2C+H&rft.aulast=Alkon&rft.aufirst=D&rft.date=1988-09-01&rft.volume=51&rft.issue=3&rft.spage=903&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increased numbers of N-nitrosodimethylamine-initiated lung tumors in mice by chronic co-administration of ethanol. AN - 78371588; 3409476 AB - Young male strain A mice received 0.5, 1.0 or 5.0 p.p.m. N-nitrosodimethylamine (NDMA) in their drinking water with or without 10 or 20% ethanol. NDMA caused primary tumors of the lung in a dose-dependent manner; these were enumerated after 16 weeks. At the two lower NDMA doses, the ethanol caused a 1.5- to 3-fold increase in the number of lung tumor bearers and a 2-3.5 increase in lung tumor multiplicity. With 5 p.p.m. NDMA concomitant exposure to 10% ethanol resulted in a 2-3.5 increase in multiplicity. In a test for a possible tumor-promoting effect of the ethanol, mice were given 5 p.p.m. NDMA for 4 weeks, followed by ethanol for 12 weeks. There was an insignificant 30% increase in numbers of tumors. By contrast, mice that had received 10% ethanol along with NDMA during the initial 4 weeks experienced a 2.5-fold increase in incidence and 6-fold increase in multiplicity of lung tumors at 16 weeks. Thus, ethanol given simultaneously with chronic oral NDMA greatly enhances tumorigenesis in the lung, by a mechanism probably related to competitive inhibition of NDMA metabolism in the liver and not attributable to promotion of these tumors. JF - Carcinogenesis AU - Anderson, L M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute-FCRF, MD 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 1717 EP - 1719 VL - 9 IS - 9 SN - 0143-3334, 0143-3334 KW - Ethanol KW - 3K9958V90M KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Animals KW - Body Weight -- drug effects KW - Mice KW - Drug Synergism KW - Ethanol -- administration & dosage KW - Lung Neoplasms -- chemically induced KW - Dimethylnitrosamine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78371588?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+numbers+of+N-nitrosodimethylamine-initiated+lung+tumors+in+mice+by+chronic+co-administration+of+ethanol.&rft.au=Anderson%2C+L+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1988-09-01&rft.volume=9&rft.issue=9&rft.spage=1717&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - cis- and trans-acting regulation of gene expression of equine infectious anemia virus. AN - 78362164; 2841502 AB - Deletion analysis of the equine infectious anemia virus long terminal repeat revealed that sequences responsive to virus-specific transactivation are located within the region spanning the transcriptional start site (-31 to +22). In addition, an active exon of a trans-acting factor (tat) was identified downstream of pol and overlapping env (nucleotides 5264 to 5461). Activation by tat is accompanied by an increase in the steady-state levels of mRNA directed by the equine infectious anemia virus long terminal repeat. JF - Journal of virology AU - Dorn, P L AU - Derse, D AD - Biological Carcinogenesis Development Program, National Cancer Institute Frederick Cancer Research Facility, Maryland 21701-1013. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 3522 EP - 3526 VL - 62 IS - 9 SN - 0022-538X, 0022-538X KW - Gene Products, tat KW - 0 KW - RNA, Viral KW - Transcription Factors KW - Index Medicus KW - Animals KW - Transfection KW - Exons KW - RNA, Viral -- biosynthesis KW - Repetitive Sequences, Nucleic Acid KW - Plasmids KW - Cell Line KW - Infectious Anemia Virus, Equine -- genetics KW - Transcription, Genetic KW - Gene Expression Regulation KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78362164?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=cis-+and+trans-acting+regulation+of+gene+expression+of+equine+infectious+anemia+virus.&rft.au=Dorn%2C+P+L%3BDerse%2C+D&rft.aulast=Dorn&rft.aufirst=P&rft.date=1988-09-01&rft.volume=62&rft.issue=9&rft.spage=3522&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 - 1988-09-20 N1 - Date created - 1988-09-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1987 Feb 27;48(4):691-701 [3643816] J Virol. 1987 Mar;61(3):743-7 [3027401] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] J Virol. 1987 Aug;61(8):2462-71 [3037109] J Virol. 1988 Jan;62(1):120-6 [2824840] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Cell. 1985 Jul;41(3):813-23 [2988790] Science. 1985 Jul 5;229(4708):74-7 [2990041] Science. 1985 Aug 2;229(4712):482-5 [2990051] Nature. 1985 Dec 12-18;318(6046):571-4 [2999613] Virology. 1986 Jan 15;148(1):226-31 [3002031] Science. 1986 May 9;232(4751):755-9 [3008338] Virology. 1986 Oct 15;154(1):1-8 [3750842] J Virol. 1986 Nov;60(2):385-93 [3021973] Virology. 1986 Dec;155(2):309-21 [2431539] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Novel glycosylation pathways of retroviral envelope proteins identified with avian reticuloendotheliosis virus. AN - 78361950; 2841469 AB - Previously, we identified two mature glycoproteins, gp90, the surface glycoprotein, and gp20, the transmembrane protein, from avian reticuloendotheliosis virus and an avian reticuloendotheliosis virus env gene-encoded intracellular polyprotein gPr77env, but the precise relationship of gPr77env to the mature envelope proteins was not determined (W.-P. Tsai, T.D. Copeland, and S. Oroszlan, Virology 155:567-583, 1986). In the present study, using metabolic labeling of viral proteins with [35S]cysteine, radioimmunoprecipitation, and carbohydrate structure analysis, we have identified a higher-molecular-weight endo-H-resistant env gene-encoded polyprotein designated gPr115env in addition to the endo-H-sensitive gPr77env. It appears that gPr77env is the primary polyprotein precursor, modified with mannosyloligosaccharides that are processed into sialic-acid-rich extraordinarily large complex-type carbohydrates (up to 17 kilodaltons for each N-linked site) on the gp90 domain but not on the gPr22 domain. In this process, gPr77env is converted into the apparently endo-H-resistant secondary polyprotein, gPr115env, which is rapidly processed into gp90 and gPr22. The proteolytic processing which occurs only after the appearance of an endo-H resistant precursor is now clearly demonstrated for a retrovirus. Some important aspects of carbohydrate structure, including the site-specific glycosylation, as well as the intracellular location and nature of the potential enzyme involved in the proteolytic cleavage of gPr115env are discussed. JF - Journal of virology AU - Tsai, W P AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/09// PY - 1988 DA - September 1988 SP - 3167 EP - 3174 VL - 62 IS - 9 SN - 0022-538X, 0022-538X KW - Carbohydrates KW - 0 KW - Glycoproteins KW - Protein Precursors KW - Retroviridae Proteins KW - Viral Envelope Proteins KW - Glycoside Hydrolases KW - EC 3.2.1.- KW - Index Medicus KW - Animals KW - Glycoproteins -- analysis KW - Glycoside Hydrolases -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Protein Precursors -- analysis KW - Glycosylation KW - Autoradiography KW - Cell Line KW - Carbohydrates -- analysis KW - Immunoassay KW - Retroviridae -- metabolism KW - Retroviridae Proteins -- metabolism KW - Reticuloendotheliosis virus -- metabolism KW - Viral Envelope Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78361950?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Novel+glycosylation+pathways+of+retroviral+envelope+proteins+identified+with+avian+reticuloendotheliosis+virus.&rft.au=Tsai%2C+W+P%3BOroszlan%2C+S&rft.aulast=Tsai&rft.aufirst=W&rft.date=1988-09-01&rft.volume=62&rft.issue=9&rft.spage=3167&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 - 1988-09-20 N1 - Date created - 1988-09-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1970 Aug 15;227(5259):680-5 [5432063] J Cell Biochem. 1984;24(2):121-30 [6373800] J Virol. 1971 Nov;8(5):778-85 [4332144] Biochem Soc Trans. 1984 Aug;12(4):599-600 [6489589] Anal Biochem. 1984 Sep;141(2):515-22 [6437277] J Cell Biol. 1984 Dec;99(6):2011-23 [6094591] Biochemistry. 1984 Nov 6;23(23):5628-37 [6439245] J Biol Chem. 1985 Jan 25;260(2):1265-70 [3968060] Virology. 1985 Jan 30;140(2):289-312 [2982236] Science. 1985 Aug 23;229(4715):726-33 [4023707] Annu Rev Biochem. 1985;54:631-64 [3896128] Biochemistry. 1985 Aug 13;24(17):4665-71 [4063349] Science. 1986 Mar 28;231(4745):1567-72 [3006247] Virology. 1986 Apr 30;150(2):491-502 [3083581] Cell. 1986 May 9;45(3):375-85 [2421920] J Cell Biol. 1986 Jul;103(1):265-75 [3013899] Science. 1986 Oct 24;234(4775):438-43 [2945253] Virology. 1986 Dec;155(2):567-83 [3024401] Science. 1987 Jan 16;235(4786):348-50 [3541206] Methods Enzymol. 1987;138:169-85 [3298950] Cell. 1987 Aug 14;50(4):523-34 [3038335] Annu Rev Biochem. 1987;56:497-534 [3304143] J Cell Biol. 1987 Sep;105(3):1191-203 [2821009] Nature. 1987 Nov 5-11;330(6143):74-7 [2959866] Proc Natl Acad Sci U S A. 1987 Nov;84(22):8120-4 [2825177] J Virol. 1988 Mar;62(3):1016-21 [2828650] Virology. 1972 Mar;47(3):551-66 [4111052] J Natl Cancer Inst. 1973 Aug;51(2):489-99 [4358134] J Virol. 1975 Jul;16(1):53-61 [166208] Eur J Biochem. 1975 Aug 15;56(2):335-41 [1175627] J Biol Chem. 1975 Nov 10;250(21):8569-75 [389] J Virol. 1976 Mar;17(3):983-90 [56462] J Virol. 1976 Jun;18(3):956-68 [178931] Biochem Biophys Res Commun. 1976 May 3;70(1):139-45 [1275931] Proc Natl Acad Sci U S A. 1976 Jul;73(7):2326-30 [1065881] J Virol. 1977 Feb;21(2):810-4 [189094] Biochemistry. 1977 Feb 22;16(4):710-7 [402147] Virology. 1977 Feb;76(2):539-53 [190766] J Biochem. 1984 Apr;95(4):1209-13 [6430882] J Virol. 1984 Oct;52(1):172-82 [6090694] Proc Natl Acad Sci U S A. 1978 Jun;75(6):2708-12 [208072] Arch Virol. 1978;58(1):61-4 [211992] J Biol Chem. 1979 Feb 25;254(4):1340-8 [216692] J Virol. 1979 Feb;29(2):735-43 [430608] Virology. 1979 Feb;93(1):20-30 [219596] J Virol. 1979 Mar;29(3):1221-5 [87519] J Virol. 1979 May;30(2):508-14 [89204] J Biol Chem. 1979 Dec 25;254(24):12531-4 [500730] Nature. 1979 Nov 29;282(5738):471-7 [503226] J Virol. 1980 Apr;34(1):168-77 [6154804] Nature. 1980 Nov 20;288(5788):236-41 [6985476] Proc Natl Acad Sci U S A. 1980 Nov;77(11):6420-4 [6935656] J Virol. 1981 Aug;39(2):646-50 [6268850] J Virol. 1981 Sep;39(3):845-54 [6169843] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Virology. 1981 Dec;115(2):262-71 [6274085] Virology. 1982 May;119(1):122-32 [6280380] J Gen Virol. 1982 Apr;59(Pt 2):329-43 [7077302] Biochim Biophys Acta. 1982 Aug 27;717(3):491-501 [7126644] J Biol Chem. 1982 Dec 10;257(23):14023-8 [6292217] J Virol. 1983 Jun;46(3):920-36 [6304351] J Cell Biol. 1983 Aug;97(2):293-300 [6350314] Virology. 1970 Aug;41(4):631-46 [4319782] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anticonvulsant activity of deaminated analogues of glutamic acid diethyl ester (GDEE). AN - 78432546; 3167573 AB - GDEE, a specific but low-potency antagonist of the quisqualate or 'Type 2' excitatory amino acid receptor, blocks seizures induced by homocysteine and quisqualic acid. Deaminated analogues of GDEE were examined for anticonvulsant activity in mice, for the purpose of determining the structural properties of GDEE required for anticonvulsant activity. The deaminated derivative of GDEE, diethyl glutarate (5 carbon chain) inhibited homocysteine thiolactone (HTL)-induced seizures with an ED50 of 533 mg/kg. A similar compound with carbon chain length increased by two (diethyl pimelate; 7 carbons) was less effective. Decreases or further increases in carbon chain length resulted in a nearly complete loss of activity. Dimethyl glutarate (5 carbons) and dimethyl adipate (6 carbons) were similar to diethyl glutarate in potency, blocking HTL-induced seizures with ED50s of about 625 and 540 mg/kg, respectively. Diethyl ethylmalonate, diethyl maleate, and diethyl fumarate were much less effective. Diethyl glutarate, but not diethyl succinate (4 carbons), blocked seizures induced by intracerebral quisqualic acid. None of the agents tested blocked pentylenetetrazole-induced seizures. Thus a number of deaminated structural variants of GDEE have anticonvulsant activity equal to that of GDEE. The amino group of GDEE appears therefore to be irrelevant for its anticonvulsant effect. JF - Brain research AU - Freed, W J AU - Braun, D E AD - NIMH Neurosciences Center, St. Elizabeths, Washington, DC 20032. Y1 - 1988/08/30/ PY - 1988 DA - 1988 Aug 30 SP - 157 EP - 162 VL - 459 IS - 1 SN - 0006-8993, 0006-8993 KW - Anticonvulsants KW - 0 KW - Glutamates KW - Glutarates KW - Homocysteine KW - 0LVT1QZ0BA KW - glutamic acid diethyl ester KW - 16450-41-2 KW - homocysteine thiolactone KW - D5H88XF24X KW - Pentylenetetrazole KW - WM5Z385K7T KW - Index Medicus KW - Glutarates -- therapeutic use KW - Animals KW - Mice KW - Homocysteine -- analogs & derivatives KW - Female KW - Seizures -- chemically induced KW - Seizures -- drug therapy KW - Glutamates -- therapeutic use KW - Anticonvulsants -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78432546?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Anticonvulsant+activity+of+deaminated+analogues+of+glutamic+acid+diethyl+ester+%28GDEE%29.&rft.au=Freed%2C+W+J%3BBraun%2C+D+E&rft.aulast=Freed&rft.aufirst=W&rft.date=1988-08-30&rft.volume=459&rft.issue=1&rft.spage=157&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 - 1988-11-21 N1 - Date created - 1988-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Behavioral evidence for increased acetylcholine receptor sensitivity after nucleus basalis magnocellularis lesions in the rat. AN - 78492889; 3181290 AB - Lesions of the nucleus basalis magnocellularis and the medial septal area have been shown to produce both deficits in memory and decreases in choline acetyltransferase levels. In order to determine whether functional changes in acetylcholine receptor sensitivity also occur, the present experiment examined the ability of acetylcholine, 40 micrograms intraventricularly, to induce motor seizures in nucleus basalis magnocellularis-medial septal area lesioned versus control rats. While choline acetyltransferase activity was only modestly reduced in lesioned rats vs control rats (30%), the seizure scores were considerably higher in lesioned vs. control rats (270%). These results suggest that there is an increased functional response to acetylcholine following bilateral nucleus basalis magnocellularis-medial septal area lesions. JF - European journal of pharmacology AU - Mastropaolo, J AU - Crawley, J N AD - Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/08/24/ PY - 1988 DA - 1988 Aug 24 SP - 301 EP - 304 VL - 153 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Receptors, Cholinergic KW - 0 KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Acetylcholine KW - N9YNS0M02X KW - Index Medicus KW - Seizures -- chemically induced KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Acetylcholine -- pharmacology KW - Choline O-Acetyltransferase -- antagonists & inhibitors KW - Male KW - Olivary Nucleus -- drug effects KW - Receptors, Cholinergic -- drug effects KW - Receptors, Cholinergic -- physiology KW - Olivary Nucleus -- physiology KW - Behavior, Animal -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78492889?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Behavioral+evidence+for+increased+acetylcholine+receptor+sensitivity+after+nucleus+basalis+magnocellularis+lesions+in+the+rat.&rft.au=Mastropaolo%2C+J%3BCrawley%2C+J+N&rft.aulast=Mastropaolo&rft.aufirst=J&rft.date=1988-08-24&rft.volume=153&rft.issue=2-3&rft.spage=301&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 - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prospects for human papillomavirus vaccines and immunotherapies. AN - 78323088; 2840515 JF - Journal of the National Cancer Institute AU - Schreier, A A AU - Allen, W P AU - Laughlin, C AU - Gruber, J AD - Biological Carcinogenesis Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08/17/ PY - 1988 DA - 1988 Aug 17 SP - 896 EP - 899 VL - 80 IS - 12 SN - 0027-8874, 0027-8874 KW - Papillomavirus Vaccines KW - 0 KW - Viral Vaccines KW - Index Medicus KW - Animals KW - Immunotherapy KW - Humans KW - Disease Models, Animal KW - Viral Vaccines -- immunology KW - Papillomaviridae -- immunology KW - Tumor Virus Infections -- therapy KW - Viral Vaccines -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78323088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prospects+for+human+papillomavirus+vaccines+and+immunotherapies.&rft.au=Schreier%2C+A+A%3BAllen%2C+W+P%3BLaughlin%2C+C%3BGruber%2C+J&rft.aulast=Schreier&rft.aufirst=A&rft.date=1988-08-17&rft.volume=80&rft.issue=12&rft.spage=896&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 - 1988-09-06 N1 - Date created - 1988-09-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence that mouse promotion-sensitivity gene pro1 is transcribed by RNA polymerase III. AN - 78653581; 3146526 AB - The murine gene pro1 confers susceptibility to tumor promoters upon transfection into an insensitive host cell. Nucleotide analysis over a minimally active domain of 1049 bp reveals signals expected for a gene transcribed by RNA polymerase II (RNAPII). Similar analysis of the complementary strand shows intragenic signals characteristic of genes transcribed by RNA polymerase III (RNAPIII). We have previously characterized a small, pro1-homologous transcript that is constitutively expressed at lower levels in promotion-insensitive JB6 epidermal cells as compared to promotion-sensitive and transformed clonal variants. To identify whether the pro1 RNAPII or RNAPIII transcription unit encodes the pro1-homologous RNA, RNA probes specific for each of the predicted transcripts were generated. The RNA probe specific for the pro1 RNAPIII transcription unit was found to detect the pro1-hybridizing RNA. Ligating the pro1 RNAPII 5'-flanking region to an interferon gamma reporter sequence failed to induce synthesis of the reporter protein. In addition, pro1 transcripts generated from the predicted RNAPII and RNAPIII transcription units were untranslatable in rabbit reticulocyte lysates. These data are consistent with pro1 associated tumor promotion occurring not through an RNAPII intermediate, but through an RNAPIII intermediate. JF - Gene AU - Garrity, R R AU - Seed, J L AU - Young, H A AU - Winterstein, D AU - Colburn, N H AD - Biological Carcinogenesis Development Program, Program Resources Inc., NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 63 EP - 72 VL - 68 IS - 1 SN - 0378-1119, 0378-1119 KW - Carcinogens KW - 0 KW - Interferon-gamma KW - 82115-62-6 KW - DNA-Directed RNA Polymerases KW - EC 2.7.7.6 KW - RNA Polymerase III KW - Index Medicus KW - Protein Biosynthesis KW - Animals KW - Interferon-gamma -- genetics KW - Transfection KW - Cells, Cultured KW - Genetic Vectors KW - Mice KW - Nucleic Acid Hybridization KW - Plasmids KW - Carcinogens -- pharmacology KW - DNA-Directed RNA Polymerases -- metabolism KW - Genes -- drug effects KW - RNA Polymerase III -- metabolism KW - Transcription, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78653581?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Evidence+that+mouse+promotion-sensitivity+gene+pro1+is+transcribed+by+RNA+polymerase+III.&rft.au=Garrity%2C+R+R%3BSeed%2C+J+L%3BYoung%2C+H+A%3BWinterstein%2C+D%3BColburn%2C+N+H&rft.aulast=Garrity&rft.aufirst=R&rft.date=1988-08-15&rft.volume=68&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inter- and intraclonal variability of polypeptides synthesized in a rat hepatoma cell line. Quantitative two-dimensional gel analysis. AN - 78365498; 3403523 AB - To examine the degree of clonal heterogeneity in the synthesis of polypeptides in neoplastic cells, single-cell subclones from the rat hepatoma cell line H4-II-E were isolated. Polypeptides from the clones were resolved on high resolution two-dimensional polyacrylamide gels (PAGE), and quantitatively analyzed with a computerized two-dimensional PAGE analysis system developed in this laboratory. Only four qualitatively different spots were found which were synthesized in one of the subclones in four out of five experiments. In contrast, 5-20% of the spots showed statistically significant quantitative differences when any one subclone was compared to any other. These differences were generally quite small, averaging about 1.5-fold in intensity, although variations of fourfold or more were observed. Different cultures of the same subclone showed quantitative differences of the same order as seen in different subclones, indicating that this variability was primarily intraclonal in nature, i.e. associated with the cultures rather than the subclones. The distribution of quantitatively variable spots indicates that 50% or more of the polypeptides in these cells may display intraclonal variability. Similar results were obtained with a second set of subclones derived from these primary ones. Time course studies were conducted where cells were maintained continuously for 12 weeks, with samples taken for two-dimensional PAGE analysis once a week. The fraction of polypeptides that vary significantly generally increased with time between sampling points. Experiments with independent cultures grown in parallel indicate that about 4% of this variability can be correlated to the age of the culture media, although the majority appears due to uncontrolled and/or random differences that arise between cultures. These results indicate that independent cultures quickly develop detectable quantitative differences in the expression of a large fraction of their polypeptides. These differences cannot, at present, be associated with the observable biology of the cells and probably reflect time-associated variations in the balance of cellular macromolecular synthesis which arise in tissue culture cells. JF - The Journal of biological chemistry AU - Miller, M J AU - Schwartz, D M AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 11227 EP - 11236 VL - 263 IS - 23 SN - 0021-9258, 0021-9258 KW - Index Medicus KW - Rats KW - Karyotyping KW - Animals KW - Clone Cells -- metabolism KW - Time Factors KW - Cell Line KW - Peptide Biosynthesis KW - Liver Neoplasms, Experimental -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78365498?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inter-+and+intraclonal+variability+of+polypeptides+synthesized+in+a+rat+hepatoma+cell+line.+Quantitative+two-dimensional+gel+analysis.&rft.au=Miller%2C+M+J%3BSchwartz%2C+D+M%3BThorgeirsson%2C+S+S&rft.aulast=Miller&rft.aufirst=M&rft.date=1988-08-15&rft.volume=263&rft.issue=23&rft.spage=11227&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 - 1988-09-16 N1 - Date created - 1988-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cadmium carcinogenesis in male Wistar [Crl:(WI)BR] rats: dose-response analysis of tumor induction in the prostate and testes and at the injection site. AN - 78336655; 3396014 AB - Carcinogenic dose-response effects of CdCl2 in male Wistar [Crl:(WI)BR] rats were studied over a 2-year period. Groups of rats received a single s.c. injection of CdCl2 at doses of 0, 1.0, 2.5, 5.0, 10.0, 20.0, or 40.0 mumol/kg in the dorsal thoracic midline. Other groups received either four separate s.c. doses of 5 mumol Cd/kg each (at 0, 48, 96, and 168 h), or low dose cadmium (5.0 mumol/kg, s.c., at 0 h) followed by a higher dose (10.0 or 20.0 mumol/kg, s.c., at 48 h). The cadmium treatments resulted in appearance of tumors at the injection site, in the testes, and in the ventral prostate. Injection site tumors (mostly sarcomas) appeared to be strictly related to accumulated dose of cadmium and approached a 45% incidence at the highest cadmium dose (40 mumol/kg). Testicular tumors (mostly Leydig cell adenomas) were found to be highly dependent on testicular degeneration caused by cadmium. The highest Leydig cell tumor incidence occurred in the 40 mumol/kg (83%) and 20 mumol/kg (72%) dosage groups. Low dose pretreatment (5.0 mumol/kg) reduced or prevented the testicular degeneration and tumor formation that would otherwise result from a subsequent higher dose of CdCl2 (20 mumol/kg). Prostatic tumors (mostly adenomas of the ventral lobe) were also found to be associated with cadmium treatment, but in a non-dose related fashion. Prostatic tumor incidence was significantly elevated at the 2.5 mumol/kg dose of CdCl2 (eight tumors/26 rats; 31%) and showed a strong positive correlation between 0.0 and 2.5 mumol/kg in both tumor incidence and multiplicity. At higher doses, including those that caused marked testicular degeneration and induced prostatic atrophy, an elevated incidence of tumors did not occur. The occurrence of hyperplastic foci of the prostate, however, showed a strong positive correlation with increasing dose after single injections of cadmium up to and including 20.0 mumol/kg. Results indicate that CdCl2 can induce preneoplastic lesions of the prostate that appear to develop into tumors only at doses well below those causing marked degeneration of the testes and atrophy of the prostate. JF - Cancer research AU - Waalkes, M P AU - Rehm, S AU - Riggs, C W AU - Bare, R M AU - Devor, D E AU - Poirier, L A AU - Wenk, M L AU - Henneman, J R AU - Balaschak, M S AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 4656 EP - 4663 VL - 48 IS - 16 SN - 0008-5472, 0008-5472 KW - Cadmium KW - 00BH33GNGH KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Precancerous Conditions -- chemically induced KW - Pancreatic Neoplasms -- chemically induced KW - Injections, Subcutaneous KW - Male KW - Sarcoma, Experimental -- chemically induced KW - Prostatic Neoplasms -- chemically induced KW - Cadmium -- toxicity KW - Testicular Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78336655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cadmium+carcinogenesis+in+male+Wistar+%5BCrl%3A%28WI%29BR%5D+rats%3A+dose-response+analysis+of+tumor+induction+in+the+prostate+and+testes+and+at+the+injection+site.&rft.au=Waalkes%2C+M+P%3BRehm%2C+S%3BRiggs%2C+C+W%3BBare%2C+R+M%3BDevor%2C+D+E%3BPoirier%2C+L+A%3BWenk%2C+M+L%3BHenneman%2C+J+R%3BBalaschak%2C+M+S&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1988-08-15&rft.volume=48&rft.issue=16&rft.spage=4656&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 - 1988-09-08 N1 - Date created - 1988-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of normal human exocervical epithelial cells immortalized in vitro by papillomavirus types 16 and 18 DNA. AN - 78336235; 2456144 AB - An in vitro system for studying the interaction between human papillomavirus (HPV) 16 and 18 recombinant DNA and normal human exocervical epithelial cells is described. Eight HPV-immortalized human exocervical epithelial cell lines were established; all the lines contained either integrated HPV16 or 18 sequences and expressed HPV mRNAs. Thus, integration and expression appear to be required for immortalization. Immortalized cells (greater than 200 population doublings to date) divided rapidly (doubling time of 30 to 46 h) and morphologically resembled primary cultures of normal human exocervical epithelial cells. They expressed a keratin pattern consistent with their origin from exocervical epithelium. When cultured at high density or in the presence of serum they terminally differentiated. Sublines resistant to terminal differentiation were selected by growth in serum-supplemented medium. Keratin pattern changes suggest they have some properties in common with cervical squamous carcinoma cells. However, HPV-immortalized cell lines were not tumorgenic in nude mice. Thus, HPV16/18 is not carcinogenic by itself. These cell lines represent an appropriate model for studying factors that regulate HPV gene expression in normal cervical epithelial cells and examining the influence of cocarcinogens on neoplastic progression. JF - Cancer research AU - Woodworth, C D AU - Bowden, P E AU - Doniger, J AU - Pirisi, L AU - Barnes, W AU - Lancaster, W D AU - DiPaolo, J A AD - Laboratory of Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 4620 EP - 4628 VL - 48 IS - 16 SN - 0008-5472, 0008-5472 KW - DNA, Viral KW - 0 KW - RNA, Messenger KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Uterine Cervical Neoplasms -- etiology KW - Animals KW - Transfection KW - Epithelium -- microbiology KW - Humans KW - RNA, Messenger -- analysis KW - Mice KW - Keratins -- analysis KW - Female KW - Cell Line KW - Cervix Uteri -- pathology KW - Cervix Uteri -- microbiology KW - DNA, Viral -- analysis KW - Cervix Uteri -- analysis KW - Papillomaviridae -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78336235?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+normal+human+exocervical+epithelial+cells+immortalized+in+vitro+by+papillomavirus+types+16+and+18+DNA.&rft.au=Woodworth%2C+C+D%3BBowden%2C+P+E%3BDoniger%2C+J%3BPirisi%2C+L%3BBarnes%2C+W%3BLancaster%2C+W+D%3BDiPaolo%2C+J+A&rft.aulast=Woodworth&rft.aufirst=C&rft.date=1988-08-15&rft.volume=48&rft.issue=16&rft.spage=4620&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 - 1988-09-08 N1 - Date created - 1988-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Malignant pheochromocytoma: effective treatment with a combination of cyclophosphamide, vincristine, and dacarbazine. AN - 78327182; 3395037 AB - To determine the efficacy and toxicity of combination chemotherapy in patients with advanced, malignant pheochromocytoma. Nonrandomized, single-arm trial. Governmental medical referral center. Fourteen patients with malignant pheochromocytoma confirmed by histologic tests. All patients had metastatic disease and elevated urinary catecholamine secretion. After optimization of antihypertensive therapy, patients received cyclophosphamide, 750 mg/m2 body surface area on day 1; vincristine, 1.4 mg/m2 on day 1, and dacarbazine, 600 mg/m2 on days 1 and 2, every 21 days. Combination chemotherapy with cyclophosphamide, vincristine, and dacarbazine produced a complete and partial response rate of 57% (median duration, 21 months; range, 7 to more than 34). Complete and partial biochemical responses were seen in 79% of patients (median duration, more than 22 months; range, 6 to more than 35). All responding patients had objective improvement in performance status and blood pressure. Toxicity included expected hematologic, neurologic, and gastrointestinal effects of chemotherapy without serious sequelae. There were four minor hypotensive episodes and one minor hypertensive episode. Combination chemotherapy with cyclophosphamide, vincristine, and dacarbazine is effective for advanced malignant pheochromocytoma. Urinary catecholamines are useful to ascertain biochemical response to therapy. JF - Annals of internal medicine AU - Averbuch, S D AU - Steakley, C S AU - Young, R C AU - Gelmann, E P AU - Goldstein, D S AU - Stull, R AU - Keiser, H R AD - National Cancer Institute, Uniformed Services, University of the Health Sciences, Bethesda, Maryland. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 267 EP - 273 VL - 109 IS - 4 SN - 0003-4819, 0003-4819 KW - Biomarkers, Tumor KW - 0 KW - Catecholamines KW - Metanephrine KW - 5001-33-2 KW - Vanilmandelic Acid KW - 55-10-7 KW - Vincristine KW - 5J49Q6B70F KW - Dacarbazine KW - 7GR28W0FJI KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Humans KW - Vincristine -- administration & dosage KW - Adult KW - Biomarkers, Tumor -- analysis KW - Vanilmandelic Acid -- analysis KW - Dacarbazine -- administration & dosage KW - Middle Aged KW - Adolescent KW - Catecholamines -- analysis KW - Female KW - Male KW - Adrenal Gland Neoplasms -- drug therapy KW - Metanephrine -- analysis KW - Pheochromocytoma -- secondary KW - Pheochromocytoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Pheochromocytoma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78327182?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Malignant+pheochromocytoma%3A+effective+treatment+with+a+combination+of+cyclophosphamide%2C+vincristine%2C+and+dacarbazine.&rft.au=Averbuch%2C+S+D%3BSteakley%2C+C+S%3BYoung%2C+R+C%3BGelmann%2C+E+P%3BGoldstein%2C+D+S%3BStull%2C+R%3BKeiser%2C+H+R&rft.aulast=Averbuch&rft.aufirst=S&rft.date=1988-08-15&rft.volume=109&rft.issue=4&rft.spage=267&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 - 1988-08-25 N1 - Date created - 1988-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biochemistry and clinical activity of N-(phosphonacetyl)-L-aspartate: a review. AN - 78326712; 3293772 JF - Cancer research AU - Grem, J L AU - King, S A AU - O'Dwyer, P J AU - Leyland-Jones, B AD - Investigational Drug Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08/15/ PY - 1988 DA - 1988 Aug 15 SP - 4441 EP - 4454 VL - 48 IS - 16 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - Organophosphorus Compounds KW - Aspartic Acid KW - 30KYC7MIAI KW - sparfosic acid KW - 78QVZ7RG8L KW - Phosphonoacetic Acid KW - N919E46723 KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Drug Resistance KW - Organophosphorus Compounds -- therapeutic use KW - Aspartic Acid -- pharmacology KW - Phosphonoacetic Acid -- adverse effects KW - Aspartic Acid -- analogs & derivatives KW - Aspartic Acid -- therapeutic use KW - Phosphonoacetic Acid -- analogs & derivatives KW - Aspartic Acid -- adverse effects KW - Phosphonoacetic Acid -- pharmacology KW - Phosphonoacetic Acid -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78326712?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Biochemistry+and+clinical+activity+of+N-%28phosphonacetyl%29-L-aspartate%3A+a+review.&rft.au=Grem%2C+J+L%3BKing%2C+S+A%3BO%27Dwyer%2C+P+J%3BLeyland-Jones%2C+B&rft.aulast=Grem&rft.aufirst=J&rft.date=1988-08-15&rft.volume=48&rft.issue=16&rft.spage=4441&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 - 1988-09-08 N1 - Date created - 1988-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human repair gene restores normal pattern of preferential DNA repair in repair defective CHO cells. AN - 78405777; 3412890 AB - The pattern of preferential DNA repair of UV-induced pyrimidine dimers was studied in repair-deficient Chinese hamster ovary (CHO) cells transfected with the human excision repair gene, ERCC-1. Repair efficiency was measured in the active dihydrofolate reductase (DHFR) gene and in its flanking, non-transcribed sequences in three cell lines: Wild type CHO cells, a UV-sensitive excision deficient CHO mutant, and the transfected line of the mutant carrying the expressed ERCC-1 gene. The CHO cells transformed with the human ERCC-1 gene repaired the active DHFR gene much more efficiently than the non-transcribed sequences, a pattern similar to that seen in wild type CHO cells. This pattern differs from that previously reported in CHO cells transfected with the denV gene of bacteriophage T4, in which both active and non-transcribed DNA sequences were efficiently repaired (Bohr and Hanawalt, Carcinogenesis 8: 1333-1336, 1987). The ERCC-1 gene product may specifically substitute for the repair enzyme present in normal hamster cells while the denV product, T4 endonuclease V, does not be appear to be constrained in its access to inactive chromatin. JF - Nucleic acids research AU - Bohr, V A AU - Chu, E H AU - van Duin, M AU - Hanawalt, P C AU - Okumoto, D S AD - Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08/11/ PY - 1988 DA - 1988 Aug 11 SP - 7397 EP - 7403 VL - 16 IS - 15 SN - 0305-1048, 0305-1048 KW - Index Medicus KW - Animals KW - Cell Line KW - Cricetinae KW - Cloning, Molecular KW - DNA Repair UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78405777?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+repair+gene+restores+normal+pattern+of+preferential+DNA+repair+in+repair+defective+CHO+cells.&rft.au=Bohr%2C+V+A%3BChu%2C+E+H%3Bvan+Duin%2C+M%3BHanawalt%2C+P+C%3BOkumoto%2C+D+S&rft.aulast=Bohr&rft.aufirst=V&rft.date=1988-08-11&rft.volume=16&rft.issue=15&rft.spage=7397&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 - 1988-10-05 N1 - Date created - 1988-10-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1982 Mar;42(3):860-3 [7059984] Cancer Res. 1987 Dec 15;47(24 Pt 1):6426-36 [3315187] Nature. 1983 Nov 10-16;306(5939):206-8 [6417541] Nature. 1984 Aug 2-8;310(5976):425-9 [6462228] Cell. 1985 Feb;40(2):359-69 [3838150] Somat Cell Mol Genet. 1985 Jan;11(1):87-92 [3919454] Proc Natl Acad Sci U S A. 1985 Nov;82(22):7656-60 [3865186] Cell. 1986 Mar 28;44(6):913-23 [2420469] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3830-3 [3459159] Mutat Res. 1986 Jul;166(1):59-69 [2425254] J Biol Chem. 1986 Dec 15;261(35):16666-72 [3023360] Nucleic Acids Res. 1986 Nov 25;14(22):8979-95 [3786142] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8878-82 [3466163] Mutat Res. 1987 Jan;183(1):69-74 [3025723] Cell. 1987 Aug 28;50(5):789-99 [3621344] Carcinogenesis. 1987 Sep;8(9):1333-6 [3621470] Cell. 1987 Oct 23;51(2):241-9 [3664636] Proc Natl Acad Sci U S A. 1983 Sep;80(18):5655-9 [6577448] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A simplified automated procedure for generation of human lymphokine-activated killer cells for use in clinical trials. AN - 78374294; 3042868 AB - The administration of lymphokine-activated killer (LAK) cells along with interleukin-2 (IL-2) can mediate regression of tumors in selected patients. A closed automated system utilizing commercial blood cell separators has been developed for washing and Ficoll-Hypaque (FH) separation of lymphocytes, for lymphocyte culture in polyolefin bags, and for concentration of LAK cells out of culture prior to infusion. We now demonstrate that preparation of LAK cells can be simplified by elimination of the FH sedimentation step. Patient leukapheresis was performed using Fenwal CS-3000 blood cell separators, with a mean cellular yield per procedure of 54 X 10(9) WBC (95% lymphocytes), 184 X 10(9) RBC, and 306 X 10(9) platelets (n = 22). These cells were then washed in the same apheresis kit with a counter-current flow of saline, thereby eliminating 85% of platelets while retaining 88% of WBC. Aliquots of the washed cells were separated on FH gradients in 50 ml centrifuge tubes, and both FH-separated and washed-only cells were cultured at 3 X 10(6)/ml with 1500 U/ml IL-2 in polyolefin bags. Cytotoxicities of 22 preparations of LAK cells from 14 patients were evaluated in 4 h 51Cr release assays. Cells that were washed-only averaged 47, 35, and 9 lytic units/10(6) cells against K562, Daudi, and fresh tumor, while FH separated cells averaged 46, 33, and 6 lytic units/10(6) cells respectively. Cellular recoveries using the wash-only technique were 25% greater than when using FH sedimentation. Omission of FH separation saves time and expense in preparation and provides greater numbers of LAK cells for use in adoptive immunotherapy. JF - Journal of immunological methods AU - Aebersold, P AU - Carter, C S AU - Hyatt, C AU - Johnson, S AU - Ottaway, K AU - Leitman, S F AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08/09/ PY - 1988 DA - 1988 Aug 09 SP - 1 EP - 7 VL - 112 IS - 1 SN - 0022-1759, 0022-1759 KW - Interleukin-2 KW - 0 KW - Index Medicus KW - Humans KW - Erythrocyte Count KW - Clinical Trials as Topic KW - Cytotoxicity Tests, Immunologic KW - Leukocyte Count KW - Autoanalysis -- methods KW - Platelet Count KW - Cell Separation -- methods KW - Lymphocyte Activation KW - Leukapheresis -- methods KW - Killer Cells, Natural -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78374294?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunological+methods&rft.atitle=A+simplified+automated+procedure+for+generation+of+human+lymphokine-activated+killer+cells+for+use+in+clinical+trials.&rft.au=Aebersold%2C+P%3BCarter%2C+C+S%3BHyatt%2C+C%3BJohnson%2C+S%3BOttaway%2C+K%3BLeitman%2C+S+F%3BRosenberg%2C+S+A&rft.aulast=Aebersold&rft.aufirst=P&rft.date=1988-08-09&rft.volume=112&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunological+methods&rft.issn=00221759&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-20 N1 - Date created - 1988-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An Hebrew language version of the Stroop test. AN - 85230548; pmid-3211671 AB - We present normative data from a Hebrew language version of the Stroop color-word test. In this sample of college-educated Israeli young adults, 18 women and 28 men with a mean age of 28.4 yr. completed a Hebrew language Stroop test. When compared with 1978 English language norms of Golden, Hebrew speakers were slower on color-word reading and color naming, similar on naming the color of incongruently colored names of colors, and showed less interference. Slowed color-word reading and color-naming may reflect the two-syllable length of the Hebrew names for one-syllable length English language colors; reduced interference may reflect the exclusion of vowels in much Hebrew printing and subjects' ability to provide competing, nonconflicting words while naming the color of words in which the hue and the lexical content do not match. JF - Perceptual and Motor Skills AU - Ingraham, L J AU - Chard, F AU - Wood, M AU - Mirsky, A F AD - Laboratory of Psychology and Psychopathology, National Institute of Mental Health, Bethesda, Maryland 20892. PY - 1988 SP - 187 EP - 192 VL - 67 IS - 1 SN - 0031-5125, 0031-5125 KW - Comparative Study KW - Reading KW - Verbal Behavior KW - Human KW - Adult KW - Israel KW - Female KW - Male KW - Color Perception KW - Language KW - Attention KW - Psychological Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85230548?accountid=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=Perceptual+and+Motor+Skills&rft.atitle=An+Hebrew+language+version+of+the+Stroop+test.&rft.au=Ingraham%2C+L+J%3BChard%2C+F%3BWood%2C+M%3BMirsky%2C+A+F&rft.aulast=Ingraham&rft.aufirst=L&rft.date=1988-08-01&rft.volume=67&rft.issue=1&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Perceptual+and+Motor+Skills&rft.issn=00315125&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Effects of botulinum toxin injections on speech in adductor spasmodic dysphonia. AN - 85164201; pmid-3399071 AB - Adductor spasmodic dysphonia involves an overadduction of the vocal folds during speech causing uncontrolled voice and pitch breaks and slow, effortful speech. The disorder is resistant to speech therapy and often recurs following initial benefit from unilateral recurrent laryngeal nerve resection. Botulinum toxin injections into multiple sites of the thyroarytenoid muscle on one side were performed in 16 patients. Speech was recorded prior to injection and three times post-injection. Symptoms were measured by two examiners from speech spectrograms without knowledge of speaker identity or recording session. Significant (p less than or equal to 0.03) reductions in pitch and voice breaks, phonatory aperiodicity, and sentence time occurred only when injections resulted in unilateral vocal fold paralysis. Symptoms returned with the restoration of vocal fold movement, 3 months later. Reduction in speed of swallowing without aspiration was reported in 80% of cases. Although speech volume was reduced, there were no instances of aphonia. JF - Neurology AU - Ludlow, Christy L AU - Naunton, R F AU - Sedory, S E AU - Schulz, Geralyn Marie AU - Hallett, M AD - Laryngeal and Speech Section, National Institute of Neurological Disorders and Stroke; Department of Speech and Hearing Sciences, Columbian College of Arts and Sciences, George Washington University PY - 1988 SP - 1220 EP - 1225 VL - 38 IS - 8 SN - 0028-3878, 0028-3878 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85164201?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=Effects+of+botulinum+toxin+injections+on+speech+in+adductor+spasmodic+dysphonia.&rft.au=Ludlow%2C+Christy+L%3BNaunton%2C+R+F%3BSedory%2C+S+E%3BSchulz%2C+Geralyn+Marie%3BHallett%2C+M&rft.aulast=Ludlow&rft.aufirst=Christy&rft.date=1988-08-01&rft.volume=38&rft.issue=8&rft.spage=1220&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=00283878&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Molecular and genetic analysis of cystic fibrosis. AN - 78667420; 3066743 JF - Genomics AU - Dean, M AD - Biological Carcinogenesis Development Program, NCI-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 93 EP - 99 VL - 3 IS - 2 SN - 0888-7543, 0888-7543 KW - Index Medicus KW - Genetic Linkage KW - Humans KW - Chromosomes, Human KW - Restriction Mapping KW - Genes KW - Cystic Fibrosis -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78667420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Molecular+and+genetic+analysis+of+cystic+fibrosis.&rft.au=Dean%2C+M&rft.aulast=Dean&rft.aufirst=M&rft.date=1988-08-01&rft.volume=3&rft.issue=2&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Genomics&rft.issn=08887543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-04-06 N1 - Date created - 1989-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of rodent sperm, vaginal cytology, and reproductive organ weight data from National Toxicology Program 13-week studies. AN - 78652199; 3220212 AB - Sperm morphology and vaginal cytology examinations (SMVCEs), which include evaluations of motility, concentration and head morphology of sperm from the cauda epididymis, and male reproductive organ weight data, were developed by the National Toxicology Program as a screening system for reproductive toxicants. An analysis was conducted of SMVCE studies carried out at the end of fifty 13-week studies (25 for rats, 25 for mice) over a 3-year period. Statistically significant changes in these studies were summarized, as were control data for each male endpoint (mean, SD, 95% confidence limits around the mean, median, and statistical power). Reproductive organ weights (testis, epididymis, cauda epididymis) and sperm motility were the most statistically powerful endpoints evaluated; sperm head morphology may also be a sensitive endpoint for detecting reproductive toxicants. For 24 chemicals tested in both rats and mice, the concordance of results [i.e., no adverse effect in either species, or at least one SMVCE endpoint (not necessarily the same one) adversely affected in both species] was 58%. These data suggest that detection of potential reproductive toxicants might be best when both species are used. Types of sperm head abnormalities and their relative proportion of the total did not differ among control and treatment groups. Estrous cycle data were obtained in the final week of forty-six 13-week studies (23 for mice, 23 for rats). Only 3 chemicals caused an increase in mean cycle length compared with the control group. More data from breeding studies in which female estrous cycle length is measured are needed to assess fully the association of cycle length with reproductive outcome; stages of the estrous cycle are so variable that they may not be useful in assessing potential toxicity. Interlaboratory variability in SMVCE values for many endpoints was documented. Very few of the chemicals that form the basis of this report have been evaluated in definitive reproductive toxicology protocols; a companion paper compares changes in SMVCE endpoints with the outcome of continuous breeding reproduction studies. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Morrissey, R E AU - Schwetz, B A AU - Lamb, J C AU - Ross, M D AU - Teague, J L AU - Morris, R W AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 343 EP - 358 VL - 11 IS - 2 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Space life sciences KW - Sperm Head -- ultrastructure KW - Body Weight KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Sperm Count KW - Reference Standards KW - Sperm Motility KW - Organ Size KW - Male KW - Female KW - Vagina -- cytology KW - Rats -- physiology KW - Mice -- physiology KW - Spermatozoa -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78652199?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evaluation+of+rodent+sperm%2C+vaginal+cytology%2C+and+reproductive+organ+weight+data+from+National+Toxicology+Program+13-week+studies.&rft.au=Morrissey%2C+R+E%3BSchwetz%2C+B+A%3BLamb%2C+J+C%3BRoss%2C+M+D%3BTeague%2C+J+L%3BMorris%2C+R+W&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1988-08-01&rft.volume=11&rft.issue=2&rft.spage=343&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Association of sperm, vaginal cytology, and reproductive organ weight data with results of continuous breeding reproduction studies in Swiss (CD-1) mice. AN - 78651597; 3220213 AB - In continuous breeding reproduction studies in which an adverse effect on fertility was detected over an 18-week treatment period, a crossover mating trial was then conducted to determine the affected sex. Results of 25 crossover breeding studies conducted using Swiss (CD-1) mice were compared with results of sperm morphology and vaginal cytology examinations (SMVCEs) conducted at the conclusion of the mating trial. SMVCE endpoints include sperm concentration, motility, and morphology, vaginal cytology, and male reproductive organ weights. In most SMVCE studies multiple endpoints were adversely affected. For male reproductive toxicants, sperm motility was decreased in 89% of the studies, and absolute right epididymis and right testis weights were affected less frequently (80% each). Among studies with no detectable reduction in male breeding performance, 87% exhibited no detectable decrease in epididymis weight. Eighty-two percent had no change in cauda epididymis weight and 80% had no significant change in sperm concentration. An increase in female cycle length was associated (100%) with an effect on breeding due to female dysfunction. Overall accuracy, defined as correct identification of toxicants and nontoxicants, was highest for epididymis weight (84%), followed by cauda epididymis weight and sperm motility (79% each), and sperm concentration (76%). Female cycle length was so variable that the overall accuracy of the parameter in 13 studies was 69%. With the variety of chemicals used in this analysis, the association of abnormal sperm morphology with reproductive outcome was 71%. Control data (mean, 95% confidence interval around the mean, median, and statistical sensitivity) for each male endpoint (parent, and offspring at 10 weeks of age following a single breeding) were summarized from each of the two laboratories that conducted the studies. For several endpoints, statistical power was dependent on the laboratory conducting the studies. In general, the statistical sensitivity was relatively high for reproductive organ weights, although it was less for smaller organs such as the prostate. On the basis of both the biological and statistical analyses, it is recommended that multiple SMVCE endpoints, including sperm measures, be included in screens for reproductive toxicants. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Morrissey, R E AU - Lamb, J C AU - Schwetz, B A AU - Teague, J L AU - Morris, R W AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 359 EP - 371 VL - 11 IS - 2 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Sperm Head -- ultrastructure KW - Animals KW - Fertility KW - Testis -- anatomy & histology KW - Sex Factors KW - Reference Standards KW - Reproduction KW - Mice KW - Male KW - Female KW - Pregnancy KW - Organ Size -- drug effects KW - Vagina -- cytology KW - Spermatozoa -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78651597?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Association+of+sperm%2C+vaginal+cytology%2C+and+reproductive+organ+weight+data+with+results+of+continuous+breeding+reproduction+studies+in+Swiss+%28CD-1%29+mice.&rft.au=Morrissey%2C+R+E%3BLamb%2C+J+C%3BSchwetz%2C+B+A%3BTeague%2C+J+L%3BMorris%2C+R+W&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1988-08-01&rft.volume=11&rft.issue=2&rft.spage=359&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The acute toxicity of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF) in the male Fischer rat. AN - 78651039; 3220203 AB - Polychlorinated dibenzofurans are ubiquitous environmental pollutants which have great potential for human exposure. To characterize the toxicity of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF), male F344 rats were administered a single oral dose of 0, 100, 250, 500, 1000, or 2000 micrograms 4PeCDF/kg. A progressive and dose-dependent loss of body weight was evident by 3 days after treatment. Signs of toxicity included piloerection, hair loss, hypoactivity, morbidity, and death. Death occurred as soon as 14 days after treatment and continued throughout the 35-day observation period. The LD50/35 was estimated to be 916 micrograms/kg with a 95% confidence interval of 565-1484 micrograms/kg. Dose-dependent increases were observed in serum cholesterol, triglyceride, and bile acid concentrations and in sorbitol dehydrogenase and aspartate aminotransferase activities. The hematocrit, hemoglobin, mean corpuscular volume, and mean corpuscular hemoglobin concentrations were depressed in a dose-dependent fashion. Hepatic ethoxyresorufin-O-deethylase (EROD) activity was increased in all treatment groups approximately 25 times above that of control animals. Lymphoid depletion in the thymus and spleen was observed in the three highest doses and thymic atrophy was present at all dose levels. Absolute liver weight and the liver:body weight ratio were significantly increased above controls. Hepatotoxicity was dose-dependent and was characterized by lipid accumulation resulting in hepatocytomegaly. Epithelial hyperplasia and focal ulcerations of the forestomach was observed in animals administered 500 micrograms 4PeCDF/kg. Spontaneous cardiomyopathy was exacerbated by treatment with 2000 micrograms/kg. Since 4PeCDF and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produce a similar spectrum of toxic effects, the biochemical mechanism(s) of toxicity for these chemicals may be similar. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Brewster, D W AU - Uraih, L C AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 236 EP - 249 VL - 11 IS - 2 SN - 0272-0590, 0272-0590 KW - Benzofurans KW - 0 KW - Bile Acids and Salts KW - Triglycerides KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Cholesterol KW - 97C5T2UQ7J KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - 2,3,4,7,8-pentachlorodibenzofuran KW - U4C2RV3124 KW - Index Medicus KW - Triglycerides -- blood KW - Animals KW - Liver -- enzymology KW - Liver -- pathology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Bile Acids and Salts -- metabolism KW - Rats KW - Cholesterol -- blood KW - Rats, Inbred F344 KW - Oxidoreductases -- metabolism KW - Body Weight -- drug effects KW - Lethal Dose 50 KW - Macaca mulatta KW - Male KW - Organ Size -- drug effects KW - Benzofurans -- blood KW - Benzofurans -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78651039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+acute+toxicity+of+2%2C3%2C4%2C7%2C8-pentachlorodibenzofuran+%284PeCDF%29+in+the+male+Fischer+rat.&rft.au=Brewster%2C+D+W%3BUraih%2C+L+C%3BBirnbaum%2C+L+S&rft.aulast=Brewster&rft.aufirst=D&rft.date=1988-08-01&rft.volume=11&rft.issue=2&rft.spage=236&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 - 1989-03-23 N1 - Date created - 1989-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental characterization and chromosomal mapping of the 5-azacytidine-sensitive fluF locus of Aspergillus nidulans. AN - 78596234; 2463470 AB - In Aspergillus nidulans, a fungus that possesses negligible, if any, levels of methylation in its genome, low concentrations of 5-azacytidine (5-AC) convert a high percentage of the cell population to fluffy phenotypic variants through a heritable modification of a single nuclear gene (M. Tamame, F. Antequera, J. R. Villanueva, and T. Santos, Mol. Cell. Biol. 3:2287-2297, 1983). This new 5-AC-altered locus, designated here fluF1, was mapped as the closest marker to the centromere that has been identified so far on the right arm of chromosome VIII. Of all mutagens tested, only 5-AC induced the fluffy phenotype with a significant frequency. Furthermore, we determined that the wild-type, dominant allele of the fluF gene was primarily accessible to modification by 5-AC at the initial stages of fungal vegetative growth. These results indicated that 5-AC does not act through random mutagenic action but, rather, that fluF constitutes a specific target for this drug during a well-defined period of fungal development. Alteration of fluF by 5-AC resulted in a dramatic modification of the developmental program of A. nidulans. The resulting fluffy clones were characterized by massive, uncontrolled proliferation of undifferentiated hyphae, a drastic delay in the onset of asexual differentiation (conidiation), and colonies with an invasive nature. These features are reminiscent of the malignant properties of tumor cells. We propose that the locus fluF plays a primary role in the control of cell proliferation in A. nidulans and that its alteration by 5-AC produces pleiotropic modifications of the developmental program of this fungus. JF - Molecular and cellular biology AU - Tamame, M AU - Antequera, F AU - Santos, E AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 3043 EP - 3050 VL - 8 IS - 8 SN - 0270-7306, 0270-7306 KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Genotype KW - Genetic Variation KW - Cell Nucleus -- ultrastructure KW - Crosses, Genetic KW - Mutation KW - Aspergillus nidulans -- drug effects KW - Azacitidine -- pharmacology KW - Genes, Fungal -- drug effects KW - Aspergillus nidulans -- genetics KW - Aspergillus nidulans -- growth & development KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78596234?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Developmental+characterization+and+chromosomal+mapping+of+the+5-azacytidine-sensitive+fluF+locus+of+Aspergillus+nidulans.&rft.au=Tamame%2C+M%3BAntequera%2C+F%3BSantos%2C+E&rft.aulast=Tamame&rft.aufirst=M&rft.date=1988-08-01&rft.volume=8&rft.issue=8&rft.spage=3043&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 - 1989-02-23 N1 - Date created - 1989-02-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genetics. 1970 Oct;66(2):267-79 [5512361] Mutat Res. 1969 Sep-Oct;8(2):255-64 [5366006] Biochim Biophys Acta. 1983 Sep 9;740(4):355-61 [6411122] Annu Rev Biochem. 1983;52:93-124 [6311083] J Bacteriol. 1983 Oct;156(1):155-60 [6352675] Mol Cell Biol. 1983 Dec;3(12):2287-97 [6197627] Mutat Res. 1984 Jan;139(1):21-4 [6197648] Cell. 1984 Jun;37(2):359-65 [6722879] Proc Natl Acad Sci U S A. 1984 Jun;81(11):3389-93 [6203119] EMBO J. 1984 May;3(5):961-7 [6203746] J Biol Chem. 1984 Jul 10;259(13):8033-6 [6330093] Cell. 1984 Oct;38(3):791-800 [6207933] Proc Natl Acad Sci U S A. 1984 Nov;81(22):6993-7 [6209710] Cell. 1985 Mar;40(3):485-6 [2578884] J Biol Chem. 1985 Apr 10;260(7):4059-68 [2579944] Nature. 1986 May 15-21;321(6067):209-13 [2423876] Mol Cell Biol. 1986 May;6(5):1698-705 [2431285] Mol Cell Biol. 1986 Aug;6(8):2944-9 [2431295] Cell. 1987 Jan 16;48(1):11-24 [2431792] Mol Cell Biol. 1987 Jun;7(6):2196-200 [2439904] Science. 1987 Oct 9;238(4824):163-70 [3310230] Adv Genet. 1953;5:141-238 [13040135] Mutat Res. 1983 Jul;121(1):47-52 [6191216] Genet Res. 1965 Nov;6(3):352-9 [5848714] Proc Natl Acad Sci U S A. 1983 Aug;80(15):4842-6 [6192443] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of covalent binding from halothane metabolism in hepatic microsomes from phenobarbital-induced and hyperthyroid rats. AN - 78521512; 3188577 AB - 1. Hepatic microsomal suspensions from rats pretreated with saline, phenobarbital or triiodothyronine were incubated with 14C-halothane under aerobic and anerobic conditions. 2. Metabolism of halothane by microsomes from phenobarbital-induced rats under anaerobic conditions resulted in covalent binding of 14C to microsomal lipids, and to a lesser extent, microsomal proteins, as seen in previous studies. Covalent binding was decreased with incubation under aerobic conditions. 3. Metabolism of halothane by microsomal suspensions from hyperthyroid rats produced much less covalent binding to microsomal lipids and proteins, with binding similar to, or less than, that observed with microsomes from saline-treated rats. The covalent binding of halothane to protein of microsomes from hyperthyroid rats was dependent upon metabolism, and was inhibited by SKF 525A, reduced glutathione, or cytosol. 4. The in vitro observations with respect to covalent binding are inconsistent with previous reports on halothane hepatotoxicity in hyperthyroid rats in vivo. This inconsistency and the relatively small extent of covalent binding with microsomes from hyperthyroid rats observed, suggests that covalent binding is not an important mechanism of halothane hepatotoxicity in the hyperthyroid rat model. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Smith, A C AU - Roberts, S M AU - James, R C AU - Berman, L M AU - Harbison, R D AD - National Cancer Institute, Bethesda, MD. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 991 EP - 1001 VL - 18 IS - 8 SN - 0049-8254, 0049-8254 KW - Proteins KW - 0 KW - Pyridines KW - Triiodothyronine KW - 06LU7C9H1V KW - metapyrone KW - 17286-92-9 KW - NADP KW - 53-59-8 KW - Glutathione KW - GAN16C9B8O KW - Halothane KW - UQT9G45D1P KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Chemical and Drug Induced Liver Injury KW - NADP -- pharmacology KW - Pyridines -- pharmacology KW - Proteins -- metabolism KW - Glutathione -- pharmacology KW - Male KW - Lipid Metabolism KW - Phenobarbital -- pharmacology KW - Halothane -- metabolism KW - Microsomes, Liver -- metabolism KW - Microsomes, Liver -- drug effects KW - Hyperthyroidism -- metabolism KW - Halothane -- toxicity KW - Hyperthyroidism -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78521512?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.atitle=Comparison+of+covalent+binding+from+halothane+metabolism+in+hepatic+microsomes+from+phenobarbital-induced+and+hyperthyroid+rats.&rft.au=Smith%2C+A+C%3BRoberts%2C+S+M%3BJames%2C+R+C%3BBerman%2C+L+M%3BHarbison%2C+R+D&rft.aulast=Smith&rft.aufirst=A&rft.date=1988-08-01&rft.volume=18&rft.issue=8&rft.spage=991&rft.isbn=&rft.btitle=&rft.title=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.issn=00498254&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-07 N1 - Date created - 1988-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcohol antagonists--the continuing quest. AN - 78519395; 3056079 JF - Alcoholism, clinical and experimental research AU - Lister, R G AU - Nutt, D J AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism/DICBR, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 566 EP - 569 VL - 12 IS - 4 SN - 0145-6008, 0145-6008 KW - Alcohol Deterrents KW - 0 KW - Azides KW - Benzodiazepines KW - 12794-10-4 KW - Ethanol KW - 3K9958V90M KW - Ro 15-4513 KW - 91917-65-6 KW - Index Medicus KW - Animals KW - Brain -- drug effects KW - Ethanol -- toxicity KW - Azides -- pharmacology KW - Benzodiazepines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78519395?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alcohol+antagonists--the+continuing+quest.&rft.au=Lister%2C+R+G%3BNutt%2C+D+J&rft.aulast=Lister&rft.aufirst=R&rft.date=1988-08-01&rft.volume=12&rft.issue=4&rft.spage=566&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 - 1988-11-30 N1 - Date created - 1988-11-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic silastic central venous catheterization for induction, maintenance and support of persistent granulocytopenia in rabbits. AN - 78513476; 3184859 AB - In order to investigate new approaches in diagnosis, prevention and treatment of infectious complicating chemotherapy-induced granulocytopenia, we developed and prospectively evaluated a method of chronic central venous catheterization for the induction, maintenance and support of persistent granulocytopenia in rabbits. The method entails a central venous silastic catheter with a subcutaneous tunnel and a heparin lock device for repeated non-traumatic sampling of blood and administration of medications. During the course of 10 months, 226 rabbits were studied. Mean duration of catheter placement was 27 days, 17 of which were spent in granulocytopenia. Two-way flow was sustained throughout the duration of placement in 205 rabbits (91%) and for 5,845 (95%) of a total 6,163 catheter-days. All but two catheters could be flushed throughout the duration of their placement. Postoperative infectious complications related to catheter insertion developed in less than 1% of the rabbits. This method of chronic catheterization safely provides long-term venous access for studies requiring frequent venous access, including the painless induction, maintenance, and support of chronic granulocytopenia in rabbits. JF - Laboratory animal science AU - Walsh, T J AU - Bacher, J AU - Pizzo, P A AD - Section of Infectious Diseases, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 467 EP - 471 VL - 38 IS - 4 SN - 0023-6764, 0023-6764 KW - Cytarabine KW - 04079A1RDZ KW - Index Medicus KW - Animals KW - Prospective Studies KW - Rabbits KW - Cytarabine -- administration & dosage KW - Female KW - Catheters, Indwelling KW - Catheterization, Central Venous KW - Disease Models, Animal KW - Agranulocytosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78513476?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chronic+silastic+central+venous+catheterization+for+induction%2C+maintenance+and+support+of+persistent+granulocytopenia+in+rabbits.&rft.au=Walsh%2C+T+J%3BBacher%2C+J%3BPizzo%2C+P+A&rft.aulast=Walsh&rft.aufirst=T&rft.date=1988-08-01&rft.volume=38&rft.issue=4&rft.spage=467&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 - 1988-12-05 N1 - Date created - 1988-12-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ankylosis of hock joints in group caged male B6C3F1 mice. AN - 78511002; 3184849 AB - Enlarged hock joints were observed during 1983 in B6C3F1 mice of chronic toxicity and carcinogenicity studies sponsored by the National Toxicology Program (NTP). Subsequently, approximately 9,500 B6C3F1 mice on 32 NTP chemical toxicity and carcinogenicity studies were evaluated for this condition by clinical examination. Group caged male B6C3F1 mice had thickening and reduced mobility of the hock joints at prevalences of 1.2% up to 6 months of age; 23% at 6 to 12 months of age; and 62% at 13 to 26 months of age. Group caged female B6C3F1 mice had a prevalence of 2% or less. Histologically, affected mice had periarticular exostoses on the bones of the hock joints, with formation of bony bridges around joints and deposition of new bone in joint spaces, resulting in partial or complete ankylosis. Individually caged male and female B6C3F1 mice were not affected. The cause of the ankylosis was not determined, but its occurrence in the NTP studies has been reduced by individual caging. JF - Laboratory animal science AU - Rao, G N AU - Lindsey, J R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 417 EP - 421 VL - 38 IS - 4 SN - 0023-6764, 0023-6764 KW - Index Medicus KW - Animals KW - Hindlimb KW - Male KW - Ankylosis -- pathology KW - Ankylosis -- epidemiology KW - Joints -- pathology KW - Rodent Diseases -- epidemiology KW - Housing, Animal KW - Ankylosis -- veterinary KW - Mice KW - Rodent Diseases -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78511002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ankylosis+of+hock+joints+in+group+caged+male+B6C3F1+mice.&rft.au=Rao%2C+G+N%3BLindsey%2C+J+R&rft.aulast=Rao&rft.aufirst=G&rft.date=1988-08-01&rft.volume=38&rft.issue=4&rft.spage=417&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 - 1988-12-05 N1 - Date created - 1988-12-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Do cage effects influence tumor incidence? An examination of laboratory animal carcinogenicity studies utilizing Fischer 344 rats. AN - 78499681; 3183292 AB - Approximately 125 carcinogenicity studies in Fischer 344 rats conducted by the National Toxicology Program (NTP) were examined to determine the frequency with which cage effects were associated with observed carcinogenic responses. All studies involving groups of 50 rats housed five per cage and showing evidence of chemically-related carcinogenicity were considered. For each of these experiments, two statistical analyses were carried out for each dosed and control group: (i) a test to determine whether or not the occurrence of tumors clustered within cages; and (ii) an evaluation to determine whether or not tumor incidences differed significantly between differing cage shelf levels. These analyses showed that the numbers of statistically significant (P less than 0.05 or P less than 0.01) effects were consistent with the number expected by chance alone. Thus, cage-related factors appeared to have little or no impact upon tumor incidence in these particular studies. Experimental design protocols now used by the NTP (which include random assignment of animals to cages; random assignment of columns of cages to dosed and control groups; and periodic rotation of cage location) further reduce the likelihood that factors associated with the housing of the animals could influence tumor incidence in current studies. JF - Journal of applied toxicology : JAT AU - Haseman, J K AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 267 EP - 273 VL - 8 IS - 4 SN - 0260-437X, 0260-437X KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Neoplasms, Experimental -- etiology KW - Female KW - Housing, Animal KW - Carcinogenicity Tests KW - Animals, Laboratory UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78499681?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+applied+toxicology+%3A+JAT&rft.atitle=Do+cage+effects+influence+tumor+incidence%3F+An+examination+of+laboratory+animal+carcinogenicity+studies+utilizing+Fischer+344+rats.&rft.au=Haseman%2C+J+K&rft.aulast=Haseman&rft.aufirst=J&rft.date=1988-08-01&rft.volume=8&rft.issue=4&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Journal+of+applied+toxicology+%3A+JAT&rft.issn=0260437X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-21 N1 - Date created - 1988-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of systemic fungal infections: recent progress and current problems. AN - 78498214; 2846299 AB - Systemic mycoses continue to emerge as life-threatening infections. Considerable progress in treating these infections is being achieved through better application of established available antifungal agents (amphotericin B, flucytosine, miconazole and ketoconazole), and through development of promising investigational agents (fluconazole, itraconazole). Systemic fungal infections, however, continue to present major problems, including clinical resistance, microbiological resistance, emergence of new pathogens, and involvement of more immunocompromised patients. The purpose of this paper, therefore, is to review the recent progress and current problems in treatment of systemic fungal infections. JF - European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology AU - Walsh, T J AU - Pizzo, A AD - Infectious Diseases Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 460 EP - 475 VL - 7 IS - 4 SN - 0934-9723, 0934-9723 KW - Antifungal Agents KW - 0 KW - Triazoles KW - Itraconazole KW - 304NUG5GF4 KW - Miconazole KW - 7NNO0D7S5M KW - Amphotericin B KW - 7XU7A7DROE KW - Fluconazole KW - 8VZV102JFY KW - Flucytosine KW - D83282DT06 KW - Ketoconazole KW - R9400W927I KW - Index Medicus KW - Chemistry KW - Miconazole -- adverse effects KW - Ketoconazole -- therapeutic use KW - Humans KW - Amphotericin B -- pharmacokinetics KW - Ketoconazole -- analogs & derivatives KW - Flucytosine -- pharmacokinetics KW - Triazoles -- pharmacokinetics KW - Miconazole -- pharmacokinetics KW - Flucytosine -- therapeutic use KW - Miconazole -- therapeutic use KW - Ketoconazole -- pharmacokinetics KW - Flucytosine -- adverse effects KW - Chemical Phenomena KW - Amphotericin B -- adverse effects KW - Triazoles -- therapeutic use KW - Ketoconazole -- adverse effects KW - Amphotericin B -- therapeutic use KW - Antifungal Agents -- pharmacokinetics KW - Antifungal Agents -- adverse effects KW - Mycoses -- drug therapy KW - Antifungal Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78498214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+clinical+microbiology+%26+infectious+diseases+%3A+official+publication+of+the+European+Society+of+Clinical+Microbiology&rft.atitle=Treatment+of+systemic+fungal+infections%3A+recent+progress+and+current+problems.&rft.au=Walsh%2C+T+J%3BPizzo%2C+A&rft.aulast=Walsh&rft.aufirst=T&rft.date=1988-08-01&rft.volume=7&rft.issue=4&rft.spage=460&rft.isbn=&rft.btitle=&rft.title=European+journal+of+clinical+microbiology+%26+infectious+diseases+%3A+official+publication+of+the+European+Society+of+Clinical+Microbiology&rft.issn=09349723&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-12-12 N1 - Date created - 1988-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A case-referent study of soft-tissue sarcoma and Hodgkin's disease. Farming and insecticide use. AN - 78469982; 3175554 AB - A population-based case-referent study in Kansas examined the relationship between exposure to insecticides and the development of soft-tissue sarcoma (STS) and Hodgkin's disease (HD). Data from telephone interviews for 133 STS cases, 121 HD cases, and 948 referents indicated that STS was associated with use of insecticides on animals, but not on crops. HD was not significantly associated with either use. STS risk was higher among the farmers who themselves mixed or applied insecticides to animals than among farmers who did not. Farmers who failed to use any protective equipment to reduce insecticide exposure were at a significantly elevated risk of STS. Risk rose with early calendar year of first use. The excess risk appeared to be primarily among fibrous and myomatous sarcomas with little association seen for lipomatous or other STS neoplasms. Myomatous sarcomas increased significantly with duration and time since first use of insecticides on animals. If the reported association between STS and insecticides is causal, the data suggest that exposure to the agent(s) responsible may have been reduced in the mid-1950s or the agent(s) have an average latency period for STS of at least 20 years. JF - Scandinavian journal of work, environment & health AU - Hoar Zahm, S AU - Blair, A AU - Holmes, F F AU - Boysen, C D AU - Robel, R J AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 224 EP - 230 VL - 14 IS - 4 SN - 0355-3140, 0355-3140 KW - Hydrocarbons, Chlorinated KW - 0 KW - Insecticides KW - Pesticides KW - Index Medicus KW - Risk Factors KW - Humans KW - Aged KW - Pesticides -- adverse effects KW - Insecticides -- adverse effects KW - Hodgkin Disease -- chemically induced KW - Soft Tissue Neoplasms -- chemically induced KW - Agricultural Workers' Diseases -- chemically induced KW - Sarcoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78469982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+case-referent+study+of+soft-tissue+sarcoma+and+Hodgkin%27s+disease.+Farming+and+insecticide+use.&rft.au=Hoar+Zahm%2C+S%3BBlair%2C+A%3BHolmes%2C+F+F%3BBoysen%2C+C+D%3BRobel%2C+R+J&rft.aulast=Hoar+Zahm&rft.aufirst=S&rft.date=1988-08-01&rft.volume=14&rft.issue=4&rft.spage=224&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 - 1988-11-08 N1 - Date created - 1988-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of interleukin 2 and phorbol myristate acetate augmentation of expression of transfected human interferon-gamma genomic DNA. AN - 78444209; 3139787 AB - We have reported that human interferon-gamma (IFN-gamma) genomic DNA is expressed after transfection into a mouse T-lymphoblastoid cell line and expression can be enhanced by both interleukin 2 (IL2) and phorbol myristate acetate (PMA). It can now be shown that PMA rapidly induces new transcription of the IFN-gamma gene and that increased human (Hu) IFN-gamma can be detected by 2 h after the addition of PMA to the mouse cells. Enhancement of IFN-gamma production by IL2 takes place with similar kinetics with increased IFN-gamma production observed at 4-6 h after IL2 addition, although the maximum amount of IFN-gamma produced in response to IL2 was significantly lower than that produced in response to PMA. Furthermore, along with increased levels of cytoplasmic IFN-gamma RNA, we were able to demonstrate increased nuclear transcription at 4 h after IL2 treatment. Stimulation of IFN-gamma mRNA by both PMA and IL2 could occur in the presence of cycloheximide, indicating that protein synthesis was not required for the initial stimulation to occur. However, the functional half-life of IFN-gamma mRNA after actinomycin D treatment was higher in cells that had been treated with PMA when compared with untreated or IL2-treated cells. This data indicates that there are quantitative differences in the ability of PMA or IL2 to augment IFN-gamma production, and that PMA may increase IFN-gamma production in the transfected cell by additional mechanisms, such as increasing mRNA stability. JF - Journal of interferon research AU - Young, H A AU - Birchenall-Sparks, M AU - Kovacs, E AU - Dorman, L AU - Ruscetti, F W AD - Laboratory of Molecular Immunoregulation, NCI-FCRF, Frederick, MD 21701. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 527 EP - 538 VL - 8 IS - 4 SN - 0197-8357, 0197-8357 KW - Interferon Inducers KW - 0 KW - Interleukin-2 KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Interferon-gamma KW - 82115-62-6 KW - DNA KW - 9007-49-2 KW - Cycloheximide KW - 98600C0908 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Drug Interactions KW - Half-Life KW - Transfection KW - Receptors, Interleukin-2 -- analysis KW - Interferon Inducers -- pharmacology KW - Cells, Cultured KW - Kinetics KW - Humans KW - Cycloheximide -- pharmacology KW - RNA, Messenger -- analysis KW - Radioimmunoassay KW - Cell Division KW - Interleukin-2 -- pharmacology KW - Interferon-gamma -- genetics KW - DNA -- genetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78444209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+interferon+research&rft.atitle=Characterization+of+interleukin+2+and+phorbol+myristate+acetate+augmentation+of+expression+of+transfected+human+interferon-gamma+genomic+DNA.&rft.au=Young%2C+H+A%3BBirchenall-Sparks%2C+M%3BKovacs%2C+E%3BDorman%2C+L%3BRuscetti%2C+F+W&rft.aulast=Young&rft.aufirst=H&rft.date=1988-08-01&rft.volume=8&rft.issue=4&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Journal+of+interferon+research&rft.issn=01978357&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-23 N1 - Date created - 1988-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Changes in cerebral receptors for gamma aminobutyric acid in patients with hepatic encephalopathy. AN - 78423417; 2843723 AB - If the gamma-aminobutyric acid (GABA) inhibitory neurotransmitter system plays an important role in the mediation of hepatic encephalopathy (HE) in man, changes in the status of receptors for GABA in the brain may occur in patients with HE. To test this possibility, brains were obtained at autopsy from 11 patients who had died of causes unrelated to liver disease and from 11 patients who had died with chronic liver disease. Eight of the liver disease group had overt HE at the time of death. The specific binding of GABA to synaptic membranes isolated from frontal cortex was determined. Mean specific binding of GABA for patients with cirrhosis without overt HE was similar to that for control patients. In contrast, corresponding means for patients who had mild HE (stages I-III) and for patients who had severe HE (stage IV) were 45% higher (p less than 0.05) and 43% lower, respectively, than that for control patients. The mean specific binding of GABA was significantly greater for patients with mild HE than in patients with severe HE (p less than 0.025). Scatchard plots of the GABA binding data were curvilinear and consistent with a model of GABA receptors with two independent binding sites. Computer-assisted analysis of the binding data indicated that the altered GABA binding observed in patients with HE is attributable to changes in the affinity rather than the density of both GABA receptors (increased affinities in mild HE, and decreased affinities in hepatic coma). These findings are compatible with the hypothesis that alterations in GABAergic neurotransmission are associated with and contribute to the syndrome of HE in man. JF - Liver AU - Ferenci, P AU - Riederer, P AU - Jellinger, K AU - Schafer, D F AU - Jones, E A AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 225 EP - 230 VL - 8 IS - 4 SN - 0106-9543, 0106-9543 KW - Receptors, GABA-A KW - 0 KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Index Medicus KW - Liver Cirrhosis, Alcoholic -- metabolism KW - Coronary Disease -- metabolism KW - Aged, 80 and over KW - Humans KW - Aged KW - Middle Aged KW - gamma-Aminobutyric Acid -- metabolism KW - Synaptic Membranes -- metabolism KW - Male KW - Female KW - Receptors, GABA-A -- metabolism KW - Brain -- metabolism KW - Hepatic Encephalopathy -- pathology KW - Hepatic Encephalopathy -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78423417?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Liver&rft.atitle=Changes+in+cerebral+receptors+for+gamma+aminobutyric+acid+in+patients+with+hepatic+encephalopathy.&rft.au=Ferenci%2C+P%3BRiederer%2C+P%3BJellinger%2C+K%3BSchafer%2C+D+F%3BJones%2C+E+A&rft.aulast=Ferenci&rft.aufirst=P&rft.date=1988-08-01&rft.volume=8&rft.issue=4&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Liver&rft.issn=01069543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-27 N1 - Date created - 1988-10-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Testicular toxicity and reduced Sertoli cell numbers in neonatal rats by di(2-ethylhexyl)phthalate and the recovery of fertility as adults. AN - 78395241; 3413790 AB - Neonatal and adult rats (1, 2, 3, 6, and 12 weeks of age) were given five daily oral doses of di(2-ethylhexyl) phthalate (DEHP) (0, 10, 100, 1000, 2000 mg/kg) and histological changes in the testes were examined 24 hr after the last dose. Relative testis weights were reduced at doses of 1000 mg/kg in 1, 2, 3, and 6-week-old but not in 12-week-old rats, while doses of 2000 mg/kg were fatal to suckling rats and caused decreased relative testis weight but not death in 6- and 12-week-old rats. In neonatal rats (1 week old), DEHP (1000 mg/kg) caused a 35% decrease in Sertoli cell numbers while 2- and 3-week-old rats showed losses of spermatocytes but not of Sertoli cells. The 6- and 12-week-old rats showed loss of both spermatids and spermatocytes at 1000 and/or 2000 mg/kg. Total testicular zinc concentrations were decreased in 12-week-old but not in suckling (3-week) or weaned (6-week) rats. The results support the hypothesis that the Sertoli cell is the primary testicular target of phthalate ester toxicity since effects were observed at an age when only Sertoli cells were present. Fertility was assessed in mating trials in adult male rats after neonatal exposure to DEHP on Days 6-10. Although Sertoli cell number was reduced 24 hr after the last dose, the numbers were normal at 6 and 13 weeks of age. However, at 6 weeks there was a dose-related decrease in maturation of the spermatids in the tubules. There were no consistent changes in fertility, implantation rate, or numbers of live fetuses in untreated females mated with the DEHP-treated males. However, there were decreases in testis weight and testicular spermatid numbers at 13 and 19 weeks but not at 11, 12, 16, or 23 weeks of age. Therefore, a loss of Sertoli cells due to DEHP exposure neonatally did not affect the fertility of the rats as adults, but may have caused subtle effects on sperm production. JF - Toxicology and applied pharmacology AU - Dostal, L A AU - Chapin, R E AU - Stefanski, S A AU - Harris, M W AU - Schwetz, B A AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 104 EP - 121 VL - 95 IS - 1 SN - 0041-008X, 0041-008X KW - Phthalic Acids KW - 0 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Sertoli Cells -- drug effects KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Sperm Count -- drug effects KW - Age Factors KW - Testis -- metabolism KW - Cell Count -- drug effects KW - Zinc -- metabolism KW - Male KW - Organ Size -- drug effects KW - Fertility -- drug effects KW - Testicular Diseases -- pathology KW - Testicular Diseases -- chemically induced KW - Diethylhexyl Phthalate -- toxicity KW - Animals, Newborn -- growth & development KW - Phthalic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78395241?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Testicular+toxicity+and+reduced+Sertoli+cell+numbers+in+neonatal+rats+by+di%282-ethylhexyl%29phthalate+and+the+recovery+of+fertility+as+adults.&rft.au=Dostal%2C+L+A%3BChapin%2C+R+E%3BStefanski%2C+S+A%3BHarris%2C+M+W%3BSchwetz%2C+B+A&rft.aulast=Dostal&rft.aufirst=L&rft.date=1988-08-01&rft.volume=95&rft.issue=1&rft.spage=104&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intrauterine radiation exposures and mental retardation. AN - 78390834; 3410697 AB - Small head size and mental retardation have been known as effects of intrauterine exposure to ionizing radiation since the 1920s. In the 1950s, studies of Japanese atomic-bomb survivors revealed that at 4-17 wk of gestation, the greater the dose, the smaller the brain (and head size), and that beginning at 0.5 Gy (50 rad) in Hiroshima, mental retardation increased in frequency with increasing dose. No other excess of birth defects was observed. Otake and Schull (1984) pointed out that the period of susceptibility to mental retardation coincided with that for proliferation and migration of neuronal elements from near the cerebral ventricles to the cortex. Mental retardation could be the result of interference with this process. Their analysis indicated that exposures at 8-15 wk to 0.01-0.02 Gy (1-2 rad) doubled the frequency of severe mental retardation. This estimate was based on small numbers of mentally retarded atomic-bomb survivors. Although nuclear accidents have occurred recently, new cases will hopefully be too rare to provide further information about the risk of mental retardation. It may be possible, however, to learn about lesser impairment. New psychometric tests may be helpful in detecting subtle deficits in intelligence or neurodevelopmental function. One such test is PEERAMID, which is being used in schools to identify learning disabilities due, for example, to deficits in attention, short- or long-term memory, or in sequencing information. This and other tests could be applied in evaluating survivors of intrauterine exposure to various doses of ionizing radiation. The results could change our understanding of the safety of low-dose exposures. JF - Health physics AU - Miller, R W AD - Clinical Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 295 EP - 298 VL - 55 IS - 2 SN - 0017-9078, 0017-9078 KW - Index Medicus KW - Radiation Dosage KW - Cephalometry -- instrumentation KW - Nuclear Warfare KW - Humans KW - Brain -- radiation effects KW - Gestational Age KW - Infant, Newborn KW - Brain -- embryology KW - Japan KW - Female KW - Pregnancy KW - Intellectual Disability -- etiology KW - Fetus -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78390834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intrauterine+radiation+exposures+and+mental+retardation.&rft.au=Miller%2C+R+W&rft.aulast=Miller&rft.aufirst=R&rft.date=1988-08-01&rft.volume=55&rft.issue=2&rft.spage=295&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 - 1988-10-07 N1 - Date created - 1988-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interferon-induced transcription of a major histocompatibility class I gene accompanies binding of inducible nuclear factors to the interferon consensus sequence. AN - 78389205; 2457903 AB - Interferon (IFN) induces transcription of major histocompatibility class I genes by way of the conserved cis-acting regulatory element, termed the IFN consensus sequence (ICS). Binding of nuclear factors to the ICS was studied in gel mobility shift assays with the 5' upstream region of the murine H-2Ld gene. We found that the ICS binds a constitutive nuclear factor present in lymphocytes and fibroblasts regardless of IFN treatment. Within 1 hr after IFN treatment, new ICS binding activity was induced, which consisted of at least two binding activities distinguished by their requirement for de novo protein synthesis. Methylation interference and competition experiments showed that both constitutive and induced factors bind to the same approximately equal to 10-base-pair binding site within the ICS. Site-directed mutagenesis of H-2Ld-chloramphenicol acetyltransferase fusion genes showed that mutations in the binding site, but not in other regions of the ICS, abolish transcriptional activation of class I genes by IFN, providing evidence that specific binding of nuclear factors to the ICS is an essential requirement for transcriptional induction. Finally, we show that IFN-inducible genes of various species share a sequence motif that is capable of competing for the nuclear factors identified here. We propose that specific protein binding to the conserved motif represents a basic mechanism of IFN-mediated transcriptional induction of a number of genes. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Shirayoshi, Y AU - Burke, P A AU - Appella, E AU - Ozato, K AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 5884 EP - 5888 VL - 85 IS - 16 SN - 0027-8424, 0027-8424 KW - Interferons KW - 9008-11-1 KW - Cycloheximide KW - 98600C0908 KW - Index Medicus KW - Animals KW - Cycloheximide -- pharmacology KW - Binding, Competitive KW - Mice KW - Amino Acid Sequence KW - Methylation KW - Transcription, Genetic -- drug effects KW - Interferons -- pharmacology KW - Genes, Regulator KW - Genes, MHC Class I UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78389205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interferon-induced+transcription+of+a+major+histocompatibility+class+I+gene+accompanies+binding+of+inducible+nuclear+factors+to+the+interferon+consensus+sequence.&rft.au=Shirayoshi%2C+Y%3BBurke%2C+P+A%3BAppella%2C+E%3BOzato%2C+K&rft.aulast=Shirayoshi&rft.aufirst=Y&rft.date=1988-08-01&rft.volume=85&rft.issue=16&rft.spage=5884&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 - 1988-10-05 N1 - Date created - 1988-10-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1982 Nov 25;257(22):13169-72 [6183260] Nature. 1982 Oct 28;299(5886):833-6 [6290893] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Eur J Immunol. 1983 Jun;13(6):495-9 [6190661] Cell. 1984 Oct;38(3):745-55 [6548414] Nature. 1985 Apr 18-24;314(6012):637-9 [3990797] Cell. 1986 Jan 17;44(1):147-58 [3000619] Nucleic Acids Res. 1985 Dec 20;13(24):8765-85 [3001650] Cell. 1986 Jan 31;44(2):261-72 [3510743] Cell. 1986 Aug 1;46(3):389-99 [3755378] Nature. 1986 Aug 21-27;322(6081):743-6 [3748155] Nature. 1986 Oct 16-22;323(6089):640-3 [3095662] Cell. 1986 Dec 26;47(6):921-8 [3096580] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9537-41 [3467324] Interferon. 1986;7:47-87 [2434435] J Cell Physiol. 1987 Feb;130(2):276-83 [3102507] Proc Natl Acad Sci U S A. 1987 May;84(10):3380-4 [3106967] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] Science. 1987 Jun 5;236(4806):1237-45 [3296191] Nature. 1987 Jun 25-Jul 1;327(6124):727-30 [3600771] Nature. 1987 Jul 9-15;328(6126):175-8 [2885756] Mol Cell Biol. 1987 Jul;7(7):2625-30 [3475569] Annu Rev Biochem. 1987;56:727-77 [2441659] Proc Natl Acad Sci U S A. 1987 Sep;84(18):6394-8 [3476954] Proc Natl Acad Sci U S A. 1988 Feb;85(3):723-7 [3422454] Mol Cell Biol. 1987 Dec;7(12):4498-504 [2830497] Mol Cell Biol. 1987 Dec;7(12):4542-8 [3501825] EMBO J. 1988 Jan;7(1):85-92 [3359997] Nucleic Acids Res. 1983 Mar 11;11(5):1213-26 [6186990] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New understanding from epidemiology--the next 25 years. AN - 78386359; 3410695 AB - The epidemiology of radiation carcinogenesis is likely to be dominated during the next 25 y by the gradual maturation of major studies of populations exposed to substantial levels of radiation dose. During this period, for example, most of the new information on cancer risk among survivors of the 1945 atomic bombings of Hiroshima and Nagasaki will pertain to persons exposed at ages under 30. From the A-bomb survivor data and from a number of medically and occupationally irradiated populations now under study, it will be possible to construct a fairly complete picture of the temporal distribution of excess cancer risk over the remaining life span following exposure, a major source of uncertainty and controversy in current risk estimates. Provided that the necessary efforts are made, it should be possible to greatly increase our understanding of which organs and tissues are vulnerable to radiation carcinogenesis, variation by age at exposure and sex, and (what is most difficult at the present time) the influence of other risk factors and possible modifying factors on the magnitude of risk associated with radiation exposure. For some sites it may be possible, as it is now for breast cancer, to rule out certain broad classes of simple dose-response models. While the data gathered during the next 25 y will be nearly the last from some very important series, their information content should be extremely high. Thus, there is every reason to improve the resources, e.g., by improving dosimetry, enlarging samples, tapping new sources of case ascertainment, and gathering information on factors other than radiation dose. Modeling in epidemiological investigations depends heavily on work in experimental radiobiology. Thus far, the exchange has been largely in one direction, since epidemiological study design is mostly a matter of extracting information from "experiments" that have already taken place. With more epidemiological information, it seems reasonable to hope that detailed hypotheses, with direct relevance to areas of epidemiological uncertainty, may be generated suitable for experimental investigation. It seems likely that findings from large studies of populations exposed to relatively low levels of radiation, for which the signal-to-noise ratio is low, and for which random error and subtle sources of bias may have more than usual influence on reported results, will continue to generate controversy.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Health physics AU - Land, C E AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20205. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 269 EP - 278 VL - 55 IS - 2 SN - 0017-9078, 0017-9078 KW - Index Medicus KW - Humans KW - Ukraine KW - Leukemia, Radiation-Induced -- etiology KW - Child KW - Nuclear Reactors KW - Accidents KW - Lung Neoplasms -- etiology KW - Lung Neoplasms -- epidemiology KW - Leukemia, Radiation-Induced -- epidemiology KW - Risk Factors KW - Nuclear Warfare KW - Environmental Exposure KW - Middle Aged KW - Time Factors KW - Female KW - Male KW - Models, Theoretical KW - Neoplasms, Radiation-Induced -- etiology KW - Neoplasms, Radiation-Induced -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78386359?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=New+understanding+from+epidemiology--the+next+25+years.&rft.au=Land%2C+C+E&rft.aulast=Land&rft.aufirst=C&rft.date=1988-08-01&rft.volume=55&rft.issue=2&rft.spage=269&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 - 1988-10-07 N1 - Date created - 1988-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spontaneous establishment and characterization of mouse keratinocyte cell lines in serum-free medium. AN - 78385939; 2457574 AB - Mouse keratinocytes cultures readily develop into established cell lines without undergoing a "crisis" in a newly-developed serum-free medium, LEP/MK2. LEP/MK2 consists of calcium-free MEM with non-essential amino acids supplemented with 8 factors. Two lines, MK1 and MKDC4, have been isolated and have now doubled more than 400 and 200 times respectively. In MK1 cells, Giemsa banding has revealed significant karyotypic changes as early as the 4th passage, leading to a near-tetraploid karyotype with random loss and gain of individual chromosomes. Minute chromosomes, but no stable markers have been observed. After these initial changes, examination of cultures at several passage levels has shown that the karyotype has remained essentially stable. The MKDC4 line, also sub-tetraploid at the 7th passage, had 4 marker chromosomes by the 47th passage. The rapid increase in chromosome number may have contributed to the "immortalization" of these lines. The response of these established keratinocyte lines to growth factors and serum-derived inhibitors changed with increasing passage level. Most notable of these changes were a reduction in the requirement for bovine pituitary extract (an absolute requirement for growth of secondary MK1 cells) and a decreased sensitivity to serum and serum-derived inhibitors, e.g., transforming growth factor-beta. The established lines, like primary and secondary keratinocytes, remain responsive to calcium-induced terminal differentiation and are non-tumorigenic in athymic, nude mice. This serum-free system is suitable for transformation studies with oncogenes and chemical carcinogens. JF - In vitro cellular & developmental biology : journal of the Tissue Culture Association AU - Kaighn, M E AU - Camalier, R F AU - Bertolero, F AU - Saffiotti, U AD - Laboratory of Experimental Pathology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 845 EP - 854 VL - 24 IS - 8 SN - 0883-8364, 0883-8364 KW - Culture Media KW - 0 KW - Growth Substances KW - Peptides KW - Tissue Extracts KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Keratins KW - 68238-35-7 KW - Transforming Growth Factors KW - 76057-06-2 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Karyotyping KW - Animals KW - Pituitary Gland -- physiology KW - Growth Substances -- administration & dosage KW - Dose-Response Relationship, Drug KW - Cell Division -- drug effects KW - Tissue Extracts -- pharmacology KW - Calcium -- pharmacology KW - Mice KW - Mice, Nude KW - Peptides -- pharmacology KW - Neoplasms, Experimental -- pathology KW - Insulin-Like Growth Factor I -- pharmacology KW - Cell Line KW - Epidermis -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78385939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Spontaneous+establishment+and+characterization+of+mouse+keratinocyte+cell+lines+in+serum-free+medium.&rft.au=Kaighn%2C+M+E%3BCamalier%2C+R+F%3BBertolero%2C+F%3BSaffiotti%2C+U&rft.aulast=Kaighn&rft.aufirst=M&rft.date=1988-08-01&rft.volume=24&rft.issue=8&rft.spage=845&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 - 1988-10-07 N1 - Date created - 1988-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Experimental cardiac allograft survival across major histocompatibility complex barriers in the rhesus monkey following T lymphocyte-depleted autologous marrow transplantation. I. In vitro T lymphocyte depletion studies. AN - 78369721; 3043776 AB - We have developed a rhesus monkey model consisting of myeloablative total-body irradiation and T lymphocyte-depleted autologous bone marrow transplantation followed by MHC-mismatched heterotopic cardiac allograft implantation that has provided an opportunity to study the role of marrow T cells in cardiac allograft rejection. In order to assess quantitatively the effects of low numbers of residual marrow T cells following depletion, methods to deplete rhesus marrow extensively and to detect residual T cells following depletion at levels below the sensitivity of standard assays have been developed. A rhesus marrow limiting dilution assay has been developed that quantifies less than 1 T cell in 10(5) marrow cells and is superior to traditional detection methods by at least 3 logs. In a direct comparison of four T cell depletion methods, effective depletion has been achieved with complement-mediated cytotoxicity (C'MC), erythrocyte rosetting, and counterflow centrifugal elutriation (CCE), the latter with a simplified single-flow rate protocol. Median marrow T cell depletions of 2.1, 1.1, and 3.1 logs, and total nucleated cell losses of 40%, 61%, and 42% respectively, have been observed. A reported use of ricin A-chain-like toxins for the enhancement of C'MC was of low efficacy with rhesus peripheral blood T cell targets. CCE followed by C'MC has resulted in a median 4.8 logs depletion with residual marrow T cell contents less than 0.001%. Thus, C'MC, E-rosetting, and particularly CCE are effective methods of T cell depletion--and, when used in combination, extensively eliminate marrow T cells. A rhesus marrow limiting dilution assay detects residual T cells at these low levels. These techniques provide a basis for the quantitative study of the role of T cells in organ graft rejection following T lymphocyte-depleted autologous marrow transplantation. JF - Transplantation AU - Moses, R D AU - Orr, K S AU - MacVittie, T J AU - Gress, R E AD - Experiemental Immunology, Branches, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 197 EP - 205 VL - 46 IS - 2 SN - 0041-1337, 0041-1337 KW - Immunotoxins KW - 0 KW - Index Medicus KW - Bone Marrow Cells KW - Centrifugation KW - Animals KW - Antibody-Dependent Cell Cytotoxicity KW - Graft Survival KW - Rosette Formation KW - Macaca mulatta KW - Complement Activation KW - Cell Separation -- methods KW - Heart Transplantation KW - T-Lymphocytes -- immunology KW - Bone Marrow Transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78369721?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Experimental+cardiac+allograft+survival+across+major+histocompatibility+complex+barriers+in+the+rhesus+monkey+following+T+lymphocyte-depleted+autologous+marrow+transplantation.+I.+In+vitro+T+lymphocyte+depletion+studies.&rft.au=Moses%2C+R+D%3BOrr%2C+K+S%3BMacVittie%2C+T+J%3BGress%2C+R+E&rft.aulast=Moses&rft.aufirst=R&rft.date=1988-08-01&rft.volume=46&rft.issue=2&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=Transplantation&rft.issn=00411337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-14 N1 - Date created - 1988-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Salvage treatment with intermediate-dose methotrexate and 5-fluorouracil in metastatic breast cancer. AN - 78364508; 3407622 AB - Twenty-six patients (25 evaluable for response) with previously treated metastatic breast cancer were treated with intermediate-dose methotrexate (300 mg/m2) followed by 5-fluorouracil (600 mg/m2) and folinic acid-SF (Leucovorin) rescue (10 mg/m2 q 6 h X 6 doses) with or without tamoxifen (20 mg) and conjugated estrogen (Premarin) (.625 mg twice daily) depending on receptor status. There were two partial responses (8%) with no difference in response between patients who did or did not receive hormones. Toxicity was primarily hematological and elevation of liver function tests. The above schedule has minimal activity in previously treated metastatic breast-cancer patients. JF - American journal of clinical oncology AU - Swain, S M AU - Steinberg, S AU - Lippman, M AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 445 EP - 447 VL - 11 IS - 4 SN - 0277-3732, 0277-3732 KW - Fluorouracil KW - U3P01618RT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Fluorouracil -- administration & dosage KW - Fluorouracil -- adverse effects KW - Methotrexate -- adverse effects KW - Humans KW - Methotrexate -- administration & dosage KW - Female KW - Breast Neoplasms -- mortality KW - Breast Neoplasms -- pathology KW - Neoplasm Metastasis KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78364508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+clinical+oncology&rft.atitle=Salvage+treatment+with+intermediate-dose+methotrexate+and+5-fluorouracil+in+metastatic+breast+cancer.&rft.au=Swain%2C+S+M%3BSteinberg%2C+S%3BLippman%2C+M&rft.aulast=Swain&rft.aufirst=S&rft.date=1988-08-01&rft.volume=11&rft.issue=4&rft.spage=445&rft.isbn=&rft.btitle=&rft.title=American+journal+of+clinical+oncology&rft.issn=02773732&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-14 N1 - Date created - 1988-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ongoing protein synthesis needed for 1,25-(OH)2D3-mediated rapid increase of cyclic GMP in human skin fibroblasts. AN - 78358254; 2456949 AB - Recently we reported that 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) through interaction with its specific receptor rapidly (within 1 min) stimulated intracellular cGMP production in cultured human skin fibroblasts. Here we show that this effect of 100 nM 1,25-(OH)2D3 is prevented by brief (30 min) inhibition of RNA synthesis (with actinomycin D or alpha-amanitin) or by brief inhibition of protein synthesis (with cycloheximide or diphtheria toxin). The protein synthesis inhibitors also blocked stimulation of cGMP by other steroids (testosterone or dexamethasone at 100 nM) but did not block cGMP stimulation by sodium nitroprusside. Since the time for the 1,25-(OH)2D3 receptor to increase cGMP seems too short to require de novo protein synthesis, we conclude that the 1,25-(OH)2D3 receptor acts together with rapidly turning over protein(s) to stimulate cGMP synthesis. JF - FEBS letters AU - Barsony, J AU - Marx, S J AD - Mineral Metabolism Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 207 EP - 210 VL - 235 IS - 1-2 SN - 0014-5793, 0014-5793 KW - Amanitins KW - 0 KW - Diphtheria Toxin KW - Nitroprusside KW - 169D1260KM KW - Dactinomycin KW - 1CC1JFE158 KW - Testosterone KW - 3XMK78S47O KW - RNA KW - 63231-63-0 KW - Dexamethasone KW - 7S5I7G3JQL KW - Cycloheximide KW - 98600C0908 KW - Calcitriol KW - FXC9231JVH KW - Cyclic GMP KW - H2D2X058MU KW - Index Medicus KW - Dactinomycin -- pharmacology KW - Transcription, Genetic -- drug effects KW - Testosterone -- pharmacology KW - RNA -- antagonists & inhibitors KW - Cells, Cultured KW - Amanitins -- pharmacology KW - Humans KW - Dexamethasone -- pharmacology KW - Cycloheximide -- pharmacology KW - Diphtheria Toxin -- pharmacology KW - Nitroprusside -- pharmacology KW - RNA -- biosynthesis KW - Protein Biosynthesis KW - Fibroblasts -- drug effects KW - Cyclic GMP -- biosynthesis KW - Fibroblasts -- metabolism KW - Calcitriol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78358254?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Ongoing+protein+synthesis+needed+for+1%2C25-%28OH%292D3-mediated+rapid+increase+of+cyclic+GMP+in+human+skin+fibroblasts.&rft.au=Barsony%2C+J%3BMarx%2C+S+J&rft.aulast=Barsony&rft.aufirst=J&rft.date=1988-08-01&rft.volume=235&rft.issue=1-2&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-16 N1 - Date created - 1988-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rodent diets for carcinogenesis studies. AN - 78353214; 3404285 AB - An optimal diet for rodents in chemical carcinogenicity studies should be nutritionally adequate for growth and maintenance without excesses of high energy and growth-enhancing nutrients. Purified diets are expensive, and standardized purified diets for long-term studies are not yet established. Purified diets caused periportal lipidosis, hemorrhagic diseases and calcification of tissues in rodents. Diet restriction will result in consumption of most food during the resting phase. This will cause increased activity during the resting phase with a shift of nocturnal cycle and associated changes in physiological processes. Diet restriction may modify the carcinogenic responses to chemicals, and the practice is labor intensive. Decreasing the fat and protein content to adequate levels with a slight increase in fiber content and making the diet available only during the normal feeding period (night) may decrease the energy consumption, slow the growth and lower the body weight gain by 10-20%, with a substantial decrease in the prevalence of spontaneous tumors in the pituitary and mammary glands. We should take advantage of the biological similarities between rodents and humans to enhance the utility of rodent studies; however, mimicking the diet and feeding procedures of humans without a thorough understanding of the physiology of the altered rodent may not be useful. Contaminant concentrations of the diets should be as low as is practical. Each lot of diet should be analyzed for macronutrients and labile micronutrients with complete micronutrient analyses of randomly selected lots. JF - The Journal of nutrition AU - Rao, G N AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 929 EP - 931 VL - 118 IS - 8 SN - 0022-3166, 0022-3166 KW - Index Medicus KW - Animals KW - Nutritive Value KW - Circadian Rhythm KW - Food Contamination KW - Female KW - Neoplasms, Experimental -- etiology KW - Rodentia -- growth & development KW - Diet -- standards UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78353214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nutrition&rft.atitle=Rodent+diets+for+carcinogenesis+studies.&rft.au=Rao%2C+G+N&rft.aulast=Rao&rft.aufirst=G&rft.date=1988-08-01&rft.volume=118&rft.issue=8&rft.spage=929&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nutrition&rft.issn=00223166&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-14 N1 - Date created - 1988-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human T lymphotropic virus I infection deregulates surface expression of the transferrin receptor. AN - 78352483; 2899599 AB - Human T-lymphotropic virus I (HTLV-I) is an etiologic agent in adult T cell leukemia. In an effort to understand the relationship between HTLV-I infection and malignant transformation, we have examined transferrin receptor expression in HTLV-I-infected cells. Transferrin receptor expression in normal T cells is tightly regulated and essential for cell proliferation. We have used matched T cell sets originating from a normal donor, consisting of tetanus toxoid-specific normal T cell clones (TM3 and TM5) and their in vitro HTLV-I-infected counterparts (TM3H and TM5H). Using these matched sets of virus-infected and normal T cells, we have determined that HTLV-I infection leads to hyperexpression of surface transferrin receptors (five- to six-fold higher than normal counterparts). Although the growth rates of the virus-infected cells did not differ significantly from their normal controls, HTLV-I-infected cells constitutively hyperexpressed surface transferrin receptors, whereas the level of surface receptor expression of normal counterpart cells varied during the cycle of antigenic stimulation. Immunoprecipitation of total (surface plus cytoplasmic) transferrin expression showed that the HTLV-I-infected cells did not possess a greater total number of transferrin receptors than their normal counterparts. This data was supported by Northern blot analysis, which showed equivalent transferrin receptor mRNA expression in HTLV-I-infected and uninfected cells. Functional analysis revealed a marked defect in 59Fe-transferrin internalization in the HTLV-I-infected cells. Furthermore, the HTLV-I-infected cells showed markedly decreased transferrin receptor phosphorylation and internalization in response to active phorbol ester. Thus the data demonstrate that in peripheral blood T cells, HTLV-I infection is accompanied by surface transferrin receptor overexpression secondary to subcellular redistribution and defective internalization. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Vidal, C AU - Matsushita, S AU - Colamonici, O R AU - Trepel, J B AU - Mitsuya, H AU - Neckers, L M AD - Laboratory of Pathology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 984 EP - 988 VL - 141 IS - 3 SN - 0022-1767, 0022-1767 KW - Membrane Glycoproteins KW - 0 KW - Receptors, Transferrin KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Lymphocyte Activation -- drug effects KW - T-Lymphocytes -- metabolism KW - Phosphorylation KW - Cells, Cultured KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Membrane -- metabolism KW - T-Lymphocytes -- immunology KW - Receptors, Transferrin -- physiology KW - Deltaretrovirus Infections -- immunology KW - Deltaretrovirus -- physiology KW - Receptors, Transferrin -- drug effects KW - Deltaretrovirus Infections -- metabolism KW - Deltaretrovirus Infections -- etiology KW - Receptors, Transferrin -- metabolism KW - Membrane Glycoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78352483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+T+lymphotropic+virus+I+infection+deregulates+surface+expression+of+the+transferrin+receptor.&rft.au=Vidal%2C+C%3BMatsushita%2C+S%3BColamonici%2C+O+R%3BTrepel%2C+J+B%3BMitsuya%2C+H%3BNeckers%2C+L+M&rft.aulast=Vidal&rft.aufirst=C&rft.date=1988-08-01&rft.volume=141&rft.issue=3&rft.spage=984&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 - 1988-08-31 N1 - Date created - 1988-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of ornithine decarboxylase activity by IL-2 and cyclic AMP. AN - 78349268; 2840461 AB - IL-2 regulates the expression and activation of the principal rate-limiting enzyme of polyamine synthesis, ornithine decarboxylase (ODC). The apparent activation of ODC occurs by two independent steps. Rapid activation of enzyme occurs within the first 10 min of lymphokine treatment of cloned IL-2-dependent murine cell lines. The initial rapid rise in enzyme activity is insensitive to protein or mRNA synthesis inhibitors. The early rise in ODC activity is followed by a protracted increase in enzyme activity, apparent protein measured by [3H]difluoromethylornithine binding, and by accumulation of steady state ODC mRNA. Stable analogues of cAMP which inhibit IL-2-stimulated proliferation, suppressed only the mRNA-dependent increase in ODC activity. Phorbol esters were shown to increase steady state levels of ODC mRNA whereas cAMP analogue clearly inhibited the growth factor-induced increase in ODC mRNA. These studies show that IL-2 regulates the expression of ODC at multiple levels, including transcription and accumulation of steady state mRNA, and post-translational activation of an enzyme important for DNA synthesis. Furthermore, anti-proliferative signals such as cAMP may effect the regulation of ODC enzyme production at the level of mRNA accumulation and stability. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Farrar, W L AU - Vinocour, M AU - Cleveland, J L AU - Harel-Bellan, A AD - Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick, MD 21701-1013. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 967 EP - 971 VL - 141 IS - 3 SN - 0022-1767, 0022-1767 KW - Interleukin-2 KW - 0 KW - RNA, Messenger KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Cyclic AMP KW - E0399OZS9N KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Lymphocyte Activation -- drug effects KW - Animals KW - Transcription, Genetic -- drug effects KW - RNA, Messenger -- metabolism KW - Humans KW - Enzyme Activation -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Cell Line KW - Ornithine Decarboxylase -- metabolism KW - Interleukin-2 -- pharmacology KW - Cyclic AMP -- pharmacology KW - T-Lymphocytes, Cytotoxic -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78349268?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+ornithine+decarboxylase+activity+by+IL-2+and+cyclic+AMP.&rft.au=Farrar%2C+W+L%3BVinocour%2C+M%3BCleveland%2C+J+L%3BHarel-Bellan%2C+A&rft.aulast=Farrar&rft.aufirst=W&rft.date=1988-08-01&rft.volume=141&rft.issue=3&rft.spage=967&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 - 1988-08-31 N1 - Date created - 1988-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Esophageal candidiasis. Managing an increasingly prevalent infection. AN - 78346700; 3041396 AB - Esophageal candidiasis is an opportunistic infection that is being recognized increasingly often in certain patients, including those who have a neoplastic disease, are undergoing protracted antibiotic therapy, or hae acquired immunodeficiency syndrome (AIDS). Impaired cell-mediated immunity may predispose the patient to esophageal mucosal colonization, whereas chemotherapy-induced granulocytopenia may predispose to disseminated candidiasis. Esophageal candidiasis should be suspected in susceptible patients with complaints of substernal odynophagia or dysphagia. The diagnosis is confirmed by endoscopically directed mucosal biopsy. Esophagitis from other causes (eg. herpes simplex virus, cytomegalovirus, or bacterial infection) may develop concomitantly with esophageal candidiasis. Treatment is determined by the clinical and immune status of the patient. Amphotericin B (Fungizone) is administered to immunocompromised patients at risk for disseminated or deeply invasive candidiasis and is indicated in nongranulocytopenic patients whose symptoms prevent reliable administration of oral antifungal agents. Ketoconazole (Nizoral) may be administered to clinically stable nongranulocytopenic patients with esophageal candidiasis limited to the mucosa. Patients with AIDS and a history of esophageal candidiasis usually benefit from long-term suppression with an oral antifungal agent. JF - Postgraduate medicine AU - Walsh, T J AU - Hamilton, S R AU - Belitsos, N AD - Infectious Diseases Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 193 EP - 6, 201-5 VL - 84 IS - 2 SN - 0032-5481, 0032-5481 KW - Antifungal Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Candidiasis, Chronic Mucocutaneous -- complications KW - Acquired Immunodeficiency Syndrome -- complications KW - Drug Interactions KW - Agranulocytosis -- complications KW - Neoplasms -- complications KW - Diagnosis, Differential KW - Risk Factors KW - Humans KW - Adult KW - Esophagoscopy KW - Antifungal Agents -- therapeutic use KW - Esophageal Diseases -- diagnosis KW - Candidiasis -- diagnosis KW - Esophageal Diseases -- therapy KW - Candidiasis -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78346700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Postgraduate+medicine&rft.atitle=Esophageal+candidiasis.+Managing+an+increasingly+prevalent+infection.&rft.au=Walsh%2C+T+J%3BHamilton%2C+S+R%3BBelitsos%2C+N&rft.aulast=Walsh&rft.aufirst=T&rft.date=1988-08-01&rft.volume=84&rft.issue=2&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Postgraduate+medicine&rft.issn=00325481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-02 N1 - Date created - 1988-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulation of DNA synthesis in cultured primary human mesothelial cells by specific growth factors. AN - 78338884; 3260881 AB - Monolayer cultures of human mesothelial cells made quiescent by serum deprivation are induced to undergo one round of DNA synthesis by platelet-derived growth factor (PDGF), epidermal growth factor (EGF), or transforming growth factor type beta 1 (TGF-beta 1). This one-time stimulation is independent of other serum components. The kinetics for induction of DNA synthesis observed for PDGF, EGF, and TGF-beta 1 are all similar to one another, with a peak of DNA synthesis occurring 24-36 h after the addition of the growth factors. Repetitive rounds of DNA synthesis and cell division do not ensue after addition of PDGF, EGF, or TGF-beta 1 alone or in combination; however, in media supplemented with chemically denatured serum, each of these factors is capable of sustaining continuous replication of mesothelial cells. Stimulation of growth by PDGF and TGF-beta 1 is unusual for an epithelial cell type, and indicates that mesothelial cells have growth regulatory properties similar to connective tissue cells. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Gabrielson, E W AU - Gerwin, B I AU - Harris, C C AU - Roberts, A B AU - Sporn, M B AU - Lechner, J F AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 2717 EP - 2721 VL - 2 IS - 11 SN - 0892-6638, 0892-6638 KW - Growth Substances KW - 0 KW - Peptides KW - Platelet-Derived Growth Factor KW - Tritium KW - 10028-17-8 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Transforming Growth Factors KW - 76057-06-2 KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Thymidine -- metabolism KW - Cells, Cultured KW - Kinetics KW - Humans KW - Platelet-Derived Growth Factor -- pharmacology KW - Epithelium -- metabolism KW - Epidermal Growth Factor -- pharmacology KW - Peptides -- pharmacology KW - Epithelium -- drug effects KW - Growth Substances -- pharmacology KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78338884?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Stimulation+of+DNA+synthesis+in+cultured+primary+human+mesothelial+cells+by+specific+growth+factors.&rft.au=Gabrielson%2C+E+W%3BGerwin%2C+B+I%3BHarris%2C+C+C%3BRoberts%2C+A+B%3BSporn%2C+M+B%3BLechner%2C+J+F&rft.aulast=Gabrielson&rft.aufirst=E&rft.date=1988-08-01&rft.volume=2&rft.issue=11&rft.spage=2717&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 - 1988-08-30 N1 - Date created - 1988-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of transfected DNA by primary murine keratinocytes. AN - 78338285; 2456357 AB - Primary murine keratinocytes can be maintained in culture for extended periods in a proliferative, basal cell state under conditions of reduced extracellular Ca2+. In response to increased Ca2+ concentrations, the cells undergo a well-defined program of terminal differentiation, thus serving as a convenient model in which to study the genes involved in regulating this and possibly other differentiation cascades by DNA-mediated gene transfer. However, because of their sensitivity to increased Ca2+ concentrations, the introduction of exogenous genomic DNA into primary keratinocytes by conventional methods is problematic. We have optimized the calcium phosphate DNA transfection procedure by introducing conditions that reduce the potency of Ca2+ as a differentiation signal. Primary epidermal cells were transfected with pSV2CAT, a plasmid that codes for the enzyme chloramphenicol acetyltransferase CAT. Enzyme activity was measured in cell extracts under varying transfection conditions. When the K+ concentration of the medium used for transfection by calcium phosphate precipitation is reduced from 6.5 to 0.01 mM, CAT activity following transfection increases 2-3 times. Exposure to the DNA precipitate for 2-4 h is optimal. By the use of fibroblast conditioned medium following transfection, enzyme activity can be detected in cell extracts for at least 21 d, suggesting that the exogenous gene is integrated. The low K+/Ca2+ transfection method is more effective than SrCl2 used as an alternative for CaCl2 in Ca2+ sensitive cells. Low K+ medium enhances cell survival for Ca2+ mediated transfection but also appears to have a beneficial effect on DNA uptake or expression. JF - The Journal of investigative dermatology AU - Harper, J R AU - Greenhalgh, D A AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 150 EP - 153 VL - 91 IS - 2 SN - 0022-202X, 0022-202X KW - Keratins KW - 68238-35-7 KW - DNA KW - 9007-49-2 KW - Acetyltransferases KW - EC 2.3.1.- KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Acetyltransferases -- biosynthesis KW - Potassium -- pharmacology KW - Mice KW - Calcium -- pharmacology KW - Acetyltransferases -- genetics KW - Mice, Inbred BALB C KW - Time Factors KW - Fibroblasts -- physiology KW - Transfection KW - Epidermis -- metabolism KW - DNA -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78338285?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Expression+of+transfected+DNA+by+primary+murine+keratinocytes.&rft.au=Harper%2C+J+R%3BGreenhalgh%2C+D+A%3BYuspa%2C+S+H&rft.aulast=Harper&rft.aufirst=J&rft.date=1988-08-01&rft.volume=91&rft.issue=2&rft.spage=150&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 - 1988-08-26 N1 - Date created - 1988-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiologic evidence for early onset of mental disorders and higher risk of drug abuse in young adults. AN - 78336578; 3394882 AB - Data from the National Institute of Mental Health (NIMH) Epidemiologic Catchment Area Program, an epidemiologic survey of five communities, showed that four major disorders commonly begin in late adolescence or young adulthood. The median age at onset for anxiety disorders is 15 years; for major depressive episode, 24 years; for drug abuse or dependence, 19 years; and for alcohol abuse or dependence, 21 years. Findings also suggest that for respondents 18-30 years old, having a major depressive episode or anxiety disorder doubles the risk for later drug abuse or dependence. JF - The American journal of psychiatry AU - Christie, K A AU - Burke, J D AU - Regier, D A AU - Rae, D S AU - Boyd, J H AU - Locke, B Z AD - Division of Clinical Research, National Institute of Mental Health, Rockville, MD 20857. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 971 EP - 975 VL - 145 IS - 8 SN - 0002-953X, 0002-953X KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Age Factors KW - Risk Factors KW - Humans KW - Adult KW - Adolescent KW - Depressive Disorder -- epidemiology KW - Substance-Related Disorders -- complications KW - Anxiety Disorders -- epidemiology KW - Depressive Disorder -- complications KW - Substance-Related Disorders -- epidemiology KW - Anxiety Disorders -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78336578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epidemiologic+evidence+for+early+onset+of+mental+disorders+and+higher+risk+of+drug+abuse+in+young+adults.&rft.au=Christie%2C+K+A%3BBurke%2C+J+D%3BRegier%2C+D+A%3BRae%2C+D+S%3BBoyd%2C+J+H%3BLocke%2C+B+Z&rft.aulast=Christie&rft.aufirst=K&rft.date=1988-08-01&rft.volume=145&rft.issue=8&rft.spage=971&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 - 1988-08-25 N1 - Date created - 1988-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - EGF receptor expression in the developing tooth is altered by exogenous retinoic acid and EGF. AN - 78333934; 3260878 AB - Retinoic acid (RA) is a teratogen producing a variety of malformations including clefts of the secondary palate and malformations of the teeth. Recent studies in our laboratory investigating the effects of RA and EGF on the medial epithelium of the palatal shelf have also provided some information on the effects of these agents on the development of the tooth. In the control, toothbud epithelial cells expressed the EGF receptor, bound EGF, and proliferated. The majority of bud stage teeth exposed to RA either in vivo or in organ culture did not detectably bind EGF, express the EGF receptor, or proliferate in the epithelial or mesenchymal components. Toothbuds exposed to exogenous EGF in organ culture also did not bind EGF, the receptor, or proliferate. EGF has been reported to inhibit morphogenesis of toothbuds in culture and when EGF was given to neonates the size of the tooth was reduced. Regulation of EGF receptor expression appears to be important in the development of the toothbud and exposure to RA or EGF disrupts this process and could contribute to the decreased tooth size, agenesis, and malformations observed in the teeth. While limited in scope, these experiments present previously unreported effects of RA and EGF on the toothbud epithelium. These observations should be of interest to those studying tooth development, and warrant further and more detailed studies. JF - Developmental biology AU - Abbott, B D AU - Pratt, R M AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 300 EP - 304 VL - 128 IS - 2 SN - 0012-1606, 0012-1606 KW - Tretinoin KW - 5688UTC01R KW - Epidermal Growth Factor KW - 62229-50-9 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Mice KW - Female KW - Pregnancy KW - Tretinoin -- pharmacology KW - Odontogenesis -- drug effects KW - Epidermal Growth Factor -- pharmacology KW - Receptor, Epidermal Growth Factor -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78333934?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology&rft.atitle=EGF+receptor+expression+in+the+developing+tooth+is+altered+by+exogenous+retinoic+acid+and+EGF.&rft.au=Abbott%2C+B+D%3BPratt%2C+R+M&rft.aulast=Abbott&rft.aufirst=B&rft.date=1988-08-01&rft.volume=128&rft.issue=2&rft.spage=300&rft.isbn=&rft.btitle=&rft.title=Developmental+biology&rft.issn=00121606&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-02 N1 - Date created - 1988-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - High correlations of norepinephrine, dopamine, and epinephrine and their major metabolite excretion rates. AN - 78329767; 3395200 AB - We have previously reported high correlations between norepinephrine and its metabolite outputs in depressed patients. In this article, we expand this finding to healthy volunteers and alcoholic patients. Furthermore, we find similar high correlations between urinary outputs of dopamine, norepinephrine, and their major metabolites. The same is true, to a lesser degree, for epinephrine and metanephrine outputs. There are implications of these findings for psychobiological research on the monoamine systems. JF - Archives of general psychiatry AU - Linnoila, M AU - Oliver, J AU - Adinoff, B AU - Potter, W Z AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 701 EP - 704 VL - 45 IS - 8 SN - 0003-990X, 0003-990X KW - Metanephrine KW - 5001-33-2 KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Vanilmandelic Acid KW - 55-10-7 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Homovanillic Acid KW - X77S6GMS36 KW - Epinephrine KW - YKH834O4BH KW - Abridged Index Medicus KW - Index Medicus KW - Methoxyhydroxyphenylglycol -- urine KW - Metanephrine -- urine KW - Circadian Rhythm KW - Humans KW - Adult KW - Depressive Disorder -- urine KW - Alcoholism -- urine KW - Middle Aged KW - Vanilmandelic Acid -- urine KW - Homovanillic Acid -- urine KW - Male KW - Female KW - Norepinephrine -- urine KW - Norepinephrine -- metabolism KW - Dopamine -- metabolism KW - Epinephrine -- urine KW - Dopamine -- urine KW - Epinephrine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78329767?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=High+correlations+of+norepinephrine%2C+dopamine%2C+and+epinephrine+and+their+major+metabolite+excretion+rates.&rft.au=Linnoila%2C+M%3BOliver%2C+J%3BAdinoff%2C+B%3BPotter%2C+W+Z&rft.aulast=Linnoila&rft.aufirst=M&rft.date=1988-08-01&rft.volume=45&rft.issue=8&rft.spage=701&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 - 1988-08-22 N1 - Date created - 1988-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Guanine nucleotide-binding proteins that enhance choleragen ADP-ribosyltransferase activity: nucleotide and deduced amino acid sequence of an ADP-ribosylation factor cDNA. AN - 78326953; 3135549 AB - Three (two soluble and one membrane) guanine nucleotide-binding proteins (G proteins) that enhance ADP-ribosylation of the Gs alpha stimulatory subunit of the adenylyl cyclase (EC 4.6.1.1) complex by choleragen have recently been purified from bovine brain. To further define the structure and function of these ADP-ribosylation factors (ARFs), we isolated a cDNA clone (lambda ARF2B) from a bovine retinal library by screening with a mixed heptadecanucleotide probe whose sequence was based on the partial amino acid sequence of one of the soluble ARFs from bovine brain. Comparison of the deduced amino acid sequence of lambda ARF2B with sequences of peptides from the ARF protein (total of 60 amino acids) revealed only two differences. Whether these are cloning artifacts or reflect the existence of more than one ARF protein remains to be determined. Deduced amino acid sequences of ARF, Go alpha (the alpha subunit of a G protein that may be involved in regulation of ion fluxes), and c-Ha-ras gene product p21 show similarities in regions believed to be involved in guanine nucleotide binding and GTP hydrolysis. ARF apparently lacks a site analogous to that ADP-ribosylated by choleragen in G-protein alpha subunits. Although both the ARF proteins and the alpha subunits bind guanine nucleotides and serve as choleragen substrates, they must interact with the toxin A1 peptide in different ways. In addition to serving as an ADP-ribose acceptor, ARF interacts with the toxin in a manner that modifies its catalytic properties. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Price, S R AU - Nightingale, M AU - Tsai, S C AU - Williamson, K C AU - Adamik, R AU - Chen, H C AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 5488 EP - 5491 VL - 85 IS - 15 SN - 0027-8424, 0027-8424 KW - Membrane Proteins KW - 0 KW - DNA KW - 9007-49-2 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 - Animals KW - Base Sequence KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Cloning, Molecular KW - Cholera Toxin -- metabolism KW - GTP-Binding Proteins -- metabolism KW - DNA -- genetics KW - Membrane Proteins -- genetics KW - Poly(ADP-ribose) Polymerases -- metabolism KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78326953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Guanine+nucleotide-binding+proteins+that+enhance+choleragen+ADP-ribosyltransferase+activity%3A+nucleotide+and+deduced+amino+acid+sequence+of+an+ADP-ribosylation+factor+cDNA.&rft.au=Price%2C+S+R%3BNightingale%2C+M%3BTsai%2C+S+C%3BWilliamson%2C+K+C%3BAdamik%2C+R%3BChen%2C+H+C%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Price&rft.aufirst=S&rft.date=1988-08-01&rft.volume=85&rft.issue=15&rft.spage=5488&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 - 1988-09-07 N1 - Date created - 1988-09-07 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J03794; GENBANK N1 - SuppNotes - Cited By: J Mol Biol. 1970 Mar;48(3):443-53 [5420325] Protein Eng. 1986 Oct-Nov;1(1):47-54 [3148932] J Cyclic Nucleotide Res. 1978 Jun;4(3):159-68 [214459] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] J Biol Chem. 1980 Feb 25;255(4):1252-8 [6766444] Biochemistry. 1980 Oct 14;19(21):4871-4 [7426631] Biochim Biophys Acta. 1981 Feb 5;672(3):248-61 [7213814] J Biol Chem. 1981 Aug 10;256(15):7990-7 [7263636] J Biol Chem. 1982 Jan 10;257(1):20-3 [6273425] Biochim Biophys Acta. 1982 Feb 2;714(2):337-43 [7055618] Nature. 1983 Mar 3;302(5903):33-7 [6298635] J Biol Chem. 1983 Oct 10;258(19):11908-14 [6311828] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] J Biol Chem. 1984 Jan 25;259(2):696-8 [6582062] J Biol Chem. 1984 May 25;259(10):6228-34 [6327671] J Biol Chem. 1984 May 25;259(10):6235-40 [6327672] Nature. 1984 Aug 16-22;310(5978):583-6 [6087162] EMBO J. 1984 Nov;3(11):2581-5 [6096132] J Mol Evol. 1984-1985;21(2):112-25 [6100188] Science. 1985 Oct 4;230(4721):32-6 [3898365] Science. 1985 Oct 4;230(4721):78-82 [3898366] Cell. 1986 Jan 31;44(2):283-92 [3943125] Annu Rev Neurosci. 1986;9:87-119 [2423011] J Biol Chem. 1986 Jun 15;261(17):7906-11 [3086320] J Biol Chem. 1987 Jan 25;262(3):1030-6 [3100524] Nature. 1987 Jan 29-Feb 4;325(6103):445-7 [2433590] Annu Rev Cell Biol. 1986;2:391-419 [3103658] Proc Natl Acad Sci U S A. 1987 May;84(10):3107-11 [3106961] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5139-42 [3110784] Annu Rev Biochem. 1987;56:615-49 [3113327] Biochem Biophys Res Commun. 1987 Aug 14;146(3):1234-9 [3113429] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7493-7 [3118369] FEBS Lett. 1987 Nov 30;224(2):365-71 [2826231] Nature. 1987 Dec 24-31;330(6150):758-60 [2827032] J Biol Chem. 1988 Feb 5;263(4):1768-72 [3123477] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1015-9 [3277185] Adv Enzymol Relat Areas Mol Biol. 1988;61:303-79 [3128060] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3307-11 [198781] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The gene encoding the nonstructural protein of B19 (human) parvovirus may be lethal in transfected cells. AN - 78316289; 2969055 AB - The B19 parvovirus is a cause of bone marrow failure in humans. B19 is toxic to erythroid progenitor cells in vitro. Viral products possibly responsible for toxicity were explored by transfection of cloned B19 genome into HeLa cells. The nonstructural (NS) protein was detected in cells 30 h after transfection. Plasmids containing the B19 genome were transfected with selectable marker genes in stable transformation assays. Plasmids that contained the left side of the B19 genome, which encodes the NS protein of the virus, inhibited antibiotic-resistant colony formation. Transformation occurred when NS protein expression was blocked by mutation. Suppression of transformation by NS protein was not tissue specific, suggesting a role for NS protein in toxicity for nonpermissive cells without parvovirus replication or virion accumulation. JF - Journal of virology AU - Ozawa, K AU - Ayub, J AU - Kajigaya, S AU - Shimada, T AU - Young, N AD - Cell Biology Section, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 2884 EP - 2889 VL - 62 IS - 8 SN - 0022-538X, 0022-538X KW - Viral Core Proteins KW - 0 KW - Viral Nonstructural Proteins KW - Index Medicus KW - Promoter Regions, Genetic KW - Transfection KW - Transformation, Genetic KW - Transcription, Genetic KW - Gene Expression Regulation KW - Molecular Weight KW - Parvoviridae -- genetics KW - Capsid -- genetics KW - Parvoviridae -- pathogenicity KW - Viral Core Proteins -- genetics KW - Genes, Viral KW - Genes, Lethal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78316289?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=The+gene+encoding+the+nonstructural+protein+of+B19+%28human%29+parvovirus+may+be+lethal+in+transfected+cells.&rft.au=Ozawa%2C+K%3BAyub%2C+J%3BKajigaya%2C+S%3BShimada%2C+T%3BYoung%2C+N&rft.aulast=Ozawa&rft.aufirst=K&rft.date=1988-08-01&rft.volume=62&rft.issue=8&rft.spage=2884&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 - 1988-08-19 N1 - Date created - 1988-08-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Blood. 1986 May;67(5):1411-7 [3008891] J Virol. 1985 Sep;55(3):886-9 [4020972] Science. 1986 Aug 22;233(4766):883-6 [3738514] J Virol. 1986 Oct;60(1):251-8 [3018288] Mol Cell Biol. 1986 Aug;6(8):2884-94 [3491293] J Virol. 1987 May;61(5):1448-56 [3033274] J Virol. 1987 Aug;61(8):2395-406 [3599180] J Virol. 1987 Aug;61(8):2627-30 [3599184] Mol Cell Biol. 1987 Apr;7(4):1320-5 [3037312] N Engl J Med. 1987 Jul 30;317(5):287-94 [3037373] Blood. 1987 Aug;70(2):384-91 [3038211] Annu Rev Biochem. 1987;56:317-32 [3113326] Mol Cell Biol. 1987 Aug;7(8):2830-7 [3670295] Lancet. 1981 Mar 21;1(8221):664-5 [6110886] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] J Clin Invest. 1984 Jan;73(1):224-30 [6317715] J Clin Invest. 1984 Dec;74(6):2024-32 [6392340] Mol Cell Biol. 1984 Dec;4(12):2929-31 [6098829] J Virol. 1986 Jun;58(3):921-36 [3701931] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of bradykinin-induced phosphoinositide turnover in neurohybrid NCB-20 cells. AN - 78313875; 2839620 AB - Phosphoinositide hydrolysis was studied in neurohybrid NCB-20 cells prelabeled with myo-[3H]inositol. Among nearly 20 neurotransmitters and neuromodulators examined, only bradykinin, carbachol, and histamine significantly increased the accumulation of [3H]inositol monophosphate (IP1) in the presence of lithium. The EC50 of bradykinin was 20 nM and the saturating concentration was approximately 1 microM. The bradykinin response was robust (10-fold) and was potently and selectively blocked by a bradykinin antagonist, B 4881 [D-Arg-(Hyp3, Thi, D-Phe)-bradykinin], with a Ki of 10 nM. This effect of bradykinin appeared to be additive to that mediated by activation of muscarinic cholinergic and histamine H1 receptors. The accumulation induced by bradykinin or carbachol was dependent on the presence of calcium in the incubation medium; less than twofold stimulation was observed in the absence of exogenous calcium. Bradykinin-induced [3H]IP1 accumulation required high concentration of lithium to elicit its maximal stimulation; the concentration of lithium required for half maximal effect was about 13 mM, similar to the value reported previously for carbachol-induced accumulation in the same cell line. In contrast, using related neurohybrid NG108-15 cells, bradykinin-induced [3H]IP1 accumulation was found to require much less lithium. IN the presence of lithium, bradykinin also evoked a transient increase in the production of [3H]-inositol bis- and trisphosphate. Basal and bradykinin-induced phosphoinositide breakdown was inhibited by 4 beta-phorbol 12,13-dibutyrate, but was unaffected by the biologically inactive 4 beta-phorbol. Pretreatment of cells with pertussis toxin induced only about 30% loss of the bradykinin-induced [3H]IP1 accumulation, without affecting basal activity.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of neurochemistry AU - Chuang, D M AU - Dillon-Carter, O AD - Laboratory of Preclinical Pharmacology, National Institute of Mental Health, St. Elizabeths Hospital, Washington, DC 20032. Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 505 EP - 513 VL - 51 IS - 2 SN - 0022-3042, 0022-3042 KW - Phorbol Esters KW - 0 KW - Phorbols KW - Phosphatidylinositols KW - Triprolidine KW - 2L8T9S52QM KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Diphenhydramine KW - 8GTS82S83M KW - Lithium KW - 9FN79X2M3F KW - Type C Phospholipases KW - EC 3.1.4.- KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Bradykinin KW - S8TIM42R2W KW - phorbol KW - XUZ76S9127 KW - Index Medicus KW - Phorbol Esters -- pharmacology KW - Animals KW - Phorbols -- pharmacology KW - Kinetics KW - GTP-Binding Proteins -- metabolism KW - Diphenhydramine -- pharmacology KW - Cell Line KW - Type C Phospholipases -- metabolism KW - Triprolidine -- pharmacology KW - Lithium -- pharmacology KW - Phosphatidylinositols -- metabolism KW - Bradykinin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78313875?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+bradykinin-induced+phosphoinositide+turnover+in+neurohybrid+NCB-20+cells.&rft.au=Chuang%2C+D+M%3BDillon-Carter%2C+O&rft.aulast=Chuang&rft.aufirst=D&rft.date=1988-08-01&rft.volume=51&rft.issue=2&rft.spage=505&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 - 1988-08-24 N1 - Date created - 1988-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preclinical pharmacology of arabinosyl-5-azacytidine in nonhuman primates. AN - 78309519; 2455594 AB - The plasma and cerebrospinal fluid (CSF) pharmacokinetics of arabinosyl-5-azacytidine (AAC) were studied in rhesus monkeys following a 15-min, 1-h, or 12-h i.v. infusion of 200 mg/kg. No clinically significant toxicity was observed with these schedules. The plasma elimination of AAC is rapid and characterized by a triphasic decay with t1/2 alpha = 3.6-5.4 min, t1/2 beta = 18-24 min, and t1/2 gamma = 94-144 min for the above infusion schedules. The CSF penetration of AAC as measured by the CSF:plasma Css ratio for the 12-h infusion was 0.15. The stability of AAC in pooled plasma, phosphate buffered saline, and RPMI 1640 culture media at 37 degrees C was compared with the terminal half-life of AAC observed in vivo. The shorter in vitro AAC half-life in plasma with or without tetrahydrouridine versus that in phosphate buffered saline suggests that the terminal half-life of AAC in vivo is most likely a result of enhanced nucleophilic attack and hydrolytic degradation of the unstable triazine ring in plasma. A triexponential equation modeling the disappearance of AAC was constructed from the in vivo experimental data. Use of this equation in computer-aided simulations of current Phase I doses and schedules of AAC correctly predicts the human plasma concentrations which have been observed. The preclinical pharmacokinetic data provided here may be useful in helping to develop rational human studies with specific concentration x time goals. JF - Cancer research AU - Heideman, R L AU - Balis, F M AU - McCully, C AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 4294 EP - 4298 VL - 48 IS - 15 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - fazarabine KW - 5V71D8JOKK KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Animals KW - Half-Life KW - Macaca mulatta KW - Drug Evaluation, Preclinical KW - Male KW - Mathematics KW - Azacitidine -- pharmacokinetics KW - Antineoplastic Agents -- cerebrospinal fluid KW - Azacitidine -- cerebrospinal fluid KW - Azacitidine -- toxicity KW - Antineoplastic Agents -- pharmacokinetics KW - Antineoplastic Agents -- toxicity KW - Antineoplastic Agents -- blood KW - Azacitidine -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78309519?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preclinical+pharmacology+of+arabinosyl-5-azacytidine+in+nonhuman+primates.&rft.au=Heideman%2C+R+L%3BBalis%2C+F+M%3BMcCully%2C+C%3BPoplack%2C+D+G&rft.aulast=Heideman&rft.aufirst=R&rft.date=1988-08-01&rft.volume=48&rft.issue=15&rft.spage=4294&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 - 1988-08-24 N1 - Date created - 1988-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Factors regulating activation and DNA alkylation by 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone and nitrosodimethylamine in rat lung and isolated lung cells, and the relationship to carcinogenicity. AN - 78307666; 3390815 AB - The molecular dosimetry for O6-methylguanine (O6MG) formation in DNA from rat lung and pulmonary cells was compared following treatment for 4 days with equimolar doses of 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a potent pulmonary carcinogen or nitrosodimethylamine (NDMA), a weak carcinogen in rat lung. The dose response for O6MG formation from NNK was biphasic; the O6MG to dose ratio, an index of alkylation efficiency, increased dramatically as the dose of carcinogen was decreased. In contrast, the dose-response curve for methylation by NDMA appeared opposite of that for NNK with alkylation efficiency increasing as a function of dose. These results suggested that high and low Km pathways exist for the activation of NNK, whereas only high Km pathways may be involved in NDMA activation. Furthermore, DNA methylation by NNK was cell selective with the highest levels in the Clara cell, whereas methylation by NDMA was not. DNA methylation in the Clara cell was 50-fold greater by NNK than by NDMA at equimolar doses (0.005 mmol/kg). Thus, differences in O6MG formation, specifically the presence of a high affinity pathway in the Clara cell for activation of NNK, may explain why following low dose exposure, NNK is a potent pulmonary carcinogen while NDMA is not. Different cytochrome P-450 isozymes also appear to be involved in the activation of NNK and NDMA. Inhibition of in vitro methylation (with calf thymus DNA and lung microsomes) by antibodies to cytochrome P-450 isozymes provided evidence that a homolog of rabbit cytochrome P-450(2) (cytochrome P-450b) may be important in the activation of NNK in rat lung, whereas cytochrome P-450(5) may activate NDMA. A 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible cytochrome P-450 isozyme (P-450c) may also be involved in the activation of NNK but not NDMA. Treatment with TCDD increased both NNK activation by pulmonary microsomes and the formation of O6MG in Clara cells and type II cells incubated in vitro with NNK. alpha-Naphthoflavone (alpha-NF), a specific inhibitor of cytochrome P-450c reversed the increase in methylation by TCDD-induced microsomes but did not inhibit in vitro activation of NNK using microsomes from untreated rats. However, NNK mediated O6MG formation in Clara cells, but not in type II cells incubated with alpha-NF, was decreased by 21%. These data indicate that both cytochrome P-450b and P-450c are probably involved in the activation of NNK in Clara cells from untreated rats.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Devereux, T R AU - Anderson, M W AU - Belinsky, S A AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 4215 EP - 4221 VL - 48 IS - 15 SN - 0008-5472, 0008-5472 KW - Antibodies KW - 0 KW - Benzoflavones KW - Carcinogens KW - Isoenzymes KW - Nitrosamines KW - Guanine KW - 5Z93L87A1R KW - alpha-naphthoflavone KW - 604-59-1 KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - O-(6)-methylguanine KW - 9B710FV2AE KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Isoenzymes -- immunology KW - Cytochrome P-450 Enzyme System -- immunology KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Guanine -- analogs & derivatives KW - Methylation KW - Isoenzymes -- metabolism KW - Guanine -- metabolism KW - Benzoflavones -- pharmacology KW - Alkylation KW - Dimethylnitrosamine -- pharmacology KW - Nitrosamines -- pharmacology KW - Carcinogens -- pharmacology KW - DNA -- metabolism KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78307666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Factors+regulating+activation+and+DNA+alkylation+by+4-%28N-methyl-N-nitrosamino%29-1-%283-pyridyl%29-1-butanone+and+nitrosodimethylamine+in+rat+lung+and+isolated+lung+cells%2C+and+the+relationship+to+carcinogenicity.&rft.au=Devereux%2C+T+R%3BAnderson%2C+M+W%3BBelinsky%2C+S+A&rft.aulast=Devereux&rft.aufirst=T&rft.date=1988-08-01&rft.volume=48&rft.issue=15&rft.spage=4215&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 - 1988-08-24 N1 - Date created - 1988-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Laboratory correlates of adoptive immunotherapy with recombinant interleukin-2 and lymphokine-activated killer cells in humans. AN - 78304512; 3260537 AB - Adoptive immunotherapy with interleukin 2 (IL-2) and lymphokine-activated killer (LAK) cells (IL-2/LAK) is a technically demanding cancer therapy dependent upon large scale isolation and culture of lymphocytes. An important question is whether this technology can be accomplished routinely outside of highly specialized centers. In addition, no systematic examination of laboratory correlates of IL-2/LAK therapy in humans has been reported to date. The objectives of this report are to address two issues relevant to IL-2/LAK therapy. (a) Can IL-2/LAK therapy be accomplished outside of previously identified centers of expertise? (b) What are the relevant laboratory/clinical parameter correlations? The six institutions in the National Cancer Institute extramural trial treated 83 evaluable patients with renal cancer, malignant melanoma, or colon cancer with IL-2/LAK by a uniform protocol. Patients received 5 days of IL-2 priming, then daily leukaphereses for 5 days starting 48 h after IL-2 to harvest cells. Mononuclear cells were isolated, then cultured in roller bottles in 1-liter aliquots for 3 to 4 days at a cell density of 1.5 x 10(6) per ml with recombinant IL-2, 1500 units per ml. Cells were harvested and administered to patients with additional IL-2. Administration of IL-2 regularly induced lymphopenia and rebound lymphocytosis. Leukapheresis yields and numbers of LAK cells generated in culture and reinfused into patients correlated directly with peak lymphocyte counts achieved by IL-2 administration. Mean mononuclear cell recovery per 5 days of leukapheresis (+/- SEM) was 14.3 +/- 0.8 x 10(10). Average volume of cells cultured per patient was 95 liters (range, 41 to 235). Mean yield of cells harvested from cultures was 53%. Mean total number of LAK cells infused per patient was 7.6 +/- 0.4 x 10(10) (range, 2 to 15.2 x 10(10]. LAK activity was measured in vitro by lysis of 51Cr-labeled natural killer-resistant Daudi and fresh tumor targets. LAK effector cells regularly lysed these targets in vitro. Neither tumor reduction nor clinical toxicity correlated with dose or with cytolytic activity of LAK cells, or with other laboratory parameters including base-line lymphocyte count and IL-2-induced lymphocytosis. We conclude: (a) large quantities of LAK effector cells with tumoricidal activity can be generated routinely at different centers; (b) neither in vitro LAK activity nor numbers of LAK cells infused were predictive of clinical efficacy or toxicity. There is a need to identify other laboratory or clinical parameters more predictive of IL-2/LAK therapeutic efficacy or toxicity. JF - Cancer research AU - Boldt, D H AU - Mills, B J AU - Gemlo, B T AU - Holden, H AU - Mier, J AU - Paietta, E AU - McMannis, J D AU - Escobedo, L V AU - Sniecinski, I AU - Rayner, A A AD - NCI Extramural IL-2/LAK Working Group, Audie L. Murphy VA Hospital, San Antonio, Texas. Y1 - 1988/08/01/ PY - 1988 DA - 1988 Aug 01 SP - 4409 EP - 4416 VL - 48 IS - 15 SN - 0008-5472, 0008-5472 KW - Interleukin-2 KW - 0 KW - Lymphokines KW - Recombinant Proteins KW - Index Medicus KW - Kidney Neoplasms -- therapy KW - Rectal Neoplasms -- therapy KW - Colonic Neoplasms -- therapy KW - Humans KW - Lymphokines -- pharmacology KW - Immunization, Passive KW - Melanoma -- therapy KW - Recombinant Proteins -- therapeutic use KW - Male KW - Leukocyte Count KW - Female KW - Interleukin-2 -- therapeutic use KW - Killer Cells, Natural -- immunology KW - Killer Cells, Natural -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78304512?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Laboratory+correlates+of+adoptive+immunotherapy+with+recombinant+interleukin-2+and+lymphokine-activated+killer+cells+in+humans.&rft.au=Boldt%2C+D+H%3BMills%2C+B+J%3BGemlo%2C+B+T%3BHolden%2C+H%3BMier%2C+J%3BPaietta%2C+E%3BMcMannis%2C+J+D%3BEscobedo%2C+L+V%3BSniecinski%2C+I%3BRayner%2C+A+A&rft.aulast=Boldt&rft.aufirst=D&rft.date=1988-08-01&rft.volume=48&rft.issue=15&rft.spage=4409&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 - 1988-08-24 N1 - Date created - 1988-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Medicine -- The Art of Humaneness: On Ethics of Traditional Chinese Medicine AN - 60987432; 89V0719 AB - The history of traditional Chinese medical ethics is described, & the Confucian ethics that formed the cultural context of traditional Chinese medicine & medical ethics are outlined. It is argued that the application of Confucian ethics in medicine prescribed the attitudes of physicians toward themselves, patients, & colleagues. 1 Appendix, 37 References. Modified HA JF - The Journal of Medicine and Philosophy AU - Qiu, Ren-Zong AD - Instit Philosophy Chinese Academy Social Sciences, 5 Juanguomen Nei Da Jie Beijing Y1 - 1988/08// PY - 1988 DA - August 1988 SP - 277 EP - 299 VL - 13 IS - 3 SN - 0360-5310, 0360-5310 KW - traditional Chinese medical ethics, Confucian influences KW - Confucianism KW - Ethics KW - Traditional Medicine KW - China KW - article KW - 2045: sociology of health and medicine; sociology of medicine (public health) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/60987432?accountid=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+Journal+of+Medicine+and+Philosophy&rft.atitle=Medicine+--+The+Art+of+Humaneness%3A+On+Ethics+of+Traditional+Chinese+Medicine&rft.au=Qiu%2C+Ren-Zong&rft.aulast=Qiu&rft.aufirst=Ren-Zong&rft.date=1988-08-01&rft.volume=13&rft.issue=3&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Medicine+and+Philosophy&rft.issn=03605310&rft_id=info:doi/ LA - English DB - Sociological Abstracts N1 - Date revised - 2007-04-01 N1 - Last updated - 2016-09-28 N1 - CODEN - JMPHDC N1 - SubjectsTermNotLitGenreText - China; Traditional Medicine; Ethics; Confucianism ER - TY - JOUR T1 - Obesity and insulin resistance: Lessons learned from the Pima indians AN - 21096709; 11312966 AB - Abstract not available. JF - Diabetes - Metabolism: Research and Reviews (Print Edition) AU - Lillioja, S AU - Bogardus, C AD - Clinical Diabetes and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona 85016 Y1 - 1988/08// PY - 1988 DA - Aug 1988 SP - 517 EP - 540 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 USA VL - 4 IS - 5 SN - 1520-7552, 1520-7552 KW - Physical Education Index KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/21096709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Diabetes+-+Metabolism%3A+Research+and+Reviews+%28Print+Edition%29&rft.atitle=Obesity+and+insulin+resistance%3A+Lessons+learned+from+the+Pima+indians&rft.au=Lillioja%2C+S%3BBogardus%2C+C&rft.aulast=Lillioja&rft.aufirst=S&rft.date=1988-08-01&rft.volume=4&rft.issue=5&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Diabetes+-+Metabolism%3A+Research+and+Reviews+%28Print+Edition%29&rft.issn=15207552&rft_id=info:doi/10.1002%2Fdmr.5610040508 LA - English DB - Physical Education Index N1 - Date revised - 2009-12-01 N1 - Last updated - 2011-12-14 DO - http://dx.doi.org/10.1002/dmr.5610040508 ER - TY - JOUR T1 - Are cell number and cell proliferation risk factors for cancer? AN - 78289879; 3385783 AB - Relatively little is known about the mechanisms underlying carcinogenesis in humans. Caloric restriction strongly inhibits the development of neoplasia in rodents, and there is evidence of a positive relationship between cancer and body weight in humans. Caloric restriction early in life is also known to permanently diminish organ cellularity. A recent link between adult stature and cancer incidence similarly implicates a lasting effect for growth and possibly for early nutrition in carcinogenesis. It is postulated that cancer risk is proportional to the number of proliferating cells, which in turn depends on both the number of cells and the rate of cell division within the tissue. This hypothesis is consistent with several aspects of human carcinogenesis, including multistage models and the epithelial origin of most cancers. JF - Journal of the National Cancer Institute AU - Albanes, D AU - Winick, M AD - Cancer Prevention Studies Branch, Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/07/20/ PY - 1988 DA - 1988 Jul 20 SP - 772 EP - 774 VL - 80 IS - 10 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - Body Weight KW - Cell Count KW - Body Height KW - Risk Factors KW - Humans KW - Models, Biological KW - Cell Division KW - Neoplasms -- pathology KW - Energy Intake KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78289879?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Are+cell+number+and+cell+proliferation+risk+factors+for+cancer%3F&rft.au=Albanes%2C+D%3BWinick%2C+M&rft.aulast=Albanes&rft.aufirst=D&rft.date=1988-07-20&rft.volume=80&rft.issue=10&rft.spage=772&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 - 1988-08-04 N1 - Date created - 1988-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Directional effects of acute total-body x-irradiation: exposure rate versus homogeneity of exposure. AN - 78285517; 3290499 AB - Survival patterns of NBL/Up mice exposed to 675-800 R of total-body x-radiation depended on direction and rate of exposure. Homogeneous dual exposures administered at 126 R/minute were more effective than those administered at 63 R/minute. Dorsal and dual exposures at 63 R/minute were equally effective, while absorption reduced the effectiveness of ventral exposures. Since cellular repair of hematopoietic tissue was initiated only during exposure, increased homogeneity without increased exposure rate would not increase effectiveness. With rate, direction, and homogeneity influencing the effectiveness of total-body exposures, fallacies inherent in converting total-body exposures to absorbed tissue dose became apparent. JF - Journal of the National Cancer Institute AU - Uphoff, D E AU - Swain, R W AU - Bowie, G M AD - Division of Cancer Biology and Diagnosis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/07/20/ PY - 1988 DA - 1988 Jul 20 SP - 769 EP - 772 VL - 80 IS - 10 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - Animals KW - Energy Transfer KW - Radiotherapy Dosage KW - Mice KW - Female KW - Whole-Body Irradiation -- methods KW - Whole-Body Irradiation -- adverse effects KW - Radiotherapy -- methods KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78285517?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Directional+effects+of+acute+total-body+x-irradiation%3A+exposure+rate+versus+homogeneity+of+exposure.&rft.au=Uphoff%2C+D+E%3BSwain%2C+R+W%3BBowie%2C+G+M&rft.aulast=Uphoff&rft.aufirst=D&rft.date=1988-07-20&rft.volume=80&rft.issue=10&rft.spage=769&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 - 1988-08-04 N1 - Date created - 1988-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Two modes of regulation of the phospholipase C-linked substance-P receptor in rat parotid acinar cells. AN - 78479370; 2460079 AB - In rat parotid acinar cells prelabelled with [3H]inositol, substance P (100 nM) induced the formation of [3H]inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]. Ins(1,4,5)P3 reached a maximum 7 s after substance P stimulation, and thereafter decreased and reached a stable value at 60 s. When the cells were exposed to substance P for 10, 30, 60, or 300 s, washed, and re-exposed to this peptide, the formation of [3H]inositol trisphosphate (InsP3) was attenuated in a time-dependent manner. In the cells pretreated as described above, the number of [3H]substance-P-binding sites (Bmax) was also decreased. Possible role(s) of Ca2+ and protein kinase (protein kinase C) control mechanisms in regulating substance P responses were investigated. Desensitization of substance P-induced InsP3 was not affected by the Ca2+ ionophore ionomycin, nor was it dependent on Ca2+ mobilization. On the other hand, in the presence of 4 beta-phorbol 12,13-dibutyrate (PDBu) and 12-O-tetradecanoyl-4 beta-phorbol 13-acetate, known activators of protein kinase C, substance P-induced InsP3 formation was inhibited. However, PDBu had no effect on [3H]substance P binding, whether present during the assay or when cells were pretreated. The persistent desensitization of InsP3 formation induced by substance P was not affected by PDBu. These results suggest that the persistent desensitization of InsP3 formation induced by substance P is a homologous process involving down-regulation of the substance P receptor; the mechanism does not appear to involve, or to be affected by, the Ca2+ or protein kinase C signalling systems. Protein kinase C activation can, however, inhibit substance P-induced InsP3 formation, which may indicate the presence of a negative-feedback control on the substance P pathway. JF - The Biochemical journal AU - Sugiya, H AU - Obie, J F AU - Putney, J W AD - Laboratory of Cellular and Molecular Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/07/15/ PY - 1988 DA - 1988 Jul 15 SP - 459 EP - 466 VL - 253 IS - 2 SN - 0264-6021, 0264-6021 KW - Inositol Phosphates KW - 0 KW - Phorbol Esters KW - Receptors, Neurokinin-1 KW - Receptors, Neurotransmitter KW - phorbol-12,13-didecanoate KW - 24928-17-4 KW - Substance P KW - 33507-63-0 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Type C Phospholipases KW - EC 3.1.4.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Protein Kinase C -- metabolism KW - Phorbol Esters -- pharmacology KW - Animals KW - Substance P -- pharmacology KW - Inositol Phosphates -- metabolism KW - In Vitro Techniques KW - Enzyme Activation -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Calcium -- pharmacology KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Binding Sites KW - Receptors, Neurotransmitter -- metabolism KW - Parotid Gland -- drug effects KW - Parotid Gland -- metabolism KW - Type C Phospholipases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78479370?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Two+modes+of+regulation+of+the+phospholipase+C-linked+substance-P+receptor+in+rat+parotid+acinar+cells.&rft.au=Sugiya%2C+H%3BObie%2C+J+F%3BPutney%2C+J+W&rft.aulast=Sugiya&rft.aufirst=H&rft.date=1988-07-15&rft.volume=253&rft.issue=2&rft.spage=459&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 - 1988-11-21 N1 - Date created - 1988-11-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem J. 1983 May 15;212(2):473-82 [6309146] Eur J Pharmacol. 1983 Jan 28;87(1):77-84 [6188620] Eur J Pharmacol. 1983 Sep 30;93(3-4):245-53 [6196211] Nature. 1984 Apr 19-25;308(5961):693-8 [6232463] Nature. 1984 May 3-9;309(5963):63-6 [6325926] Nature. 1984 Jun 28-Jul 4;309(5971):795-7 [6204206] Mol Pharmacol. 1984 Sep;26(2):261-6 [6237255] Biochem J. 1984 Oct 1;223(1):237-43 [6333870] Nature. 1984 Nov 22-28;312(5992):315-21 [6095092] J Biol Chem. 1985 Mar 25;260(6):3281-8 [3919020] Biochem J. 1985 Jan 1;225(1):263-6 [3883986] Nature. 1985 Sep 12-18;317(6033):124-9 [2993919] Biochem Biophys Res Commun. 1986 Jan 29;134(2):868-75 [3004469] J Biol Chem. 1986 Apr 25;261(12):5307-13 [3082882] Biochemistry. 1986 Mar 25;25(6):1371-7 [3008828] Nature. 1986 Apr 17-23;320(6063):631-4 [3010126] Proc Natl Acad Sci U S A. 1986 May;83(9):2797-801 [2871555] Biochem Biophys Res Commun. 1986 Apr 14;136(1):362-8 [3010971] Biochem Biophys Res Commun. 1986 May 29;137(1):50-60 [3013192] Cell. 1986 Sep 12;46(6):951-8 [3019558] J Biol Chem. 1987 Feb 5;262(4):1638-43 [3543007] Eur J Biochem. 1987 Mar 2;163(2):417-21 [3028803] J Biol Chem. 1987 Mar 5;262(7):3098-105 [3029100] Annu Rev Cell Biol. 1986;2:149-78 [3548765] J Biol Chem. 1987 May 5;262(13):6121-7 [3032956] J Biol Chem. 1987 Jul 5;262(19):9026-32 [3036840] Biochem J. 1987 Aug 1;245(3):631-9 [2822028] Biochem J. 1987 Jun 15;244(3):647-53 [2451500] J Biol Chem. 1978 Sep 10;253(17):5892-4 [28319] J Biol Chem. 1980 Mar 25;255(6):2273-6 [7358670] Mol Pharmacol. 1980 Jul;18(1):78-83 [6157980] J Pharmacol Exp Ther. 1982 Apr;221(1):247-53 [7062287] J Biol Chem. 1982 Jul 10;257(13):7847-51 [7085651] Biochem J. 1982 Sep 15;206(3):555-60 [6184051] J Physiol. 1982 Oct;331:557-65 [6185669] Nature. 1983 Nov 3-9;306(5938):67-9 [6605482] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Congenital poisoning by polychlorinated biphenyls and their contaminants in Taiwan. AN - 78301282; 3133768 AB - In 1979, a mass poisoning occurred in Taiwan from cooking oil contaminated by thermally degraded polychlorinated biphenyls. Because these chemicals persist in human tissue, children born to female patients after the outbreak were exposed in utero. In 1985, 117 children born to affected women and 108 unexposed controls were examined and evaluated. The exposed children were shorter and lighter than controls; they had abnormalities of gingiva, skin, nails, teeth, and lungs more frequently than did controls. The exposed children showed delay of developmental milestones, deficits on formal developmental testing, and abnormalities on behavioral assessment. These findings are most consistent with a generalized disorder of ectodermal tissue. This syndrome is one of very few documented to result from transplacental exposure to pollutant chemicals. JF - Science (New York, N.Y.) AU - Rogan, W J AU - Gladen, B C AU - Hung, K L AU - Koong, S L AU - Shih, L Y AU - Taylor, J S AU - Wu, Y C AU - Yang, D AU - Ragan, N B AU - Hsu, C C AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/07/15/ PY - 1988 DA - 1988 Jul 15 SP - 334 EP - 336 VL - 241 IS - 4863 SN - 0036-8075, 0036-8075 KW - Oils KW - 0 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - Maternal-Fetal Exchange KW - Growth Disorders -- chemically induced KW - Taiwan KW - Pigmentation Disorders -- congenital KW - Conjunctivitis -- chemically induced KW - Pigmentation Disorders -- chemically induced KW - Nails, Malformed KW - Humans KW - Conjunctivitis -- congenital KW - Female KW - Pregnancy KW - Lactation KW - Oils -- adverse effects KW - Polychlorinated Biphenyls -- poisoning UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78301282?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Congenital+poisoning+by+polychlorinated+biphenyls+and+their+contaminants+in+Taiwan.&rft.au=Rogan%2C+W+J%3BGladen%2C+B+C%3BHung%2C+K+L%3BKoong%2C+S+L%3BShih%2C+L+Y%3BTaylor%2C+J+S%3BWu%2C+Y+C%3BYang%2C+D%3BRagan%2C+N+B%3BHsu%2C+C+C&rft.aulast=Rogan&rft.aufirst=W&rft.date=1988-07-15&rft.volume=241&rft.issue=4863&rft.spage=334&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 - 1988-08-09 N1 - Date created - 1988-08-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-4/B cell stimulatory factor 1 stimulates T cell growth by an IL-2-independent mechanism. AN - 78287351; 3133410 AB - Resting T cells are stimulated to synthesize DNA by IL-4 and phorbol myristate acetate (PMA). This response of T cells to IL-4 plus PMA is independent of the action of IL-2 as judged by 1) the lack of IL-2 in supernatants of stimulated cells, 2) the failure to detect IL-2 mRNA in stimulated cells by in situ hybridization, 3) the inability of anti-IL-2R antibody and of anti-IL-2 antibody to block responses to IL-4 plus PMA, and 4) the failure of cyclosporin A to block responses. T cells also respond to anti-CD3 antibodies and IL-4 in the presence of anti-IL-2R antibodies. IL-4 stimulation of growth of the long term T cell line HT-2 also appears to be independent of the action of IL-2. No IL-2 mRNA is found in IL-4-stimulated HT-2 cells by Northern blotting; the response of HT-2 cells to IL-4 is not blocked by anti-IL-2R antibodies; the response of HT-2 cells to IL-4 is not inhibited by cyclosporin A. Although IL-4 stimulation of T cells is independent of IL-2, IL-4 plus PMA treatment of resting T cells does cause enhanced expression of IL-2R and prepares cells to proliferate to IL-2 alone. In both these properties IL-4 resembles IL-2. These experiments lead us to conclude that IL-4 can act as an alternative to IL-2 as authentic T cell growth factor. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Brown, M AU - Hu-Li, J AU - Paul, W E AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/07/15/ PY - 1988 DA - 1988 Jul 15 SP - 504 EP - 511 VL - 141 IS - 2 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Interleukin-2 KW - Interleukins KW - RNA, Messenger KW - Receptors, Immunologic KW - Receptors, Interleukin-2 KW - Interleukin-4 KW - 207137-56-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Cell Division -- drug effects KW - Interphase -- drug effects KW - Mice KW - Mice, Inbred BALB C KW - RNA, Messenger -- biosynthesis KW - Mice, Inbred DBA KW - Lymphocyte Activation -- drug effects KW - Receptors, Immunologic -- drug effects KW - Receptors, Immunologic -- immunology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Drug Synergism KW - Antibodies, Monoclonal -- physiology KW - Cell Line KW - Female KW - Cell-Free System KW - T-Lymphocytes -- metabolism KW - T-Lymphocytes -- cytology KW - Interleukins -- pharmacology KW - B-Lymphocytes -- immunology KW - T-Lymphocytes -- immunology KW - Interleukin-2 -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78287351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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-4%2FB+cell+stimulatory+factor+1+stimulates+T+cell+growth+by+an+IL-2-independent+mechanism.&rft.au=Brown%2C+M%3BHu-Li%2C+J%3BPaul%2C+W+E&rft.aulast=Brown&rft.aufirst=M&rft.date=1988-07-15&rft.volume=141&rft.issue=2&rft.spage=504&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 - 1988-08-03 N1 - Date created - 1988-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A chronic inflammatory response. Its role in supporting the development of c-myb and c-myc related promonocytic and monocytic tumors in BALB/c mice. AN - 78285425; 2838552 AB - This study demonstrates that an inflammatory response caused by the injection of pristane into the peritoneal cavity of mice provides a useful system for rapid induction of myeloid tumors by retroviruses. Two such tumors, which developed in the peritoneal cavity with average latencies of 68 to 71 d and incidences of greater than 50%, are 1) the McML, mature monocyte-macrophage tumors induced by retroviral constructs containing exons 2 and 3 of c-myc cDNA, and 2) the MML, promonocytic tumors induced by Moloney murine leukemia virus infection and its integration into the c-myb locus. Development of both neoplasms is clearly dependent on the intense i.p. inflammatory response, inasmuch as mice given the viruses and not pristane fail to develop these tumors. Although both types of tumors appear in the peritoneal cavity, the MML tumors that arise by i.v. injection of Moloney murine leukemia virus may actually originate via infection, and perhaps transformation, of precursor hemopoietic cells outside the peritoneal cavity, followed by migration of the cells to the peritoneal cavity. This is suggested by the fact that i.v.v but not i.p. injection of virus is an efficient method of producing these particular myeloid tumors. Although both McML and MML tumors require the inflammatory environment for their development, treatment of mice with a nonsteroid anti-inflammatory drug, indomethacin, has no effect on McML monocyte/macrophage tumors but completely prevents the development of the MML promonocyte tumors. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Wolff, L AU - Mushinski, J F AU - Shen-Ong, G L AU - Morse, H C AD - Laboratory of Genetics, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/07/15/ PY - 1988 DA - 1988 Jul 15 SP - 681 EP - 689 VL - 141 IS - 2 SN - 0022-1767, 0022-1767 KW - DNA, Neoplasm KW - 0 KW - Terpenes KW - pristane KW - 26HZV48DT1 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Moloney murine leukemia virus KW - Mice KW - DNA, Neoplasm -- isolation & purification KW - Mice, Inbred BALB C KW - Phenotype KW - Terpenes -- administration & dosage KW - Macrophages -- pathology KW - Chronic Disease KW - Cell Line KW - Female KW - Retroviridae Infections -- genetics KW - Retroviridae Infections -- pathology KW - Leukemia, Monocytic, Acute -- pathology KW - Leukemia, Monocytic, Acute -- etiology KW - Leukemia, Myeloid -- genetics KW - Inflammation -- etiology KW - Inflammation -- genetics KW - Leukemia, Myeloid -- etiology KW - Leukemia, Monocytic, Acute -- genetics KW - Leukemia, Myeloid -- pathology KW - Proto-Oncogenes KW - Inflammation -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78285425?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+chronic+inflammatory+response.+Its+role+in+supporting+the+development+of+c-myb+and+c-myc+related+promonocytic+and+monocytic+tumors+in+BALB%2Fc+mice.&rft.au=Wolff%2C+L%3BMushinski%2C+J+F%3BShen-Ong%2C+G+L%3BMorse%2C+H+C&rft.aulast=Wolff&rft.aufirst=L&rft.date=1988-07-15&rft.volume=141&rft.issue=2&rft.spage=681&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 - 1988-08-03 N1 - Date created - 1988-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of a cell surface-expressed disulfide-linked dimer involved in murine T cell activation. AN - 78284135; 2838547 AB - We have produced a hamster mAb, H1.2F3, which was derived by immunization with a murine TCR-gamma delta + epidermal T cell line. H1.2F3 immunoprecipitates a cell surface-expressed disulfide-linked dimer that has a m.w. of 85,000 under non-reducing conditions and consists of subunits of 35,000 to 39,000 m.w. This dimer is distinct from the CD3-associated TCR-gamma delta complex (CD3/TCR), inasmuch as H1.2F3 does not co-precipitate or co-modulate with the CD3/TCR complex and recognizes an Ag with a single-peptide backbone of 22,000 m.w. after N-Glycanase treatment. H1.2F3 is weakly reactive with a small percentage of cells from unfractionated thymus, spleen, or lymph node, but reactivity with both T and B lymphocytes is markedly enhanced by a brief period of stimulation with Con A or PMA in vitro. This enhancement requires de novo protein synthesis. Enhanced expression of the H1.2F3 Ag can also be induced in vivo by injection of Con A or anti-CD3. H1.2F3 is a potent stimulator of T, but not B, cell proliferation in the presence of PMA and FcR-bearing accessory cells. These functional and biochemical studies strongly suggest that the Ag recognized by H1.2F3 is the murine homologue of the human CD28 Ag recognized by mAb 9.3. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Yokoyama, W M AU - Koning, F AU - Kehn, P J AU - Pereira, G M AU - Stingl, G AU - Coligan, J E AU - Shevach, E M AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/07/15/ PY - 1988 DA - 1988 Jul 15 SP - 369 EP - 376 VL - 141 IS - 2 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD27 KW - Antigens, Surface KW - Disulfides KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Antibodies, Monoclonal -- biosynthesis KW - Animals KW - Aging KW - Mice, Inbred C3H KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Antigen-Presenting Cells -- immunology KW - Antibodies, Monoclonal -- physiology KW - Molecular Weight KW - Structure-Activity Relationship KW - Protein Conformation KW - Cricetinae KW - Lymphocyte Activation KW - T-Lymphocytes -- metabolism KW - Antigens, Surface -- isolation & purification KW - T-Lymphocytes -- physiology KW - T-Lymphocytes -- immunology KW - Antigens, Surface -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78284135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+a+cell+surface-expressed+disulfide-linked+dimer+involved+in+murine+T+cell+activation.&rft.au=Yokoyama%2C+W+M%3BKoning%2C+F%3BKehn%2C+P+J%3BPereira%2C+G+M%3BStingl%2C+G%3BColigan%2C+J+E%3BShevach%2C+E+M&rft.aulast=Yokoyama&rft.aufirst=W&rft.date=1988-07-15&rft.volume=141&rft.issue=2&rft.spage=369&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 - 1988-08-03 N1 - Date created - 1988-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neoadjuvant chemotherapy in previously untreated patients with advanced head and neck squamous cell cancer. AN - 78269974; 2454721 AB - Between May 1981 and January 1986, 130 consecutive patients with advanced untreated head and neck squamous cell cancer (HNSCC) received neoadjuvant chemotherapy (NAC) with two or three courses of the CABO combination (methotrexate 40 mg/m2 intravenously (IV) on days 1 and 15; CDDP 50 mg/m2 IV on day 4; bleomycin 10 mg IV on days 1, 8, and 15; and vincristine 2 mg IV on days 1, 8, and 15 every 3 weeks) prior to surgery and/or radiotherapy. Of the 123 patients evaluable for response to chemotherapy, 19 (15.4%) had a complete remission and 59 (48%) a partial response, yielding a 63.4% overall response rate. Response rate was significantly correlated with the performance status (PS) (P = 0.001), the stage (P = 0.005), and the T class (P = 0.02); 107 patients completed subsequent local treatment (87 with radiotherapy and 20 with surgery +/- radiotherapy). The median survival of the 124 patients evaluable for survival was 14.7 months and the overall survival rate at 3 years was 24%. The median survival and the overall survival at 3 years for the surgical subgroup were 24.7 months and 38% and for the radiotherapy subgroup were 14.3 months and 22%. These results were compared with those obtained in a historical control group of 79 patients treated in our institute with short courses of chemotherapy regimens, which did not include cisplatin, followed by radiotherapy (29 patients) or local treatments alone (26 patients with radiotherapy and 24 patients with surgery +/- radiotherapy) between January 1976 and December 1980. Most of the patient characteristics were evenly distributed (age, sex, and primary sites) except that more advanced lesions were included in the NAC group (Stage IV: 85% versus 62%; T4: 65% versus 42%; N2-3: 48% versus 29%). The overall survival was significantly higher in patients receiving NAC than in the historical control group, comparing both the groups taken as a whole (P less than 0.05) and the surgery +/- radiotherapy (P less than 0.05) and the radiotherapy (P less than 0.02) subgroups. This experience suggests a positive role of NAC on survival. However, this improvement in outcome compared with a historical control group cannot be regarded as definitive evidence for benefit to patients. Randomized studies using active regimens are required to confirm these data. JF - Cancer AU - Cognetti, F AU - Pinnarò, P AU - Carlini, P AU - Ruggeri, E M AU - Ambesi Impiombato, F AU - Del Vecchio, M R AU - Giannarelli, D AU - Perrino, A AD - Department of Medical Oncology I, National Cancer Institute, Regina Elena, Rome, Italy. Y1 - 1988/07/15/ PY - 1988 DA - 1988 Jul 15 SP - 251 EP - 261 VL - 62 IS - 2 SN - 0008-543X, 0008-543X KW - Bleomycin KW - 11056-06-7 KW - Vincristine KW - 5J49Q6B70F KW - Cisplatin KW - Q20Q21Q62J KW - Methotrexate KW - YL5FZ2Y5U1 KW - Abridged Index Medicus KW - Index Medicus KW - Vincristine -- adverse effects KW - Bleomycin -- administration & dosage KW - Humans KW - Vincristine -- administration & dosage KW - Aged KW - Bleomycin -- adverse effects KW - Cisplatin -- administration & dosage KW - Evaluation Studies as Topic KW - Methotrexate -- adverse effects KW - Middle Aged KW - Follow-Up Studies KW - Cisplatin -- adverse effects KW - Methotrexate -- administration & dosage KW - Female KW - Male KW - Carcinoma, Squamous Cell -- mortality KW - Head and Neck Neoplasms -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Head and Neck Neoplasms -- drug therapy KW - Carcinoma, Squamous Cell -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78269974?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neoadjuvant+chemotherapy+in+previously+untreated+patients+with+advanced+head+and+neck+squamous+cell+cancer.&rft.au=Cognetti%2C+F%3BPinnar%C3%B2%2C+P%3BCarlini%2C+P%3BRuggeri%2C+E+M%3BAmbesi+Impiombato%2C+F%3BDel+Vecchio%2C+M+R%3BGiannarelli%2C+D%3BPerrino%2C+A&rft.aulast=Cognetti&rft.aufirst=F&rft.date=1988-07-15&rft.volume=62&rft.issue=2&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-10 N1 - Date created - 1988-08-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergistic antitumor effects of immunotherapy with recombinant interleukin-2 and recombinant tumor necrosis factor-alpha. AN - 78267002; 3260130 AB - The antitumor activity of combination therapy with recombinant tumor necrosis-alpha (rhTNF-alpha) and recombinant interleukin-2 (rhIL-2) was assessed against established immunogenic (MCA-106) and nonimmunogenic (MCA-102) sarcomas at both s.c. and visceral (hepatic) sites. C57BL/6 (B6) mice were treated with a single i.v. dose of rhTNF-alpha (2, 4, 6, or 8 micrograms) followed by rhIL-2 (25,000 U) i.p. thrice daily for 5 consecutive days. Synergistic effects as measured by regression of tumor, prolongation of survival, and improved cure rates were found using the combination of rhTNF-alpha plus rhIL-2 compared to rhTNF-alpha alone or rhIL-2 alone in the treatment of the immunogenic sarcoma MCA-106. No significant antitumor effects were observed against the nonimmunogenic MCA-102 sarcoma. These findings were similar for both s.c. and large single hepatic tumor models. The effect of the timing of rhIL-2 injections in relation to rhTNF-alpha administration (concurrent, 2, 4, or 6 days post single rhTNF-alpha dose) was also evaluated. Substantial tumor regression and increased survival times were seen in mice with s.c. tumors when rhIL-2 therapy was delayed as much as 48 h after rhTNF-alpha administration. No antitumor response was noted with the combination compared to rhTNF-alpha alone when rhIL-2 was delayed for greater than 4 days. No increase in lethal toxicity during treatment course of the combination of rhTNF-alpha and rhIL-2 was noted at any schedule compared to single agent rhTNF-alpha therapy. A possible role of rhTNF-alpha in regulation of IL-2-dependent antitumor activity in vivo is discussed. JF - Cancer research AU - McIntosh, J K AU - Mulé, J J AU - Merino, M J AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/07/15/ PY - 1988 DA - 1988 Jul 15 SP - 4011 EP - 4017 VL - 48 IS - 14 SN - 0008-5472, 0008-5472 KW - Interleukin-2 KW - 0 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - Drug Therapy, Combination KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Female KW - Sarcoma, Experimental -- therapy KW - Liver Neoplasms -- therapy KW - Interleukin-2 -- therapeutic use KW - Immunotherapy KW - Tumor Necrosis Factor-alpha -- therapeutic use KW - Recombinant Proteins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78267002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+antitumor+effects+of+immunotherapy+with+recombinant+interleukin-2+and+recombinant+tumor+necrosis+factor-alpha.&rft.au=McIntosh%2C+J+K%3BMul%C3%A9%2C+J+J%3BMerino%2C+M+J%3BRosenberg%2C+S+A&rft.aulast=McIntosh&rft.aufirst=J&rft.date=1988-07-15&rft.volume=48&rft.issue=14&rft.spage=4011&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 - 1988-08-11 N1 - Date created - 1988-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of the activity of immunotoxins made with either ricin A chain or Pseudomonas exotoxin in human ovarian and epidermoid carcinoma cell lines. AN - 78264788; 3260128 AB - The present study evaluates whether the in vitro activity of immunotoxins can be enhanced by verapamil or by various antagonists of calmodulin (dansylcadaverine, trifluoperazine, chlorpromazine). The following immunotoxins made with either Pseudomonas exotoxin (PE), recombinant ricin A chain (rRTA), or ricin A chain (RTA) were used: HB21-PE and 454A12-rRTA that both recognize the human transferrin receptor; and 260F9-rRTA and 454C11-RTA that both react with human ovarian and breast cancer cells. The cytotoxicity of these immunotoxins was determined in human ovarian carcinoma cell lines and KB cells. Verapamil, that was demonstrated previously to enhance the cell-killing activity of PE immunotoxins, enhanced the activity of several ricin A chain immunotoxins, including 454A12-rRTA, 260F9-rRTA, and 454C11-RTA. Comparing 50% inhibitory dose values for inhibition of protein synthesis by 454A12-rRTA, enhancement ranged from 2- to greater than 25-fold, was dependent on the concentration of verapamil, and was greatest at short incubation times. In addition, the cytotoxicity of HB21-PE and of selected RTA immunotoxins was increased up to 30-fold by the addition of various calmodulin antagonists. The enhancing drugs did not decrease the specificity of the immunotoxins. JF - Cancer research AU - Pirker, R AU - FitzGerald, D J AU - Willingham, M C AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/07/15/ PY - 1988 DA - 1988 Jul 15 SP - 3919 EP - 3923 VL - 48 IS - 14 SN - 0008-5472, 0008-5472 KW - Bacterial Toxins KW - 0 KW - Calmodulin KW - Exotoxins KW - Immunotoxins KW - Virulence Factors KW - Trifluoperazine KW - 214IZI85K3 KW - Ricin KW - 9009-86-3 KW - Verapamil KW - CJ0O37KU29 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - monodansylcadaverine KW - I9N81SC5HD KW - Cadaverine KW - L90BEN6OLL KW - Chlorpromazine KW - U42B7VYA4P KW - Index Medicus KW - Cadaverine -- pharmacology KW - Trifluoperazine -- pharmacology KW - Humans KW - Cadaverine -- analogs & derivatives KW - Calmodulin -- antagonists & inhibitors KW - Verapamil -- pharmacology KW - Drug Synergism KW - Female KW - Chlorpromazine -- pharmacology KW - Cell Line KW - Carcinoma, Squamous Cell -- pathology KW - Ovarian Neoplasms -- pathology KW - Immunotoxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78264788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+activity+of+immunotoxins+made+with+either+ricin+A+chain+or+Pseudomonas+exotoxin+in+human+ovarian+and+epidermoid+carcinoma+cell+lines.&rft.au=Pirker%2C+R%3BFitzGerald%2C+D+J%3BWillingham%2C+M+C%3BPastan%2C+I&rft.aulast=Pirker&rft.aufirst=R&rft.date=1988-07-15&rft.volume=48&rft.issue=14&rft.spage=3919&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 - 1988-08-11 N1 - Date created - 1988-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequence of the 5' end of the developmentally regulated rat P450 PB1 (P450IIC6) gene. AN - 78326119; 3399405 JF - Nucleic acids research AU - Umeno, M AU - Morris, S AU - Matsunaga, E AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/07/11/ PY - 1988 DA - 1988 Jul 11 SP - 6249 VL - 16 IS - 13 SN - 0305-1048, 0305-1048 KW - Index Medicus KW - Animals KW - Base Sequence KW - Molecular Sequence Data KW - Transcription, Genetic KW - Male KW - Female KW - Rats -- growth & development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78326119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sequence+of+the+5%27+end+of+the+developmentally+regulated+rat+P450+PB1+%28P450IIC6%29+gene.&rft.au=Umeno%2C+M%3BMorris%2C+S%3BMatsunaga%2C+E%3BGelboin%2C+H+V%3BGonzalez%2C+F+J&rft.aulast=Umeno&rft.aufirst=M&rft.date=1988-07-11&rft.volume=16&rft.issue=13&rft.spage=6249&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 - 1988-08-31 N1 - Date created - 1988-08-31 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X06712; GENBANK N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Biol Chem. 1986 Aug 15;261(23):10667-72 [3015936] Nature. 1985 Oct 31-Nov 6;317(6040):765-6 [4058584] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Estimation of in-vivo miscoding rates. AN - 78452480; 3050120 AB - The replication of premutagenic DNA lesions generates mutant progeny in patterns that distinguish lesions that rarely produce a mutation per DNA replication from those that frequently do so. The quantitative aspects of this distinction were tested in studies of heat-mutagenized bacteriophage T4. Previous T4 studies had demonstrated that transition mutations produced at G.C base-pairs depended upon heat-induced DNA lesions distinct from those responsible for transversions at G.C pairs. In this study the transversion mutations are shown to arise in patterns predicted for mutations produced from lesions that miscode rarely (fewer than 10% per replication). In contrast, the transition mutations arise in patterns predicted for mutations produced from lesions that miscode at about 20 to 60% per replication. The fact that the two classes of DNA lesions are distinguishable as predicted by the quantitative model suggests that such studies may in general be useful in quantifying the behavior of mutation-generating DNA lesions. The method employed also estimates the frequency of premutagenic lesions in DNA. JF - Journal of molecular biology AU - Ripley, L S AD - Laboratory of Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/07/05/ PY - 1988 DA - 1988 Jul 05 SP - 17 EP - 34 VL - 202 IS - 1 SN - 0022-2836, 0022-2836 KW - DNA, Viral KW - 0 KW - Index Medicus KW - Heterozygote KW - Genetic Code KW - T-Phages -- genetics KW - Escherichia coli -- genetics KW - DNA Replication KW - Hot Temperature KW - DNA Damage KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78452480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Estimation+of+in-vivo+miscoding+rates.&rft.au=Ripley%2C+L+S&rft.aulast=Ripley&rft.aufirst=L&rft.date=1988-07-05&rft.volume=202&rft.issue=1&rft.spage=17&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 - 1988-11-21 N1 - Date created - 1988-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clone size distributions of mutations induced by ethyl methanesulfonate in bacteriophage T4. AN - 78451353; 3172207 AB - Size distributions of mutant clones can reveal important aspects of the mutation process. Previously published data on mutant clones induced by ethyl methanesulfonate (EMS) in bacteriophage T4 generated a distribution that was essentially flat, implying a mutagenic mechanism involving only rare mispairing by reacted bases. Here, methods for estimating the spontaneous component of such a distribution are used to generate a corrected distribution. The corrected distribution is strongly peaked, implying frequent (but not obligatory) mispairing. Frequent mispairing is in accord with current views of the fates of DNA lesions believed to mediate EMS-induced mutagenesis. JF - Journal of molecular biology AU - Drake, J W AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/07/05/ PY - 1988 DA - 1988 Jul 05 SP - 11 EP - 16 VL - 202 IS - 1 SN - 0022-2836, 0022-2836 KW - Ethyl Methanesulfonate KW - 9H154DI0UP KW - Index Medicus KW - Hydrogen Bonding KW - Clone Cells -- drug effects KW - Ethyl Methanesulfonate -- pharmacology KW - T-Phages -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78451353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Clone+size+distributions+of+mutations+induced+by+ethyl+methanesulfonate+in+bacteriophage+T4.&rft.au=Drake%2C+J+W&rft.aulast=Drake&rft.aufirst=J&rft.date=1988-07-05&rft.volume=202&rft.issue=1&rft.spage=11&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 - 1988-11-21 N1 - Date created - 1988-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protein kinase C: subcellular redistribution by increased Ca2+ influx. Evidence that Ca2+-dependent subcellular redistribution of protein kinase C is involved in potentiation of beta-adrenergic stimulation of pineal cAMP and cGMP by K+ and A23187. AN - 78261074; 2897966 AB - Phenylephrine is known to stimulate translocation of protein kinase C in rat pinealocytes (Sugden, D., Vanecek, J., Klein, D.C., Thomas, T.P., and Anderson, W. B. (1985) Nature 314, 359-361). In the present study, the receptor mediating this effect was found to belong to the alpha 1-adrenoceptor subclass. Activation of this receptor is also known to produce a sustained increase in [Ca2+]i by increasing net influx (Sugden, A. L., Sugden, D., and Klein, D. C. (1985) J. Biol. Chem. 261, 11608-11612), which points to the possible importance of Ca2+ influx in the subcellular redistribution (activation) of protein kinase C in intact cells. This possibility was investigated by reducing extracellular Ca2+ ((Ca2+]o) with EGTA or by inhibiting Ca2+ influx with inorganic Ca2+ blockers. These treatments reduced alpha 1-adrenoceptor-mediated translocation of protein kinase C. This suggested that elevation of Ca2+ influx alone triggers activation of protein kinase C. In support of this, it was found that treatments which elevate Ca2+ influx, including increased extracellular K+ and addition of the Ca2+ ionophore A23187, cause redistribution of protein kinase C. The effect of K+ was blocked by nifedipine and that of A23187 by EGTA, indicating that effects of these agents are Ca2+-dependent. The possible role of phospholipase C activation in these effects was examined by measuring the formation of [3H]diacylglycerol by cells labeled with [3H]arachidonic acid. Although [3H]diacylglycerol formation was easily detected in the presence or absence of an effective concentration of an inhibitor of diacylglycerol kinase, none of the agents which cause rapid translocation of protein kinase C were found to cause a rapid increase in the generation of [3H]diacylglycerol. These findings establish that an increase in Ca2+ influx is sufficient to trigger translocation of protein kinase C. In addition, we found that a very close correlation exists between translocation of protein kinase C by phenylephrine, K+, and A23187 and their ability to potentiate beta-adrenergic stimulation of cAMP and cGMP accumulation. This provides strong support to the proposal that translocation of protein kinase C is required for potentiation of beta-adrenergic stimulation of pinealocyte cAMP and cGMP accumulation. JF - The Journal of biological chemistry AU - Ho, A K AU - Thomas, T P AU - Chik, C L AU - Anderson, W B AU - Klein, D C AD - Section on Neuroendocrinology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/07/05/ PY - 1988 DA - 1988 Jul 05 SP - 9292 EP - 9297 VL - 263 IS - 19 SN - 0021-9258, 0021-9258 KW - Adrenergic beta-Antagonists KW - 0 KW - Receptors, Adrenergic, beta KW - Calcimycin KW - 37H9VM9WZL KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Cyclic GMP KW - H2D2X058MU KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Norepinephrine -- pharmacology KW - Kinetics KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium -- pharmacology KW - Subcellular Fractions -- enzymology KW - Adrenergic beta-Antagonists -- pharmacology KW - Female KW - Protein Kinase C -- metabolism KW - Pineal Gland -- metabolism KW - Cyclic GMP -- metabolism KW - Cyclic AMP -- metabolism KW - Pineal Gland -- enzymology KW - Receptors, Adrenergic, beta -- physiology KW - Receptors, Adrenergic, beta -- drug effects KW - Pineal Gland -- drug effects KW - Calcium -- pharmacology KW - Calcimycin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78261074?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Protein+kinase+C%3A+subcellular+redistribution+by+increased+Ca2%2B+influx.+Evidence+that+Ca2%2B-dependent+subcellular+redistribution+of+protein+kinase+C+is+involved+in+potentiation+of+beta-adrenergic+stimulation+of+pineal+cAMP+and+cGMP+by+K%2B+and+A23187.&rft.au=Ho%2C+A+K%3BThomas%2C+T+P%3BChik%2C+C+L%3BAnderson%2C+W+B%3BKlein%2C+D+C&rft.aulast=Ho&rft.aufirst=A&rft.date=1988-07-05&rft.volume=263&rft.issue=19&rft.spage=9292&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 - 1988-07-27 N1 - Date created - 1988-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thyrotropin stimulation of lysosomal tyrosine transport in rat FRTL-5 thyroid cells. AN - 78259239; 2837483 AB - Tyrosine countertransport was used to demonstrate the hormonal stimulation of neutral amino acid transport across the lysosomal membrane of FRTL-5 cells. Cells grown with thyrotropin (1 X 10(-10) M) had 7-fold (+/- S.E.) higher tyrosine countertransport activity in their lysosomes than cells grown without thyrotropin. Thyrotropin also stimulated the uptake into tyrosine-loaded lysosomes of other neutral amino acids recognized by the tyrosine carrier, namely, phenylalanine (3-fold) and leucine (6-fold). In contrast lysosomal cystine countertransport was not affected by thyrotropin. Addition of thyrotropin to cells grown without thyrotropin showed that the stimulation of tyrosine counter-transport (a) required at least 48 h to reach the level of the thyrotropin-supplemented cells, (b) depended upon protein synthesis, since cycloheximide (20 microM) was inhibitory, and (c) depended upon RNA synthesis, since actinomycin D (1 nM) was inhibitory. Cells grown without thyrotropin but with dibutyryl cyclic AMP (1 mM) or cholera toxin (1 nM) exhibited enhanced lysosomal countertransport of tyrosine, suggesting that cyclic AMP may act as a messenger. This represents the first demonstration of hormonal responsiveness in a lysosomal transport system and may reflect the importance of salvage and reutilization of lysosomal degradation products for the thyroid epithelial cell. JF - The Journal of biological chemistry AU - Harper, G S AU - Kohn, L D AU - Bernardini, I AU - Bernar, J AU - Tietze, F AU - Andersson, H C AU - Gahl, W A AD - Section on Human Biochemical Genetics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/07/05/ PY - 1988 DA - 1988 Jul 05 SP - 9320 EP - 9325 VL - 263 IS - 19 SN - 0021-9258, 0021-9258 KW - Dactinomycin KW - 1CC1JFE158 KW - Tyrosine KW - 42HK56048U KW - Phenylalanine KW - 47E5O17Y3R KW - Cystine KW - 48TCX9A1VT KW - Bucladesine KW - 63X7MBT2LQ KW - Thyrotropin KW - 9002-71-5 KW - Cholera Toxin KW - 9012-63-9 KW - Cycloheximide KW - 98600C0908 KW - Cyclic AMP KW - E0399OZS9N KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - Animals KW - Phenylalanine -- metabolism KW - Cholera Toxin -- pharmacology KW - Thyroid Gland KW - Bucladesine -- pharmacology KW - Biological Transport -- drug effects KW - Rats KW - Cystine -- metabolism KW - Dactinomycin -- pharmacology KW - Cycloheximide -- pharmacology KW - Kinetics KW - Leucine -- metabolism KW - Cyclic AMP -- metabolism KW - Cell Line KW - Thyrotropin -- pharmacology KW - Lysosomes -- metabolism KW - Tyrosine -- metabolism KW - Lysosomes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78259239?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Thyrotropin+stimulation+of+lysosomal+tyrosine+transport+in+rat+FRTL-5+thyroid+cells.&rft.au=Harper%2C+G+S%3BKohn%2C+L+D%3BBernardini%2C+I%3BBernar%2C+J%3BTietze%2C+F%3BAndersson%2C+H+C%3BGahl%2C+W+A&rft.aulast=Harper&rft.aufirst=G&rft.date=1988-07-05&rft.volume=263&rft.issue=19&rft.spage=9320&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 - 1988-07-27 N1 - Date created - 1988-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activity of immunotoxins constructed with modified Pseudomonas exotoxin A lacking the cell recognition domain. AN - 78254593; 3132465 AB - Pseudomonas exotoxin (PE) contains three domains whose functions are cell recognition, membrane translocation, and ADP ribosylation of elongation factor 2. PE40 is a form of PE which is missing the cell recognition domain. To study the properties of PE40, it was expressed in Escherichia coli using a vector which contains a T7 phage promoter, an OmpA signal sequence, and that portion of the PE gene encoding PE40. Upon induction with isopropyl-1-thio-beta-D-galactopyranoside, large amounts of PE40 were secreted, and highly purified PE40 was prepared from the culture medium. PE40 was chemically coupled to different monoclonal antibodies, and protein synthesis inhibition activities of these immunotoxins was assessed on various cell lines. These activities were compared with the activities of the corresponding immunotoxins made with native PE. These data indicate that PE40 may be useful in the construction of certain immunotoxins. JF - The Journal of biological chemistry AU - Kondo, T AU - FitzGerald, D AU - Chaudhary, V K AU - Adhya, S AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/07/05/ PY - 1988 DA - 1988 Jul 05 SP - 9470 EP - 9475 VL - 263 IS - 19 SN - 0021-9258, 0021-9258 KW - Amino Acids KW - 0 KW - Bacterial Toxins 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 - Animals KW - Genes, Bacterial KW - Genes KW - Protein Synthesis Inhibitors -- pharmacology KW - Cells, Cultured KW - Kinetics KW - Amino Acids -- analysis KW - Escherichia coli -- genetics KW - Mice KW - Amino Acid Sequence KW - Plasmids KW - Cell Line KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Pseudomonas aeruginosa -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78254593?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activity+of+immunotoxins+constructed+with+modified+Pseudomonas+exotoxin+A+lacking+the+cell+recognition+domain.&rft.au=Kondo%2C+T%3BFitzGerald%2C+D%3BChaudhary%2C+V+K%3BAdhya%2C+S%3BPastan%2C+I&rft.aulast=Kondo&rft.aufirst=T&rft.date=1988-07-05&rft.volume=263&rft.issue=19&rft.spage=9470&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 - 1988-07-27 N1 - Date created - 1988-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential regulation of mu-opiate receptors in heroin- and morphine-dependent rats. AN - 78299974; 2839362 AB - Rats made dependent on heroin and morphine exhibit both qualitative and quantitative differences in the characteristics of radioligand binding to mu-opioid receptors in the central nervous system. In brain membranes prepared from control animals, [3H]dihydromorphine (DHM) binding was best described by a two-site model, while in morphine-dependent rats, [3H]DHM binding was best described by a single-site model. In contrast, [3H]DHM binding to membranes from heroin-dependent animals was best described by a two-site model, with an increased density of the high-affinity, and no change in the low-affinity population compared to controls. Furthermore, both the number of binding sites for [3H]DAGO (a ligand that selectively labels a population of high-affinity mu-opiate receptors) and the sensitivity of [3H]DHM to sodium ions was increased in heroin; but not in morphine-dependent rats. These studies demonstrate that opiate receptors are differentially regulated in heroin- and morphine-dependent animals. Such neurochemical changes in mu-opiate receptors may underlie differences in the behavioral and pharmacological profiles of heroin and morphine reported in man. JF - FEBS letters AU - Bolger, G T AU - Skolnick, P AU - Rice, K C AU - Weissman, B A AD - Laboratory of Neuroscience, NIDDK, Bethesda, MD 20892. Y1 - 1988/07/04/ PY - 1988 DA - 1988 Jul 04 SP - 22 EP - 26 VL - 234 IS - 1 SN - 0014-5793, 0014-5793 KW - Enkephalins KW - 0 KW - Receptors, Opioid KW - Receptors, Opioid, mu KW - Enkephalin, Ala(2)-MePhe(4)-Gly(5)- KW - 100929-53-1 KW - Naloxone KW - 36B82AMQ7N KW - Heroin KW - 70D95007SX KW - Morphine KW - 76I7G6D29C KW - Sodium KW - 9NEZ333N27 KW - Dihydromorphine KW - C3S5FRP6JW KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Naloxone -- pharmacology KW - Animals KW - Dihydromorphine -- metabolism KW - Enkephalins -- metabolism KW - Cell Membrane -- metabolism KW - Male KW - Sodium -- pharmacology KW - Receptors, Opioid -- metabolism KW - Receptors, Opioid -- drug effects KW - Brain -- metabolism KW - Substance-Related Disorders -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78299974?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Differential+regulation+of+mu-opiate+receptors+in+heroin-+and+morphine-dependent+rats.&rft.au=Bolger%2C+G+T%3BSkolnick%2C+P%3BRice%2C+K+C%3BWeissman%2C+B+A&rft.aulast=Bolger&rft.aufirst=G&rft.date=1988-07-04&rft.volume=234&rft.issue=1&rft.spage=22&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-17 N1 - Date created - 1988-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of laser irradiation on immature olfactory neuroepithelial explants from the rat. AN - 85190626; pmid-3386379 AB - The photobiological effect of low-output laser irradiation on the maturation and regeneration of immature olfactory bipolar receptor cells of the rat was studied. The maturation and regeneration of the receptor cells of rat fetuses were quantified in neuroepithelial explants with morphometric analysis. The number of explants with outgrowth and the number and length of neuritic outgrowths were determined on a regular basis for 12 days. Explants in the experimental group were irradiated with a helium-neon laser using different incident energy densities (IED). Explants in the fluorescent light control group were exposed to fluorescent light for the same periods of time as those in the experimental group were exposed to laser irradiation. Explants in another control group were not exposed to laser or fluorescent light irradiation. The IED of 0.5 J/cm2 laser irradiation has been found to increase significantly the number of explants with outgrowth and the number and length of the outgrowths. Other laser IEDs or fluorescent light irradiation did not influence maturation or regeneration. JF - The Laryngoscope AU - Mester, A F AU - Snow, J B 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 - 1988 SP - 743 EP - 745 VL - 98 IS - 7 SN - 0023-852X, 0023-852X KW - Rats KW - Rats, Inbred Strains KW - In Vitro KW - Support, U.S. Gov't, P.H.S. KW - Nerve Regeneration KW - Embryo and Fetal Development KW - Animal KW - Olfactory Mucosa KW - Receptors, Sensory KW - Lasers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85190626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Laryngoscope&rft.atitle=Effects+of+laser+irradiation+on+immature+olfactory+neuroepithelial+explants+from+the+rat.&rft.au=Mester%2C+A+F%3BSnow%2C+J+B&rft.aulast=Mester&rft.aufirst=A&rft.date=1988-07-01&rft.volume=98&rft.issue=7&rft.spage=743&rft.isbn=&rft.btitle=&rft.title=The+Laryngoscope&rft.issn=0023852X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Metabolism of [14C]MPTP in mouse and monkey implicates MPP+, and not bound metabolites, as the operative neurotoxin. AN - 78808071; 2979736 AB - The distribution, identification, and binding of [phenyl-14C]- or [methyl-14C]MPTP metabolites have been determined in brains of mouse and monkey exposed to toxic doses of MPTP. The distribution of radiolabeled metabolites was heterogeneous, with levels of MPP+ 1-100 mumol/L in dissected and homogenized monkey brain tissues. MPP+ constituted greater than 98% of all tissue radioactivity remaining at 1-3 days in the monkey and was identified in both cortical and striatal tissue. The relevance of the 2% of unextractable ("bound") radiolabeled metabolite was assessed in mouse brain by using pargyline or mazindol pretreatments which block dopamine depletion. The amount of binding increased rather than decreased when [phenyl-14C]MPTP was used along with pargyline or mazindol but was unchanged when [methyl-14C]MPTP was employed. This demonstrates that bound metabolites are inversely correlated to neurotoxicity as well as being N-demethylated. Two extractable metabolites, demethylated MPTP (PTP) and 1-methyl-4-phenyl-2-pyridone, were found at 30-min survival times in mouse brain and probably derive from peripheral metabolism of MPTP. At 4 h, mouse brain profiles of extractable metabolites resembled those from monkey brain, containing MPP+ as the predominant (greater than 90%) constituent. The similarity of MPP+ concentrations in mouse and monkey brain homogenates with those concentrations of MPP+ known to produce biological effects in vitro, along with the inverse relationship between bound metabolites and neurotoxicity, supports the intermediacy of MPP+ as the operative neurotoxin. JF - Chemical research in toxicology AU - Yang, S C AU - Johannessen, J N AU - Markey, S P AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20892. PY - 1988 SP - 228 EP - 233 VL - 1 IS - 4 SN - 0893-228X, 0893-228X KW - Carbon Radioisotopes KW - 0 KW - Neurotoxins KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Animals KW - Cerebral Cortex -- metabolism KW - Biotransformation KW - MPTP Poisoning KW - Mice, Inbred C57BL KW - Radioisotope Dilution Technique KW - Mice KW - Macaca mulatta KW - Tissue Distribution KW - Male KW - Female KW - 1-Methyl-4-phenylpyridinium -- toxicity KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- metabolism KW - Brain -- metabolism KW - 1-Methyl-4-phenylpyridinium -- metabolism KW - Neurotoxins -- toxicity KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78808071?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Metabolism+of+%5B14C%5DMPTP+in+mouse+and+monkey+implicates+MPP%2B%2C+and+not+bound+metabolites%2C+as+the+operative+neurotoxin.&rft.au=Yang%2C+S+C%3BJohannessen%2C+J+N%3BMarkey%2C+S+P&rft.aulast=Yang&rft.aufirst=S&rft.date=1988-07-01&rft.volume=1&rft.issue=4&rft.spage=228&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-09 N1 - Date created - 1992-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of 7,12-dimethylbenz[a]anthracene-adenine nucleoside adducts. AN - 78807211; 2979734 AB - Chromatographic comparisons were made between radioactive adducts derived from the DNA of cells treated with [3H]7,12-dimethylbenz[a]anthracene and adducts derived from calf thymus DNA or nucleotides which had been treated in vitro with the synthetic syn 3,4-dihydrodiol 1,2-epoxide of this same carcinogen. This confirmed that three of the adducts formed in cells were derived from reaction of this particular dihydrodiol epoxide with deoxyadenosine while a fourth adduct was derived from its reaction with deoxyguanosine. After reaction of the dihydrodiol epoxide with polyadenylic acid, two ribonucleoside adducts were characterized by spectroscopic methods and were shown to have arisen from the cis opening of the epoxide ring at C1 by the amino group of adenine residues. JF - Chemical research in toxicology AU - Cheng, S C AU - Prakash, A S AU - Pigott, M A AU - Hilton, B D AU - Roman, J M AU - Lee, H M AU - Harvey, R G AU - Dipple, A AD - BRI-Basic Research Program, NCI-Frederick Cancer Research Facility, Maryland 21701. PY - 1988 SP - 216 EP - 221 VL - 1 IS - 4 SN - 0893-228X, 0893-228X KW - Deoxyadenosines KW - 0 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - DNA KW - 9007-49-2 KW - Deoxyguanosine KW - G9481N71RO KW - Adenosine KW - K72T3FS567 KW - Index Medicus KW - Fetus KW - Animals KW - Cattle KW - Cells, Cultured KW - Mice KW - Nucleic Acid Hybridization KW - Adenosine -- metabolism KW - Deoxyguanosine -- metabolism KW - DNA -- metabolism KW - Deoxyadenosines -- metabolism KW - 9,10-Dimethyl-1,2-benzanthracene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78807211?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Characterization+of+7%2C12-dimethylbenz%5Ba%5Danthracene-adenine+nucleoside+adducts.&rft.au=Cheng%2C+S+C%3BPrakash%2C+A+S%3BPigott%2C+M+A%3BHilton%2C+B+D%3BRoman%2C+J+M%3BLee%2C+H+M%3BHarvey%2C+R+G%3BDipple%2C+A&rft.aulast=Cheng&rft.aufirst=S&rft.date=1988-07-01&rft.volume=1&rft.issue=4&rft.spage=216&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-09 N1 - Date created - 1992-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential responsiveness of cerebellar Purkinje neurons to GABA and benzodiazepine receptor ligands in an animal model of hepatic encephalopathy. AN - 78752246; 2854841 AB - The role of the GABA-benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy was investigated by recording the electrophysiological responses of single cerebellar Purkinje neurons from rabbits with hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure. Both the GABAmimetic muscimol and the benzodiazepine receptor agonist flunitrazepam were 3-4 times more potent in depressing the spontaneous activity of Purkinje neurons from rabbits with hepatic encephalopathy than from control animals. Furthermore, qualitatively different responses of Purkinje neurons to benzodiazepine receptor antagonists (Ro 15-1788 and Ro 14-7437) were found in controls and rabbits with hepatic encephalopathy. These compounds markedly excited Purkinje neurons from rabbits with hepatic encephalopathy, but had either no effect (Ro 14-7437) or partially suppressed (Ro 15-1788) the spontaneous activity of neurons from control animals. In addition, incubation of Purkinje neurons from rabbits with hepatic encephalopathy with subthreshold concentrations of Ro 14-7437 reduced their sensitivity to muscimol, whereas treatment of control neurons with Ro 14-7437 had no effect on their sensitivity to muscimol. Finally, Purkinje neurons from hepatic encephalopathy and control rabbits displayed no difference in sensitivity to the depressant actions of the alpha-adrenoceptor agonist phenylephrine. These findings demonstrate a differential responsiveness of Purkinje neurons from an animal model of hepatic encephalopathy to ligands that interact with the GABA-benzodiazepine receptor complex. Furthermore, the observations made in this experimental model are consistent with the involvement of the GABA-benzodiazepine receptor complex in mediating hepatic encephalopathy, and provide a potential explanation for the reported efficacy of benzodiazepine receptor antagonists in ameliorating this syndrome. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience AU - Basile, A S AU - Gammal, S H AU - Mullen, K D AU - Jones, E A AU - Skolnick, P AD - Laboratory of Neuroscience, NIDDK, Bethesda, Maryland 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 2414 EP - 2421 VL - 8 IS - 7 SN - 0270-6474, 0270-6474 KW - GABA Antagonists KW - 0 KW - Ligands KW - Receptors, GABA-A KW - Benzodiazepines KW - 12794-10-4 KW - Muscimol KW - 2763-96-4 KW - Flumazenil KW - 40P7XK9392 KW - Flunitrazepam KW - 620X0222FQ KW - Galactosamine KW - 7535-00-4 KW - Ro 14-7437 KW - 78756-03-3 KW - Index Medicus KW - Animals KW - Benzodiazepines -- antagonists & inhibitors KW - Rabbits KW - Flunitrazepam -- pharmacology KW - Benzodiazepines -- pharmacology KW - Muscimol -- pharmacology KW - Male KW - Flumazenil -- pharmacology KW - Receptors, GABA-A -- physiology KW - Purkinje Cells -- drug effects KW - Hepatic Encephalopathy -- physiopathology KW - Hepatic Encephalopathy -- pathology KW - Purkinje Cells -- physiology KW - Hepatic Encephalopathy -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78752246?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differential+responsiveness+of+cerebellar+Purkinje+neurons+to+GABA+and+benzodiazepine+receptor+ligands+in+an+animal+model+of+hepatic+encephalopathy.&rft.au=Basile%2C+A+S%3BGammal%2C+S+H%3BMullen%2C+K+D%3BJones%2C+E+A%3BSkolnick%2C+P&rft.aulast=Basile&rft.aufirst=A&rft.date=1988-07-01&rft.volume=8&rft.issue=7&rft.spage=2414&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 - 1989-06-29 N1 - Date created - 1989-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of kidney tumors in the male F344/N rat after treatment with dimethyl methylphosphonate. AN - 78609869; 3209020 AB - Dimethyl methylphosphonate (DMMP), a chemical that has been used as a flame retardant and as a nerve gas simulant to mimic the physical but not biologic properties of nerve gases, was administered by gavage in corn oil for up to 2 years at doses of 0, 500, or 1000 mg/kg/day to male and female F344/N rats and at doses of 0, 1000, or 2000 mg/kg/day to male and female B6C3F1 mice. Survival in dosed male rats was reduced, due in part to kidney toxicity, and lesions in the kidney included increased severity of spontaneous nephropathy, calcification, hyperplasia of the tubular and transitional epithelium, tubular cell adenocarcinomas, and transitional cell papillomas and carcinomas. Survival in female rats was similar among groups; survival in mice was reduced and this reduced survival decreased the sensitivity for detecting a carcinogenic response. There were no dose-related neoplastic responses in female rats or male or female mice. The spectrum of kidney lesions seen in the male rat given DMMP is similar to that seen after the long-term administration of a variety of other chemicals including unleaded gasoline, hydrocarbon solvents, and 1,4-dichlorobenzene. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Dunnick, J K AU - Eustis, S L AU - Haseman, J K AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina 27709. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 91 EP - 99 VL - 11 IS - 1 SN - 0272-0590, 0272-0590 KW - Organophosphorus Compounds KW - 0 KW - dimethyl methylphosphonate KW - 20Z996230U KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Carcinoma, Transitional Cell -- pathology KW - Animals KW - Rats, Inbred F344 KW - Adenocarcinoma -- chemically induced KW - Body Weight -- drug effects KW - Mice KW - Carcinoma, Transitional Cell -- chemically induced KW - Male KW - Female KW - Adenocarcinoma -- pathology KW - Kidney Neoplasms -- pathology KW - Kidney Neoplasms -- chemically induced KW - Organophosphorus Compounds -- toxicity KW - Kidney Neoplasms -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78609869?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Development+of+kidney+tumors+in+the+male+F344%2FN+rat+after+treatment+with+dimethyl+methylphosphonate.&rft.au=Dunnick%2C+J+K%3BEustis%2C+S+L%3BHaseman%2C+J+K&rft.aulast=Dunnick&rft.aufirst=J&rft.date=1988-07-01&rft.volume=11&rft.issue=1&rft.spage=91&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 - 1989-02-21 N1 - Date created - 1989-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of renal cortical slices from the Fischer 344 rat as an in vitro model to evaluate nephrotoxicity. AN - 78605158; 2905310 AB - The toxicity of several classical acute nephrotoxicants was evaluated in an in vitro system using renal cortical slices prepared from adult male Fischer 344 rats. Gentamicin, cephaloridine, 4-ipomeanol, potassium dichromate (K2Cr2O7), mercuric chloride (HgCl2), carbon tetrachloride (CCl4), and hexachlorobutadiene (HCBD) were preincubated with slices for 2 hr at 37 degrees C at concentrations ranging from 1 x 10(-6) to 1 x 10(-1) M. Following preincubation, slices were removed, rinsed in medium lacking the nephrotoxicant, and subsequently incubated for 90 min at 25 degrees C for physiological assessment of proximal tubular functions. Using a single preparation, slices were monitored for organic ion accumulation, gluconeogenesis, lipid peroxidation, and total glutathione (reduced and oxidized) concentrations. In addition, preincubation and incubation media were assessed for the presence of renal enzymes originating from brush border, cytosol, and lysosomes. The relative degree of toxicity in this model was consistent with nephrotoxic potency in vivo where HgCl2, K2Cr2O7 greater than HCBD greater than CCl4, cephaloridine greater than gentamicin greater than 4-ipomeanol. Effects on organic ion accumulation, gluconeogenesis, and glutathione concentrations occurred simultaneously for each toxicant. Toxicants produced different effects on enzyme release and malondialdehyde formation. These results suggest that toxicity produced in vitro is representative of in vivo nephrotoxicity and support the further use of this model to evaluate mechanisms of nephrotoxicity. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Smith, J H AD - Division of Cancer Treatment, National Institutes of Health, Bethesda, Maryland 20205. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 132 EP - 142 VL - 11 IS - 1 SN - 0272-0590, 0272-0590 KW - Culture Media KW - 0 KW - Lipid Peroxides KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - alpha-Glucosidases KW - EC 3.2.1.20 KW - Acetylglucosaminidase KW - EC 3.2.1.52 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - gamma-Glutamyltransferase -- metabolism KW - alpha-Glucosidases -- metabolism KW - Disease Models, Animal KW - Alkaline Phosphatase -- metabolism KW - Acetylglucosaminidase -- metabolism KW - Lipid Peroxides -- metabolism KW - Male KW - L-Lactate Dehydrogenase -- metabolism KW - Kidney Diseases -- pathology KW - Kidney Cortex -- enzymology KW - Kidney Cortex -- pathology KW - Kidney Cortex -- metabolism KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78605158?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+use+of+renal+cortical+slices+from+the+Fischer+344+rat+as+an+in+vitro+model+to+evaluate+nephrotoxicity.&rft.au=Smith%2C+J+H&rft.aulast=Smith&rft.aufirst=J&rft.date=1988-07-01&rft.volume=11&rft.issue=1&rft.spage=132&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 - 1989-02-21 N1 - Date created - 1989-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of a bar code scanner to improve the utility and flexibility of record and verify systems used in radiation therapy. AN - 78602855; 3211055 AB - Record and verify systems used in radiation therapy serve a useful purpose in verification of machine parameters for each radiation field and monitoring the treatment as it is administered. There are, however, limitations as to the completeness of this monitoring. These restrictions are primarily due to design limitations of accelerators, which provide only a limited number of hardwired signals for use by such systems. The extent of the signals provided varies among manufacturers. As a result, some commonly used treatment accessories, such as blocking trays, may not be recognized by these systems. Additionally, current commercial record and verify systems cannot be expanded to accommodate institution-specific, customized treatment accessories or devices for positioning or immobilization of patients. This paper describes a complementary approach to providing device detection using a bar code scanner to read coded labels mounted on treatment accessories and download the data into the record and verify system for processing. A microcomputer-based system employing a portable bar code scanner was developed to evaluate the potential of this concept. Implications of adding bar code scanners to record and verify systems are discussed. JF - Medical physics AU - Miller, R W AU - van de Geijn, J AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland 20892. PY - 1988 SP - 611 EP - 613 VL - 15 IS - 4 SN - 0094-2405, 0094-2405 KW - Index Medicus KW - Humans KW - Radiation Monitoring -- instrumentation KW - Radiotherapy -- methods KW - Radiotherapy -- instrumentation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78602855?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+use+of+a+bar+code+scanner+to+improve+the+utility+and+flexibility+of+record+and+verify+systems+used+in+radiation+therapy.&rft.au=Miller%2C+R+W%3Bvan+de+Geijn%2C+J&rft.aulast=Miller&rft.aufirst=R&rft.date=1988-07-01&rft.volume=15&rft.issue=4&rft.spage=611&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 - 1989-02-22 N1 - Date created - 1989-02-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Substance P: the relationship between receptor distribution in rat lung and the capacity of substance P to stimulate vascular permeability. AN - 78584366; 2462377 AB - The interaction of substance P (SP) with specific receptors in intact lung tissue was autoradiographically visualized, using slide-mounted tissue sections of rat lung tissue. SP receptors are highly concentrated in the central airways and are not detectable in peripheral bronchi, vessels, and alveoli. Within central airways, receptor distribution is most concentrated in the epithelium and small vessels in the lamina propria. Smooth muscle in airway or blood vessel walls expressed no detectable SP receptors. Immunohistochemical staining for SP revealed SP-containing nerves in the same areas where the receptors are localized. Displacement curves of SP bound to rat lung indicated that the C-terminal fragment was much more effective than the N-terminal fragment at competing for SP binding. Injection of 0.3 to 30 nmol/kg SP dramatically increased vascular permeability in the trachea and to a lesser extent in the hilus. Peripheral lung failed to respond to SP with increased vascular permeability unless toxic concentrations of SP were employed. SP increased the transudation of protein into the trachea within 5 min of injection, and the extravasated protein persisted through at least 2 h. Both SP and SP(3-11) were capable of stimulating increased vascular permeability, but SP(1-4) was inactive. SP caused mast cell degranulation as reflected in increased plasma histamine levels after SP or SP(3-11) injection, but SP(1-4) had no effect. In order to determine if histamine release caused by SP contributed to the vascular permeability response, the effects of H1 and H2 antihistamine treatment were studied.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The American review of respiratory disease AU - Sertl, K AU - Wiedermann, C J AU - Kowalski, M L AU - Hurtado, S AU - Plutchok, J AU - Linnoila, I AU - Pert, C B AU - Kaliner, M A AD - Allergic Diseases Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 151 EP - 159 VL - 138 IS - 1 SN - 0003-0805, 0003-0805 KW - Receptors, Neurokinin-1 KW - 0 KW - Receptors, Neurotransmitter KW - Substance P KW - 33507-63-0 KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Immunohistochemistry -- methods KW - Autoradiography -- methods KW - Male KW - Female KW - Receptors, Neurotransmitter -- metabolism KW - Substance P -- metabolism KW - Capillary Permeability KW - Lung -- metabolism KW - Substance P -- physiology KW - Pulmonary Circulation KW - Lung -- innervation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78584366?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Substance+P%3A+the+relationship+between+receptor+distribution+in+rat+lung+and+the+capacity+of+substance+P+to+stimulate+vascular+permeability.&rft.au=Sertl%2C+K%3BWiedermann%2C+C+J%3BKowalski%2C+M+L%3BHurtado%2C+S%3BPlutchok%2C+J%3BLinnoila%2C+I%3BPert%2C+C+B%3BKaliner%2C+M+A&rft.aulast=Sertl&rft.aufirst=K&rft.date=1988-07-01&rft.volume=138&rft.issue=1&rft.spage=151&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 - 1989-01-24 N1 - Date created - 1989-01-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Covalent binding of platinum to renal protein from sensitive and resistant guinea pigs treated with cisplatin: possible role in nephrotoxicity. AN - 78460248; 3175342 AB - Covalent binding of platinum from the anticancer drug cisplatin has been determined in subcellular organelles from kidney and liver of guinea pig strains sensitive and resistant to the systemic toxicity of cisplatin. Organ distribution of platinum was similar between the two strains, but the sensitive animals (pigmented) excreted only half as much platinum in 24 hr as did the resistent animals (albino). Subcellular distribution of platinum in mitochondria, microsomes, and cytosol was approximately equal for both strains, but the sensitive animals had twice as much platinum bound covalently to cytosolic acid-insoluble protein as did the resistant animals. In the albino guinea pigs, concentrations of total platinum and of covalently bound platinum were greater in kidney subcellular organelles than in either liver or lung organelles, which may help explain the sensitivity of the kidney to the toxic effects of cisplatin. JF - Research communications in chemical pathology and pharmacology AU - Litterst, C L AU - Schweitzer, V G AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 35 EP - 48 VL - 61 IS - 1 SN - 0034-5164, 0034-5164 KW - Platinum KW - 49DFR088MY KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Cytosol -- metabolism KW - Animals KW - Guinea Pigs KW - In Vitro Techniques KW - Drug Resistance KW - Protein Binding KW - Female KW - Platinum -- metabolism KW - Kidney -- metabolism KW - Cisplatin -- toxicity KW - Kidney -- drug effects KW - Cisplatin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78460248?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Research+communications+in+chemical+pathology+and+pharmacology&rft.atitle=Covalent+binding+of+platinum+to+renal+protein+from+sensitive+and+resistant+guinea+pigs+treated+with+cisplatin%3A+possible+role+in+nephrotoxicity.&rft.au=Litterst%2C+C+L%3BSchweitzer%2C+V+G&rft.aulast=Litterst&rft.aufirst=C&rft.date=1988-07-01&rft.volume=61&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Research+communications+in+chemical+pathology+and+pharmacology&rft.issn=00345164&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-31 N1 - Date created - 1988-10-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prevalence and patterns of combined alcohol and marijuana use. AN - 78457935; 3172788 AB - The prevalence of combined alcohol and marijuana use in the U.S. population was determined from the 1982 National Household Survey on Drug Abuse. Past month use of both alcohol and marijuana was reported by 14% of men and 6% of women; in this group, occasional or more frequent use of these drugs in combination was reported by 79% of men and 67% of women. Among individuals aged 18-25 years, 24% of men and 12% of women reported using alcohol and marijuana in combination. More men than women and more individuals aged 18-25 and 26-34 compared with younger and older individuals used these drugs in combination. JF - Journal of studies on alcohol AU - Norton, R AU - Colliver, J AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 378 EP - 380 VL - 49 IS - 4 SN - 0096-882X, 0096-882X KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - United States KW - Age Factors KW - Sex Factors KW - Humans KW - Health Surveys KW - Adult KW - Aged KW - Middle Aged KW - Drug Synergism KW - Adolescent KW - Male KW - Female KW - Alcohol Drinking -- ethnology KW - Cannabis KW - Marijuana Smoking KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78457935?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prevalence+and+patterns+of+combined+alcohol+and+marijuana+use.&rft.au=Norton%2C+R%3BColliver%2C+J&rft.aulast=Norton&rft.aufirst=R&rft.date=1988-07-01&rft.volume=49&rft.issue=4&rft.spage=378&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 - 1988-11-21 N1 - Date created - 1988-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alcohol-related problems, marital disruption and depressive symptoms among adult children of alcohol abusers in the United States. AN - 78453002; 3172779 AB - Dependent problem drinking, marital disruption and depressive symptoms of sons and daughters of alcohol abusers are examined in a representative sample of 1,772 adults in the United States. Controlling for the sociodemographic characteristics of the adult sons and daughters in logistic regression analyses and for the alcohol-related problems (e.g., alcohol dependence) of the sons and daughters in the analyses of marital disruption and depressive symptoms, the results suggest that having parents who have been alcohol abusers places sons at risk for dependent problem drinking, both sons and daughters at risk for divorce or separation and daughters at risk for depressive symptomatology. JF - Journal of studies on alcohol AU - Parker, D A AU - Harford, T C AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 306 EP - 313 VL - 49 IS - 4 SN - 0096-882X, 0096-882X KW - Index Medicus KW - United States KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Divorce KW - Depression KW - Parent-Child Relations KW - Social Problems KW - Alcoholism -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78453002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alcohol-related+problems%2C+marital+disruption+and+depressive+symptoms+among+adult+children+of+alcohol+abusers+in+the+United+States.&rft.au=Parker%2C+D+A%3BHarford%2C+T+C&rft.aulast=Parker&rft.aufirst=D&rft.date=1988-07-01&rft.volume=49&rft.issue=4&rft.spage=306&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 - 1988-11-21 N1 - Date created - 1988-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synthetic peptides derived from IRBP induce EAU and EAP in Lewis rats. AN - 78407167; 3262040 AB - In an earlier study we isolated three cyanogen bromide cleavage fragments of bovine IRBP that exhibited high levels of immunopathogenicity, producing inflammatory changes in the eyes (EAU) and pineal gland (EAP) of Lewis rats. These fragments have been localized within the IRBP sequence. In order to identify these putative immunopathogenic epitopes of IRBP, nine selected peptide sequences were synthesized and tested for the induction of disease in Lewis rats. Seven of the peptides were found inactive in producing disease while two closely related peptides, designated R4 (23-mer) and R9 (27-mer) were found to reproducibly induce EAU and EAP in immunized rats. No good correlation was found between the immunopathogenicity of the nine tested peptides and their amphipathicity: peptides R4 and R9 were not predicted to form strong amphipathic helices, while peptides selected for their high predicted helical amphipathicity were not immunopathogenic. EAU induced by peptides R4 and R9 was less severe and had a longer onset time than the disease induced by whole IRBP. In addition, the inflammatory changes induced by R4 and R9 in the posterior segment of the eye were less acute than those induced by whole IRBP and included granuloma formation and perivasculitis, features which are not generally seen in rats immunized with whole IRBP. Thus, the changes induced by R4 and R9 more closely resemble those which are characteristically found in human eyes affected by certain uveitic diseases than do changes produced by the intact protein. JF - Current eye research AU - Sanui, H AU - Redmond, T M AU - Hu, L H AU - Kuwabara, T AU - Margalit, H AU - Cornette, J L AU - Wiggert, B AU - Chader, G J AU - Gery, I AD - Laboratory of Immunol, National Eye Institute, Bethesda, MD 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 727 EP - 735 VL - 7 IS - 7 SN - 0271-3683, 0271-3683 KW - Eye Proteins KW - 0 KW - Peptide Fragments KW - Retinol-Binding Proteins KW - interstitial retinol-binding protein KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred Lew KW - Dose-Response Relationship, Drug KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Male KW - Retinol-Binding Proteins -- pharmacology KW - Pineal Gland -- pathology KW - Retinitis -- immunology KW - Autoimmune Diseases -- chemically induced KW - Uveitis -- immunology KW - Retinitis -- chemically induced KW - Peptide Fragments -- immunology KW - Uveitis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78407167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+eye+research&rft.atitle=Synthetic+peptides+derived+from+IRBP+induce+EAU+and+EAP+in+Lewis+rats.&rft.au=Sanui%2C+H%3BRedmond%2C+T+M%3BHu%2C+L+H%3BKuwabara%2C+T%3BMargalit%2C+H%3BCornette%2C+J+L%3BWiggert%2C+B%3BChader%2C+G+J%3BGery%2C+I&rft.aulast=Sanui&rft.aufirst=H&rft.date=1988-07-01&rft.volume=7&rft.issue=7&rft.spage=727&rft.isbn=&rft.btitle=&rft.title=Current+eye+research&rft.issn=02713683&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-21 N1 - Date created - 1988-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolic and hemodynamic effects of antihypertensive treatment with ketanserin. AN - 78404610; 3415801 AB - Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 hours), blood pressures measured 12 hours after dosing were not significantly different from those obtained after placebo. However, 2 hours after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (P less than 0.01) and 6 +/- 5 mm Hg (P less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. Except for a slight decline in serum prolactin levels 12 hours after dosing with ketanserin, no changes were observed in pituitary hormone levels, serum testosterone, plasma catecholamines, plasma renin activity, aldosterone, or lipoproteins. Stroke volume, measured 2 hours after dosing, increased with ketanserin therapy, but cardiac output, systemic resistance, and heart rate were unchanged. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24 hours of antihypertensive activity. JF - American journal of hypertension AU - Levinson, P D AU - Zimlichman, R AU - Goldstein, D S AU - Brewer, H B AU - Keiser, H R AD - Hypertension-Endocrine Branche, National Heart, Lung, and Blood Institute, Bethesda, Maryland. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 245S EP - 248S VL - 1 IS - 3 Pt 3 SN - 0895-7061, 0895-7061 KW - Prolactin KW - 9002-62-4 KW - Ketanserin KW - 97F9DE4CT4 KW - Index Medicus KW - Prolactin -- blood KW - Heart Rate -- drug effects KW - Humans KW - Adult KW - Middle Aged KW - Blood Pressure -- drug effects KW - Male KW - Female KW - Hemodynamics -- drug effects KW - Ketanserin -- therapeutic use KW - Hypertension -- physiopathology KW - Ketanserin -- adverse effects KW - Hypertension -- metabolism KW - Hypertension -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78404610?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+hypertension&rft.atitle=Metabolic+and+hemodynamic+effects+of+antihypertensive+treatment+with+ketanserin.&rft.au=Levinson%2C+P+D%3BZimlichman%2C+R%3BGoldstein%2C+D+S%3BBrewer%2C+H+B%3BKeiser%2C+H+R&rft.aulast=Levinson&rft.aufirst=P&rft.date=1988-07-01&rft.volume=1&rft.issue=3+Pt+3&rft.spage=245S&rft.isbn=&rft.btitle=&rft.title=American+journal+of+hypertension&rft.issn=08957061&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-19 N1 - Date created - 1988-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment and prevention of basal cell carcinoma with oral isotretinoin. AN - 78393575; 3165982 AB - Twelve patients with multiple basal cell carcinomas resulting from varying causes were treated with high-dose oral isotretinoin (mean daily dosage: 3.1 mg/kg/day) for a mean of 8 months. Of the 270 tumors monitored in these patients, only 8% underwent complete clinical and histologic regression. All patients developed moderate to severe acute toxicities, leading five patients to withdraw from the study. Retinoid skeletal toxicity was identified in two patients who were examined after long-term therapy. Lower doses of isotretinoin (0.25 to 1.5 mg/kg/day) were ineffective for chemotherapy but demonstrated a chemopreventive effect in a subset of three patients who received these lower doses for 3 to 8 years. Two of these three patients have been observed after discontinuation of therapy. In one patient with a history of arsenic exposure, only one new tumor has appeared in a 27-month posttreatment observation period; in the other patient with the nevoid basal cell carcinoma syndrome, 29 new tumors have appeared within a 13-month period. This suggests that the need for long-term maintenance therapy with isotretinoin for chemoprevention of basal cell carcinoma may depend on the underlying cause of the skin cancers. JF - Journal of the American Academy of Dermatology AU - Peck, G L AU - DiGiovanna, J J AU - Sarnoff, D S AU - Gross, E G AU - Butkus, D AU - Olsen, T G AU - Yoder, F W AD - Dermatology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 176 EP - 185 VL - 19 IS - 1 Pt 2 SN - 0190-9622, 0190-9622 KW - Tretinoin KW - 5688UTC01R KW - Isotretinoin KW - EH28UP18IF KW - Index Medicus KW - Administration, Oral KW - Humans KW - Adult KW - Isomerism KW - Aged KW - Middle Aged KW - Male KW - Female KW - Remission Induction KW - Skin Neoplasms -- drug therapy KW - Carcinoma, Basal Cell -- prevention & control KW - Neoplasms, Multiple Primary -- prevention & control KW - Neoplasms, Multiple Primary -- drug therapy KW - Carcinoma, Basal Cell -- drug therapy KW - Tretinoin -- administration & dosage KW - Skin Neoplasms -- prevention & control KW - Tretinoin -- therapeutic use KW - Tretinoin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78393575?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Academy+of+Dermatology&rft.atitle=Treatment+and+prevention+of+basal+cell+carcinoma+with+oral+isotretinoin.&rft.au=Peck%2C+G+L%3BDiGiovanna%2C+J+J%3BSarnoff%2C+D+S%3BGross%2C+E+G%3BButkus%2C+D%3BOlsen%2C+T+G%3BYoder%2C+F+W&rft.aulast=Peck&rft.aufirst=G&rft.date=1988-07-01&rft.volume=19&rft.issue=1+Pt+2&rft.spage=176&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Academy+of+Dermatology&rft.issn=01909622&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Who talks to physicians about mental health and substance abuse problems? AN - 78374119; 3404298 AB - This is an analysis of data from the NIMH-sponsored Epidemiologic Catchment Area community-based study, investigating who reported discussing mental health or substance abuse problems with nonpsychiatric physicians. Data were from 7,092 respondents in four sites, all of whom had received care only in the nonpsychiatric sector in the previous six months. A multiple logistic model found that those individuals who had psychiatric disorders, and female, middle-aged, and Hispanic respondents, were more likely to have discussed emotional or mental health problems with their physicians. Respondents with alcohol abuse and substance abuse disorders did not report any more discussion of mental health problems than did respondents without alcohol or substance abuse disorders. Only 36% of the respondents who said they had discussed mental health problems were found to have psychiatric disorders by the Diagnostic Interview Survey (DIS), but many of those without disorders reported more anxiety symptoms. An analysis was done to predict which respondents with DIS-defined psychiatric disorders did not report discussing mental health problems with their nonpsychiatric physicians. Those less than 35 years of age, those older than 65 years of age, males, and those with only one recent visit to a provider were statistically at high risk for not discussing their psychiatric problems. JF - Journal of general internal medicine AU - Ford, D E AU - Kamerow, D B AU - Thompson, J W AD - Primary Care Research Program, National Institute of Mental Health, Rockville, Maryland 20857. PY - 1988 SP - 363 EP - 369 VL - 3 IS - 4 SN - 0884-8734, 0884-8734 KW - Index Medicus KW - United States KW - Models, Psychological KW - Humans KW - Statistics as Topic KW - Male KW - Female KW - Catchment Area (Health) KW - Physicians, Family KW - Patients -- psychology KW - Substance-Related Disorders KW - Mental Health KW - Physician-Patient Relations UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78374119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+general+internal+medicine&rft.atitle=Who+talks+to+physicians+about+mental+health+and+substance+abuse+problems%3F&rft.au=Ford%2C+D+E%3BKamerow%2C+D+B%3BThompson%2C+J+W&rft.aulast=Ford&rft.aufirst=D&rft.date=1988-07-01&rft.volume=3&rft.issue=4&rft.spage=363&rft.isbn=&rft.btitle=&rft.title=Journal+of+general+internal+medicine&rft.issn=08848734&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-22 N1 - Date created - 1988-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tolerance to tumor necrosis factor in rats and the relationship to endotoxin tolerance and toxicity. AN - 78350602; 3294337 AB - Treatment of rats with recombinant human TNF initially causes a marked decrease in food intake, a loss of body weight, and a negative nitrogen balance. These alterations normalize with continued twice daily intraperitoneal injections of the same dose. Rats tolerized to TNF in this manner are refractory to a lethal dose of TNF. Also, TNF-pretreated and -tolerized rats have prolonged survival and reversed histopathologic changes after injection of a lethal dose of endotoxin compared with control animals. The TNF-tolerant state is dependent on the dose of TNF used and the length of TNF pretreatment. TNF-induced tolerance is relatively short lived, being present 2-4 d after TNF pretreatment and dissipating by 2 wk. Rats made tolerant to endotoxin are also tolerant to a lethal dose of TNF. A bidirectional crossreacting tolerance exists between TNF and endotoxin. The mechanism of TNF tolerance is unclear, but it does not appear to be due to a humoral immune response or a perturbation of the uptake and clearance of injected TNF. JF - The Journal of experimental medicine AU - Fraker, D L AU - Stovroff, M C AU - Merino, M J AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/07/01/ PY - 1988 DA - 1988 Jul 01 SP - 95 EP - 105 VL - 168 IS - 1 SN - 0022-1007, 0022-1007 KW - Endotoxins KW - 0 KW - Immunoglobulin G KW - Immunoglobulin M KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Nitrogen KW - N762921K75 KW - Index Medicus KW - Rats KW - Eating KW - Body Weight KW - Drug Tolerance KW - Animals KW - Rats, Inbred F344 KW - Recombinant Proteins -- pharmacology KW - Kinetics KW - Escherichia coli KW - Immunoglobulin M -- biosynthesis KW - Nitrogen -- metabolism KW - Immunoglobulin G -- biosynthesis KW - Male KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Tumor Necrosis Factor-alpha -- immunology KW - Endotoxins -- toxicity KW - Endotoxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78350602?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tolerance+to+tumor+necrosis+factor+in+rats+and+the+relationship+to+endotoxin+tolerance+and+toxicity.&rft.au=Fraker%2C+D+L%3BStovroff%2C+M+C%3BMerino%2C+M+J%3BNorton%2C+J+A&rft.aulast=Fraker&rft.aufirst=D&rft.date=1988-07-01&rft.volume=168&rft.issue=1&rft.spage=95&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 - 1988-09-02 N1 - Date created - 1988-09-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 1966 Nov 1;124(5):983-1000 [5926304] Immunol Today. 1988 Jan;9(1):28-31 [3076757] Science. 1985 Aug 30;229(4716):869-71 [3895437] Nature. 1986 Apr 17-23;320(6063):584-8 [3010124] Prostaglandins. 1986 Apr;31(4):639-50 [3088676] Science. 1986 Oct 24;234(4775):470-4 [3764421] Am J Physiol. 1986 Oct;251(4 Pt 1):E470-6 [3532821] J Biol Chem. 1986 Nov 15;261(32):14871-4 [3021754] J Immunol. 1987 Feb 1;138(3):957-62 [3492537] J Immunol. 1987 Feb 1;138(3):963-74 [3805720] N Engl J Med. 1987 Feb 12;316(7):379-85 [3543677] Metabolism. 1987 May;36(5):469-74 [3574135] Surg Gynecol Obstet. 1987 May;164(5):415-22 [3576418] Cancer Res. 1987 Aug 15;47(16):4318-22 [3300963] J Immunol. 1987 Nov 1;139(9):2989-92 [2822800] J Exp Med. 1987 Dec 1;166(6):1788-97 [2824656] J Clin Oncol. 1987 Dec;5(12):1942-51 [3681377] Lancet. 1987 Nov 28;2(8570):1229-32 [2890853] Nature. 1987 Dec 17-23;330(6149):662-4 [3317066] Important Adv Oncol. 1987;:105-30 [2841229] J Immunol Methods. 1984 Mar 30;68(1-2):167-75 [6707477] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prostaglandin-sensitive adenylyl cyclase of cultured preadipocytes and mature adipocytes of the rat: probable role of Gi in determination of stimulatory or inhibitory action. AN - 78342052; 2840437 AB - Preadipocytes of rats were obtained from the stromal-vascular fraction of collagenase-digested perirenal fat pads and grown in serum-containing medium. By day 8 of culture the cells reached confluence and by 12 days were lipid-laden. The adenylyl cyclase of the plasma membranes was compared to that of mature fat cells. Unlike the membranes from adipocytes, the preadipocytes showed adenylyl cyclase activity that was stimulated by GTP. Stimulation of preadipocyte membranes by Gpp(NH)p, NaF, and forskolin was comparable to that of membranes from adipocytes, but the response to epinephrine and isoproterenol was minimal (approximately 1.5-fold for preadipocytes vs. 4-5-fold for adipocytes). In contrast, GTP-dependent stimulation of adenylyl cyclase of preadipocytes by PGE1 was nearly 8-fold. Stimulation occurred even in the presence of both GTP and 140 mM NaCl, a condition that leads to inhibition by PGE1 of adenylyl cyclase in membranes of adipocytes. Other characteristics of the adenylyl cyclase of preadipocyte membranes that differ from those of adipocytes include lack of inhibition by GTP of forskolin-activated activity, and, following treatment with pertussis toxin, enhanced stimulation by PGE1. ADP-ribosylation of Gi and Gs with pertussis and cholera toxins, respectively, indicated that the membranes of preadipocytes contained only 5-11% of the Gi of adipocytes and a much lower ratio of Gi:Gs. These findings suggest that cultured preadipocytes have an incompletely developed Gi pathway that may account for the stimulatory effect of prostaglandins on the adenylyl cyclase of these cells as opposed to the inhibitory action of PG in mature fat cells. JF - Journal of cellular physiology AU - Lu, Z D AU - Piñeyro, M A AU - Kirkland, J L AU - Li, Z H AU - Gregerman, R I AD - Endocrinology Section, National Institute on Aging, Francis Scott Key Medical Center, Baltimore, Maryland. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 1 EP - 12 VL - 136 IS - 1 SN - 0021-9541, 0021-9541 KW - Adenylate Cyclase Toxin KW - 0 KW - Arachidonic Acids KW - Prostaglandins KW - Virulence Factors, Bordetella KW - Colforsin KW - 1F7A44V6OU KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Arachidonic Acid KW - 27YG812J1I KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - Sodium KW - 9NEZ333N27 KW - Cyclic AMP KW - E0399OZS9N KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Alprostadil KW - F5TD010360 KW - Index Medicus KW - Membranes -- drug effects KW - Alprostadil -- pharmacology KW - Animals KW - Fibroblasts -- drug effects KW - Fibroblasts -- enzymology KW - Cholera Toxin -- pharmacology KW - Adenosine Diphosphate Ribose -- metabolism KW - Guanosine Triphosphate -- pharmacology KW - Sodium -- pharmacology KW - Arachidonic Acids -- pharmacology KW - Rats KW - Virulence Factors, Bordetella -- pharmacology KW - Membranes -- enzymology KW - Rats, Inbred F344 KW - Colforsin -- pharmacology KW - Lung -- drug effects KW - Cyclic AMP -- metabolism KW - Lung -- enzymology KW - Male KW - GTP-Binding Proteins -- metabolism KW - Adipose Tissue -- drug effects KW - Adenylyl Cyclases -- metabolism KW - Adipose Tissue -- enzymology KW - Prostaglandins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78342052?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prostaglandin-sensitive+adenylyl+cyclase+of+cultured+preadipocytes+and+mature+adipocytes+of+the+rat%3A+probable+role+of+Gi+in+determination+of+stimulatory+or+inhibitory+action.&rft.au=Lu%2C+Z+D%3BPi%C3%B1eyro%2C+M+A%3BKirkland%2C+J+L%3BLi%2C+Z+H%3BGregerman%2C+R+I&rft.aulast=Lu&rft.aufirst=Z&rft.date=1988-07-01&rft.volume=136&rft.issue=1&rft.spage=1&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 - 1988-09-02 N1 - Date created - 1988-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occupation and lung cancer in Shanghai: a case-control study. AN - 78330610; 3395581 AB - Occupation was evaluated as a potential risk factor for lung cancer as part of a large population based case-control study conducted in the ten urban districts of Shanghai. A total of 733 newly diagnosed cases of male lung cancer and 760 controls selected from the general population was interviewed to obtain lifetime occupational histories and information on smoking and other factors. Of the approximately 25 major industrial titles examined, significantly raised risks, adjusted for smoking, were found for employment in agricultural production (odds ratio (OR) = 1.6, 95% confidence interval (CI) = 1.0-2.6). A concomitant increase was detected for farmers (OR = 1.6, 95% CI = 1.0-2.5) when 35 major occupational titles were examined. There was a 70% excess among workers in the chemical industry (OR = 1.7, 95% CI = 0.9-3.1) and a significant decrease among textile industry workers (OR = 0.7, 95% CI = 0.5-1.0). Raised risks of 30% to 80% were associated with reported job exposures to wood and coal dusts, smoke from burning fuels, and chemical fumes. Employment categories were also examined for 672 cases and 735 controls among women, but small numbers in many of the industrial and occupational categories precluded detailed analyses. The largest excess risk among women (OR = 5.1, 95% CI 1.3-23.5) was among glass products workers. Although cigarette smoking was the dominant cause of lung cancer among men and a significant risk factor among women in Shanghai, these findings suggest the importance of certain workplace exposures and offer leads to occupational carcinogens. JF - British journal of industrial medicine AU - Levin, L I AU - Zheng, W AU - Blot, W J AU - Gao, Y T AU - Fraumeni, J F AD - National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 450 EP - 458 VL - 45 IS - 7 SN - 0007-1072, 0007-1072 KW - Index Medicus KW - Risk Factors KW - Humans KW - Agricultural Workers' Diseases -- etiology KW - Adult KW - Smoking -- adverse effects KW - Middle Aged KW - Occupations KW - Male KW - Female KW - China KW - Chemical Industry KW - Lung Neoplasms -- etiology KW - Occupational Diseases -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78330610?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Occupation+and+lung+cancer+in+Shanghai%3A+a+case-control+study.&rft.au=Levin%2C+L+I%3BZheng%2C+W%3BBlot%2C+W+J%3BGao%2C+Y+T%3BFraumeni%2C+J+F&rft.aulast=Levin&rft.aufirst=L&rft.date=1988-07-01&rft.volume=45&rft.issue=7&rft.spage=450&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 - 1988-09-02 N1 - Date created - 1988-09-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Ind Med. 1986 Feb;43(2):84-90 [3947573] Natl Cancer Inst Monogr. 1985 Dec;69:11-3 [3834319] Br J Ind Med. 1986 May;43(5):332-8 [3707871] Am J Epidemiol. 1986 Jul;124(1):53-66 [3717140] Br J Ind Med. 1986 Aug;43(8):516-21 [3730301] Br J Ind Med. 1965 Jan;22:72-7 [14261709] Ann N Y Acad Sci. 1965 Dec 31;132(1):156-65 [5219878] J Occup Med. 1973 Sep;15(9):717-9 [4738625] Environ Res. 1975 Apr;9(2):196-207 [1140180] Prev Med. 1976 Jun;5(2):295-315 [935079] J Occup Med. 1976 Nov;18(11):743-54 [993866] Int J Epidemiol. 1979 Dec;8(4):375-82 [541161] Chest. 1981 Jan;79(1):6-11 [7449508] Br J Cancer. 1981 Feb;43(2):183-95 [7470381] Am Ind Hyg Assoc J. 1981 May;42(5):329-40 [7013460] J Toxicol Environ Health. 1981 Nov-Dec;8(5-6):1027-40 [7338938] Cancer. 1982 Jul 15;50(2):364-71 [7083144] J Natl Cancer Inst. 1983 Mar;70(3):421-6 [6300496] Natl Cancer Inst Monogr. 1982;62:43-6 [7167193] J Natl Cancer Inst. 1983 Jul;71(1):1-4 [6575197] J Natl Cancer Inst. 1983 Jul;71(1):31-7 [6575207] Am J Ind Med. 1984;5(5):343-57 [6720695] Scand J Work Environ Health. 1984 Aug;10(4):211-7 [6494840] Am J Ind Med. 1985;7(5-6):395-402 [4003402] Br J Ind Med. 1985 Jun;42(6):411-4 [4005195] Cancer. 1985 Aug 15;56(4):910-7 [2990660] Lancet. 1985 Oct 26;2(8461):934-5 [2865429] Br J Ind Med. 1985 Nov;42(11):723-33 [4063215] Scand J Soc Med. 1985;13(4):147-52 [4089567] Am J Epidemiol. 1986 Feb;123(2):235-49 [3946373] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of DNA repair capacity of mammalian cells by carcinogen treatment. AN - 78323002; 3135602 AB - To determine whether DNA excision repair is enhanced in mammalian cells in response to DNA damage, as it is in bacteria as part of the SOS response, we used an expression vector-host cell reactivation assay to measure cellular DNA repair capacity. When UV-damaged chloramphenicol acetyltransferase (CAT) vector DNA was introduced into monkey cells (CV-1), the level of CAT activity was inversely related to the UV fluence due to inhibition of CAT gene expression by UV photoproducts. When CV-1 cells were treated with either UV radiation or mitomycin C, 24-48 h before transfection, CAT expression from the UV-irradiated plasmid was increased. This increase also occurred in a line of normal human cells, but not in repair-deficient human xeroderma pigmentosum cells. We confirmed that this increase in CAT expression was due to repair, and not to production of damage-free templates by recombination; the frequency of generation of supF+ recombinants after transfection with UV-irradiated pZ189 vectors carrying different point mutations in the supF gene did not significantly increase in carcinogen-treated CV-1 cells. From these results we conclude that carcinogen treatment enhances the excision-repair capacity of normal mammalian cells. JF - Somatic cell and molecular genetics AU - Protić, M AU - Roilides, E AU - Levine, A S AU - Dixon, K AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 351 EP - 357 VL - 14 IS - 4 SN - 0740-7750, 0740-7750 KW - Mitomycins KW - 0 KW - Mitomycin KW - 50SG953SK6 KW - Acetyltransferases KW - EC 2.3.1.- KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Xeroderma Pigmentosum KW - Animals KW - Ultraviolet Rays KW - Humans KW - Transfection KW - Genetic Vectors KW - Cercopithecus aethiops KW - Recombination, Genetic KW - Acetyltransferases -- analysis KW - Mutation KW - Cell Line KW - DNA Repair KW - Mitomycins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78323002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Somatic+cell+and+molecular+genetics&rft.atitle=Enhancement+of+DNA+repair+capacity+of+mammalian+cells+by+carcinogen+treatment.&rft.au=Proti%C4%87%2C+M%3BRoilides%2C+E%3BLevine%2C+A+S%3BDixon%2C+K&rft.aulast=Proti%C4%87&rft.aufirst=M&rft.date=1988-07-01&rft.volume=14&rft.issue=4&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Somatic+cell+and+molecular+genetics&rft.issn=07407750&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-31 N1 - Date created - 1988-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The mutagenic activity of selected compounds at the TK locus: rodent vs. human cells. AN - 78319557; 3292900 AB - The mutagenic (TFT resistance) and toxic responses of mouse lymphoma (MOLY) L5178Y cells and human lymphoblast (HULY) TK6 cells were compared for 13 chemicals. The mutagenic activities of 8 of the 13 chemicals (62%) examined in the HULY and MOLY assays are in agreement - the results being judged positive in both assays. However, a dramatic difference is observed when the two conditions of metabolic activation are considered separately; the overall concordance of 8/13 has been achieved by combining a 13/13 (100%) agreement in the absence of S9 with a 1/6 (17%) agreement in the presence of S9. In the absence of S9, the concentration ranges, lowest significant doses, and shapes of the concentration-response curves for both toxicity and mutagenicity were similar in spite of the differences in exposure times (4 h for MOLY, 20 for HULY) and expression times (2 days for MOLY, 3 days for HULY). The general agreement observed in the absence of S9 contrasted with the differences manifested in its presence. 6 compounds which were negative in the absence of S9 were tested in both the MOLY and HULY assays in the presence of S9. Of the 6 chemicals, only 1 was positive in both MOLY and HULY under the latter condition; 4 others were positive in MOLY and negative in HULY whereas 1 was positive in HULY and negative in MOLY. JF - Mutation research AU - Caspary, W J AU - Langenbach, R AU - Penman, B W AU - Crespi, C AU - Myhr, B C AU - Mitchell, A D AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 61 EP - 81 VL - 196 IS - 1 SN - 0027-5107, 0027-5107 KW - Mutagens KW - 0 KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Biotransformation KW - Leukemia L5178 -- genetics KW - Humans KW - Genes -- drug effects KW - Mice KW - Species Specificity KW - Cell Survival KW - Mutagenicity Tests KW - Thymidine Kinase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78319557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+mutagenic+activity+of+selected+compounds+at+the+TK+locus%3A+rodent+vs.+human+cells.&rft.au=Caspary%2C+W+J%3BLangenbach%2C+R%3BPenman%2C+B+W%3BCrespi%2C+C%3BMyhr%2C+B+C%3BMitchell%2C+A+D&rft.aulast=Caspary&rft.aufirst=W&rft.date=1988-07-01&rft.volume=196&rft.issue=1&rft.spage=61&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 - 1988-08-24 N1 - Date created - 1988-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Beta-carbolines as antagonists of the discriminative stimulus effects of diazepam in rats. AN - 78315758; 3392659 AB - Rats were trained to discriminate between saline and 1.0 mg/kg of diazepam in a two-choice procedure where responding was maintained under a fixed-ratio, 5-response schedule of stimulus shock termination. beta-Carboline-3-carboxylate-methyl ester (beta CCM), beta-carboline-3-carboxylate-ethyl ester (beta CCE) and beta-carboline-3-carboxylate-t-butyl ester (beta CCtB), compounds with alkylcarboxy substitutions on the 3-position of the beta-carboline ring structure, were effective antagonists of the discriminative effects of diazepam. The 3-hydroxymethyl-substituted compound (3HMC) was relatively ineffective in antagonizing the discriminative effects of diazepam. The order of potency in antagonizing the 1.0 mg/kg training dose of diazepam was beta CCtB greater than beta CCM greater than beta CCE much greater than 3 HMC. The greater potency of beta CCtB likely reflects its resistance to metabolism in vivo. beta CCE and beta CCtB produced dose-related, parallel shifts in the dose-response curve for the discriminative effects of diazepam, but the magnitude of the shifts was limited: the two highest doses of beta CCE and beta CCtB produced shifts that were not significantly different in magnitude. These latter results suggest that these beta-carbolines antagonize only a portion of the component(s) of action of diazepam in producing discriminative stimuli. In contrast, the 7-substituted beta-carbolines harmane, harmol and harmine were ineffective in antagonizing the discriminative effects of diazepam up to doses of the beta-carbolines which disrupted the ability of the animals to respond.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Journal of pharmacology and experimental therapeutics AU - Shannon, H E AU - Hagen, T J AU - Guzman, F AU - Cook, J A AD - National Institute on Drug Abuse, Division of Research, Addiction Research Center, Lexington, Kentucky. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 275 EP - 281 VL - 246 IS - 1 SN - 0022-3565, 0022-3565 KW - Carbolines KW - 0 KW - Picrotoxin KW - 124-87-8 KW - harmol KW - 487-03-6 KW - Harmine KW - 4FHH5G48T7 KW - 3-hydroxymethyl-beta-carboline KW - 65474-79-5 KW - beta-carboline-3-carboxylic acid ethyl ester KW - 74214-62-3 KW - harman KW - 82D6J0535P KW - tert-butyl beta-carboline-3-carboxylate KW - 93835-05-3 KW - beta-carboline-3-carboxylic acid methyl ester KW - I2A008F6YL KW - Diazepam KW - Q3JTX2Q7TU KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Picrotoxin -- pharmacology KW - Harmine -- analogs & derivatives KW - Harmine -- pharmacology KW - Male KW - Discrimination Learning -- drug effects KW - Diazepam -- pharmacology KW - Carbolines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78315758?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Beta-carbolines+as+antagonists+of+the+discriminative+stimulus+effects+of+diazepam+in+rats.&rft.au=Shannon%2C+H+E%3BHagen%2C+T+J%3BGuzman%2C+F%3BCook%2C+J+A&rft.aulast=Shannon&rft.aufirst=H&rft.date=1988-07-01&rft.volume=246&rft.issue=1&rft.spage=275&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 - 1988-08-17 N1 - Date created - 1988-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pneumocystis carinii pneumonia: therapy and prophylaxis. AN - 78313749; 2969023 JF - The Journal of infectious diseases AU - Kovacs, J A AU - Masur, H AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 254 EP - 259 VL - 158 IS - 1 SN - 0022-1899, 0022-1899 KW - Anti-Bacterial Agents KW - 0 KW - Drug Combinations KW - Quinazolines KW - Sulfadiazine KW - 0N7609K889 KW - Pentamidine KW - 673LC5J4LQ KW - Trimethoprim, Sulfamethoxazole Drug Combination KW - 8064-90-2 KW - Dapsone KW - 8W5C518302 KW - Trimethoprim KW - AN164J8Y0X KW - Sulfamethoxazole KW - JE42381TNV KW - Trimetrexate KW - UPN4ITI8T4 KW - Pyrimethamine KW - Z3614QOX8W KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Pyrimethamine -- therapeutic use KW - Sulfadiazine -- therapeutic use KW - Dapsone -- administration & dosage KW - Drug Combinations -- administration & dosage KW - Trimethoprim -- adverse effects KW - Humans KW - Drug Combinations -- therapeutic use KW - Sulfamethoxazole -- administration & dosage KW - Trimethoprim -- administration & dosage KW - Sulfamethoxazole -- therapeutic use KW - Recurrence KW - Drug Therapy, Combination KW - Pentamidine -- administration & dosage KW - Sulfamethoxazole -- adverse effects KW - Quinazolines -- therapeutic use KW - Drug Combinations -- adverse effects KW - Trimethoprim -- therapeutic use KW - Dapsone -- therapeutic use KW - Pentamidine -- therapeutic use KW - Pneumonia, Pneumocystis -- prevention & control KW - Anti-Bacterial Agents -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- complications KW - Pneumonia, Pneumocystis -- drug therapy KW - Pneumonia, Pneumocystis -- etiology KW - Anti-Bacterial Agents -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78313749?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pneumocystis+carinii+pneumonia%3A+therapy+and+prophylaxis.&rft.au=Kovacs%2C+J+A%3BMasur%2C+H&rft.aulast=Kovacs&rft.aufirst=J&rft.date=1988-07-01&rft.volume=158&rft.issue=1&rft.spage=254&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 - 1988-08-17 N1 - Date created - 1988-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of single-drug and combination antifungal therapy in an experimental model of candidiasis in rabbits with prolonged neutropenia. AN - 78312744; 3392423 AB - We developed an experimental model of candidiasis in rabbits with prolonged neutropenia. Rabbits were made neutropenic with cytosine arabinoside (Ara-C) administered through an indwelling silastic catheter that had been surgically implanted in the external jugular vein. Neutropenia was sustained with intravenous Ara-C, and bacterial complications were prevented with parenteral ceftazidime plus ampicillin. Candidiasis was established by intravenously administering Candida albicans or Candida tropicalis (1-2 x 10(5) colony-forming units) and resulted in hepatic and splenic lesions that mimicked those associated with hepatosplenic candidiasis in humans. The kidney proved to be the site most refractory to eradication of Candida spp. and offered a target organ for assessing antifungal therapy. We evaluated amphotericin B, 5-flucytosine, ketoconazole, and rifampin, alone and in combination. Although each agent reduced the colony counts of Candida in the liver, spleen, and lung, the combination of amphotericin B and 5-flucytosine was the only regimen effective in eradicating renal candidiasis. JF - The Journal of infectious diseases AU - Thaler, M AU - Bacher, J AU - O'Leary, T AU - Pizzo, P A AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 80 EP - 88 VL - 158 IS - 1 SN - 0022-1899, 0022-1899 KW - Antifungal Agents KW - 0 KW - Cytarabine KW - 04079A1RDZ KW - Amphotericin B KW - 7XU7A7DROE KW - Flucytosine KW - D83282DT06 KW - Ketoconazole KW - R9400W927I KW - Rifampin KW - VJT6J7R4TR KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Animals KW - Cytarabine -- toxicity KW - Ketoconazole -- administration & dosage KW - Amphotericin B -- administration & dosage KW - Rabbits KW - Rifampin -- administration & dosage KW - Flucytosine -- administration & dosage KW - Drug Evaluation, Preclinical KW - Female KW - Candidiasis -- drug therapy KW - Agranulocytosis -- complications KW - Neutropenia -- complications KW - Candidiasis -- pathology KW - Antifungal Agents -- administration & dosage KW - Neutropenia -- diagnosis KW - Candidiasis -- etiology KW - Antifungal Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78312744?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evaluation+of+single-drug+and+combination+antifungal+therapy+in+an+experimental+model+of+candidiasis+in+rabbits+with+prolonged+neutropenia.&rft.au=Thaler%2C+M%3BBacher%2C+J%3BO%27Leary%2C+T%3BPizzo%2C+P+A&rft.aulast=Thaler&rft.aufirst=M&rft.date=1988-07-01&rft.volume=158&rft.issue=1&rft.spage=80&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 - 1988-08-17 N1 - Date created - 1988-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of gene amplification by arsenic. AN - 78297610; 3388020 AB - Arsenic is a well-established carcinogen in humans, but there is little evidence for its carcinogenicity in animals and it is inactive as an initiator or tumor promoter in two-stage models of carcinogenicity in mice. Two arsenic salts (sodium arsenite and sodium arsenate) induced a high frequency of methotrexate-resistant 3T6 cells, which were shown to have amplified copies of the dihydrofolate reductase gene. The ability of arsenic to induce gene amplification may relate to its carcinogenic effects in humans since amplification of oncogenes is observed in many human tumors. The inability of arsenic to induce gene mutations may relate to the negative results of arsenic in long-term animal studies and suggests that these experiments may not detect some environmental agents that act late in the carcinogenic process in humans. JF - Science (New York, N.Y.) AU - Lee, T C AU - Tanaka, N AU - Lamb, P W AU - Gilmer, T M AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/07/01/ PY - 1988 DA - 1988 Jul 01 SP - 79 EP - 81 VL - 241 IS - 4861 SN - 0036-8075, 0036-8075 KW - Arsenates KW - 0 KW - Arsenites KW - Sodium Compounds KW - sodium arsenite KW - 48OVY2OC72 KW - sodium arsenate KW - 7631-89-2 KW - DNA KW - 9007-49-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Arsenic KW - N712M78A8G KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Animals KW - Oncogenes KW - Neoplasms, Experimental -- chemically induced KW - Neoplasms, Experimental -- genetics KW - Humans KW - DNA -- genetics KW - Drug Resistance KW - Mice KW - Nucleic Acid Hybridization KW - Cell Line KW - Arsenates -- pharmacology KW - Arsenic -- pharmacology KW - Gene Amplification -- drug effects KW - Tetrahydrofolate Dehydrogenase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78297610?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Induction+of+gene+amplification+by+arsenic.&rft.au=Lee%2C+T+C%3BTanaka%2C+N%3BLamb%2C+P+W%3BGilmer%2C+T+M%3BBarrett%2C+J+C&rft.aulast=Lee&rft.aufirst=T&rft.date=1988-07-01&rft.volume=241&rft.issue=4861&rft.spage=79&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 - 1988-08-02 N1 - Date created - 1988-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of the carbohydrate-binding specificities of cholera toxin and Escherichia coli heat-labile enterotoxins LTh-I, LT-IIa, and LT-IIb. AN - 78284383; 3290106 AB - The heat-labile enterotoxins of Vibrio cholerae and Escherichia coli are related in structure and function. They are oligomers consisting of A and B polypeptide subunits. They bind to gangliosides, and they activate adenylate cyclase. The toxins form two antigenically distinct groups; members of each group cross-react but are not necessarily identical. Serogroup I includes cholera toxin (CT) and type I heat-labile enterotoxin (LT-I) of E. coli. LTh-I and LTp-I are antigenic variants of LT-I produced by strains of E. coli from humans and pigs, respectively. Serogroup II contains the type II heat-labile enterotoxin (LT-II) of E. coli. Two antigenic variants designated LT-IIa and LT-IIb have been described. The binding of CT, LTh-I, LT-IIa, and LT-IIb to gangliosides was analyzed by immunostaining thin-layer chromatograms and by solid-phase radioimmunoassay. The four toxins have different glycolipid-binding specificities. LTh-I and CT bind strongly to ganglioside GM1 and less strongly to ganglioside GD1b. However, LTh-I, unlike CT, also binds weakly to GM2 and asialo GM1. LTh-I, like CT, probably binds to the terminal sugar sequence Gal beta 1-3GalNAc beta 1-4(NeuAc alpha 2-3)Gal . . ., where GalNAc is N-acetylgalactosamine and NeuAc is N-acetylneuraminic acid. LT-IIa probably binds to the same sugar sequence to which CT and LTh-I bind, with the additional contribution to binding of a second NeuAc as in GD1b and GD2. Also, LT-IIa must bind the Gal beta 1-3GalNAc . . . sequence in such a way that its binding is relatively unaffected by attachment of NeuAc to the terminal galactose residue as in GD1a, GT1b, and GQ1b. LT-IIb probably binds to the terminal sugar sequence NeuAc alpha 2-3Gal beta 1-4GalNAc . . ., as it binds to gangliosides GD1a and GT1b but not to GM1. JF - Infection and immunity AU - Fukuta, S AU - Magnani, J L AU - Twiddy, E M AU - Holmes, R K AU - Ginsburg, V AD - Laboratory of Structural Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 1748 EP - 1753 VL - 56 IS - 7 SN - 0019-9567, 0019-9567 KW - Bacterial Toxins KW - 0 KW - Enterotoxins KW - Escherichia coli Proteins KW - Glycolipids KW - Glycosphingolipids KW - Receptors, Cell Surface KW - Receptors, Immunologic KW - glycolipid receptor KW - heat-labile enterotoxin, E coli KW - G(M1) Ganglioside KW - 37758-47-7 KW - asialo GM1 ganglioside KW - 71012-19-6 KW - Cholera Toxin KW - 9012-63-9 KW - Neuraminidase KW - EC 3.2.1.18 KW - Index Medicus KW - Fetus KW - Animals KW - Cattle KW - Adrenal Glands -- cytology KW - Glycosphingolipids -- metabolism KW - Brain KW - Mice KW - Structure-Activity Relationship KW - Carbohydrate Conformation KW - Receptors, Immunologic -- drug effects KW - Escherichia coli -- metabolism KW - Bacterial Toxins -- metabolism KW - Enterotoxins -- metabolism KW - Receptors, Immunologic -- analysis KW - Glycolipids -- metabolism KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78284383?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+the+carbohydrate-binding+specificities+of+cholera+toxin+and+Escherichia+coli+heat-labile+enterotoxins+LTh-I%2C+LT-IIa%2C+and+LT-IIb.&rft.au=Fukuta%2C+S%3BMagnani%2C+J+L%3BTwiddy%2C+E+M%3BHolmes%2C+R+K%3BGinsburg%2C+V&rft.aulast=Fukuta&rft.aufirst=S&rft.date=1988-07-01&rft.volume=56&rft.issue=7&rft.spage=1748&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 - 1988-08-01 N1 - Date created - 1988-08-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1974 Jan 25;183(4122):334-6 [4587905] Biomed Chromatogr. 1986 Feb;1(1):31-7 [3506816] Anal Biochem. 1980 Dec;109(2):399-402 [7224165] Infect Immun. 1981 Nov;34(2):337-40 [6171517] J Biol Chem. 1981 Dec 25;256(24):13223-5 [7309759] Methods Enzymol. 1982;83:139-91 [7047999] Proc Natl Acad Sci U S A. 1982 Jun;79(11):3470-4 [6954491] Infect Immun. 1982 Nov;38(2):424-33 [7141703] Infect Immun. 1983 Jul;41(1):383-90 [6345396] J Natl Cancer Inst. 1983 Aug;71(2):231-51 [6576183] Infect Immun. 1983 Sep;41(3):1056-61 [6350177] Infect Immun. 1983 Dec;42(3):914-23 [6196297] Microbiol Rev. 1983 Dec;47(4):596-620 [6363900] FEBS Lett. 1984 Apr 24;169(2):241-6 [6325242] Microbiol Rev. 1984 Sep;48(3):199-221 [6436655] Infect Immun. 1984 Dec;46(3):759-64 [6209224] Gastroenterology. 1985 Jul;89(1):27-35 [3891496] J Biochem. 1985 Mar;97(3):729-35 [3926755] J Bacteriol. 1986 Feb;165(2):348-52 [3511028] FEBS Lett. 1986 Jun 9;201(2):229-32 [3709810] Infect Immun. 1986 Sep;53(3):464-73 [3017862] Infect Immun. 1986 Nov;54(2):529-36 [2429930] Infect Immun. 1986 Nov;54(2):587-9 [3533784] Biochem J. 1986 Sep 1;238(2):313-22 [3541910] Methods Enzymol. 1987;138:220-32 [3298951] Rev Infect Dis. 1987 May-Jun;9(3):544-61 [2440089] Infect Immun. 1987 Aug;55(8):1854-8 [3112012] Arch Biochem Biophys. 1987 Aug 15;257(1):217-29 [3115180] J Bacteriol. 1987 Nov;169(11):5180-7 [2822667] Biochem Biophys Res Commun. 1978 Feb 28;80(4):849-57 [637870] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suspiciousness induced by four-hour intravenous infusions of cocaine. Preliminary findings. AN - 78262087; 3270328 AB - Cocaine hydrochloride was administered to experienced users as an intravenous (IV) loading dose of 40 to 80 mg, followed by four-hour continuous IV infusions of either cocaine or placebo. Rates of cocaine infusion were individualized to maintain steady-state cocaine concentrations for the duration of the infusion. During the infusions, subjects rated themselves on questions that assessed their suspiciousness and paranoia, and nurse-observers took descriptive notes on the subjects' behavior; these notes were later scored on a scale for guarded, suspicious, and paranoid behavior. Nurses observed and rated moderately suspicious behavior when cocaine IV bolus loading doses were followed by cocaine infusions, but not when loading doses were followed by saline solution infusions; subjects did not rate themselves as suspicious during any of the study conditions. Suspiciousness during low-dose cocaine infusions significantly correlated with the amount of cocaine previously administered to the subjects. Suspiciousness during infusions was not related to plasma cocaine concentrations, preadmission drug use, or psychiatric symptoms and history. Cocaine infusions may be a useful tool to pursue the biology of stimulant psychoses. JF - Archives of general psychiatry AU - Sherer, M A AU - Kumor, K M AU - Cone, E J AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 673 EP - 677 VL - 45 IS - 7 SN - 0003-990X, 0003-990X KW - Placebos KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Abridged Index Medicus KW - Index Medicus KW - Infusions, Intravenous KW - Double-Blind Method KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Male KW - Paranoid Disorders -- psychology KW - Cocaine -- toxicity KW - Psychoses, Substance-Induced -- psychology KW - Psychoses, Substance-Induced -- etiology KW - Paranoid Disorders -- chemically induced KW - Cocaine -- blood KW - Cocaine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78262087?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Suspiciousness+induced+by+four-hour+intravenous+infusions+of+cocaine.+Preliminary+findings.&rft.au=Sherer%2C+M+A%3BKumor%2C+K+M%3BCone%2C+E+J%3BJaffe%2C+J+H&rft.aulast=Sherer&rft.aufirst=M&rft.date=1988-07-01&rft.volume=45&rft.issue=7&rft.spage=673&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 - 1988-07-28 N1 - Date created - 1988-07-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: NIH Guide Grants Contracts. 1993 Jun 25;22(23):1-4 [8390275] Erratum In: Arch Gen Psychiatry 1989 Dec;46(12):1152 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alprazolam augmentation of the antipsychotic effects of fluphenazine in schizophrenic patients. Preliminary results. AN - 78260784; 3289524 AB - Alprazolam was added, under double-blind conditions, to stable fluphenazine hydrochloride regimens in 12 symptomatic, chronically ill inpatients with schizophrenia. The addition of alprazolam was associated with significant, albeit modest, reductions in global psychosis, thought disorder, and paranoia ratings, with a return to pretreatment levels on discontinuation of alprazolam treatment. Improvement in "negative symptoms" such as emotional withdrawal paralleled the changes in "positive symptoms" but did not, in itself, reach statistical significance. There were no significant changes in group mean plasma levels of homovanillic acid or 3-methoxy-4-hydroxyphenylglycol during alprazolam treatment, although group mean serum cortisol levels were significantly decreased by alprazolam treatment. Patients who responded favorably to alprazolam treatment were significantly more psychotic or anxious before treatment, were older, showed significant alprazolam-associated reductions in plasma levels of homovanillic acid, and had significantly more prominent prefrontal cortex atrophy on computed tomographic scans than patients in whom alprazolam was without therapeutic effect. These preliminary data, based on a small sample, suggest that some patients with schizophrenia who are only partially responsive to standard neuroleptic treatment may benefit from the addition of triazolobenzodiazepines, such as alprazolam. JF - Archives of general psychiatry AU - Wolkowitz, O M AU - Breier, A AU - Doran, A AU - Kelsoe, J AU - Lucas, P AU - Paul, S M AU - Pickar, D AD - Section on Clinical Studies, National Institute of Mental Health, Bethesda, Md. 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 664 EP - 671 VL - 45 IS - 7 SN - 0003-990X, 0003-990X KW - Fluphenazine KW - S79426A41Z KW - Dopamine KW - VTD58H1Z2X KW - Alprazolam KW - YU55MQ3IZY KW - Abridged Index Medicus KW - Index Medicus KW - Double-Blind Method KW - Humans KW - Tomography, X-Ray Computed KW - Clinical Trials as Topic KW - Dopamine -- metabolism KW - Brain -- metabolism KW - Brain -- diagnostic imaging KW - Drug Therapy, Combination KW - Psychiatric Status Rating Scales KW - Brain -- pathology KW - Adult KW - Schizophrenic Psychology KW - Drug Synergism KW - Female KW - Male KW - Fluphenazine -- pharmacology KW - Alprazolam -- therapeutic use KW - Schizophrenia -- metabolism KW - Alprazolam -- pharmacology KW - Fluphenazine -- therapeutic use KW - Schizophrenia -- drug therapy KW - Schizophrenia -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78260784?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alprazolam+augmentation+of+the+antipsychotic+effects+of+fluphenazine+in+schizophrenic+patients.+Preliminary+results.&rft.au=Wolkowitz%2C+O+M%3BBreier%2C+A%3BDoran%2C+A%3BKelsoe%2C+J%3BLucas%2C+P%3BPaul%2C+S+M%3BPickar%2C+D&rft.aulast=Wolkowitz&rft.aufirst=O&rft.date=1988-07-01&rft.volume=45&rft.issue=7&rft.spage=664&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 - 1988-07-28 N1 - Date created - 1988-07-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Arch Gen Psychiatry. 1989 Nov;46(11):1052-3 [2818141] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential effects of bryostatins and phorbol esters on arachidonic acid metabolite release and epidermal growth factor binding in C3H 10T1/2 cells. AN - 78257125; 3132318 AB - The bryostatins, a group of macrocyclic lactones isolated on the basis of their antineoplastic activity, protein kinase C in vitro and block phorbol ester binding to this enzyme. In some cellular systems, bryostatins mimic phorbol ester action. In other systems, however, the bryostatins display only marginal agonistic action and, instead, inhibit phorbol ester-induced responses. At least in primary mouse epidermal cells, a transient duration of action of bryostatin 1 could rationalize these differences. To determine whether this model of transient activation could explain the dual actions of bryostatin 1 in other cell systems, we have examined the effects of bryostatin 1 on short-term responses in C3H 10T1/2 mouse fibroblasts. Even at very short exposures (30 min), bryostatin 1 blocked phorbol ester-induced arachidonic acid metabolite release and induced only minimal release when assayed alone. In contrast, epidermal growth factor binding was markedly and rapidly decreased in bryostatin 1-treated C3H 10T1/2 cells, and this decrease showed only limited reversal 16 h after initial exposure. Bryostatins 2, 3, 4, 10, and several of their derivatives caused variable arachidonic acid metabolite release (10 to 60% of phorbol ester control) and correspondingly variable inhibition of phorbol ester action. Our findings on arachidonic acid metabolite release argue against transient activation of the protein kinase C pathway as the sole explanation of bryostatin 1 action. They indicate, moreover, differences in the structure-activity relations of the bryostatins for the phorbol ester-mimetic and phorbol ester-inhibitory actions. JF - Cancer research AU - Dell'Aquila, M L AU - Herald, C L AU - Kamano, Y AU - Pettit, G R AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/07/01/ PY - 1988 DA - 1988 Jul 01 SP - 3702 EP - 3708 VL - 48 IS - 13 SN - 0008-5472, 0008-5472 KW - Arachidonic Acids KW - 0 KW - Bryostatins KW - Lactones KW - Macrolides KW - Phorbol Esters KW - Calcimycin KW - 37H9VM9WZL KW - bryostatin 1 KW - 37O2X55Y9E KW - Epidermal Growth Factor KW - 62229-50-9 KW - bryostatin 2 KW - 87745-28-6 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Calcium -- physiology KW - Mice KW - Calcimycin -- pharmacology KW - Time Factors KW - Cell Line KW - Structure-Activity Relationship KW - Phorbol Esters -- pharmacology KW - Receptor, Epidermal Growth Factor -- metabolism KW - Phorbol Esters -- antagonists & inhibitors KW - Protein Kinase C -- physiology KW - Arachidonic Acids -- metabolism KW - Epidermal Growth Factor -- metabolism KW - Lactones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78257125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differential+effects+of+bryostatins+and+phorbol+esters+on+arachidonic+acid+metabolite+release+and+epidermal+growth+factor+binding+in+C3H+10T1%2F2+cells.&rft.au=Dell%27Aquila%2C+M+L%3BHerald%2C+C+L%3BKamano%2C+Y%3BPettit%2C+G+R%3BBlumberg%2C+P+M&rft.aulast=Dell%27Aquila&rft.aufirst=M&rft.date=1988-07-01&rft.volume=48&rft.issue=13&rft.spage=3702&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 - 1988-07-20 N1 - Date created - 1988-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of prolactin-stimulated Nb2 lymphoma cell mitogenesis by cholera toxin and pertussis toxin. AN - 78254340; 3383778 AB - We have investigated whether cholera toxin (CT)- or pertussis toxin (IAP)-sensitive G proteins are involved in ovine (o) PRL-stimulated mitogenesis in the lactogen-dependent rat Nb2 node lymphoma cell line. Addition of IAP to medium caused a biphasic effect on oPRL-stimulated cell number. Low doses (10(-3) ng/ml) enhanced (mean +/- SEM, 15 +/- 3%) whereas higher doses (greater than or equal to 10 ng/ml) inhibited (24 +/- 3%) mitogenesis stimulated by a submaximal dose of oPRL (0.1 ng/ml) compared to control values. The cAMP analog 8-bromo-cAMP also had a biphasic effect on cell division stimulated by submaximal doses of PRL. Low doses (10(-5) M) enhanced whereas higher doses (10(-3) M) inhibited Nb2 cell growth in response to PRL. Incubation with CT only inhibited oPRL-stimulated mitogenesis in a dose-dependent manner. Maximal inhibition (63 +/- 7%) occurred at a concentration of 10 ng/ml or more. Phorbol myristate acetate (PMA) enhanced mitogenesis stimulated by PRL alone and in the presence of either stimulatory or inhibitory doses of IAP, but PMA did not block IAP inhibition. In contrast, PMA had no effect on cells incubated with CT; the inhibition of PRL-stimulated cell division by CT remained unchanged. Lactogenic receptor-binding sites per cell and affinity were not significantly affected by PMA, IAP, or CT, suggesting a postreceptor mechanism of action. In summary, these data demonstrate that cAMP modifies PRL-stimulated Nb2 cell mitogenesis. The differences between IAP and CT (i.e. biphasic effect, degree of inhibition, and differential effect of PMA) suggest that these agents could also modulate PRL actions in the Nb2 cell through different mechanisms, including a cAMP-independent pathway. JF - Endocrinology AU - Larsen, J L AU - Dufau, M L AD - Molecular Endocrinology Section, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/07// PY - 1988 DA - July 1988 SP - 438 EP - 444 VL - 123 IS - 1 SN - 0013-7227, 0013-7227 KW - Virulence Factors, Bordetella KW - 0 KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Prolactin KW - 9002-62-4 KW - Cholera Toxin KW - 9012-63-9 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Lymphoma KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Cell Line KW - Virulence Factors, Bordetella -- pharmacology KW - Cholera Toxin -- pharmacology KW - Cell Division -- drug effects KW - Prolactin -- antagonists & inhibitors KW - Prolactin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78254340?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modulation+of+prolactin-stimulated+Nb2+lymphoma+cell+mitogenesis+by+cholera+toxin+and+pertussis+toxin.&rft.au=Larsen%2C+J+L%3BDufau%2C+M+L&rft.aulast=Larsen&rft.aufirst=J&rft.date=1988-07-01&rft.volume=123&rft.issue=1&rft.spage=438&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-07-29 N1 - Date created - 1988-07-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Desensitization of pituitary gonadotropes by mediators of LH release. AN - 78304384; 3134022 AB - Desensitization of pituitary gonadotropes by exposure to 10 nM gonadotropin-releasing hormone (GnRH) for 6 h severely impaired the luteinizing hormone (LH) response to a second 3-h treatment with GnRH, and reduced the secretory responses to 50 microM arachidonic acid (AA), 100 nM tetradecanoyl phorbol-13-acetate (TPA), and AA + TPA. Pretreatment with AA blocked subsequent responses to AA but not to other secretagogues. Pretreatment with TPA attenuated the LH response to TPA, but not to GnRH, AA, and AA + TPA. After exposure to AA + TPA, all subsequent responses were abolished. Each of the secretagogues reduced GnRH receptor binding, but only GnRH-induced receptor loss and desensitization were reversed by simultaneous incubation with a GnRH antagonist. Similar results were obtained when 16-h pretreatment periods were used, or when the data were normalized for the concomitant reduction of cellular LH content. These findings indicate that GnRH-receptor loss and depletion of LH content are not the sole causes of GnRH-induced desensitization. Receptor uncoupling and impairment of AA- and protein kinase C-dependent pathways may also be involved in this process. JF - Biochemical and biophysical research communications AU - Chang, J P AU - Graeter, J S AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/06/30/ PY - 1988 DA - 1988 Jun 30 SP - 919 EP - 924 VL - 153 IS - 3 SN - 0006-291X, 0006-291X KW - Arachidonic Acids KW - 0 KW - Arachidonic Acid KW - 27YG812J1I KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Luteinizing Hormone KW - 9002-67-9 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gonadotropin-Releasing Hormone -- pharmacology KW - Female KW - Arachidonic Acids -- pharmacology KW - Pituitary Gland, Anterior -- metabolism KW - Luteinizing Hormone -- metabolism KW - Pituitary Gland, Anterior -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78304384?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Desensitization+of+pituitary+gonadotropes+by+mediators+of+LH+release.&rft.au=Chang%2C+J+P%3BGraeter%2C+J+S%3BCatt%2C+K+J&rft.aulast=Chang&rft.aufirst=J&rft.date=1988-06-30&rft.volume=153&rft.issue=3&rft.spage=919&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 - 1988-08-03 N1 - Date created - 1988-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 7,12-Dimethylbenz[a]anthracene-DNA adducts in mouse skin, dermis and epidermis. AN - 78266297; 3133108 AB - Female NIH Swiss mice were treated topically with either 0.01 or 0.1 mumol 7,12-[3H]dimethylbenz[a]anthracene and DNA was isolated either from the whole skin, the dermis or the epidermis. Levels of binding to DNA and levels of individual adducts formed were similar in all 3 tissue fractions for a given dose of carcinogen with levels for the epidermis being marginally greater than in the other fractions. In all tissue fractions, the syn dihydrodiol epoxide-deoxyribonucleoside adducts were responsible for a greater fraction of total binding at the higher, than at the lower, carcinogen dose. The mechanism of metabolic activation of 7,12-dimethylbenz[a]anthracene for DNA binding is, therefore, qualitatively the same in both the dermis and epidermis. Quantification of adducts suggests some subtle differences between the DMBA activating systems in dermis and epidermis. JF - Cancer letters AU - Pigott, M AU - Dipple, A AD - BRI-Basic Research Program, NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1988/06/30/ PY - 1988 DA - 1988 Jun 30 SP - 291 EP - 297 VL - 40 IS - 3 SN - 0304-3835, 0304-3835 KW - 3,4-dihydrodiol-1,2-epoxy 9,10-dimethyl-1,2-benzanthracene deoxyadenosine adduct KW - 0 KW - 3,4-dihydrodiol-1,2-epoxy-9,10-dimethyl-1,2-benzanthracene-deoxyguanosine adduct KW - Deoxyadenosines KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - DNA KW - 9007-49-2 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Deoxyadenosines -- analysis KW - Animals KW - Stereoisomerism KW - Deoxyadenosines -- analogs & derivatives KW - Epidermis -- metabolism KW - Mice KW - Deoxyguanosine -- analysis KW - Female KW - Chromatography, High Pressure Liquid KW - Deoxyguanosine -- analogs & derivatives KW - 9,10-Dimethyl-1,2-benzanthracene -- analogs & derivatives KW - Skin -- metabolism KW - DNA -- metabolism KW - 9,10-Dimethyl-1,2-benzanthracene -- metabolism KW - 9,10-Dimethyl-1,2-benzanthracene -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78266297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=7%2C12-Dimethylbenz%5Ba%5Danthracene-DNA+adducts+in+mouse+skin%2C+dermis+and+epidermis.&rft.au=Pigott%2C+M%3BDipple%2C+A&rft.aulast=Pigott&rft.aufirst=M&rft.date=1988-06-30&rft.volume=40&rft.issue=3&rft.spage=291&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 - 1988-08-04 N1 - Date created - 1988-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prevention of skin cancer in xeroderma pigmentosum with the use of oral isotretinoin. AN - 78239509; 3287161 AB - To confirm reports that skin cancer can be prevented with retinoids, we conducted a three-year controlled prospective study of oral isotretinoin (also called 13-cis retinoic acid) in five patients with xeroderma pigmentosum who had a history of multiple cutaneous basal-cell or squamous-cell carcinomas. Patients were treated with isotretinoin at a dosage of 2 mg per kilogram of body weight per day for two years and then followed for an additional year, without the drug. Before, during, and after treatment, biopsies of all suspicious lesions were performed, and skin cancers were surgically removed. The patients had a total of 121 tumors (mean, 24; range, 8 to 43) in the two-year interval before treatment. During two years of treatment with isotretinoin, there were 25 tumors (mean, 5; range, 3 to 9), with an average reduction in skin cancers of 63 percent (P = 0.019). After the drug was discontinued, the tumor frequency increased a mean of 8.5-fold (range, 2- to 19-fold) over the frequency during treatment (P = 0.007). Although all patients experienced mucocutaneous toxic effects, and triglyceride, liver-function, or skeletal abnormalities developed in some, high-dose oral isotretinoin was effective in the chemoprophylaxis of skin cancers in patients with xeroderma pigmentosum. JF - The New England journal of medicine AU - Kraemer, K H AU - DiGiovanna, J J AU - Moshell, A N AU - Tarone, R E AU - Peck, G L AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Md 20892. Y1 - 1988/06/23/ PY - 1988 DA - 1988 Jun 23 SP - 1633 EP - 1637 VL - 318 IS - 25 SN - 0028-4793, 0028-4793 KW - Tretinoin KW - 5688UTC01R KW - Isotretinoin KW - EH28UP18IF KW - Abridged Index Medicus KW - Index Medicus KW - Administration, Oral KW - Carcinoma, Basal Cell -- prevention & control KW - Prospective Studies KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Carcinoma, Squamous Cell -- prevention & control KW - Child KW - Adolescent KW - Male KW - Female KW - Tretinoin -- administration & dosage KW - Xeroderma Pigmentosum -- complications KW - Skin Neoplasms -- prevention & control KW - Tretinoin -- therapeutic use KW - Tretinoin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78239509?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Prevention+of+skin+cancer+in+xeroderma+pigmentosum+with+the+use+of+oral+isotretinoin.&rft.au=Kraemer%2C+K+H%3BDiGiovanna%2C+J+J%3BMoshell%2C+A+N%3BTarone%2C+R+E%3BPeck%2C+G+L&rft.aulast=Kraemer&rft.aufirst=K&rft.date=1988-06-23&rft.volume=318&rft.issue=25&rft.spage=1633&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-07-06 N1 - Date created - 1988-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - RO 15-4513 does not protect rats against the lethal effects of ethanol. AN - 78424331; 3416920 AB - In two separate research centres the ability of RO 15-4513 to protect rats against the lethal effects of ethanol (7.5 and 15 g/kg) was investigated. In neither study did RO 15-4513 offer protection against ethanol-induced lethality or the loss of righting reflex caused by these doses of ethanol. These data fail to replicate the results of an earlier report and suggest that RO 15-4513 is unlikely to be clinically useful treating acute severe ethanol toxicity. JF - European journal of pharmacology AU - Nutt, D J AU - Lister, R G AU - Rusche, D AU - Bonetti, E P AU - Reese, R E AU - Rufener, R AD - Laboratory of Clinical Studies, NIAAA/DICBR, Bethesda, MD 20892. Y1 - 1988/06/22/ PY - 1988 DA - 1988 Jun 22 SP - 127 EP - 129 VL - 151 IS - 1 SN - 0014-2999, 0014-2999 KW - Azides KW - 0 KW - Benzodiazepines KW - 12794-10-4 KW - Ethanol KW - 3K9958V90M KW - Ro 15-4513 KW - 91917-65-6 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Reflex -- drug effects KW - Time Factors KW - Male KW - Postural Balance -- drug effects KW - Ethanol -- antagonists & inhibitors KW - Azides -- pharmacology KW - Ethanol -- toxicity KW - Benzodiazepines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78424331?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=RO+15-4513+does+not+protect+rats+against+the+lethal+effects+of+ethanol.&rft.au=Nutt%2C+D+J%3BLister%2C+R+G%3BRusche%2C+D%3BBonetti%2C+E+P%3BReese%2C+R+E%3BRufener%2C+R&rft.aulast=Nutt&rft.aufirst=D&rft.date=1988-06-22&rft.volume=151&rft.issue=1&rft.spage=127&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 - 1988-10-21 N1 - Date created - 1988-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Central muscarinic cholinergic antagonists block wet-dog shakes produced by the TRH analog MK-771 in the rat. AN - 78355135; 3135919 AB - Thyrotropin-releasing hormone (TRH) is known to elicit wet-dog shakes in rats through a central mechanism of action. In the present study, the ability of muscarinic cholinergic antagonists to inhibit TRH-mediated wet-dog shakes was examined. The longer-acting TRH analog, MK-771, at doses of 1.0, 1.5 and 3.0 mg/kg elicited wet-dog shakes in a dose-dependent manner. The centrally-acting muscarinic cholinergic antagonists, atropine and scopolamine, at doses of 5 and 0.8 mg/kg, respectively, significantly reduced the ability of only the highest dose of MK-771 to elicit wet-dog shakes. When the peripherally-acting antagonists, methylscopolamine and methylatropine, were examined, they were not found to significantly reduce wet-dog shakes produced by MK-771 at doses of 5 and 0.8 mg/kg, respectively. The results of this study suggest that cholinergic antagonists inhibit MK-771-induced wet-dog shakes in a noncompetitive manner and support the view that TRH-mediated wet-dog shakes are modulated by central muscarinic cholinergic systems. JF - Brain research AU - Sills, M A AU - Mellow, A M AU - Sunderland, T AU - Jacobowitz, D M AD - Section on Histopharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/06/21/ PY - 1988 DA - 1988 Jun 21 SP - 385 EP - 388 VL - 453 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Receptors, Muscarinic KW - 0 KW - Thiazolidines KW - Scopolamine Hydrobromide KW - 451IFR0GXB KW - Thyrotropin-Releasing Hormone KW - 5Y5F15120W KW - pyro(l-alpha-aminoadipyl)-L-histidyl-L-thiazolidine-4-carboxamide KW - 64784-01-6 KW - Atropine KW - 7C0697DR9I KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Injections, Intraperitoneal KW - Animals KW - Dose-Response Relationship, Drug KW - Male KW - Thyrotropin-Releasing Hormone -- physiology KW - Thyrotropin-Releasing Hormone -- pharmacology KW - Thyrotropin-Releasing Hormone -- analogs & derivatives KW - Scopolamine Hydrobromide -- pharmacology KW - Movement Disorders -- physiopathology KW - Movement Disorders -- chemically induced KW - Receptors, Muscarinic -- drug effects KW - Atropine -- pharmacology KW - Receptors, Muscarinic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78355135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Central+muscarinic+cholinergic+antagonists+block+wet-dog+shakes+produced+by+the+TRH+analog+MK-771+in+the+rat.&rft.au=Sills%2C+M+A%3BMellow%2C+A+M%3BSunderland%2C+T%3BJacobowitz%2C+D+M&rft.aulast=Sills&rft.aufirst=M&rft.date=1988-06-21&rft.volume=453&rft.issue=1-2&rft.spage=385&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 - 1988-09-15 N1 - Date created - 1988-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Administration of MPTP acutely increases glucose utilization in the substantia nigra of primates. AN - 78351141; 3261197 AB - The quantitative 2-[14C]deoxyglucose autoradiographic method was used to map the regional distribution of the acute effects of administration of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), on local cerebral glucose utilization in rhesus monkeys. Metabolic activity was increased (+80%) in the substantia nigra pars compacta, which has been shown to be the main target site of MPTP toxicity. Metabolic activity was also increased in the nucleus paranigralis, nucleus parabrachialis pigmentosus, and ventral lamella of the inferior olive. In contrast, substantial decreases in glucose utilization were found diffusely distributed throughout many of the other structures examined, most prominently in portions of the cerebral cortex, thalamus, and cerebellum. JF - Brain research AU - Palombo, E AU - Porrino, L J AU - Bankiewicz, K S AU - Crane, A M AU - Kopin, I J AU - Sokoloff, L AD - Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/06/21/ PY - 1988 DA - 1988 Jun 21 SP - 227 EP - 234 VL - 453 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Deoxy Sugars KW - 0 KW - Pyridines KW - Deoxyglucose KW - 9G2MP84A8W KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Index Medicus KW - Brain Stem -- drug effects KW - Animals KW - Limbic System -- drug effects KW - Brain Stem -- metabolism KW - Limbic System -- metabolism KW - Macaca mulatta KW - Basal Ganglia -- drug effects KW - Male KW - Female KW - Basal Ganglia -- metabolism KW - Substantia Nigra -- metabolism KW - Substantia Nigra -- drug effects KW - Pyridines -- pharmacology KW - Deoxyglucose -- metabolism KW - Deoxy Sugars -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78351141?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Administration+of+MPTP+acutely+increases+glucose+utilization+in+the+substantia+nigra+of+primates.&rft.au=Palombo%2C+E%3BPorrino%2C+L+J%3BBankiewicz%2C+K+S%3BCrane%2C+A+M%3BKopin%2C+I+J%3BSokoloff%2C+L&rft.aulast=Palombo&rft.aufirst=E&rft.date=1988-06-21&rft.volume=453&rft.issue=1-2&rft.spage=227&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 - 1988-09-15 N1 - Date created - 1988-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cornigerine, a potent antimitotic Colchicum alkaloid of unusual structure. Interactions with tubulin. AN - 78303106; 3390207 AB - Cornigerine is a natural product analog of colchicine produced by Colchicum cornigerum in which the vicinal 2- and 3-methoxy groups are condensed into a methylenedioxy bridge. This produces a fourth ring and a structure which resembles a hybrid of colchicine, podophyllotoxin, and steganacin. Cornigerine was somewhat more toxic than colchicine with L1210 murine leukemia cells and caused them to accumulate in metaphase arrest. Cornigerine resembled colchicine in its interactions with tubulin in vitro, and it was also somewhat more potent than colchicine in these drug-tubulin interactions. Cornigerine inhibited tubulin polymerization both with and without microtubule-associated proteins, inhibited the binding of radiolabeled colchicine to tubulin, and stimulated tubulin-dependent GTP hydrolysis. Indirect evidence suggested that the binding of cornigerine to tubulin is relatively slow and temperature-dependent, like the binding of colchicine to the protein. JF - Biochemical pharmacology AU - Hamel, E AU - Ho, H H AU - Kang, G J AU - Lin, C M AD - Laboratory of Pharmacology and Experimental Therapeutics, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06/15/ PY - 1988 DA - 1988 Jun 15 SP - 2445 EP - 2449 VL - 37 IS - 12 SN - 0006-2952, 0006-2952 KW - Tubulin KW - 0 KW - cornigerine KW - 6877-25-4 KW - Guanosine Triphosphate KW - 86-01-1 KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Animals KW - Cell Survival -- drug effects KW - Mice KW - Herb-Drug Interactions KW - Hydrolysis KW - Structure-Activity Relationship KW - Guanosine Triphosphate -- metabolism KW - Plants, Medicinal -- analysis KW - Colchicine -- pharmacology KW - Colchicum -- analysis KW - Tubulin -- metabolism KW - Colchicine -- analogs & derivatives KW - Mitosis -- drug effects KW - Colchicine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78303106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cornigerine%2C+a+potent+antimitotic+Colchicum+alkaloid+of+unusual+structure.+Interactions+with+tubulin.&rft.au=Hamel%2C+E%3BHo%2C+H+H%3BKang%2C+G+J%3BLin%2C+C+M&rft.aulast=Hamel&rft.aufirst=E&rft.date=1988-06-15&rft.volume=37&rft.issue=12&rft.spage=2445&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 - 1988-07-29 N1 - Date created - 1988-07-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - G proteins in clinical medicine. AN - 78258109; 2454242 JF - Hospital practice (Office ed.) AU - Spiegel, A M AD - Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda. Y1 - 1988/06/15/ PY - 1988 DA - 1988 Jun 15 SP - 93 EP - 100, 105-6, 111-2 VL - 23 IS - 6 SN - 8750-2836, 8750-2836 KW - Ion Channels KW - 0 KW - Receptors, Cell Surface KW - Virulence Factors, Bordetella KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - GTP Phosphohydrolases KW - EC 3.6.1.- KW - GTP-Binding Proteins KW - Abridged Index Medicus KW - Index Medicus KW - Genes, ras KW - Virulence Factors, Bordetella -- pharmacology KW - Animals KW - Humans KW - GTP Phosphohydrolases -- metabolism KW - Cholera Toxin -- pharmacology KW - Pseudohypoparathyroidism -- genetics KW - Pseudohypoparathyroidism -- metabolism KW - Cyclic AMP -- physiology KW - Ion Channels -- physiology KW - Receptors, Cell Surface -- physiology KW - Cell Membrane -- enzymology KW - GTP-Binding Proteins -- physiology KW - Cell Membrane -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78258109?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=G+proteins+in+clinical+medicine.&rft.au=Spiegel%2C+A+M&rft.aulast=Spiegel&rft.aufirst=A&rft.date=1988-06-15&rft.volume=23&rft.issue=6&rft.spage=93&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 - 1988-07-21 N1 - Date created - 1988-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential carbohydrate processing and secretion of thyrotropin and free alpha subunit. Effects of 1-deoxynojirimycin. AN - 78244907; 2453512 AB - In pulse-chase experiments we compared the kinetics of early carbohydrate processing and subsequent secretion of thyroid-stimulating hormone (TSH) and free alpha subunit under control conditions and after treatment with 1-deoxynojirimycin, an inhibitor of glucosidases I and II. Under control conditions TSH achieved resistance to endo-beta-N-acetylglucosaminidase H (endo H) more rapidly than free alpha (t1/2 0.3 h versus 0.9 h); however, free alpha was secreted more rapidly than TSH (t1/2 2.2 h versus 3.4 h). With 1-deoxynojirimycin, oligosaccharides co-migrating with G3Man9GlcNAc and G2Man9GlcNAc were demonstrated on TSH for the first time, suggesting that previous pulse-chase studies did not disclose these intermediates due to rapid removal of glucose residues from the common G3Man9GlcNAc2 precursor. 1-Deoxynojirimycin delayed the rate of attainment of endo H resistance for both TSH and free alpha, but there was no effect on subunit combination. With 5 mM 1-deoxynojirimycin the amount of secreted free alpha was reduced to 65% of control; secreted TSH was reduced markedly to 17% of control without intracellular accumulation, suggesting increased intracellular degradation. There was no significant toxicity from these doses of 1-deoxynojirimycin on the production or secretion of the two major nonglycosylated pituitary proteins, growth hormone and prolactin, or on at least 10 other secretory proteins. Basal differences in the relative rates of TSH and free alpha processing and secretion as well as differential sensitivity to 1-deoxynojirimycin suggest separate secretory pathways for these two closely related proteins. JF - The Journal of biological chemistry AU - Stannard, B S AU - Gesundheit, N AU - Ronin, C AU - Burnside, J AU - Weintraub, B D AD - Molecular, Cellular, and Nutritional Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1988/06/15/ PY - 1988 DA - 1988 Jun 15 SP - 8309 EP - 8317 VL - 263 IS - 17 SN - 0021-9258, 0021-9258 KW - Glycoprotein Hormones, alpha Subunit KW - 0 KW - Pituitary Hormones, Anterior KW - 1-Deoxynojirimycin KW - 19130-96-2 KW - Thyrotropin KW - 9002-71-5 KW - Hexosaminidases KW - EC 3.2.1.- KW - Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase KW - EC 3.2.1.96 KW - Glucosamine KW - N08U5BOQ1K KW - Index Medicus KW - Animals KW - Hexosaminidases -- metabolism KW - Thyroid Neoplasms -- metabolism KW - Thyroid Diseases -- metabolism KW - Mice KW - Models, Biological KW - Chromatography, High Pressure Liquid KW - Glucosamine -- pharmacology KW - Glucosamine -- analogs & derivatives KW - Kinetics KW - Pituitary Gland -- metabolism KW - Pituitary Hormones, Anterior -- secretion KW - Thyrotropin -- secretion KW - Carbohydrate Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78244907?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+carbohydrate+processing+and+secretion+of+thyrotropin+and+free+alpha+subunit.+Effects+of+1-deoxynojirimycin.&rft.au=Stannard%2C+B+S%3BGesundheit%2C+N%3BRonin%2C+C%3BBurnside%2C+J%3BWeintraub%2C+B+D&rft.aulast=Stannard&rft.aufirst=B&rft.date=1988-06-15&rft.volume=263&rft.issue=17&rft.spage=8309&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 - 1988-07-13 N1 - Date created - 1988-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quantitative associations between DNA damage in human placenta and maternal smoking and birth weight. AN - 78242468; 3373547 AB - Specimens of human placental DNA were tested for chemical addition products (adducts) by recently developed 32P-postlabeling and immunologic assays, and results were compared with data concerning maternal exposures and birth weight. A total of 7 different adducts were detected in the 53 specimens of human placental tissue examined by the 32P-postlabeling assay. Three of these adducts were found almost exclusively in smokers. Among smokers there were positive dose-response relationships between levels of the smoking-related adducts and biochemical estimates of doses of maternal exposure to cigarette smoke during pregnancy. Levels of 1 adduct found only in smokers appeared to relate directly to amounts of caffeine consumption by the mother. In addition to these relationships with maternal exposures, levels of smoking-related adducts were inversely associated with the birth weight of offspring. Results from this study suggest that even at their current formative stage of development, assays for DNA adducts may help identify determinants of DNA damage to human tissues and improve our ability to demonstrate dose-response relationships for the effects of environmental exposures to potentially carcinogenic agents. JF - Journal of the National Cancer Institute AU - Everson, R B AU - Randerath, E AU - Santella, R M AU - Avitts, T A AU - Weinstein, I B AU - Randerath, K AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1988/06/15/ PY - 1988 DA - 1988 Jun 15 SP - 567 EP - 576 VL - 80 IS - 8 SN - 0027-8874, 0027-8874 KW - Carcinogens KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Population KW - Birth Weight KW - Maternal Health KW - Age Factors KW - Low Birth Weight KW - Physiology KW - Social Behavior KW - Health KW - Infant, Premature KW - Infant KW - Body Weight KW - Smoking KW - Population Characteristics KW - Behavior KW - Child Development KW - Demographic Factors KW - Youth KW - Biology KW - Carcinogens -- metabolism KW - Humans KW - Adult KW - Statistics as Topic KW - Female KW - Prenatal Exposure Delayed Effects KW - Pregnancy KW - DNA Damage KW - DNA -- metabolism KW - Placenta -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78242468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Quantitative+associations+between+DNA+damage+in+human+placenta+and+maternal+smoking+and+birth+weight.&rft.au=Everson%2C+R+B%3BRanderath%2C+E%3BSantella%2C+R+M%3BAvitts%2C+T+A%3BWeinstein%2C+I+B%3BRanderath%2C+K&rft.aulast=Everson&rft.aufirst=R&rft.date=1988-06-15&rft.volume=80&rft.issue=8&rft.spage=567&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 - 1988-06-29 N1 - Date created - 1988-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-selective cyclic AMP analogues are antagonistic to estrogen stimulation of growth and proto-oncogene expression in human breast-cancer cells. AN - 78232208; 2836320 AB - Cyclic AMP (cAMP) analogues that selectively bind to either one of the two binding sites of cAMP-dependent protein kinase demonstrate a potent inhibition of the growth stimulated by estrogen in MCF-7 human breast-cancer cells in culture. The site-selective analogues, which are more potent activators of protein kinase than the analogues studied earlier, exhibit growth inhibition at micromolar concentrations. Among the analogues tested, 8-Cl-cAMP (Site I-selective) and N6-benzyl-cAMP (Site 2-selective) are the 2 most potent inhibitors, causing 40-70% inhibition of the estrogen-stimulated growth at 10-20 microM concentrations with no sign of toxicity. 8-Cl-cAMP (1 microM) in combination with N6-benzyl-cAMP (0.5 microM) almost completely blocks estrogen-stimulated growth, demonstrating synergism between the Site 1- and Site 2-selective analogues. The growth inhibition parallels an increase in the R11 cAMP receptor protein with a decrease in the R1 receptor as well as reduction of c-myc and c-ras oncoproteins, whereas growth inhibition by tamoxifen does not affect the levels of the cAMP receptor proteins or the c-myc and c-ras protein levels. Site-selective cAMP analogues are antagonistic to estrogen stimulation of breast-cancer cell growth through a mechanism different from that of tamoxifen. JF - International journal of cancer AU - Katsaros, D AU - Ally, S AU - Cho-Chung, Y S AD - Cellular Biochemistry Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06/15/ PY - 1988 DA - 1988 Jun 15 SP - 863 EP - 867 VL - 41 IS - 6 SN - 0020-7136, 0020-7136 KW - Proto-Oncogene Proteins KW - 0 KW - Receptors, Cyclic AMP KW - Tamoxifen KW - 094ZI81Y45 KW - Estradiol KW - 4TI98Z838E KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Tamoxifen -- pharmacology KW - Cells, Cultured KW - Humans KW - Proto-Oncogene Proteins -- metabolism KW - Cell Division -- drug effects KW - Receptors, Cyclic AMP -- metabolism KW - Time Factors KW - Cell Line KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- pathology KW - Estradiol -- pharmacology KW - Cyclic AMP -- analogs & derivatives KW - Proto-Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78232208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Site-selective+cyclic+AMP+analogues+are+antagonistic+to+estrogen+stimulation+of+growth+and+proto-oncogene+expression+in+human+breast-cancer+cells.&rft.au=Katsaros%2C+D%3BAlly%2C+S%3BCho-Chung%2C+Y+S&rft.aulast=Katsaros&rft.aufirst=D&rft.date=1988-06-15&rft.volume=41&rft.issue=6&rft.spage=863&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 - 1988-07-11 N1 - Date created - 1988-07-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolism of the Z and E isomers of N-nitroso-N-methyl-(2-oxopropyl)amine by rat hepatocytes. AN - 78223476; 3370636 AB - The metabolism of N-nitroso-N-methyl-N-(2-oxopropyl)amine was examined using freshly isolated hepatocytes from Fischer 344 rats. As determined by high performance liquid chromatography, it was found that the E isomer was preferentially metabolized when the parent mixture was used. When the two isomers were studied separately, the E isomer was efficiently metabolized in the hepatocytic system, whereas the Z isomer was not. The kinetics of disappearance of the Z isomer during metabolism was identical to that for the reequilibration of the Z isomer to the mixture of isomers in the absence of a metabolizing system. JF - Cancer research AU - Farrelly, J G AU - Stewart, M L AU - Farnsworth, D W AU - Saavedra, J E AD - NCI-Frederick Cancer Research Facility, Basic Research Program, Maryland 21701. Y1 - 1988/06/15/ PY - 1988 DA - 1988 Jun 15 SP - 3347 EP - 3349 VL - 48 IS - 12 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - Nitrosamines KW - N-nitrosomethyl-2-oxopropylamine KW - 55984-51-5 KW - Index Medicus KW - Rats KW - Animals KW - Stereoisomerism KW - In Vitro Techniques KW - Carcinogens -- metabolism KW - Nitrosamines -- metabolism KW - Liver -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78223476?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Metabolism+of+the+Z+and+E+isomers+of+N-nitroso-N-methyl-%282-oxopropyl%29amine+by+rat+hepatocytes.&rft.au=Farrelly%2C+J+G%3BStewart%2C+M+L%3BFarnsworth%2C+D+W%3BSaavedra%2C+J+E&rft.aulast=Farrelly&rft.aufirst=J&rft.date=1988-06-15&rft.volume=48&rft.issue=12&rft.spage=3347&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 - 1988-06-29 N1 - Date created - 1988-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of protein kinase C in phosphorylation of vinculin in adriamycin-resistant HL-60 leukemia cells. AN - 78215104; 3130982 AB - In response to phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA), HL-60 cells differentiate to macrophage-like cells and exhibit the ability to phosphorylate vinculin in vitro. Adriamycin-resistant HL-60 (HL-60/ADR) cells similarly demonstrate this characteristic without prior treatment with TPA. Since protein kinase C (PK-C) is a cellular TPA receptor, we have examined the role of this enzyme in the inherent ability of HL-60/ADR cells to phosphorylate vinculin. DEAE-cellulose chromatography of cell extracts revealed that HL-60/ADR cells contained 2-fold more PK-C than did the parental cell line. All PK-C activity was found in the cytosol of wild type HL-60 cells, whereas 85% of PK-C activity was cytosolic and 15% was membrane-bound in HL-60/ADR cells. After a 2-day treatment with 10 nM TPA, PK-C activity was reduced 80-90% in both cell lines regardless of its intracellular distribution. Immunoblotting of cell extracts from HL-60/ADR cells or HL-60 cells following treatment with TPA revealed increased levels of a 52-kDa species of similar mass to M-kinase. Coincident with these changes after TPA treatment was a reduction in Ca2+ and phospholipid-independent phosphorylation of vinculin in vitro in extracts from HL-60/ADR cells, whereas HL-60 cells exhibited an elevation of this phosphoprotein. The phosphorylation of vinculin in TPA-treated HL-60 cells or untreated HL-60/ADR cells was blocked by antibodies to protein kinase C. These results suggest that it is not the absolute level of protein kinase C but rather the proteolytic activation of PK-C to a Ca2+ and phospholipid-independent form which is associated with the utilization of vinculin as an endogenous substrate. JF - Cancer research AU - Aquino, A AU - Hartman, K D AU - Knode, M C AU - Grant, S AU - Huang, K P AU - Niu, C H AU - Glazer, R I AD - Laboratory of Biological Chemistry, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/06/15/ PY - 1988 DA - 1988 Jun 15 SP - 3324 EP - 3329 VL - 48 IS - 12 SN - 0008-5472, 0008-5472 KW - Muscle Proteins KW - 0 KW - Vinculin KW - 125361-02-6 KW - Doxorubicin KW - 80168379AG KW - Protein Kinase C KW - EC 2.7.11.13 KW - Endopeptidases KW - EC 3.4.- KW - Neprilysin KW - EC 3.4.24.11 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Tumor Cells, Cultured KW - Phosphorylation KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Drug Resistance KW - Cell Differentiation -- drug effects KW - Endopeptidases -- physiology KW - Muscle Proteins -- metabolism KW - Doxorubicin -- pharmacology KW - Leukemia, Myeloid, Acute -- metabolism KW - Protein Kinase C -- physiology KW - Protein Kinase C -- immunology KW - Leukemia, Myeloid, Acute -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78215104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+protein+kinase+C+in+phosphorylation+of+vinculin+in+adriamycin-resistant+HL-60+leukemia+cells.&rft.au=Aquino%2C+A%3BHartman%2C+K+D%3BKnode%2C+M+C%3BGrant%2C+S%3BHuang%2C+K+P%3BNiu%2C+C+H%3BGlazer%2C+R+I&rft.aulast=Aquino&rft.aufirst=A&rft.date=1988-06-15&rft.volume=48&rft.issue=12&rft.spage=3324&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 - 1988-06-29 N1 - Date created - 1988-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential effects of maitotoxin on ATP secretion and on phosphoinositide breakdown in rat pheochromocytoma cells. AN - 78268066; 2838322 AB - Maitotoxin (MTX) induced exocytotic secretion of ATP from PC12 rat pheochromocytoma cells. The threshold for stimulation of secretion was at concentrations of about 2 ng/ml of MTX. Maximal release occurred at 40 ng/ml. MTX-induced ATP release required the presence of calcium in the extracellular medium and could be inhibited by nifedipine, a specific blocker of voltage-dependent calcium channels. In addition to the effects on ATP secretion from PC12 cells, MTX stimulated the breakdown of phosphoinositides, as measured by the accumulation of [3H]inositol phosphates. Maximal stimulation of phosphoinositide breakdown was reached at only 0.5-1.0 ng/ml MTX. MTX at concentrations required to evoke ATP release (greater than 2 ng/ml) had lesser or no effect on phosphoinositide breakdown. Although stimulation of phosphoinositide breakdown by MTX was dependent on extracellular calcium, it was insensitive to the calcium channel blockers nifedipine, D-600 and cobalt ions. The different concentration range required to elicit these responses and the varying sensitivity to calcium channel blockers indicate that MTX-evoked secretion and MTX-stimulated phosphoinositide breakdown are independent phenomena in PC12 cells. JF - FEBS letters AU - Gusovsky, F AU - Daly, J W AU - Yasumoto, T AU - Rojas, E AD - Laboratory of Bioorganic Chemistry, NIDDK, Bethesda, MD 20892. Y1 - 1988/06/06/ PY - 1988 DA - 1988 Jun 06 SP - 139 EP - 142 VL - 233 IS - 1 SN - 0014-5793, 0014-5793 KW - Inositol Phosphates KW - 0 KW - Marine Toxins KW - Oxocins KW - Phosphatidylinositols KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - maitotoxin KW - 9P59GES78D KW - Nifedipine KW - I9ZF7L6G2L KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Nifedipine -- pharmacology KW - Animals KW - Tumor Cells, Cultured KW - Inositol Phosphates -- metabolism KW - Dose-Response Relationship, Drug KW - Calcium -- pharmacology KW - Marine Toxins -- pharmacology KW - Phosphatidylinositols -- metabolism KW - Adrenal Gland Neoplasms -- metabolism KW - Adenosine Triphosphate -- secretion KW - Pheochromocytoma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78268066?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Differential+effects+of+maitotoxin+on+ATP+secretion+and+on+phosphoinositide+breakdown+in+rat+pheochromocytoma+cells.&rft.au=Gusovsky%2C+F%3BDaly%2C+J+W%3BYasumoto%2C+T%3BRojas%2C+E&rft.aulast=Gusovsky&rft.aufirst=F&rft.date=1988-06-06&rft.volume=233&rft.issue=1&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-01 N1 - Date created - 1988-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regional cerebral palmitate incorporation after unilateral auditory deprivation in immature and adult Fischer-344 rats. AN - 85237306; pmid-3366202 AB - Regional cerebral incorporation of intravenously injected [U-14C]palmitate was measured from 1 day to 13 weeks after left cochlear destruction in 11-day- and 3 month-old, awake Fischer-344 rats. In 11-day-old animals, statistically significant left-right differences in incorporation were absent 1 day after cochlear destruction and were found only in parts of the cochlear nucleus and inferior colliculus after 1 week. After 6 to 13 weeks, consistent with functional neuroanatomy of central auditory regions, incorporation was reduced by 6 to 9% in the left cochlear nucleus and left lateral superior olivary nucleus, compared with corresponding right-side regions. The right medial superior olivary nucleus, medial nucleus of the trapezoid body, lateral lemniscus nucleus, inferior colliculus, medial geniculate body, and auditory cortex had 5 to 9% less incorporation than did corresponding left-side regions. Fewer significant differences after chronic auditory deprivation occurred in 3-month-old rats than in 11-day-old rats following cochlear destruction. Reduced incorporation corresponded to reported changes in cell morphology, which also were greater in immature than mature rats following auditory deprivation. The results suggest that the palmitate method can be used to identify long-term regional changes in the turnover of brain lipids after sensory deprivation. JF - Experimental Neurology AU - Tone, O AU - Miller, J C AU - Bell, J M AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute on Aging, Bethesda, Maryland 20892. PY - 1988 SP - 491 EP - 505 VL - 100 IS - 3 SN - 0014-4886, 0014-4886 KW - Rats KW - Cochlea KW - Animals, Newborn KW - Rats, Inbred F344 KW - Comparative Study KW - Palmitic Acids KW - Palmitates KW - Auditory Pathways KW - Sensory Deprivation KW - Brain KW - Animal KW - Tissue Distribution KW - Hearing KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85237306?accountid=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+Neurology&rft.atitle=Regional+cerebral+palmitate+incorporation+after+unilateral+auditory+deprivation+in+immature+and+adult+Fischer-344+rats.&rft.au=Tone%2C+O%3BMiller%2C+J+C%3BBell%2C+J+M%3BRapoport%2C+S+I&rft.aulast=Tone&rft.aufirst=O&rft.date=1988-06-01&rft.volume=100&rft.issue=3&rft.spage=491&rft.isbn=&rft.btitle=&rft.title=Experimental+Neurology&rft.issn=00144886&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Cholesteryl ester storage disease: a patient with massive splenomegaly and splenic abscess. AN - 85215285; pmid-3376925 AB - Cholesteryl ester storage disease (CESD), a rare lysosomal storage disorder characterized by functional deficiency of acid lipase activity, classically features hepatomegaly in conjunction with lipid-laden macrophages containing excessive quantities of cholesteryl esters. We present a patient whose clinical course was complicated by massive, symptomatic splenomegaly, and an unsuspected splenic abscess. Computed tomographic and magnetic resonance imaging are correlated. Histologic, electron microscopic, and biochemical features are presented. To our knowledge, this is the first report of splenic abscess in CESD. JF - The American Journal of Gastroenterology AU - Edelstein, R A AU - Filling-Katz, M R AU - Pentchev, P AU - Gal, A AU - Chandra, R AU - Shawker, T AU - Guzzetta, P AU - Comly, M AU - Kaneski, C AU - Brady, R O AD - Developmental and Metabolic Neurology Branch, National Institutes of Health, Bethesda, Maryland. PY - 1988 SP - 687 EP - 692 VL - 83 IS - 6 SN - 0002-9270, 0002-9270 KW - Lipid Metabolism, Inborn Errors KW - Pedigree KW - Abscess KW - Human KW - Liver KW - Spleen KW - Case Report KW - Child KW - Splenomegaly KW - Cholesterol Esters KW - Splenic Diseases KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85215285?accountid=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=Cholesteryl+ester+storage+disease%3A+a+patient+with+massive+splenomegaly+and+splenic+abscess.&rft.au=Edelstein%2C+R+A%3BFilling-Katz%2C+M+R%3BPentchev%2C+P%3BGal%2C+A%3BChandra%2C+R%3BShawker%2C+T%3BGuzzetta%2C+P%3BComly%2C+M%3BKaneski%2C+C%3BBrady%2C+R+O&rft.aulast=Edelstein&rft.aufirst=R&rft.date=1988-06-01&rft.volume=83&rft.issue=6&rft.spage=687&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 - Ultrastructural localization of GABA-immunoreactive terminals in the anteroventral cochlear nucleus of the guinea pig. AN - 85171338; pmid-2898468 AB - The immunocytochemical distribution of gamma-aminobutyric acid (GABA) was studied by electron microscopy in the anteroventral cochlear nucleus (AVCN) of the guinea pig using affinity-purified antibodies made against GABA conjugated to bovine serum albumin. Our observations confirm that spherical cells are the predominant cell type in the guinea pig AVCN and receive numerous axosomatic contacts (Schwartz and Gulley, (1978) J. Anat. 153, 489-508). Stellate cells receive few axosomatic contacts. Electron microscopic immunocytochemistry shows that GABA immunoreactivity is present in synaptic terminals in the AVCN. Of the several classes of presynaptic terminals present in the AVCN as characterized by vesicle type (large round; oval/pleomorphic; flat; small round) only those containing oval/pleomorphic vesicles were GABA-immunoreactive. However, GABA immunoreactivity may not be present in all these terminals because some oval/pleomorphic terminals are unlabelled. Immunoreactive terminals are widespread in the AVCN; they are abundant on spherical cell bodies, rarely seen on stellate cell bodies and are also found scattered throughout the neuropile. JF - Hearing Research AU - Oberdorfer, M D AU - Parakkal, M H AU - Altschuler, R A AU - Wenthold, R J AD - National Eye Institute, Bethesda, MD 20892. PY - 1988 SP - 229 EP - 238 VL - 33 IS - 3 SN - 0378-5955, 0378-5955 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85171338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hearing+Research&rft.atitle=Ultrastructural+localization+of+GABA-immunoreactive+terminals+in+the+anteroventral+cochlear+nucleus+of+the+guinea+pig.&rft.au=Oberdorfer%2C+M+D%3BParakkal%2C+M+H%3BAltschuler%2C+R+A%3BWenthold%2C+R+J&rft.aulast=Oberdorfer&rft.aufirst=M&rft.date=1988-06-01&rft.volume=33&rft.issue=3&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Hearing+Research&rft.issn=03785955&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Clinical, histologic, and immunopathologic comparison of pemphigus vulgaris and pemphigus foliaceus. AN - 78805144; 2978970 JF - Seminars in dermatology AU - Koulu, L AU - Stanley, J R AD - Dermatology Branch, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 82 EP - 90 VL - 7 IS - 2 SN - 0278-145X, 0278-145X KW - Adrenal Cortex Hormones KW - 0 KW - Immunoglobulin G KW - Index Medicus KW - Adrenal Cortex Hormones -- therapeutic use KW - Immunoglobulin G -- analysis KW - Drug Eruptions -- etiology KW - Acantholysis -- enzymology KW - Mouth Mucosa -- pathology KW - Humans KW - Immunoglobulin G -- immunology KW - Fluorescent Antibody Technique KW - Pemphigus -- pathology KW - Pemphigus -- immunology KW - Pemphigus -- chemically induced KW - Pemphigus -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78805144?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+dermatology&rft.atitle=Clinical%2C+histologic%2C+and+immunopathologic+comparison+of+pemphigus+vulgaris+and+pemphigus+foliaceus.&rft.au=Koulu%2C+L%3BStanley%2C+J+R&rft.aulast=Koulu&rft.aufirst=L&rft.date=1988-06-01&rft.volume=7&rft.issue=2&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Seminars+in+dermatology&rft.issn=0278145X&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 - Oncogene activation in spontaneous and chemically induced rodent tumors: implications for risk analysis. AN - 78582526; 3203636 AB - The validity of rodent tumor end points in assessing the potential hazards of chemical exposure to humans is a somewhat controversial but very important issue since most chemicals are classified as potentially hazardous to humans on the basis of long-term carcinogenesis studies in rodents. The ability to distinguish between genotoxic, cytotoxic, or receptor-mediated promotion effects of chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in spontaneously occurring and chemically induced rodent tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of rodent tumors. Different patterns of activated oncogenes were found not only in spontaneous versus chemically induced mouse liver tumors but also in a variety of spontaneous rat tumors versus chemically induced rat lung tumors. In the absence of cytotoxic effects, it could be argued that the chemicals in question activated protooncogenes by a direct genotoxic mechanism. These results provided a basis for the analysis of activated oncogenes in spontaneous and chemically induced rodent tumors to provide information at a molecular level to aid in the extrapolation of rodent carcinogenesis data to human risk assessment. JF - Environmental health perspectives AU - Reynolds, S H AU - Stowers, S J AU - Patterson, R M AU - Maronpot, R R AU - Anderson, M W AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 175 EP - 177 VL - 78 SN - 0091-6765, 0091-6765 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Risk Factors KW - Humans KW - Mice KW - Neoplasms -- veterinary KW - Oncogenes KW - Neoplasms, Experimental -- chemically induced KW - Neoplasms -- chemically induced KW - Rodent Diseases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78582526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oncogene+activation+in+spontaneous+and+chemically+induced+rodent+tumors%3A+implications+for+risk+analysis.&rft.au=Reynolds%2C+S+H%3BStowers%2C+S+J%3BPatterson%2C+R+M%3BMaronpot%2C+R+R%3BAnderson%2C+M+W&rft.aulast=Reynolds&rft.aufirst=S&rft.date=1988-06-01&rft.volume=78&rft.issue=&rft.spage=175&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 - 1989-02-06 N1 - Date created - 1989-02-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1983 Nov 18;222(4625):771-8 [6356358] Annu Rev Genet. 1984;18:553-612 [6397126] Science. 1985 May 3;228(4699):596-7 [3983645] Nature. 1985 May 30-Jun 5;315(6018):382-5 [3923365] Science. 1987 Sep 11;237(4820):1309-16 [3629242] Proc Natl Acad Sci U S A. 1986 Jan;83(1):33-7 [3510430] Proc Natl Acad Sci U S A. 1986 Aug;83(16):6048-52 [3016738] Cancer Res. 1987 Jun 15;47(12):3212-9 [3581065] Cell. 1985 Aug;42(1):23-38 [2990725] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human bronchial epithelial cells with integrated SV40 virus T antigen genes retain the ability to undergo squamous differentiation. AN - 78505753; 2846394 AB - Human bronchial epithelial cells transformed by either DNA virus infection (SV40 or Adenovirus 12-SV40 hybrid virus) or transfection with the SV40 large T antigen gene were studied for their ability to undergo squamous differentiation when exposed to 12-O-tetradecanoylphorbol-13 acetate (TPA), transforming growth factor-beta 1 (TGF-beta 1), or fetal bovine serum (FBS), agents that induce the squamous differentiation of normal human bronchial epithelial cells. Squamous differentiation occurred in all ten T-antigen-positive cell cultures when they were exposed to either FBS or TGF-beta 1, but none differentiated when exposed to TPA. From one cell line, designated BEAS-2B, two subclones were isolated, one of which was induced to undergo squamous differentiation by FBS, and a second that failed to undergo squamous differentiation and was mitogenically stimulated when exposed to serum. These phenotypically different subclones provide a new in vitro cellular system for delineating the mechanism(s) of human bronchial epithelial cell squamous differentiation in response to FBS or TGF-beta 1. JF - Differentiation; research in biological diversity AU - Ke, Y AU - Reddel, R R AU - Gerwin, B I AU - Miyashita, M AU - McMenamin, M AU - Lechner, J F AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 60 EP - 66 VL - 38 IS - 1 SN - 0301-4681, 0301-4681 KW - Antigens, Viral KW - 0 KW - Serum Albumin, Bovine KW - 12-O-tetradeca-2,4,6,8-tetranoylphorbol-13-acetate KW - 64604-09-7 KW - Transforming Growth Factors KW - 76057-06-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Tetradecanoylphorbol Acetate -- analogs & derivatives KW - Cells, Cultured KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Serum Albumin, Bovine -- pharmacology KW - Cell Differentiation KW - Transforming Growth Factors -- pharmacology KW - Colony-Forming Units Assay KW - Cell Line KW - Tumor Cells, Cultured -- cytology KW - Tumor Cells, Cultured -- immunology KW - Bronchi -- cytology KW - Tumor Cells, Cultured -- drug effects KW - Antigens, Viral -- metabolism KW - Bronchi -- drug effects KW - Bronchi -- immunology KW - Parainfluenza Virus 1, Human -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78505753?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+bronchial+epithelial+cells+with+integrated+SV40+virus+T+antigen+genes+retain+the+ability+to+undergo+squamous+differentiation.&rft.au=Ke%2C+Y%3BReddel%2C+R+R%3BGerwin%2C+B+I%3BMiyashita%2C+M%3BMcMenamin%2C+M%3BLechner%2C+J+F%3BHarris%2C+C+C&rft.aulast=Ke&rft.aufirst=Y&rft.date=1988-06-01&rft.volume=38&rft.issue=1&rft.spage=60&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 - 1988-12-22 N1 - Date created - 1988-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The statistical analysis of a carcinogen mixture experiment. II. Carcinogens with different target organs, N-methyl-N'-nitro-N-nitrosoguanidine, N-butyl-N-(4-hydroxybutyl)nitrosamine, dipentylnitrosamine, and nitrilotriacetic acid. AN - 78475333; 3176036 AB - This paper describes factorial experiments designed to determine whether two carcinogens that act on different organ systems act synergistically to produce cancers in Fischer 344 rats. Four carcinogens, N-methyl-N'-nitrosoguanidine (MNNG), N-butanol-N-butylnitrosamine (NBBN), nitilotriacetic acid (NTA), and dipentylnitrosamine (DPN) were studied in pairwise combinations. Each of the six possible pairs was studied by means of a 4 X 4 factorial experiment, each agent being fed at zero and at three non-zero doses. Methods of analysis designed explicitly for this study were derived to study interaction. These methods were supplemented by standard statistical methods appropriate for single agent studies. Antagonism was demonstrated in some chemical mixtures containing NTA. Other chemical mixtures did not interact. Findings for male and female animals were generally, but not always, in agreement. JF - Toxicology and industrial health AU - Fears, T R AU - Elashoff, R M AU - Schneiderman, M A AD - Biostatistics Branch, National Cancer Institute, Washington, D.C. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 221 EP - 255 VL - 4 IS - 2 SN - 0748-2337, 0748-2337 KW - Carcinogens KW - 0 KW - Nitrosamines KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - N,N-diamylnitrosamine KW - 13256-06-9 KW - Butylhydroxybutylnitrosamine KW - 3817-11-6 KW - Nitrilotriacetic Acid KW - KA90006V9D KW - Index Medicus KW - Nitrosamines -- toxicity KW - Animals KW - Butylhydroxybutylnitrosamine -- toxicity KW - Drug Interactions KW - Cocarcinogenesis KW - Sex Factors KW - Methylnitronitrosoguanidine -- toxicity KW - Kidney Neoplasms -- chemically induced KW - Nitrilotriacetic Acid -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Rats KW - Nitrosamines -- administration & dosage KW - Nitrilotriacetic Acid -- administration & dosage KW - Rats, Inbred F344 KW - Stomach Neoplasms -- chemically induced KW - Butylhydroxybutylnitrosamine -- administration & dosage KW - Data Interpretation, Statistical KW - Methylnitronitrosoguanidine -- administration & dosage KW - Female KW - Male KW - Urinary Bladder Neoplasms -- chemically induced KW - Carcinogens -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78475333?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+statistical+analysis+of+a+carcinogen+mixture+experiment.+II.+Carcinogens+with+different+target+organs%2C+N-methyl-N%27-nitro-N-nitrosoguanidine%2C+N-butyl-N-%284-hydroxybutyl%29nitrosamine%2C+dipentylnitrosamine%2C+and+nitrilotriacetic+acid.&rft.au=Fears%2C+T+R%3BElashoff%2C+R+M%3BSchneiderman%2C+M+A&rft.aulast=Fears&rft.aufirst=T&rft.date=1988-06-01&rft.volume=4&rft.issue=2&rft.spage=221&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 - 1988-11-22 N1 - Date created - 1988-11-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An illustration of dangers of ignoring survival differences in carcinogenic data. AN - 78454736; 3171079 AB - This paper illustrates the effects of survival differences on the routine analysis of 2-year animal carcinogenesis experiments using quantal response. Not adjusting for decreased survival in the higher dosed groups results in a decrease in the actual significance level for the quantal response trend test, and a corresponding decrease in sensitivity for detecting a true treatment effect. Similar results hold for estimation of carcinogenic risk. Tables of the range of survival differences found in recent National Toxicology Program carcinogenesis studies are presented. JF - Journal of applied toxicology : JAT AU - Bailer, A J AU - Portier, C J AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, NC 27709. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 185 EP - 189 VL - 8 IS - 3 SN - 0260-437X, 0260-437X KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Mice KW - Male KW - Female KW - Carcinogens -- toxicity KW - Neoplasms, Experimental -- mortality KW - Data Interpretation, Statistical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78454736?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+applied+toxicology+%3A+JAT&rft.atitle=An+illustration+of+dangers+of+ignoring+survival+differences+in+carcinogenic+data.&rft.au=Bailer%2C+A+J%3BPortier%2C+C+J&rft.aulast=Bailer&rft.aufirst=A&rft.date=1988-06-01&rft.volume=8&rft.issue=3&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=Journal+of+applied+toxicology+%3A+JAT&rft.issn=0260437X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-23 N1 - Date created - 1988-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of receptor-mediated signal transduction by diacylglycerol mimetics in astrocytes. AN - 78385697; 3136922 AB - 1. When rat astrocytes in primary culture were incubated with bradykinin, inositol phosphate formation and arachidonic acid release were stimulated. 2. By themselves, phorbol esters inhibited inositol phosphate formation, but phorbol esters and other cell-permeant diacylglycerol analogues stimulated arachidonic acid release. Preincubation of the cells with phorbol esters or diacylglycerol analogues blocked bradykinin-stimulated inositol phosphate formation but augmented bradykinin-stimulated arachidonic acid release. 3. The present results suggest that, in astrocytes, bradykinin activates at least two signal transduction pathways bradykinin stimulates a phosphatidylinositol-specific phospholipase C leading to enhanced inositol phosphate formation, and bradykinin stimulates a second phospholipase to enhance arachidonic acid release. The pathways may be distinguished using phorbol esters and other diacylglycerol mimetics. 4. The possibility is raised that diacylglycerol, formed in response to bradykinin, may serve as a transducer of receptor-receptor interactions by altering the ability of receptors to stimulate phospholipase activity. JF - Cellular and molecular neurobiology AU - Burch, R M AU - Kniss, D A AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 251 EP - 257 VL - 8 IS - 2 SN - 0272-4340, 0272-4340 KW - Arachidonic Acids KW - 0 KW - Diglycerides KW - Glycerides KW - Inositol Phosphates KW - Phorbol Esters KW - Arachidonic Acid KW - 27YG812J1I KW - Type C Phospholipases KW - EC 3.1.4.- KW - Bradykinin KW - S8TIM42R2W KW - Index Medicus KW - Rats KW - Animals KW - Inositol Phosphates -- metabolism KW - Cells, Cultured KW - Arachidonic Acids -- metabolism KW - Type C Phospholipases -- physiology KW - Phorbol Esters -- pharmacology KW - Cerebral Cortex -- cytology KW - Diglycerides -- pharmacology KW - Cerebral Cortex -- physiology KW - Cerebral Cortex -- drug effects KW - Astrocytes -- drug effects KW - Astrocytes -- physiology KW - Bradykinin -- pharmacology KW - Glycerides -- pharmacology KW - Astrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78385697?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+molecular+neurobiology&rft.atitle=Modulation+of+receptor-mediated+signal+transduction+by+diacylglycerol+mimetics+in+astrocytes.&rft.au=Burch%2C+R+M%3BKniss%2C+D+A&rft.aulast=Burch&rft.aufirst=R&rft.date=1988-06-01&rft.volume=8&rft.issue=2&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Cellular+and+molecular+neurobiology&rft.issn=02724340&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor-beta: possible roles in carcinogenesis. AN - 78375960; 3044431 AB - TGF-beta is the prototype of a large family of multifunctional regulatory proteins. The principal sources of the peptide, platelets and bone, suggest that it plays a role in healing and remodeling processes. In vitro, TGF-beta is chemotactic for monocytes and fibroblasts and can greatly enhance accumulation of extracellular matrix components by fibroblasts. Its ability to stimulate the formation of granulation tissue locally and the demonstration of specific time- and tissue-dependent expression in embryogenesis suggest that similar mechanisms are operative in vivo. By analogy to its effects in wound healing and embryogenesis, it is proposed that TGF-beta, secreted by tumour cells, can augment tumour growth indirectly by effects on the stromal elements. These effects include suppression of the immune response, and enhancement of both angiogenesis and formation of connective tissue. Many tumour cells have escaped from direct growth inhibitory effects of TGF-beta by a variety of mechanisms including inability to activate the latent form of the peptide, loss of cellular receptors for TGF-beta, and loss of functional intracellular signal transduction pathways. JF - British journal of cancer AU - Roberts, A B AU - Thompson, N L AU - Heine, U AU - Flanders, C AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 594 EP - 600 VL - 57 IS - 6 SN - 0007-0920, 0007-0920 KW - Peptides KW - 0 KW - Transforming Growth Factors KW - 76057-06-2 KW - Index Medicus KW - Animals KW - Chemistry KW - Embryonic and Fetal Development KW - Chemical Phenomena KW - Mice KW - Peptides -- physiology KW - Neoplasms -- etiology KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78375960?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transforming+growth+factor-beta%3A+possible+roles+in+carcinogenesis.&rft.au=Roberts%2C+A+B%3BThompson%2C+N+L%3BHeine%2C+U%3BFlanders%2C+C%3BSporn%2C+M+B&rft.aulast=Roberts&rft.aufirst=A&rft.date=1988-06-01&rft.volume=57&rft.issue=6&rft.spage=594&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 - 1988-09-26 N1 - Date created - 1988-09-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Adv Cancer Res. 1972;16:181-234 [4563044] Cell. 1987 Oct 23;51(2):189-97 [3499229] J Biol Chem. 1983 Jun 10;258(11):7155-60 [6602130] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3676-80 [6602340] Proc Natl Acad Sci U S A. 1983 Oct;80(20):6264-8 [6604914] Cancer Res. 1983 Dec;43(12 Pt 1):5915-21 [6640540] Biochemistry. 1983 Dec 6;22(25):5692-8 [6607069] J Biol Chem. 1987 Oct 25;262(30):14655-62 [2889729] Cancer Res. 1987 Dec 15;47(24 Pt 1):6595-9 [3499977] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2396-400 [6326125] Nature. 1984 Jun 28-Jul 4;309(5971):804-6 [6330562] Science. 1984 Nov 9;226(4675):705-7 [6093254] Proc Natl Acad Sci U S A. 1985 Jan;82(1):119-23 [3871521] Nature. 1985 Feb 28-Mar 6;313(6005):745-7 [3883191] Mol Cell Biol. 1985 Jan;5(1):242-7 [3856735] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2267-71 [3857579] Nature. 1985 Aug 22-28;316(6030):701-5 [3861940] Nature. 1985 Aug 29-Sep 4;316(6031):823-6 [2993906] J Clin Invest. 1985 Sep;76(3):1042-56 [3876354] Nature. 1985 Oct 3-9;317(6036):438-40 [2995828] Nature. 1985 Dec 19-1986 Jan 1;318(6047):659-63 [2417121] Biochem Biophys Res Commun. 1985 Dec 31;133(3):1026-34 [3866579] J Cell Physiol. 1986 Feb;126(2):312-8 [3455929] Cancer Res. 1986 Apr;46(4 Pt 2):2068-71 [2418960] J Biol Chem. 1986 Mar 25;261(9):4337-45 [3456347] J Cell Biol. 1986 Apr;102(4):1217-23 [3457014] J Immunol. 1986 May 15;136(10):3916-20 [2871107] J Exp Med. 1986 May 1;163(5):1037-50 [2871125] Nature. 1986 Jun 19-25;321(6072):776-9 [3012369] Nature. 1986 Jun 19-25;321(6072):779-82 [3086749] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4167-71 [2424019] Cancer Res. 1986 Sep;46(9):4665-71 [3089593] J Biol Chem. 1986 Aug 15;261(23):10478-81 [3488314] J Cell Physiol. 1986 Aug;128(2):322-8 [3488321] J Clin Invest. 1986 Aug;78(2):329-32 [3525608] Biochem Biophys Res Commun. 1986 Jul 16;138(1):476-82 [3461784] J Biol Chem. 1986 Sep 15;261(26):12362-7 [3528157] J Cell Biol. 1986 Dec;103(6 Pt 1):2403-10 [3491081] J Immunol. 1986 Dec 15;137(12):3855-60 [2878044] Mol Cell Biol. 1986 May;6(5):1679-86 [2431284] Cell. 1987 Dec 4;51(5):861-7 [3479264] Cell. 1987 Dec 4;51(5):869-77 [3479265] J Cell Biol. 1987 Dec;105(6 Pt 2):2861-76 [3320058] EMBO J. 1987 Dec 1;6(12):3673-7 [3322813] N Engl J Med. 1986 Dec 25;315(26):1650-9 [3537791] J Exp Med. 1987 Jan 1;165(1):251-6 [3491869] Br J Cancer. 1986 Nov;54(5):779-85 [2432915] Cancer Res. 1987 Feb 1;47(3):707-12 [3467839] Cell. 1987 Feb 13;48(3):409-15 [2879635] Cell Biol Int Rep. 1986 Dec;10(12):915-22 [3467860] J Biol Chem. 1987 May 15;262(14):6443-6 [3471760] EMBO J. 1987 Jun;6(6):1633-6 [3497030] J Cell Biol. 1987 Jul;105(1):457-63 [3475276] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5788-92 [2886992] Cancer Res. 1987 Sep 1;47(17):4590-4 [2887281] J Biol Chem. 1987 Sep 5;262(25):12127-31 [3476488] J Cell Biol. 1987 Aug;105(2):965-75 [2887577] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6020-4 [2888109] EMBO J. 1987 Jul;6(7):1899-904 [2820711] FASEB J. 1987 Oct;1(4):312-7 [3498658] J Cell Biol. 1987 Sep;105(3):1039-45 [3308901] J Exp Med. 1987 Oct 1;166(4):991-8 [3498791] Nature. 1987 Oct 8-14;329(6139):539-41 [2889143] J Cell Physiol. 1982 Feb;110(2):169-74 [6279682] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Validity testing of the TDx Cocaine Metabolite Assay with human specimens obtained after intravenous cocaine administration. AN - 78374852; 3410396 AB - Clinical specimens obtained from human subjects after intravenous cocaine administration were analyzed by the TDx Cocaine Metabolite Assay (TDx) and by GC/MS for benzoylecgonine. The TDx results were significantly correlated with results by GC/MS assay with no evidence of bias in the TDx assay. All cocaine metabolite positive specimens (greater than or equal to 300 ng/ml) were confirmed by GC/MS. Detection times to the last positive specimen by TDx assay and GC/MS assay of four subjects after a 20-mg intravenous dose of cocaine ranged from 29.3 to 39.1 h and 27.9 and 36.6 h, respectively. Overall, the TDx assay was found to be highly specific and accurate for the detection and measurement of benzoylecgonine in urine. JF - Forensic science international AU - Cone, E J AU - Menchen, S L AU - Mitchell, J AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 265 EP - 275 VL - 37 IS - 4 SN - 0379-0738, 0379-0738 KW - benzoylecgonine KW - 5353I8I6YS KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Injections, Intravenous KW - Humans KW - Gas Chromatography-Mass Spectrometry KW - Time Factors KW - Male KW - Cocaine -- analogs & derivatives KW - Cocaine -- urine KW - Substance-Related Disorders -- urine KW - Cocaine -- metabolism KW - Cocaine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78374852?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Forensic+science+international&rft.atitle=Validity+testing+of+the+TDx+Cocaine+Metabolite+Assay+with+human+specimens+obtained+after+intravenous+cocaine+administration.&rft.au=Cone%2C+E+J%3BMenchen%2C+S+L%3BMitchell%2C+J&rft.aulast=Cone&rft.aufirst=E&rft.date=1988-06-01&rft.volume=37&rft.issue=4&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Forensic+science+international&rft.issn=03790738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Review of occupational epidemiology of chromium chemicals and respiratory cancer. AN - 78364536; 3043655 AB - Several epidemiologic studies have investigated the association between cancer risk and employment in chromium producing and using industries. Strong and consistent associations have been found between employment in the primary chemical producing industry and the risk for respiratory cancer. Workers employed in chromate pigment production and possibly spray painters of chromate pigment paints appear to be at excess risk of respiratory cancer. Chrome platers may also be at excess risk, although the evidence is limited. A few studies indicate that chromium alloy welding may also be an exposure source of concern. Some studies of ferrochromium alloy workers have shown an excess risk for respiratory cancer, although the risk may in part be due to concomitant exposures. The evidence indicates that the hexavalent form of chromium is the primary agent of chromium carcinogenesis. Solubility and other characteristics of chromium compounds may also play a role in determining risk. JF - The Science of the total environment AU - Hayes, R B AD - Occupational Studies Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06/01/ PY - 1988 DA - 1988 Jun 01 SP - 331 EP - 339 VL - 71 IS - 3 SN - 0048-9697, 0048-9697 KW - Carcinogens KW - 0 KW - Chromium KW - 0R0008Q3JB KW - Index Medicus KW - Risk Factors KW - Humans KW - Respiratory Tract Neoplasms -- chemically induced KW - Occupational Diseases -- epidemiology KW - Respiratory Tract Neoplasms -- epidemiology KW - Occupational Diseases -- chemically induced KW - Chromium -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78364536?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Science+of+the+total+environment&rft.atitle=Review+of+occupational+epidemiology+of+chromium+chemicals+and+respiratory+cancer.&rft.au=Hayes%2C+R+B&rft.aulast=Hayes&rft.aufirst=R&rft.date=1988-06-01&rft.volume=71&rft.issue=3&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=The+Science+of+the+total+environment&rft.issn=00489697&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-16 N1 - Date created - 1988-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human and simian immunodeficiency retroviruses: activation and differential transactivation of gene expression. AN - 78330915; 2840105 AB - New West African human immunodeficiency viruses (HIV-2s) and simian immunodeficiency virus (SIV) contain functional transactivator (tat) gene and tat response elements. Their long terminal repeats (LTR) and tat genes are more related among themselves than to HIV-1 LTR and tat gene. The viral gene expression of HIV-2 as well as SIV can be stimulated by T cell activators, such as mitogens and phorbol esters. HIV-2 and SIV display a much broader transactivation response specificity than does HIV-1. The LTR-directed gene expression of HIV-2/SIV is not only transactivated by their own tat gene and by HIV-1 tat gene but also by factors in human T cell leukemia/lymphoma virus type I (HTLV-I) and simian virus 40 (SV40) infected cells, involving HTLV-I tat gene and SV40 T antigens, respectively. HIV-1 LTR-directed gene expression is much less transactivated by HIV-2/SIV tat genes and by factors in HTLV-I- and SV40-infected cells. Immune activation and heterologous transactivation of the LTR-directed gene expression may be relevant to the latency of virus infection and progression toward the acquired immunodeficiency syndrome (AIDS). JF - AIDS research and human retroviruses AU - Arya, S K AD - Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 175 EP - 186 VL - 4 IS - 3 SN - 0889-2229, 0889-2229 KW - Phytohemagglutinins KW - 0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Repetitive Sequences, Nucleic Acid KW - Phytohemagglutinins -- pharmacology KW - Haplorhini KW - Cell Line KW - Retroviridae Infections -- veterinary KW - Genes, Viral KW - Gene Expression Regulation KW - Retroviridae -- genetics KW - Monkey Diseases -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78330915?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+and+simian+immunodeficiency+retroviruses%3A+activation+and+differential+transactivation+of+gene+expression.&rft.au=Arya%2C+S+K&rft.aulast=Arya&rft.aufirst=S&rft.date=1988-06-01&rft.volume=4&rft.issue=3&rft.spage=175&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 - 1988-09-02 N1 - Date created - 1988-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of treatment-induced mortality and tumor-induced mortality on tests for carcinogenicity in small samples. AN - 78309928; 3390507 AB - Statistical tests of carcinogenicity are shown to have varying degrees of robustness to the effects of mortality. Mortality induced by two different mechanisms is studied--mortality due to the tumor of interest, and mortality due to treatment independent of the tumor. The two most commonly used tests, the life-table test and the Cochran-Armitage linear trend test, are seen to be highly sensitive to increases in treatment lethality using small-sample simulations. Increases in tumor lethality are seen to affect the performance of commonly used prevalence tests such as logistic regression. A simple survival-adjusted quantal response test appears to be the most robust of all the procedures considered. JF - Biometrics AU - Bailer, A J AU - Portier, C J AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 417 EP - 431 VL - 44 IS - 2 SN - 0006-341X, 0006-341X KW - Index Medicus KW - Animals KW - Stochastic Processes KW - Models, Theoretical KW - Biometry -- methods KW - Neoplasms, Experimental -- chemically induced KW - Mutagenicity Tests -- methods KW - Neoplasms, Experimental -- therapy KW - Neoplasms, Experimental -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78309928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+treatment-induced+mortality+and+tumor-induced+mortality+on+tests+for+carcinogenicity+in+small+samples.&rft.au=Bailer%2C+A+J%3BPortier%2C+C+J&rft.aulast=Bailer&rft.aufirst=A&rft.date=1988-06-01&rft.volume=44&rft.issue=2&rft.spage=417&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-19 N1 - Date created - 1988-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Panic attacks and alcohol withdrawal: can subjects differentiate the symptoms? AN - 78308994; 3390501 JF - Biological psychiatry AU - George, D T AU - Zerby, A AU - Noble, S AU - Nutt, D J AD - National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 240 EP - 243 VL - 24 IS - 2 SN - 0006-3223, 0006-3223 KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Diagnosis, Differential KW - Humans KW - Adult KW - Somatoform Disorders -- psychology KW - Male KW - Female KW - Fear KW - Alcohol Withdrawal Delirium -- psychology KW - Psychoses, Alcoholic -- psychology KW - Panic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78308994?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Panic+attacks+and+alcohol+withdrawal%3A+can+subjects+differentiate+the+symptoms%3F&rft.au=George%2C+D+T%3BZerby%2C+A%3BNoble%2C+S%3BNutt%2C+D+J&rft.aulast=George&rft.aufirst=D&rft.date=1988-06-01&rft.volume=24&rft.issue=2&rft.spage=240&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 - 1988-08-23 N1 - Date created - 1988-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Estimating tumor incidence rates in animal carcinogenicity experiments. AN - 78308528; 3390506 AB - Tumor incidence is the primary measure of carcinogenesis. This article focuses on estimating time-dependent incidence rates in animal experiments with few sacrifices. When the context of observation is known for none or all of the animals dying with the tumor of interest, previous results are obtained under relaxed assumptions. The link with existing semiparametric and nonparametric procedures based on latent failure times is exploited by using these methods to compute maximum likelihood estimates of the incidence rates without introducing latent random variables. Nonparametric estimators that are appropriate when all contexts of observation are known are generalized to the case in which the contexts of observation are unknown for a subset of the tumor-bearing animals. 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 - 1988/06// PY - 1988 DA - June 1988 SP - 405 EP - 415 VL - 44 IS - 2 SN - 0006-341X, 0006-341X KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Models, Theoretical KW - Neoplasms, Experimental -- epidemiology KW - Biometry -- methods KW - Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78308528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Estimating+tumor+incidence+rates+in+animal+carcinogenicity+experiments.&rft.au=Dinse%2C+G+E&rft.aulast=Dinse&rft.aufirst=G&rft.date=1988-06-01&rft.volume=44&rft.issue=2&rft.spage=405&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-19 N1 - Date created - 1988-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Exploring simple independent action in multifactor tables of proportions. AN - 78308444; 3390513 AB - The problem of assessing synergistic or antagonistic departure from simple independent action in multifactor tables of proportions is discussed. A generalized linear model is employed in which additivity corresponds to simple independent action. Data-analytic strategies are proposed for exploring departures from simple independent action in various extensions of the 2 X 2 table of proportions. This methodology is illustrated with a series of models fitted to cellular differentiation and murine toxicity data. JF - Biometrics AU - Piegorsch, W W AU - Weinberg, C R AU - Margolin, B H AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 595 EP - 603 VL - 44 IS - 2 SN - 0006-341X, 0006-341X KW - Index Medicus KW - Lymphoma -- mortality KW - Probability KW - Lymphoma -- therapy KW - Animals KW - Humans KW - In Vitro Techniques KW - Mice KW - Cell Differentiation -- drug effects KW - Models, Biological KW - Models, Theoretical KW - Biometry -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78308444?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Exploring+simple+independent+action+in+multifactor+tables+of+proportions.&rft.au=Piegorsch%2C+W+W%3BWeinberg%2C+C+R%3BMargolin%2C+B+H&rft.aulast=Piegorsch&rft.aufirst=W&rft.date=1988-06-01&rft.volume=44&rft.issue=2&rft.spage=595&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-19 N1 - Date created - 1988-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Respiratory tract lesions in F344/N rats and B6C3F1 mice after inhalation exposure to 1,2-epoxybutane. AN - 78294759; 3388431 AB - 1,2-Epoxybutane, a short-chain epoxide used as a stabilizer in chlorinated hydrocarbon solvents, was administered by inhalation exposure as a vapor 6 h/day, 5 day/week, for 24 months at exposure concentrations of 0, 200 or 400 ppm to F344/N rats and 0, 50, or 100 ppm to B6C3F1 mice. Survival of all groups of rats was 50% or greater until week 98 but was reduced in exposed groups by the end of the study. Survival in male mice was comparable among groups. Survival in female mice was greater than 50% until week 86, but was then reduced in the high-exposure group of mice. Exposure-related inflammatory, degenerative, and proliferative lesions occurred in the nasal cavity of both rats and mice. Seven papillary adenomas occurred in the nasal passages of high-exposure male rats and 2 in the nasal passages of high-exposure female rats. Alveolar/bronchiolar adenoma or carcinoma (combined) occurred with increased incidence in exposed male rats relative to controls. No exposure-related neoplastic lesions were seen in mice. After inhalation exposure, 1,2-epoxybutane was carcinogenic in rodents as were other epoxides or related compounds including propylene oxide, 1,3-butadiene, and ethylene oxide. The site of carcinogenic activity was considered to be related to length of the carbon chain. JF - Toxicology AU - Dunnick, J K AU - Eustis, S L AU - Piegorsch, W W AU - Miller, R A AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, NC 27709. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 69 EP - 82 VL - 50 IS - 1 SN - 0300-483X, 0300-483X KW - Carcinogens KW - 0 KW - Epoxy Compounds KW - Ethers, Cyclic KW - 1,2-epoxybutane KW - 106-88-7 KW - Index Medicus KW - Rats KW - Nasal Mucosa -- pathology KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Body Weight -- drug effects KW - Mice KW - Nasal Mucosa -- drug effects KW - Administration, Inhalation KW - Species Specificity KW - Male KW - Female KW - Ethers, Cyclic -- toxicity KW - Nose Diseases -- chemically induced KW - Nose Neoplasms -- pathology KW - Nose Neoplasms -- chemically induced KW - Epoxy Compounds -- toxicity KW - Nose Diseases -- pathology KW - Lung Neoplasms -- chemically induced KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78294759?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Respiratory+tract+lesions+in+F344%2FN+rats+and+B6C3F1+mice+after+inhalation+exposure+to+1%2C2-epoxybutane.&rft.au=Dunnick%2C+J+K%3BEustis%2C+S+L%3BPiegorsch%2C+W+W%3BMiller%2C+R+A&rft.aulast=Dunnick&rft.aufirst=J&rft.date=1988-06-01&rft.volume=50&rft.issue=1&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-11 N1 - Date created - 1988-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolic basis for a drug hypersensitivity: antibodies in sera from patients with halothane hepatitis recognize liver neoantigens that contain the trifluoroacetyl group derived from halothane. AN - 78291794; 3385639 AB - Previous studies have demonstrated that antibodies in sera from patients with halothane hepatitis recognize halothane-induced liver microsomal polypeptide neoantigens, and have suggested that these antibodies may play a role in the pathogenesis of the hepatitis. In the present study, the mechanism of neoantigen generation was investigated. Liver microsomes from rats treated in vivo with halothane or deuterated halothane were tested by immunoblotting for reactivity with patients' sera and with an antiserum specific for the covalently bound trifluoroacetyl (TFA) halide metabolite of halothane. Rat liver microsomes incubated aerobically or anaerobically with halothane or deuterated halothane in vitro, +/- NADPH and/or NADH, were also analyzed. The results obtained demonstrate that neoantigen expression involves oxidative halothane metabolism by cytochromes P-450 to TFA halide and covalent binding of the TFA group to the proteins. Incubation of microsomes from halothane-treated rats with 1 M piperidine cleaved the TFA groups from the proteins and abolished antigenicity, confirming this conclusion. Recognition of the neoantigens by the patients' antibodies was inhibited only partially using the hapten derivative N-E-TFA-L-lysine. It appears that the patients' antibodies recognize epitopes consisting of the TFA group plus associated structural features of the protein carriers (100 kDa, 76 kDa, 59 kDa, 57 kDa and 54 kDa), not the TFA hapten alone. To our knowledge, this constitutes the first characterization of drug metabolite-tissue protein neoantigens implicated in a drug hypersensitivity. The approach described may be of general utility for characterization of drug-induced neoantigens associated with other drug hypersensitivities. JF - The Journal of pharmacology and experimental therapeutics AU - Kenna, J G AU - Satoh, H AU - Christ, D D AU - Pohl, L R AD - Laboratory of Chemical Pharmacology, National Heart, Lung and Blood Institute, Bethesda, Maryland. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 1103 EP - 1109 VL - 245 IS - 3 SN - 0022-3565, 0022-3565 KW - Antigens KW - 0 KW - Haptens KW - Halothane KW - UQT9G45D1P KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Humans KW - Male KW - Halothane -- metabolism KW - Drug Hypersensitivity -- immunology KW - Liver -- immunology KW - Halothane -- immunology KW - Halothane -- toxicity KW - Antigens -- analysis KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78291794?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Metabolic+basis+for+a+drug+hypersensitivity%3A+antibodies+in+sera+from+patients+with+halothane+hepatitis+recognize+liver+neoantigens+that+contain+the+trifluoroacetyl+group+derived+from+halothane.&rft.au=Kenna%2C+J+G%3BSatoh%2C+H%3BChrist%2C+D+D%3BPohl%2C+L+R&rft.aulast=Kenna&rft.aufirst=J&rft.date=1988-06-01&rft.volume=245&rft.issue=3&rft.spage=1103&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 - 1988-07-29 N1 - Date created - 1988-07-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of Ro15-4513 and other benzodiazepine receptor inverse agonists on alcohol-induced intoxication in the rat. AN - 78282456; 2455039 AB - The ability of the imidazobenzodiazepine Ro15-4513 to antagonize the behavioral intoxication produced by ethanol and related short-chain alcohols was examined in the rat. Ro15-4513 dose dependently (0.5-10 mg/kg i.p.: IC50, 1.5 mg/kg) inhibited the intoxication induced by ethanol (2 g/kg), as well as t-amyl alcohol (0.36 g/kg) and methanol (4.66 g/kg). The effects of Ro15-4513 in blocking ethanol-induced intoxication were blocked by the benzodiazepine receptor antagonists Ro15-1788 and CGS-8216. However, Ro15-4513 was ineffective in antagonizing the intoxication observed after higher doses of ethanol (4 g/kg). In contrast, ethanol-induced intoxication was not antagonized by the benzodiazepine receptor antagonists Ro15-1788 (10 mg/kg) or CGS-8216 (20 mg/kg), nor by the inverse agonists FG-7142 (10-30 mg/kg) or beta CCE (10 mg/kg). When administered after ethanol, Ro15-4513 also reversed ethanol-induced intoxication in a dose-dependent manner (2.5-10 mg/kg i.p.: IC50, 5 mg/kg), an effect which was also blocked by Ro15-1788 and CGS-8216. However, neither beta CCE (10 mg/kg) or FG-7142 (less than or equal to 30 mg/kg) alone reversed ethanol-induced intoxication. Moreover, beta CCE (10 mg/kg), when administered just before Ro15-4513, completely antagonized the actions of Ro15-4513 in reversing ethanol-induced intoxication. These data suggest that the ability of Ro15-4513 to antagonize, and to reverse, ethanol-induced intoxication is mediated via central benzodiazepine receptors.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Journal of pharmacology and experimental therapeutics AU - Suzdak, P D AU - Paul, S M AU - Crawley, J N AD - Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 880 EP - 886 VL - 245 IS - 3 SN - 0022-3565, 0022-3565 KW - Azides KW - 0 KW - Carbolines KW - Chlorides KW - Ion Channels KW - Pyrazoles KW - Receptors, GABA-A KW - Benzodiazepines KW - 12794-10-4 KW - Ethanol KW - 3K9958V90M KW - FG 7142 KW - 60PO70N1BP KW - beta-carboline-3-carboxylic acid ethyl ester KW - 74214-62-3 KW - 2-phenylpyrazolo(4,3-c)quinolin-3(5H)-one KW - 77779-60-3 KW - Ro 15-4513 KW - 91917-65-6 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Pyrazoles -- pharmacology KW - Animals KW - Ion Channels -- drug effects KW - Ethanol -- toxicity KW - Chlorides -- metabolism KW - Carbolines -- pharmacology KW - Male KW - Alcoholic Intoxication -- prevention & control KW - Azides -- pharmacology KW - Receptors, GABA-A -- drug effects KW - Benzodiazepines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78282456?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Effects+of+Ro15-4513+and+other+benzodiazepine+receptor+inverse+agonists+on+alcohol-induced+intoxication+in+the+rat.&rft.au=Suzdak%2C+P+D%3BPaul%2C+S+M%3BCrawley%2C+J+N&rft.aulast=Suzdak&rft.aufirst=P&rft.date=1988-06-01&rft.volume=245&rft.issue=3&rft.spage=880&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 - 1988-07-29 N1 - Date created - 1988-07-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of migrainelike headaches by the serotonin agonist m-chlorophenylpiperazine. AN - 78258560; 3378382 AB - In a study of serotonin (5-HT) function in patients with eating disorders and healthy control subjects, severe headaches with features of common migraine occurred unexpectedly in 28 of 52 subjects (54%) 8 to 12 hours after receiving a single oral dose of the 5-HT receptor agonist m-chlorophenylpiperazine (m-CPP), 0.5 mg/kg. None of the same subjects developed similar late-occurring headaches after placebo or the 5-HT precursor, L-tryptophan, 100 mg/kg given intravenously. The frequency of these migrainelike headaches was not significantly different between patients with bulimia or anorexia nervosa and control subjects, but incidence of headaches was significantly greater in subjects with a personal or family history of migraine, with almost all predisposed individuals (18 of 20, 90%) developing severe symptoms. Headache ratings were also significantly correlated (rho = 0.70; p less than 0.0001) with peak concentrations of m-CPP in plasma. These observations indicate that m-CPP may provide a novel probe for studies of the pathophysiology of migraine headaches. JF - Clinical pharmacology and therapeutics AU - Brewerton, T D AU - Murphy, D L AU - Mueller, E A AU - Jimerson, D C AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Md. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 605 EP - 609 VL - 43 IS - 6 SN - 0009-9236, 0009-9236 KW - Piperazines KW - 0 KW - Receptors, Serotonin KW - 1-(3-chlorophenyl)piperazine KW - REY0CNO998 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Adult KW - Female KW - Receptors, Serotonin -- drug effects KW - Migraine Disorders -- etiology KW - Migraine Disorders -- chemically induced KW - Piperazines -- pharmacology KW - Piperazines -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78258560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Induction+of+migrainelike+headaches+by+the+serotonin+agonist+m-chlorophenylpiperazine.&rft.au=Brewerton%2C+T+D%3BMurphy%2C+D+L%3BMueller%2C+E+A%3BJimerson%2C+D+C&rft.aulast=Brewerton&rft.aufirst=T&rft.date=1988-06-01&rft.volume=43&rft.issue=6&rft.spage=605&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 - 1988-07-22 N1 - Date created - 1988-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Histogenesis and clonality of pancreatic tumors induced by v-myc and v-raf oncogenes in NFS/N mice. AN - 78256541; 3381877 AB - Newborn NFS/N mice were inoculated with pseudotypes of murine retroviruses containing murine v-raf, avian v-myc, or both v-raf and v-myc within a single construct. Foci of dysplastic acinar cells, similar to those observed in rats given chemical carcinogens, were induced in 77% of mice inoculated with the raf/myc construct with a latency as short as 15 days. However, all animals given this construct also developed fibrosarcomas, erythroblastosis, and lymphomas and died within 70 days of infection, before pancreatic acinar carcinomas developed. Dysplastic foci were also observed in mice infected with viruses containing v-raf or v-myc alone with latencies of 3-4 weeks, and carcinomas were seen after an average latency of 150 days in 31% of mice infected with either of two viruses expressing v-myc alone. Two primary carcinomas were transplanted in mice, and in vitro cell lines were developed from one of the transplants. DNA prepared from seven primary carcinomas, the two transplanted tumors, and the in vitro cell lines was hybridized with a v-myc probe. Each tumor had a unique pattern of proviral integrations that was retained, with the gain or loss of single sites, in the transplants and derivative cell lines. The clonal nature of the advanced pancreatic acinar carcinomas is discussed in relation to their histogenesis and the transforming potentials of the raf and myc oncogenes. JF - The American journal of pathology AU - Fredrickson, T N AU - Hartley, J W AU - Wolford, N K AU - Resau, J H AU - Rapp, U R AU - Morse, H C AD - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 444 EP - 451 VL - 131 IS - 3 SN - 0002-9440, 0002-9440 KW - DNA KW - 9007-49-2 KW - Abridged Index Medicus KW - Index Medicus KW - Neoplasm Transplantation KW - Clone Cells KW - Mice, Inbred Strains KW - Animals KW - Tumor Cells, Cultured KW - DNA -- analysis KW - Mice KW - Retroviridae -- genetics KW - Cell Line KW - Pancreatic Neoplasms -- pathology KW - Pancreatic Neoplasms -- analysis KW - Oncogenes KW - Pancreatic Neoplasms -- genetics KW - Genes, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78256541?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Histogenesis+and+clonality+of+pancreatic+tumors+induced+by+v-myc+and+v-raf+oncogenes+in+NFS%2FN+mice.&rft.au=Fredrickson%2C+T+N%3BHartley%2C+J+W%3BWolford%2C+N+K%3BResau%2C+J+H%3BRapp%2C+U+R%3BMorse%2C+H+C&rft.aulast=Fredrickson&rft.aufirst=T&rft.date=1988-06-01&rft.volume=131&rft.issue=3&rft.spage=444&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 - 1988-07-26 N1 - Date created - 1988-07-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1986 Jul;46(7):3211-24 [3011242] J Cell Biochem. 1986;30(3):195-218 [3084503] J Exp Med. 1986 Aug 1;164(2):443-57 [3088206] Proc Natl Acad Sci U S A. 1986 Sep;83(18):6868-72 [3018749] Int Rev Exp Pathol. 1984;26:177-229 [6400513] Cell. 1987 Mar 27;48(6):1023-34 [3470144] J Natl Cancer Inst. 1961 Apr;26:1011-39 [13788102] Cancer Res. 1972 Jul;32(7):1595-7 [4337835] Eur J Biochem. 1973 Jul 2;36(1):32-8 [4200179] J Mol Biol. 1975 Nov 5;98(3):503-17 [1195397] Lab Invest. 1976 May;34(5):501-9 [818451] Arch Pathol Lab Med. 1976 Aug;100(8):405-14 [60092] Am J Pathol. 1979 Feb;94(2):333-48 [426031] Cancer Lett. 1979 Aug;7(4):197-202 [509403] J Natl Cancer Inst. 1980 Aug;65(2):383-9 [6931255] Lab Invest. 1982 May;46(5):527-34 [6804715] Nature. 1983 Nov 10-16;306(5939):194-6 [6646201] Cell. 1983 Dec;35(2 Pt 1):359-67 [6197179] Proc Natl Acad Sci U S A. 1984 Aug;81(15):4940-4 [6589638] Environ Health Perspect. 1984 Jun;56:213-7 [6434300] Environ Health Perspect. 1984 Jun;56:219-27 [6383798] J Virol. 1985 Jul;55(1):23-33 [4009794] Cancer Res. 1985 Sep;45(9):4372-9 [4028021] Cancer Res. 1986 Jun;46(6):3196-9 [2421891] Cell. 1986 May 23;45(4):485-95 [3011271] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A statistical analysis for the mouse lymphoma cell forward mutation assay. AN - 78256256; 3374512 AB - This paper illustrates the usefulness of solvent control trials and presents a statistical analysis for mouse L5178Y lymphoma data. Examination of solvent control trials establishes that the natural logarithm of mutant frequency is approximately normally distributed and that both the mean and variance of mutant frequency vary by trial. There is little evidence of downturns at higher doses in the dose-response curves studied; therefore, a trend test is proposed for the detection of an increasing dose-response curve. A Monte Carlo investigation confirms that the proposed trend test is better able to detect an increasing dose-response than 4 alternate methods of analysis. JF - Mutation research AU - Murphy, S A AU - Caspary, W J AU - Margolin, B H AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 145 EP - 154 VL - 203 IS - 3 SN - 0027-5107, 0027-5107 KW - Solvents KW - 0 KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Mice KW - Leukemia L5178 -- genetics KW - Mutation KW - Leukemia, Experimental -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78256256?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+statistical+analysis+for+the+mouse+lymphoma+cell+forward+mutation+assay.&rft.au=Murphy%2C+S+A%3BCaspary%2C+W+J%3BMargolin%2C+B+H&rft.aulast=Murphy&rft.aufirst=S&rft.date=1988-06-01&rft.volume=203&rft.issue=3&rft.spage=145&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 - 1988-07-05 N1 - Date created - 1988-07-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acyclovir-induced renal failure. Clinical course and histology. AN - 78243603; 3376977 AB - Four patients with a chronic fatigue syndrome experienced five episodes of acute renal insufficiency associated with high-dose (500 mg/m2) intravenous acyclovir administered intravenously as one-hour infusions. Nephrotoxicity developed despite precautions to avoid volume contraction. Examination of the urinary sediment of three patients by polarizing microscopy showed birefringent needle-shaped crystals within leukocytes. In the most severely affected patient, a serum creatinine concentration of 8.6 mg/dl developed and the patient underwent percutaneous renal biopsy that revealed foci of interstitial inflammation without tubular necrosis. Urine, blood, and renal tissue levels of acyclovir were high. One patient was rechallenged with low-dose intravenous acyclovir and the four patients later received oral acyclovir, all without adverse effect. The combined data from these patients support crystalluria and obstructive nephropathy as a mechanism of acyclovir-induced renal failure in humans. This experience emphasizes the importance of maintaining adequate hydration during high-dose acyclovir therapy. JF - The American journal of medicine AU - Sawyer, M H AU - Webb, D E AU - Balow, J E AU - Straus, S E AD - Medical Virology Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 1067 EP - 1071 VL - 84 IS - 6 SN - 0002-9343, 0002-9343 KW - Acyclovir KW - X4HES1O11F KW - Abridged Index Medicus KW - Index Medicus KW - Crystallization KW - Kidney -- pathology KW - Infusions, Intravenous KW - Humans KW - Adult KW - Acute Kidney Injury -- pathology KW - Acute Kidney Injury -- chemically induced KW - Acyclovir -- administration & dosage KW - Acyclovir -- adverse effects KW - Acute Kidney Injury -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78243603?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Acyclovir-induced+renal+failure.+Clinical+course+and+histology.&rft.au=Sawyer%2C+M+H%3BWebb%2C+D+E%3BBalow%2C+J+E%3BStraus%2C+S+E&rft.aulast=Sawyer&rft.aufirst=M&rft.date=1988-06-01&rft.volume=84&rft.issue=6&rft.spage=1067&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 - 1988-06-28 N1 - Date created - 1988-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oncogenic potential in fibroblasts from individuals genetically predisposed to cancer. AN - 78242659; 3374506 AB - There is now considerable evidence to suggest that genetic factors can influence the incidence of cancer. Although expression of this susceptibility to cancer appears to be tissue-specific, the normal skin fibroblasts from individuals predisposed to cancer (predisposed fibroblasts) have also been shown to express the risk of the target cell in the development of cancer. In the context of the 2-stage theory of chemical carcinogenesis predisposed fibroblasts may, therefore, exist in a pre-neoplastic or initiated state. The purpose of the present study was to determine whether predisposed fibroblasts would be oncogenically transformed in vitro by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) alone. TPA treatment induced similar changes in cellular morphology, cytoskeleton, and epidermal growth-factor binding, in predisposed and normal cells. None of these cell lines acquired anchorage-independent growth or an unlimited growth potential in culture after chronic application of TPA. Fluorescent microscopy with an F-actin probe, in the absence of TPA, showed a disorganization of the microfilament and intermediate filament network in skin fibroblasts from individuals with familial polyposis coli, hereditary and sporadic retinoblastoma, basal cell nevus syndrome, and Gardner's syndrome, as compared to normal skin fibroblasts. Single and 2-dimensional electrophoresis also indicated that the incorporation of 35S-methionine into actin in predisposed fibroblasts was 2-fold greater than in normal fibroblasts, and the turnover rate of actin in predisposed fibroblasts was less than 5 h, compared to 48 h in normal fibroblasts. These observations clearly suggest that predisposed fibroblasts may not exist in a pre-neoplastic or initiated state, and that the mechanism of genetic susceptibility to cancer may be different from that of chemical carcinogenesis. In contrast, the results of this study indicate that genetic susceptibility to a variety of cancers may be associated with a rapid turnover of actin and a disorganization of the microfilament and intermediate filament networks. JF - Mutation research AU - Antecol, M H AD - National Cancer Institute, Laboratory of Viral Carcinogenesis, Frederick, MD 21701. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 293 EP - 311 VL - 199 IS - 2 SN - 0027-5107, 0027-5107 KW - Actins KW - 0 KW - Vimentin KW - Index Medicus KW - Vimentin -- analysis KW - Disease Susceptibility KW - Cells, Cultured KW - Humans KW - Intermediate Filaments -- ultrastructure KW - Cell Line, Transformed KW - Actins -- analysis KW - Male KW - Female KW - Cell Division KW - Fibroblasts -- cytology KW - Neoplasms -- etiology KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78242659?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oncogenic+potential+in+fibroblasts+from+individuals+genetically+predisposed+to+cancer.&rft.au=Antecol%2C+M+H&rft.aulast=Antecol&rft.aufirst=M&rft.date=1988-06-01&rft.volume=199&rft.issue=2&rft.spage=293&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 - 1988-07-05 N1 - Date created - 1988-07-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Leu-8 antigen expression is diminished during cell activation but does not correlate with effector function of activated T lymphocytes. AN - 78240465; 3286763 AB - Previous studies have suggested that there is an inverse relationship between cell activation and the expression of the Leu-8 Ag, a cell surface protein that distinguishes functionally distinct T cell populations. This was confirmed in vitro, because when resting PBL were activated with PHA there was a rapid decline in expression of the Leu-8 Ag on all lymphocyte subpopulations. A decline in Leu-8 reactivity occurred after stimulation of lymphocytes with PHA, anti-CD3 plus PMA and ionomycin plus PMA, and an intermediate decline in Leu-8 expression occurred after stimulation with Con A. However, there was little loss of expression of Leu-8 after stimulation of lymphocytes with PWM or allogeneic lymphocytes. The decline in Leu-8 expression on activated lymphocytes occurred earlier than the decline in expression of CD45R. After removal of the activation stimuli, peripheral blood T cells or Jurkat cells rapidly re-expressed Leu-8. Finally, when the expression of Leu-8 on peripheral blood CD4+, Leu-8+ T cells was reduced by prior activation with PHA, these cells continued to exhibit suppressor function for PWM-stimulated Ig synthesis. Thus, there is a rapid decline in expression of the Leu-8 Ag but no change in regulatory function of CD4+, Leu-8+ T cells during cell activation. These results suggest that the molecule recognized by anti-Leu-8 plays a role in lymphocyte activation but not directly in the effector function of CD4+, Leu8+ T cells. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kanof, M E AU - James, S P AD - Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/06/01/ PY - 1988 DA - 1988 Jun 01 SP - 3701 EP - 3706 VL - 140 IS - 11 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Surface KW - Lymphocyte Function-Associated Antigen-1 KW - Phytohemagglutinins KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Phenotype KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Phytohemagglutinins -- pharmacology KW - Antibodies, Monoclonal -- physiology KW - T-Lymphocytes -- classification KW - Lymphocyte Activation KW - T-Lymphocytes -- immunology KW - Antigens, Surface -- immunology KW - Antigens, Surface -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78240465?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Leu-8+antigen+expression+is+diminished+during+cell+activation+but+does+not+correlate+with+effector+function+of+activated+T+lymphocytes.&rft.au=Kanof%2C+M+E%3BJames%2C+S+P&rft.aulast=Kanof&rft.aufirst=M&rft.date=1988-06-01&rft.volume=140&rft.issue=11&rft.spage=3701&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 - 1988-06-29 N1 - Date created - 1988-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protective, restorative, and therapeutic properties of recombinant human IL-1 in rodent models. AN - 78239810; 3259600 AB - Human rIL-1 alpha and -1 beta are shown to increase significantly the CFU-culture activity in the spleen as well as at other sites after i.v. or i.p. administration. IL-1 can also significantly increase survival and can "rescue" a number of animals if administered either before or after lethal doses of cyclophosphamide or gamma-irradiation. The protective and reconstitutive activities of the rIL-1 are shown to correlate with increased CFU-culture frequency and total number, as well as increased cellularity in the bone marrow and peripheral blood, suggesting that this is one of their mechanisms of action. The sequence and timing of administration of human rIL-1 is critical for the protection or rescue of animals receiving DNA-damaging agents; maximal activity is achieved when IL-1 is given 20 h before insult or 48 h after alkylating agent administration. Minimal therapeutic activity is observed with IL-1 as a single agent for the treatment of metastatic disease compared with other biologic response modifiers including IFN-gamma. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Castelli, M P AU - Black, P L AU - Schneider, M AU - Pennington, R AU - Abe, F AU - Talmadge, J E AD - Preclinical Screening Laboratory, National Cancer Institute-Frederick Cancer Research Facility, MD 21701. Y1 - 1988/06/01/ PY - 1988 DA - 1988 Jun 01 SP - 3830 EP - 3837 VL - 140 IS - 11 SN - 0022-1767, 0022-1767 KW - Interleukin-1 KW - 0 KW - Recombinant Proteins KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Radiation Injuries, Experimental -- mortality KW - Animals KW - Drug Administration Schedule KW - Humans KW - Lung Neoplasms -- drug therapy KW - Cyclophosphamide -- toxicity KW - Mice KW - Bone Marrow Cells KW - Leukopenia -- chemically induced KW - Kinetics KW - Neoplasm Metastasis KW - Mice, Inbred C57BL KW - Lethal Dose 50 KW - Neoplasms, Experimental -- drug therapy KW - Radiation Injuries, Experimental -- prevention & control KW - Female KW - Leukopenia -- drug therapy KW - Interleukin-1 -- administration & dosage KW - Interleukin-1 -- therapeutic use KW - Disease Models, Animal KW - Bone Marrow -- drug effects KW - Recombinant Proteins -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78239810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Protective%2C+restorative%2C+and+therapeutic+properties+of+recombinant+human+IL-1+in+rodent+models.&rft.au=Castelli%2C+M+P%3BBlack%2C+P+L%3BSchneider%2C+M%3BPennington%2C+R%3BAbe%2C+F%3BTalmadge%2C+J+E&rft.aulast=Castelli&rft.aufirst=M&rft.date=1988-06-01&rft.volume=140&rft.issue=11&rft.spage=3830&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 - 1988-06-29 N1 - Date created - 1988-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of non-volatile scavengers of hydroxyl radicals on thymine radical formation induced by gamma-rays and ultrasound. AN - 78234073; 2836327 AB - In order to investigate the mechanism of sonolysis of nucleic acid constituents, the yield of thymine radicals generated by 50 kHz ultrasound in Ar-saturated aqueous solution was compared with that formed by gamma-radiolysis in N2O-saturated solutions in the presence of various non-volatile scavengers, which cannot act in the gas phase of the cavitation bubbles. For comparison of thymine radical yields by sonolysis and gamma radiolysis, the method of spin trapping with 3,5-dibromo-4-nitrosobenzenesulphonate (a water-soluble, non-volatile, aromatic nitroso spin trap) combined with ESR was used. The efficiency of OH radical scavenging is expressed by the reciprocal value of C1/2, the scavenger concentration at which the thymine radical yield is decreased by 50 per cent. In gamma radiolysis the scavenging efficiencies of the solutes depend on their rate constants with OH radicals. For sonolysis the C1/2 values were similar to those obtained for gamma radiolysis except for the hydrophobic 5,5-dimethyl-1-pyrroline-N-oxide. These results suggest that thymine radicals induced by ultrasound are produced in the bulk of the solution as well as in the interfacial region. JF - International journal of radiation biology and related studies in physics, chemistry, and medicine AU - Kondo, T AU - Krishna, C M AU - Riesz, P AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 891 EP - 899 VL - 53 IS - 6 SN - 0020-7616, 0020-7616 KW - Azides KW - 0 KW - Carboxylic Acids KW - Cobalt Radioisotopes KW - Cyclic N-Oxides KW - Free Radicals KW - Hydroxides KW - Solutions KW - Water KW - 059QF0KO0R KW - Potassium Iodide KW - 1C4QK22F9J KW - 5,5-dimethyl-1-pyrroline-1-oxide KW - 7170JZ1QF3 KW - hydroxide ion KW - 9159UV381P KW - Sodium Azide KW - 968JJ8C9DV KW - Glucose KW - IY9XDZ35W2 KW - Thymine KW - QR26YLT7LT KW - Index Medicus KW - Gamma Rays KW - Electron Spin Resonance Spectroscopy KW - Water -- radiation effects KW - Ultrasonics KW - Thymine -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78234073?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+and+related+studies+in+physics%2C+chemistry%2C+and+medicine&rft.atitle=Effect+of+non-volatile+scavengers+of+hydroxyl+radicals+on+thymine+radical+formation+induced+by+gamma-rays+and+ultrasound.&rft.au=Kondo%2C+T%3BKrishna%2C+C+M%3BRiesz%2C+P&rft.aulast=Kondo&rft.aufirst=T&rft.date=1988-06-01&rft.volume=53&rft.issue=6&rft.spage=891&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+biology+and+related+studies+in+physics%2C+chemistry%2C+and+medicine&rft.issn=00207616&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-07-11 N1 - Date created - 1988-07-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radioimmunoscintigraphy of colon cancer with iodine-131-labeled B72.3 monoclonal antibody. AN - 78231933; 3373312 AB - The monoclonal antibody B72.3 is a murine IgG1 that is reactive with a wide range of carcinomas while demonstrating little or no reactivity to normal adult tissues. We have shown (27) quantitative analyses demonstrating selective targeting of [131I]B72.3 IgG to metastatic colorectal cancer. We have also shown (28) that (a) B72.3 localization in metastases correlated with the percentage of tumor cells in the biopsy specimen; (b) B72.3 could localize in carcinomas of various degrees of differentiation with best localization in well-differentiated tumors and (c) [131I]B72.3 could penetrate tumor masses, as determined by autoradiographic studies. We report here the various parameters effecting radioimmunoscintigraphy with [131I]B72.3 IgG. Sixteen of 35 patients with colorectal carcinoma had positive scans (without blood-pool subtraction). High circulating TAG-72 antigen levels correlated with positive scans. No dose dependent differences were seen in biodistribution or tumor imaging. The plasma clearance and urinary excretion of [131I]B72.3 and [125I]BL-3 (nonspecific control) were not significantly different. No toxicity was noted. Approximately one-half of patients developed human anti-mouse immune response. JF - Journal of nuclear medicine : official publication, Society of Nuclear Medicine AU - Carrasquillo, J A AU - Sugarbaker, P AU - Colcher, D AU - Reynolds, J C AU - Esteban, J AU - Bryant, G AU - Keenan, A M AU - Perentesis, P AU - Yokoyama, K AU - Simpson, D E AD - Department of Nuclear Medicine, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 1022 EP - 1030 VL - 29 IS - 6 SN - 0161-5505, 0161-5505 KW - Antibodies, Monoclonal KW - 0 KW - Iodine Radioisotopes KW - Index Medicus KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Radionuclide Imaging KW - Colonic Neoplasms -- secondary KW - Colonic Neoplasms -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78231933?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Radioimmunoscintigraphy+of+colon+cancer+with+iodine-131-labeled+B72.3+monoclonal+antibody.&rft.au=Carrasquillo%2C+J+A%3BSugarbaker%2C+P%3BColcher%2C+D%3BReynolds%2C+J+C%3BEsteban%2C+J%3BBryant%2C+G%3BKeenan%2C+A+M%3BPerentesis%2C+P%3BYokoyama%2C+K%3BSimpson%2C+D+E&rft.aulast=Carrasquillo&rft.aufirst=J&rft.date=1988-06-01&rft.volume=29&rft.issue=6&rft.spage=1022&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 - 1988-07-05 N1 - Date created - 1988-07-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A randomized trial of standard chemotherapy v a high-dose chemotherapy regimen in the treatment of poor prognosis nonseminomatous germ-cell tumors. AN - 78230835; 2453619 AB - We performed a prospective randomized trial of a high-dose chemotherapy regimen v standard cisplatin-based chemotherapy in poor prognosis nonseminomatous germ-cell cancer patients. The high-dose regimen consisting of twice the standard dose of cisplatin (P), along with vinblastine (Ve), bleomycin (B), and the epipodophylotoxin etoposide (VP-16) (V) (PVeBV) was compared to the classic regimen with normal dose cisplatin, vinblastine, and bleomycin (PVeB). Eligibility criteria included large abdominal masses, liver metastases, multiple pulmonary metastases, brain metastases, marked elevations in serum tumor markers (alpha-fetoprotein greater than 1,000 ng/mL or the beta-subunit of human chorionic gonadotropin greater than 10,000 mIU), unfavorable histology (pure choriocarcinoma), or extragonadal germ-cell tumors. Fifty-two consecutive patients with poor prognostic features were randomized to receive either PVeBV or PVeB. The median follow-up is 4 years. Treatment with the high-dose regimen increased the complete remission rate (88% v 67%, P = .14) and was associated with a lower relapse rate (17% v 41%, P = .2). The median survival of patients receiving standard therapy was 30 months, while the median survival for patients receiving the high-dose regimen has not been reached. Actuarial 5-year survival for patients treated with the high-dose regimen is 78%, compared with 48% for patients receiving standard therapy (two-sided Mantel-Cox test = .06). Disease-free survival was also superior for patients randomized to PVeBV (P = .03). Sixty-eight percent of patients (23 of 34) randomized to PVeBV are alive and continuously disease-free, compared with 33% (six of 18) for PVeB (P = .02). The major difference in toxicity between the high-dose regimen and standard therapy was the severity of myelosuppression and the incidence of severe hearing loss. Ninety-one percent of patients treated with PVeBV had a WBC count less than 1,000/microL, compared with 50% of patients receiving PVeB (P less than .05). Hearing aids were recommended for 12 patients who received PVeBV and two who received PVeB. The increased effectiveness of the PVeBV regimen in poor prognosis germ-cell cancer patients may relate to the double-dose cisplatin, the addition of VP-16, or to a synergistic effect of these two drugs. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Ozols, R F AU - Ihde, D C AU - Linehan, W M AU - Jacob, J AU - Ostchega, Y AU - Young, R C AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 1031 EP - 1040 VL - 6 IS - 6 SN - 0732-183X, 0732-183X KW - Bleomycin KW - 11056-06-7 KW - Vinblastine KW - 5V9KLZ54CY KW - Etoposide KW - 6PLQ3CP4P3 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - AIDS/HIV KW - Drug Administration Schedule KW - Random Allocation KW - Bleomycin -- administration & dosage KW - Dose-Response Relationship, Drug KW - Humans KW - Prognosis KW - Clinical Trials as Topic KW - Bleomycin -- adverse effects KW - Cisplatin -- administration & dosage KW - Etoposide -- administration & dosage KW - Pulmonary Fibrosis -- chemically induced KW - Vinblastine -- administration & dosage KW - Etoposide -- adverse effects KW - Vinblastine -- adverse effects KW - Cisplatin -- adverse effects KW - Neoplasm Recurrence, Local KW - Bone Marrow -- drug effects KW - Neoplasms, Germ Cell and Embryonal -- mortality KW - Neoplasms, Germ Cell and Embryonal -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78230835?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+randomized+trial+of+standard+chemotherapy+v+a+high-dose+chemotherapy+regimen+in+the+treatment+of+poor+prognosis+nonseminomatous+germ-cell+tumors.&rft.au=Ozols%2C+R+F%3BIhde%2C+D+C%3BLinehan%2C+W+M%3BJacob%2C+J%3BOstchega%2C+Y%3BYoung%2C+R+C&rft.aulast=Ozols&rft.aufirst=R&rft.date=1988-06-01&rft.volume=6&rft.issue=6&rft.spage=1031&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 - 1988-07-08 N1 - Date created - 1988-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Early signals for keratinocyte differentiation: role of Ca2+-mediated inositol lipid metabolism in normal and neoplastic epidermal cells. AN - 78227116; 2453303 AB - Differentiation of cultured keratinocytes is regulated by the Ca2+ concentration of the culture medium. Below 0.1 mM Ca2+, a monolayer of basal cells is formed which fully differentiates in response to a rise in medium Ca2+. A role for protein kinase C in this differentiation program has been suggested because phorbol esters induce epidermal differentiation in cells grown in reduced Ca2+ medium, and exogenously added phospholipase C (which increases cellular diacylglycerol) mimics phorbol ester action. These findings suggested that the external Ca2+ signal may lead to protein kinase C activation via stimulation of cellular phospholipase C activity. The effect of the external Ca2+ signal on phospholipase C was studied in cultures prelabeled with [3H]-inositol. Within 2 min after addition of Ca2+ to 1 mM, an increase in inositol phosphates was measured. This correlated with a decrease in radiolabeled phosphoinositides, suggesting that these were the source of the increased inositol phosphates. After 3 h in 1 mM Ca2+ medium, each of the inositol phosphates remained increased to 130-140% of control levels. Inositol phosphate metabolism in neoplastic epidermal cells was quantitatively similar to normal cells in response to the Ca2+ signal. Stimulation of phosphatidylinositol (PIP) metabolism appears to be mediated by a rise in intracellular free Ca2+ because Ca2+ ionophores A23187 and ionomycin also cause a similar rise in inositol phosphate levels. Phorbol esters did not increase PIP turnover but instead stimulated phosphatidylcholine metabolism. The induction of epidermal differentiation by phorbol esters was enhanced by ionomycin, suggesting that both protein kinase C activation, elevation of intracellular calcium and PIP turnover were important components of the signal for epidermal differentiation. These results demonstrate that the second messenger system for Ca2+-mediated keratinocyte differentiation may be through a direct effect on phospholipase C activity. JF - Carcinogenesis AU - Jaken, S AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 1033 EP - 1038 VL - 9 IS - 6 SN - 0143-3334, 0143-3334 KW - Ethers KW - 0 KW - Calcimycin KW - 37H9VM9WZL KW - Inositol KW - 4L6452S749 KW - Ionomycin KW - 56092-81-0 KW - Keratins KW - 68238-35-7 KW - Choline KW - N91BDP6H0X KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Ethers -- pharmacology KW - Cells, Cultured KW - Choline -- metabolism KW - Mice KW - Calcimycin -- pharmacology KW - Cell Differentiation -- drug effects KW - Keratins -- metabolism KW - Epidermis -- drug effects KW - Epidermis -- cytology KW - Epidermis -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Skin Neoplasms -- pathology KW - Calcium -- pharmacology KW - Inositol -- metabolism KW - Skin Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78227116?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Early+signals+for+keratinocyte+differentiation%3A+role+of+Ca2%2B-mediated+inositol+lipid+metabolism+in+normal+and+neoplastic+epidermal+cells.&rft.au=Jaken%2C+S%3BYuspa%2C+S+H&rft.aulast=Jaken&rft.aufirst=S&rft.date=1988-06-01&rft.volume=9&rft.issue=6&rft.spage=1033&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-07-11 N1 - Date created - 1988-07-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Polydipsia and hyponatremia in psychiatric patients. AN - 78222963; 3285701 AB - Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH. Treatment modalities currently available include fluid restriction and medications. JF - The American journal of psychiatry AU - Illowsky, B P AU - Kirch, D G AD - Clinical Brain Disorders Branch, National Institute of Mental Health, St. Elizabeths Hospital, Washington, DC 20032. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 675 EP - 683 VL - 145 IS - 6 SN - 0002-953X, 0002-953X KW - Abridged Index Medicus KW - Index Medicus KW - Drinking KW - Humans KW - Adult KW - Middle Aged KW - Inappropriate ADH Syndrome -- complications KW - Hyponatremia -- physiopathology KW - Hyponatremia -- etiology KW - Water Intoxication -- physiopathology KW - Mental Disorders -- psychology KW - Water Intoxication -- etiology KW - Mental Disorders -- complications KW - Mental Disorders -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78222963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Polydipsia+and+hyponatremia+in+psychiatric+patients.&rft.au=Illowsky%2C+B+P%3BKirch%2C+D+G&rft.aulast=Illowsky&rft.aufirst=B&rft.date=1988-06-01&rft.volume=145&rft.issue=6&rft.spage=675&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 - 1988-06-21 N1 - Date created - 1988-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - NIH conference. New approaches to the immunotherapy of cancer using interleukin-2. AN - 78221657; 3285747 AB - Experimental studies in animals have shown that therapy with high-dose interleukin-2 either alone or in combination with lymphokine-activated killer cells can reduce established pulmonary and hepatic metastases. Based on these experiments, recent clinical trials have shown that therapy with high-dose interleukin-2 alone or in combination with lymphokine-activated killer cells can mediate the regression of established metastatic disease in selected patients with advanced malignancy. Of 221 patients with advanced cancer treated with this immunotherapy, 16 have had a complete regression of all metastatic cancer, and an additional 26 have had a partial regression (greater than 50% reduction) of cancer. Toxicity from treatment was primarily due to increased capillary permeability, which led to fluid extravasation and organ dysfunction. Based on these findings, new approaches are being explored, including the use of tumor-infiltrating lymphocytes and combinations of lymphokines. These studies show that the regression of established growing cancer can be mediated by manipulating the immune system. JF - Annals of internal medicine AU - Rosenberg, S A AU - Lotze, M T AU - Mulé, J J AD - Clinical Center Communication, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 853 EP - 864 VL - 108 IS - 6 SN - 0003-4819, 0003-4819 KW - Interleukin-2 KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Humans KW - Immunization, Passive KW - Neoplasm Metastasis -- therapy KW - Mice KW - Killer Cells, Natural -- immunology KW - Immunotherapy -- methods KW - Interleukin-2 -- administration & dosage KW - Interleukin-2 -- therapeutic use KW - Neoplasms -- therapy KW - Interleukin-2 -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78221657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=NIH+conference.+New+approaches+to+the+immunotherapy+of+cancer+using+interleukin-2.&rft.au=Rosenberg%2C+S+A%3BLotze%2C+M+T%3BMul%C3%A9%2C+J+J&rft.aulast=Rosenberg&rft.aufirst=S&rft.date=1988-06-01&rft.volume=108&rft.issue=6&rft.spage=853&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 - 1988-06-15 N1 - Date created - 1988-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reaction of N-hydroxylamine and N-acetoxy derivatives of 2-amino-3-methylimidazolo[4,5-f]quinoline with DNA. Synthesis and identification of N-(deoxyguanosin-8-yl)-IQ. AN - 78220012; 3370750 AB - The N-hydroxylamine of the carcinogen 2-amino-3-methylimidazolo[4,5-f]quinoline (IQ) covalently bound to calf thymus DNA at pH 7, and the binding was 11% higher under acidic conditions (pH 5). The extent of N-hydroxy-IQ binding to single-stranded polynucleotides at neutral pH was in the following order: polyguanylic acid much greater than polyadenylic acid greater than polycytidylic acid = polyuridylic acid. The binding of the carcinogen to DNA, polyguanylic acid and polyadenylic acid at neutral pH was enhanced 6-, 4- and 2-fold respectively by the presumed in situ formation of N-acetoxy-IQ from N-hydroxy-IQ and acetic anhydride. N-(Deoxyguanosin-8-yl)-IQ was synthesized by reaction at pH 7 of N-acetoxy-IQ (formed in situ with N-hydroxy-IQ and acetic anhydride) with deoxyguanosine and the structure characterized by NMR, mass spectral and UV absorption spectral analyses. Reverse phase HPLC of enzymatically hydrolyzed DNA which had been reacted with N-hydroxy-IQ in vitro showed a major adduct which was chromatographically identical to synthetic N-(deoxyguanosin-8-yl)-IQ. In addition, N-acetoxy-IQ, generated chemically by acetic anhydride or enzymatically with mammalian acetyltransferase, formed one major adduct with DNA which was chromatographically identical to the synthetic N-(deoxyguanosin-8-yl)-IQ. The results indicate that N-hydroxy-IQ and N-acetoxy-IQ react with DNA forming primarily the N-(deoxyguanosin-8-yl)-IQ adduct. JF - Carcinogenesis AU - Snyderwine, E G AU - Roller, P P AU - Adamson, R H AU - Sato, S AU - Thorgeirsson, S S AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 1061 EP - 1065 VL - 9 IS - 6 SN - 0143-3334, 0143-3334 KW - Acetates KW - 0 KW - Carcinogens KW - Hydroxylamines KW - Quinolines KW - N-(deoxyguanosin-8-yl)-2-amino-3-methylimidazolo(4,5-f)quinoline KW - 115747-35-8 KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - DNA KW - 9007-49-2 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Chromatography, High Pressure Liquid KW - Magnetic Resonance Spectroscopy KW - Quinolines -- chemical synthesis KW - Deoxyguanosine -- chemical synthesis KW - Deoxyguanosine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78220012?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Reaction+of+N-hydroxylamine+and+N-acetoxy+derivatives+of+2-amino-3-methylimidazolo%5B4%2C5-f%5Dquinoline+with+DNA.+Synthesis+and+identification+of+N-%28deoxyguanosin-8-yl%29-IQ.&rft.au=Snyderwine%2C+E+G%3BRoller%2C+P+P%3BAdamson%2C+R+H%3BSato%2C+S%3BThorgeirsson%2C+S+S&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1988-06-01&rft.volume=9&rft.issue=6&rft.spage=1061&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-07-11 N1 - Date created - 1988-07-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Influence of estrogens on mouse uterine epidermal growth factor precursor protein and messenger ribonucleic acid. AN - 78219708; 3286224 AB - Estrogens stimulate the in vivo proliferation of epithelial cells of the mouse uterus. The cumulative evidence from several earlier studies suggests that the mitogenic effect of estrogens is mediated indirectly through a polypeptide growth factor. The primary focus of the present investigation was to determine whether an epidermal growth factor (EGF)-related polypeptide originates in the uterus of the immature or adult mouse under normal or altered estrogen status. Hybridization experiments revealed the presence of the 4.7-kilobase prepro-EGF mRNA in uteri of immature CD-1 mice. The level of this mRNA was augmented at least 2-fold in immature mice treated for 4 days with estrogen, but levels remained markedly low compared to those in submaxillary gland or kidney. Two preparations of pooled uterine luminal fluid from estrogen-treated immature mice contained EGF immunoreactivity (1.2 and 1.7 ng/ml) that was stable in response to acid (50 mM acetic acid) and heat. Negligible EGF (less than 20 pg/uterus) was detected in acid extracts of uteri from ovariectomized or cycling adult mice. After injection of 17 beta-estradiol (0.2 or 2.0 micrograms, ip), the levels of acid-extractable uterine EGF in ovariectomized adult mice up to 48 h after treatment were not different from those obtained with vehicle alone. Immunolocalization of EGF in the mouse uterus was demonstrated only after paraffin sections were first briefly treated with pronase. Staining was observed along the borders of luminal and glandular epithelial cells, especially at the apical region of the cells. Some staining was also observed in the myometrium; stromal cells were negative. Synthesis of the reactive material was apparently estrogen independent, since localization was retained in uteri of both ovariectomized and immature mice. Immunoblots of preparations of membranes from uterine homogenates or epithelial cells revealed a band at mol wt of about 130,000, which, along with other findings of the present study, suggests that EGF occurs predominantly as the membrane-bound precursor form in this organ, as has been previously shown for the kidney. Although the biological role of the precursor in the uterus is not known, we speculate that estrogens function in an autocrine circuit by stimulating processing of the membrane-bound EGF precursor. EGF elaborated by this mechanism might conceivably react with known complementary receptors on uterine epithelial cells to stimulate proliferation. JF - Endocrinology AU - DiAugustine, R P AU - Petrusz, P AU - Bell, G I AU - Brown, C F AU - Korach, K S AU - McLachlan, J A AU - Teng, C T AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 2355 EP - 2363 VL - 122 IS - 6 SN - 0013-7227, 0013-7227 KW - Estrogens KW - 0 KW - Protein Precursors KW - RNA, Messenger KW - epidermal growth factor precursor KW - Estradiol KW - 4TI98Z838E KW - Epidermal Growth Factor KW - 62229-50-9 KW - Diethylstilbestrol KW - 731DCA35BT KW - DNA KW - 9007-49-2 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Estradiol -- pharmacology KW - Mice KW - Tissue Distribution KW - Nucleic Acid Hybridization KW - Kinetics KW - Diethylstilbestrol -- pharmacology KW - Estrus -- metabolism KW - Ovariectomy KW - Female KW - Immunoenzyme Techniques KW - Male KW - Immunoassay KW - Uterus -- metabolism KW - Protein Precursors -- metabolism KW - RNA, Messenger -- metabolism KW - Estrogens -- pharmacology KW - Protein Precursors -- genetics KW - Epidermal Growth Factor -- genetics KW - Epidermal Growth Factor -- metabolism KW - Uterus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78219708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Influence+of+estrogens+on+mouse+uterine+epidermal+growth+factor+precursor+protein+and+messenger+ribonucleic+acid.&rft.au=DiAugustine%2C+R+P%3BPetrusz%2C+P%3BBell%2C+G+I%3BBrown%2C+C+F%3BKorach%2C+K+S%3BMcLachlan%2C+J+A%3BTeng%2C+C+T&rft.aulast=DiAugustine&rft.aufirst=R&rft.date=1988-06-01&rft.volume=122&rft.issue=6&rft.spage=2355&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-06-28 N1 - Date created - 1988-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Syrup of ipecac. The case for distribution from physicians' offices. AN - 78215216; 2897159 AB - Data from a nationally representative sample of household interviews were analyzed to examine public preparedness for childhood poisoning episodes. Eighty-eight percent (61% to 77% in nonwhite groups) of respondents from households with children younger than 10 years had heard of poison control centers and 70% (50% to 57% in nonwhites) stated that they had the telephone number of such a center. In contrast only 25% stated they had syrup of ipecac in their home. Among blacks and Hispanics this proportion was 9%. To explore possible reasons for this we telephoned a sample of 65 physicians listed in the greater Washington, DC, telephone directory as providers of care for infants and children. Of the 45 (69%) who agreed to be interviewed, 73% informed their patients about poison control centers and 53% provided the appropriate telephone number. Although 78% believed parents should have ipecac in the house, only three (7%) of 45 actually dispensed ipecac to parents. We conclude that ipecac is not widely available in the homes of American children. By regularly dispensing it in the course of pediatric care, physicians could largely remedy this deficiency. JF - American journal of diseases of children (1960) AU - Malloy, M H AU - Rhoads, G G AD - Epidemiology Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 640 EP - 642 VL - 142 IS - 6 SN - 0002-922X, 0002-922X KW - Ipecac KW - 8012-96-2 KW - Abridged Index Medicus KW - Index Medicus KW - Socioeconomic Factors KW - Attitude of Health Personnel KW - Pediatrics KW - Humans KW - Data Collection KW - Child KW - Parents KW - Poison Control Centers KW - Ipecac -- therapeutic use KW - Poisoning -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78215216?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+diseases+of+children+%281960%29&rft.atitle=Syrup+of+ipecac.+The+case+for+distribution+from+physicians%27+offices.&rft.au=Malloy%2C+M+H%3BRhoads%2C+G+G&rft.aulast=Malloy&rft.aufirst=M&rft.date=1988-06-01&rft.volume=142&rft.issue=6&rft.spage=640&rft.isbn=&rft.btitle=&rft.title=American+journal+of+diseases+of+children+%281960%29&rft.issn=0002922X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-06-22 N1 - Date created - 1988-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inoculation of baboons and macaques with simian immunodeficiency virus/Mne, a primate lentivirus closely related to human immunodeficiency virus type 2. AN - 78205325; 3285032 AB - A primate lymphotropic lentivirus was isolated on the human T-cell line HuT 78 after cocultivation of a lymph node from a pig-tailed macaque (Macaca nemestrina) that had died with malignant lymphoma. This isolate, originally designated M. nemestrina immunodeficiency virus (MnIV) and now classified as simian immunodeficiency virus (SIV/Mne), was inoculated intravenously into three juvenile rhesus monkeys (Macaca mulatta), three juvenile pig-tailed macaques (M. nemestrina), and two juvenile baboons (Papio cynocephalus). All six macaques became viremic by 3 weeks after inoculation, whereas neither of the baboons developed viremia. One pig-tailed macaque died at 15 weeks with suppurative peritonitis secondary to ulcerative, necrotizing colitis. Immunologic abnormalities included a marked decrease in CD4+ peripheral blood lymphocytes. Although five macaques mounted an antibody response to SIV/Mne, the animal that died at 15 weeks remained antibody negative. Three other macaques (two rhesus and one pig-tailed) died 66 to 87 weeks after inoculation after exhibiting progressive weight loss, anemia, and diarrhea. Histopathologic findings at necropsy included various manifestations of immune deficiency, nephropathy, subacute encephalitis, pancreatitis, adenocarcinoma, and lymphoid atrophy. SIV/Mne could be readily isolated from the spleens and lymph nodes of all necropsied macaques, and from the cerebrospinal fluid, brains, bone marrow, livers, and pancreas of some of the animals. SIV antigens were localized by avidin-biotin immunohistochemistry to pancreatic islet cells and to bone marrow endothelial cells. The data suggest that African baboons may be resistant to infection by SIV/Mne, whereas Asian macaques are susceptible to infection with this pathogenic primate lentivirus. JF - Journal of virology AU - Benveniste, R E AU - Morton, W R AU - Clark, E A AU - Tsai, C C AU - Ochs, H D AU - Ward, J M AU - Kuller, L AU - Knott, W B AU - Hill, R W AU - Gale, M J AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1988/06// PY - 1988 DA - June 1988 SP - 2091 EP - 2101 VL - 62 IS - 6 SN - 0022-538X, 0022-538X KW - Antibodies, Viral KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Antigens, Viral KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Glomerulonephritis -- pathology KW - Lymph Nodes -- microbiology KW - Immunosorbent Techniques KW - Species Specificity KW - T-Lymphocytes -- immunology KW - Leukocyte Count KW - Bone Marrow -- immunology KW - Antigens, Viral -- analysis KW - Lymph Nodes -- immunology KW - Antibodies, Viral -- analysis KW - Retroviridae -- pathogenicity KW - Macaca -- microbiology KW - Macaca -- immunology KW - Papio -- immunology KW - Retroviridae -- immunology KW - Acquired Immunodeficiency Syndrome -- immunology KW - Acquired Immunodeficiency Syndrome -- microbiology KW - Papio -- microbiology KW - Acquired Immunodeficiency Syndrome -- veterinary UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78205325?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inoculation+of+baboons+and+macaques+with+simian+immunodeficiency+virus%2FMne%2C+a+primate+lentivirus+closely+related+to+human+immunodeficiency+virus+type+2.&rft.au=Benveniste%2C+R+E%3BMorton%2C+W+R%3BClark%2C+E+A%3BTsai%2C+C+C%3BOchs%2C+H+D%3BWard%2C+J+M%3BKuller%2C+L%3BKnott%2C+W+B%3BHill%2C+R+W%3BGale%2C+M+J&rft.aulast=Benveniste&rft.aufirst=R&rft.date=1988-06-01&rft.volume=62&rft.issue=6&rft.spage=2091&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 - 1988-06-20 N1 - Date created - 1988-06-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1970 Aug 15;227(5259):680-5 [5432063] Vet Pathol. 1987 Sep;24(5):454-6 [2823446] Int J Cancer. 1976 Jan 15;17(1):62-70 [175022] J Immunol Methods. 1976;13(3-4):215-26 [796385] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Blood. 1980 Feb;55(2):243-52 [6444359] J Exp Med. 1982 May 1;155(5):1561-6 [6978377] Science. 1983 May 20;220(4599):868-71 [6189183] N Engl J Med. 1983 Aug 25;309(8):453-8 [6224088] Science. 1984 Apr 20;224(4646):289-2 [6200929] Science. 1984 May 4;224(4648):497-500 [6200935] Science. 1985 Jun 7;228(4704):1201-4 [3159089] Science. 1985 Oct 4;230(4721):71-3 [2412295] Proc Natl Acad Sci U S A. 1985 Oct;82(20):7053-7 [2996002] Proc Natl Acad Sci U S A. 1985 Nov;82(21):7389-93 [2932738] Science. 1985 Nov 22;230(4728):951-4 [2997923] Science. 1986 Apr 11;232(4747):238-43 [3006256] Nature. 1986 May 22-28;321(6068):435-7 [3012358] J Natl Cancer Inst. 1986 Jul;77(1):127-39 [3014195] Lab Invest. 1986 Jul;55(1):43-50 [3014214] Science. 1986 Jul 18;233(4761):343-6 [2425430] J Clin Invest. 1986 Aug;78(2):439-47 [3016028] Science. 1986 Sep 5;233(4768):1084-6 [3016902] Proc Natl Acad Sci U S A. 1986 Sep;83(18):7089-93 [3018755] Int J Cancer. 1986 Oct 15;38(4):563-74 [2428760] J Clin Invest. 1986 Nov;78(5):1229-36 [3771794] J Virol. 1986 Nov;60(2):483-90 [3021982] Proc Natl Acad Sci U S A. 1986 Dec;83(23):9124-8 [3024167] Science. 1986 Dec 19;234(4783):1563-6 [2431484] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9754-8 [3491989] Am J Pathol. 1987 Feb;126(2):199-207 [3030113] J Infect Dis. 1987 May;155(5):870-6 [3644852] Lab Invest. 1987 Apr;56(4):401-9 [3031367] Nature. 1987 Apr 9-15;326(6113):610-3 [3104797] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] Cell. 1987 May 8;49(3):307-19 [3646094] N Engl J Med. 1987 May 7;316(19):1180-5 [3472076] Am J Pathol. 1987 May;127(2):199-205 [3472469] Clin Immunol Immunopathol. 1987 Jul;44(1):93-106 [2439243] Nature. 1987 Aug 6-12;328(6130):539-43 [3497350] Nature. 1987 Aug 6-12;328(6130):543-7 [3649576] Tumori. 1972 May-Jun;58(3):143-56 [4345734] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Smoking and drinking in relation to oral and pharyngeal cancer. AN - 78203385; 3365707 AB - A case-control study of oral and pharyngeal cancer conducted in four areas of the United States provided information on the tobacco and alcohol use of 1114 patients and 1268 population-based controls. Because of the large study size, it could be shown that the risks of these cancers among nondrinkers increased with amount smoked, and conversely that the risks among nonsmokers increased with the level of alcohol intake. Among consumers of both products, risks of oropharyngeal cancer tended to combine more in a multiplicative than additive fashion and were increased more than 35-fold among those who consumed two or more packs of cigarettes and more than four alcoholic drinks/day. Cigarette, cigar, and pipe smoking were separately implicated, although it was shown for the first time that risk was not as high among male lifelong filter cigarette smokers. Cessation of smoking was associated with a sharply reduced risk of this cancer, with no excess detected among those having quit for 10 or more years, suggesting that smoking affects primarily a late stage in the process of oropharyngeal carcinogenesis. The risks varied by type of alcoholic beverage, being higher among those consuming hard liquor or beer than wine. The relative risk patterns were generally similar among whites and blacks, and among males and females, and showed little difference when oral and pharyngeal cancers were analyzed separately. From calculations of attributable risk, we estimate that tobacco smoking and alcohol drinking combine to account for approximately three-fourths of all oral and pharyngeal cancers in the United States. JF - Cancer research AU - Blot, W J AU - McLaughlin, J K AU - Winn, D M AU - Austin, D F AU - Greenberg, R S AU - Preston-Martin, S AU - Bernstein, L AU - Schoenberg, J B AU - Stemhagen, A AU - Fraumeni, J F AD - National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/06/01/ PY - 1988 DA - 1988 Jun 01 SP - 3282 EP - 3287 VL - 48 IS - 11 SN - 0008-5472, 0008-5472 KW - Index Medicus KW - United States KW - Age Factors KW - Sex Factors KW - Humans KW - European Continental Ancestry Group KW - Aged KW - African Americans KW - Middle Aged KW - Male KW - Female KW - Pharyngeal Neoplasms -- epidemiology KW - Pharyngeal Neoplasms -- etiology KW - Mouth Neoplasms -- etiology KW - Smoking -- adverse effects KW - Alcohol Drinking KW - Mouth Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78203385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Smoking+and+drinking+in+relation+to+oral+and+pharyngeal+cancer.&rft.au=Blot%2C+W+J%3BMcLaughlin%2C+J+K%3BWinn%2C+D+M%3BAustin%2C+D+F%3BGreenberg%2C+R+S%3BPreston-Martin%2C+S%3BBernstein%2C+L%3BSchoenberg%2C+J+B%3BStemhagen%2C+A%3BFraumeni%2C+J+F&rft.aulast=Blot&rft.aufirst=W&rft.date=1988-06-01&rft.volume=48&rft.issue=11&rft.spage=3282&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 - 1988-06-15 N1 - Date created - 1988-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transcriptional control of high molecular weight keratin gene expression in multistage mouse skin carcinogenesis. AN - 78199645; 2452688 AB - Monospecific antikeratin antisera and specific complementary DNA probes were used to analyze expression of keratin genes in newborn mouse skin and skin papillomas and carcinomas by indirect immunofluorescence, immunoblotting, and in situ hybridization. Tumors were induced by initiation with 7,12-dimethylbenz[a]anthracene and promotion with 12-O-tetradecanoylphorbol-13-acetate. Type I epidermal keratin K14 protein (Mr 55,000) is found in all living layers of the newborn skin but is most abundant in the lower strata. K1 (Mr 67,000) and K10 (Mr 59,000) proteins are predominantly suprabasal and K1 is processed in the stratum corneum. Transcripts for K14 were confined largely to the basal cell layer by in situ hybridization. Transcripts for K1 and K10 were highly expressed in suprabasal cells including the granular cell layer. In benign tumors, distribution of K14 protein is similar to that in newborn skin, while the abundance of K1 and K10 appears to be somewhat reduced although the tissue distribution remains suprabasal. Transcription of K14 is aberrant in benign tumors and transcripts persist throughout much of the suprabasal cell layers. Transcripts of K1 and K10 are normally distributed in papillomas but grain density is less intense than in newborn epidermis. Keratin expression in carcinomas is highly disturbed. K14 protein and transcripts are highly expressed in all strata in carcinomas while protein and transcripts for K1 and K10 are essentially absent. These results suggest that papilloma cells fail to respond to or generate signals to regulate K14 expression in the differentiating suprabasal cell layers and may not fully express their suprabasal cell keratins. Carcinomas fail to express suprabasal cell keratins and this is regulated at the transcriptional level. The loss of suprabasal keratin expression may provide a marker for malignant conversion in the mouse skin carcinogenesis model. JF - Cancer research AU - Roop, D R AU - Krieg, T M AU - Mehrel, T AU - Cheng, C K AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/06/01/ PY - 1988 DA - 1988 Jun 01 SP - 3245 EP - 3252 VL - 48 IS - 11 SN - 0008-5472, 0008-5472 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Keratins KW - 68238-35-7 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals, Newborn KW - Animals KW - Mice KW - Nucleic Acid Hybridization KW - Female KW - Skin Neoplasms -- genetics KW - Keratins -- genetics KW - Genes KW - Papilloma -- pathology KW - Carcinoma -- pathology KW - Skin -- metabolism KW - Skin Neoplasms -- pathology KW - Transcription, Genetic KW - Gene Expression Regulation KW - Papilloma -- genetics KW - Cell Transformation, Neoplastic KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78199645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transcriptional+control+of+high+molecular+weight+keratin+gene+expression+in+multistage+mouse+skin+carcinogenesis.&rft.au=Roop%2C+D+R%3BKrieg%2C+T+M%3BMehrel%2C+T%3BCheng%2C+C+K%3BYuspa%2C+S+H&rft.aulast=Roop&rft.aufirst=D&rft.date=1988-06-01&rft.volume=48&rft.issue=11&rft.spage=3245&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 - 1988-06-15 N1 - Date created - 1988-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lectins modulate the internalization of recombinant interferon-alpha A and the induction of 2',5'-oligo(A) synthetase. AN - 78202749; 2966801 AB - After binding to specific cell surface receptors, interferon-alpha (IFN-alpha) along with its receptor is internalized by the cells. However, the physiological significance of the internalization of IFN is not known. We have found that the lectin concanavalin A (ConA), which does not inhibit the binding of 125I-rIFN-alpha A, inhibits both the internalization of 125I-rIFN-alpha A and the rIFN-alpha A-induced increase in the levels of 2',5'-oligo(A) synthetase mRNA and enzymatic activity in the B lymphoblastoid cell line Daudi. The reduced level of IFN-induced 2',5'-oligo(A) synthetase in ConA-treated cells was due neither to direct inhibition of the enzymatic activity nor to generalized inhibition of protein or RNA synthesis. The dose-response curves were similar for the effect of ConA to inhibit 125I-rIFN-alpha A internalization and 2',5'-oligo(A) synthetase induction. The correlation between the ConA-mediated inhibition of both 125I-rIFN-alpha A internalization and 2',5'-oligo(A) synthetase induction suggests that internalization of rIFN-alpha A plays a role in the responses to rIFN-alpha A. However, since ConA inhibits protein mobility in the plasma membrane, it is possible that ConA is also preventing aggregation of IFN receptors or interactions between IFN receptors and signal transducing proteins in the plasma membrane that may be necessary for responses to IFN. JF - The Journal of biological chemistry AU - Faltynek, C R AU - Princler, G L AU - Ruscetti, F W AU - Birchenall-Sparks, M AD - Biological Carcinogenesis Development Program, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/05/25/ PY - 1988 DA - 1988 May 25 SP - 7112 EP - 7117 VL - 263 IS - 15 SN - 0021-9258, 0021-9258 KW - Interferon Type I KW - 0 KW - Phytohemagglutinins KW - Receptors, Immunologic KW - Receptors, Interferon KW - Recombinant Proteins KW - Concanavalin A KW - 11028-71-0 KW - 2',5'-Oligoadenylate Synthetase KW - EC 2.7.7.84 KW - Index Medicus KW - Receptors, Immunologic -- metabolism KW - Kinetics KW - Humans KW - Enzyme Induction KW - Cell Line KW - Recombinant Proteins -- metabolism KW - Interferon Type I -- metabolism KW - 2',5'-Oligoadenylate Synthetase -- biosynthesis KW - Phytohemagglutinins -- pharmacology KW - Concanavalin A -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78202749?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Lectins+modulate+the+internalization+of+recombinant+interferon-alpha+A+and+the+induction+of+2%27%2C5%27-oligo%28A%29+synthetase.&rft.au=Faltynek%2C+C+R%3BPrincler%2C+G+L%3BRuscetti%2C+F+W%3BBirchenall-Sparks%2C+M&rft.aulast=Faltynek&rft.aufirst=C&rft.date=1988-05-25&rft.volume=263&rft.issue=15&rft.spage=7112&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 - 1988-06-20 N1 - Date created - 1988-06-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The Giardia lamblia trophozoite contains sets of closely related chromosomes. AN - 19635110; 8745390 AB - Size variations in homologous chromosomes from six Giardia lamblia isolates have been demonstrated. Four or five intensely stained (major) bands as well as a variable number of lightly stained (minor) bands are present in pulsed field gradient separations. Southern blot analysis with total chromosomal DNA as well as chromosome specific probes indicates that each minor band cross-hybridizes with a major band. Minor bands of doubly cloned organisms appear identical to those of parent clones, indicating that the minor bands do not reflect the presence of variant members within the total population of trophozoites. Densitometric comparisons of chromosome bands from known numbers of Plasmodium falciparum ring stage forms and known numbers of Giardia trophozoites suggest that minor bands MBa and MBb are present in each Giardia trophozoite. Comparison of Not I restriction fragments from the major and minor bands reveals common restriction fragments. Taken together, the data imply that sets of closely related chromosomes occur in the Giardia trophozoite. Images JF - Nucleic Acids Research AU - Adam, R D AU - Nash, T E AU - Wellems, T E AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/05/25/ PY - 1988 DA - 1988 May 25 SP - 4555 EP - 4567 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 16 IS - 10 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Biochemistry Abstracts 2: Nucleic Acids KW - Clones KW - Parasites KW - Data processing KW - Giardia lamblia KW - Probes KW - Plasmodium falciparum KW - Chromosomes KW - DNA KW - Nucleic acids KW - Trophozoites KW - G 07790:Other Microorganisms KW - Q1 08185:Genetics and evolution KW - N 14835:Protein-Nucleic Acids Association KW - Q5 08501:General KW - K 03310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19635110?accountid=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=Nucleic+Acids+Research&rft.atitle=The+Giardia+lamblia+trophozoite+contains+sets+of+closely+related+chromosomes.&rft.au=Adam%2C+R+D%3BNash%2C+T+E%3BWellems%2C+T+E&rft.aulast=Adam&rft.aufirst=R&rft.date=1988-05-25&rft.volume=16&rft.issue=10&rft.spage=4555&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 - 2014-05-07 N1 - SubjectsTermNotLitGenreText - Clones; Parasites; Chromosomes; DNA; Nucleic acids; Data processing; Probes; Trophozoites; Giardia lamblia; Plasmodium falciparum ER - TY - JOUR T1 - Increased glucose utilization in superficial layers of the rat spinal dorsal horn during precipitated morphine withdrawal. AN - 78357831; 3402536 AB - The 2-deoxy-D-[1-14C]glucose method was used to map effects of morphine withdrawal on glucose utilization in the rat spinal cord. Naloxone (0.5 mg s.c.) given to morphinized rats (225 mg morphine over 7 days) produced a withdrawal syndrome, and increased glucose utilization in the superficial layers of the dorsal horn in the cervical and thoracic spinal cord. The findings are consistent with an increased input from small diameter primary afferent fibers during the morphine withdrawal syndrome. JF - European journal of pharmacology AU - Bell, J A AU - Kimes, A S AU - London, E D AD - Neuropharmacology Laboratory, Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1988/05/20/ PY - 1988 DA - 1988 May 20 SP - 171 EP - 174 VL - 150 IS - 1-2 SN - 0014-2999, 0014-2999 KW - Naloxone KW - 36B82AMQ7N KW - Morphine KW - 76I7G6D29C KW - Glucose KW - IY9XDZ35W2 KW - Clonidine KW - MN3L5RMN02 KW - Index Medicus KW - Rats KW - Naloxone -- pharmacology KW - Animals KW - Rats, Inbred F344 KW - Clonidine -- pharmacology KW - Male KW - Substance Withdrawal Syndrome -- metabolism KW - Spinal Cord -- metabolism KW - Glucose -- metabolism KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78357831?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+glucose+utilization+in+superficial+layers+of+the+rat+spinal+dorsal+horn+during+precipitated+morphine+withdrawal.&rft.au=Bell%2C+J+A%3BKimes%2C+A+S%3BLondon%2C+E+D&rft.aulast=Bell&rft.aufirst=J&rft.date=1988-05-20&rft.volume=150&rft.issue=1-2&rft.spage=171&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 - 1988-09-16 N1 - Date created - 1988-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chromatographic separation and isolation of the enantiomers of diethylstilbestrol metabolites. AN - 78350480; 3403657 JF - Journal of chromatography AU - Chae, K AU - Levy, L A AU - Korach, K S AD - Laboratory of Reproductive and Developmental Toxicology, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1988/05/20/ PY - 1988 DA - 1988 May 20 SP - 484 EP - 487 VL - 439 IS - 2 KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Stereoisomerism KW - Chromatography, High Pressure Liquid KW - Diethylstilbestrol -- metabolism KW - Diethylstilbestrol -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78350480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography&rft.atitle=Chromatographic+separation+and+isolation+of+the+enantiomers+of+diethylstilbestrol+metabolites.&rft.au=Chae%2C+K%3BLevy%2C+L+A%3BKorach%2C+K+S&rft.aulast=Chae&rft.aufirst=K&rft.date=1988-05-20&rft.volume=439&rft.issue=2&rft.spage=484&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-15 N1 - Date created - 1988-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of the cell-binding domain of human fibronectin: separable, synergistic sites mediate adhesive function. AN - 78219663; 3286012 AB - Polypeptide sequences required for function of the cell-binding domain of human fibronectin were analyzed by site-directed mutagenesis. Site-specific deletion of the putative recognition sequence Arg-Gly-Asp-Ser or an Asp-to-Glu mutation decreased the adhesive activity of fibronectin fusion proteins expressed in E. coli by greater than or equal to 97%. A second functional site over 0.5 kb away was identified by deletion mutagenesis. These mutants also showed a greater than or equal to 96% loss of activity, indicating cooperativity between sites. The two classes of mutant protein displayed synergism of activity in a trans complementation assay. Effective actin microfilament bundle organization was also dependent on the combined function of both sites. Thus, fibroblast adhesion and intracellular response to the fibronectin cell-binding domain involve two synergistic sites, each of major quantitative importance. JF - Cell AU - Obara, M AU - Kang, M S AU - Yamada, K M AD - Membrane Biochemistry Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/05/20/ PY - 1988 DA - 1988 May 20 SP - 649 EP - 657 VL - 53 IS - 4 SN - 0092-8674, 0092-8674 KW - Actins KW - 0 KW - Fibronectins KW - Oligopeptides KW - Peptide Fragments KW - Recombinant Fusion Proteins KW - arginyl-glycyl-aspartyl-serine KW - AC6UDA2MFC KW - Index Medicus KW - Actins -- physiology KW - Chromosome Deletion KW - Cells, Cultured KW - Humans KW - Recombinant Fusion Proteins -- genetics KW - Molecular Sequence Data KW - Genetic Complementation Test KW - Amino Acid Sequence KW - Mutation KW - Fluorescent Antibody Technique KW - Recombinant Fusion Proteins -- physiology KW - Fibroblasts KW - Peptide Fragments -- genetics KW - Fibronectins -- physiology KW - Oligopeptides -- genetics KW - Oligopeptides -- physiology KW - Fibronectins -- metabolism KW - Fibronectins -- genetics KW - Peptide Fragments -- physiology KW - Cell Adhesion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78219663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell&rft.atitle=Site-directed+mutagenesis+of+the+cell-binding+domain+of+human+fibronectin%3A+separable%2C+synergistic+sites+mediate+adhesive+function.&rft.au=Obara%2C+M%3BKang%2C+M+S%3BYamada%2C+K+M&rft.aulast=Obara&rft.aufirst=M&rft.date=1988-05-20&rft.volume=53&rft.issue=4&rft.spage=649&rft.isbn=&rft.btitle=&rft.title=Cell&rft.issn=00928674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-06-29 N1 - Date created - 1988-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Separation of the 24 kDa substrate for botulinum C3 ADP-ribosyltransferase and the cholera toxin ADP-ribosylation factor. AN - 78253731; 3132159 AB - Botulinum C3 ADP-ribosyltransferase modifies a approximately 24 kDa membrane protein believed to bind guanine nucleotides. Cholera toxin ADP-ribosylation factors are approximately 19 kDa GTP-binding proteins that directly activate the toxin. To evaluate a possible relationship between C3 ADP-ribosyltransferase substrate and ADP-ribosylation factor, they were partially purified from bovine brain. ADP-ribosylation factor, but not C3 ADP-ribosyltransferase substrate, stimulated auto-ADP-ribosylation of the choleragen A1 subunit whereas C3 ADP-ribosyltransferase substrate, but not ADP-ribosylation factor, was ADP-ribosylated by C3 ADP-ribosyltransferase. Thus, although both may be GTP-binding proteins, no functional similarity between ADP-ribosylation factor and C3 ADP-ribosyltransferase substrate was found. JF - Biochemical and biophysical research communications AU - Tsai, S C AU - Adamik, R AU - Moss, J AU - Aktories, K AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/05/16/ PY - 1988 DA - 1988 May 16 SP - 957 EP - 961 VL - 152 IS - 3 SN - 0006-291X, 0006-291X KW - Membrane Proteins KW - 0 KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Cholera Toxin KW - 9012-63-9 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - Pentosyltransferases KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - Cattle KW - Electrophoresis, Polyacrylamide Gel KW - Membrane Proteins -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Molecular Weight KW - Pentosyltransferases -- metabolism KW - Adenosine Diphosphate Ribose -- metabolism KW - Clostridium botulinum -- enzymology KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78253731?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Separation+of+the+24+kDa+substrate+for+botulinum+C3+ADP-ribosyltransferase+and+the+cholera+toxin+ADP-ribosylation+factor.&rft.au=Tsai%2C+S+C%3BAdamik%2C+R%3BMoss%2C+J%3BAktories%2C+K&rft.aulast=Tsai&rft.aufirst=S&rft.date=1988-05-16&rft.volume=152&rft.issue=3&rft.spage=957&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 - 1988-06-24 N1 - Date created - 1988-06-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of human c-raf-1 oncogene proteins in E. coli. AN - 78249528; 2837178 AB - Full length and truncated versions of the human c-raf-1 cDNA were cloned into the inducible E. coli expression vector pJL6. C-raf proteins of 73 kD, 57 kD and 39 kD were produced upon induction. p73 differs from normal p73 c-raf by deletion of the two first N-terminal amino acids and their replacement by 16 amino acids encoded by the vector. The p57 and p39 represent N-terminal deletions which leave the transforming protein kinase domain intact. These proteins could be readily purified from E. coli lysates by immunoprecipitation with raf-specific antisera. JF - Biochemical and biophysical research communications AU - Kolch, W AU - Bonner, T I AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701-1013. Y1 - 1988/05/16/ PY - 1988 DA - 1988 May 16 SP - 1045 EP - 1049 VL - 152 IS - 3 SN - 0006-291X, 0006-291X KW - Amino Acids KW - 0 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - Index Medicus KW - Chromosome Deletion KW - DNA Restriction Enzymes -- metabolism KW - Humans KW - Amino Acids -- analysis KW - Molecular Weight KW - Oncogenes KW - Escherichia coli -- genetics KW - Gene Expression Regulation KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78249528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+human+c-raf-1+oncogene+proteins+in+E.+coli.&rft.au=Kolch%2C+W%3BBonner%2C+T+I%3BRapp%2C+U+R&rft.aulast=Kolch&rft.aufirst=W&rft.date=1988-05-16&rft.volume=152&rft.issue=3&rft.spage=1045&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 - 1988-06-24 N1 - Date created - 1988-06-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A flexible peptide spacer increases the efficacy of holoricin anti-T cell immunotoxins. AN - 78184456; 2896212 AB - Immunotoxins, constructed by chemically cross-linking an antibody and protein toxin, do not possess the high efficacy of the native toxin. Decreases in toxicity are due in part to the steric constraints imposed on the two macromolecules, which result in both decreased antibody binding and toxin function. In examining the structural features that influence efficacy in holotoxin-antibody conjugates, it was found that the incorporation of a 29-residue polypeptide, derived from the insulin B chain between the antibody and ricin moiety, resulted in an increase in both potency and efficacy. In a murine model system, potency of the peptide spacer conjugate was increased nearly 10-fold; however, when examined by the procedure used to purge bone marrow, the peptide spacer conjugate was not demonstrably more toxic to nontarget cells than the nonspacer conjugate. Thus, in addition to increases of efficacy and potency, this novel immunotoxin demonstrated increased specificity by approximately 10-fold. To test the general utility of peptide spacer inclusion, a T101-ricin conjugate was constructed with the peptide spacer. It yielded a protein synthesis inhibition rate of -0.6 log/h on MOLT-3 cells, greater than 10-fold more efficacious than a previously constructed nonspacer T101-ricin conjugate examined under similar conditions. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Marsh, J W AU - Neville, D M AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/05/15/ PY - 1988 DA - 1988 May 15 SP - 3674 EP - 3678 VL - 140 IS - 10 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Surface KW - Antigens, Thy-1 KW - Immunotoxins KW - Peptides KW - Ricin KW - 9009-86-3 KW - Abridged Index Medicus KW - Index Medicus KW - Kinetics KW - Humans KW - Dose-Response Relationship, Immunologic KW - Cell Line KW - Antigens, Surface -- immunology KW - Structure-Activity Relationship KW - Protein Conformation KW - Ricin -- toxicity KW - Immunotoxins -- toxicity KW - Antibodies, Monoclonal -- toxicity KW - Ricin -- immunology KW - Peptides -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78184456?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+flexible+peptide+spacer+increases+the+efficacy+of+holoricin+anti-T+cell+immunotoxins.&rft.au=Marsh%2C+J+W%3BNeville%2C+D+M&rft.aulast=Marsh&rft.aufirst=J&rft.date=1988-05-15&rft.volume=140&rft.issue=10&rft.spage=3674&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 - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Allogeneic non-T spleen cells restore the responsiveness of normal T cell clones stimulated with antigen and chemically modified antigen-presenting cells. AN - 78175738; 2834436 AB - Stimulation of IL-2-producing T cell clones with chemically modified APC and Ag induces a state of proliferative unresponsiveness, i.e., subsequent stimulation with normal APC and Ag fails to elicit IL-2 production. One possible effect of chemical modification on the APC is the destruction of its ability to provide costimulatory signals. To test this, various potential costimulators were added to T cells at the time of exposure to Ag and chemically modified APC. None of the cytokines tested, including IL-1, had a positive effect; however, addition of allogeneic spleen cells allowed a T cell proliferative response and prevented the induction of subsequent unresponsiveness. Fractionation of the spleen cells showed that low density B cells and macrophages were the best source of costimulatory activity. Allogeneic resting B cells provided some costimulatory activity and resting T cells, none at all. Attempts to mimic costimulatory signals with the phorbol ester PMA were only partially successful. PMA prevented the induction of T cell unresponsiveness but failed to allow T cell proliferation in response to Ag plus chemically modified APC. Our results suggest that IL-2 production by normal T cell clones is dependent not only on T cell receptor occupancy, but also on short range costimulatory signals that are provided to different degrees by various non-T accessory cells. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Jenkins, M K AU - Ashwell, J D AU - Schwartz, R H AD - Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/05/15/ PY - 1988 DA - 1988 May 15 SP - 3324 EP - 3330 VL - 140 IS - 10 SN - 0022-1767, 0022-1767 KW - Cytochrome c Group KW - 0 KW - Interleukin-1 KW - Interleukin-3 KW - Isoantigens KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Ethyldimethylaminopropyl Carbodiimide KW - RJ5OZG6I4A KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-1 -- pharmacology KW - Interleukin-3 -- pharmacology KW - Mice, Inbred C57BL KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Communication KW - Mice KW - Ethyldimethylaminopropyl Carbodiimide -- pharmacology KW - Lymphocyte Cooperation KW - Clone Cells -- immunology KW - Lymphocyte Activation -- drug effects KW - Spleen -- cytology KW - Cytochrome c Group -- immunology KW - Isoantigens -- immunology KW - Antigen-Presenting Cells -- immunology KW - Antigen-Presenting Cells -- drug effects KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78175738?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Allogeneic+non-T+spleen+cells+restore+the+responsiveness+of+normal+T+cell+clones+stimulated+with+antigen+and+chemically+modified+antigen-presenting+cells.&rft.au=Jenkins%2C+M+K%3BAshwell%2C+J+D%3BSchwartz%2C+R+H&rft.aulast=Jenkins&rft.aufirst=M&rft.date=1988-05-15&rft.volume=140&rft.issue=10&rft.spage=3324&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 - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Case-control study of diet and mesothelioma in Louisiana. AN - 78173803; 3359447 AB - Data were analyzed from a case-control interview study of malignant mesothelioma in Louisiana, which gathered information on usual diet and on lifetime occupational exposure to asbestos. Thirty-seven patients with malignant mesothelioma of the pleura (n = 32) or peritoneum (n = 5) were matched to controls according to age, sex, race, and factors related to case ascertainment (hospital and date of diagnosis, or parish and date of death). Twenty-one of the 37 cases were judged by masked occupational review to have been exposed to asbestos (57%), compared to seven of 37 controls (19%). Seven additional cases and 10 additional controls had occupational histories suggestive of asbestos exposure. With regard to usual diet before illness, cases reported less frequent consumption of homegrown produce (p = 0.005), cruciferous vegetables (p = 0.005), and all vegetables combined (p = 0.09) than did the controls. An estimate of usual carotene intake was also significantly lower in cases (p = 0.03). Dose-dependent reductions in risk were seen with increasing consumption of vegetables, especially cruciferous vegetables (p for trend = 0.013). These associations were not explained by differences in asbestos exposure as measured by the occupational review. The results indicate that consumption of vegetables or some vegetable-related constituent may have a protective effect on developing mesothelioma. JF - Cancer research AU - Schiffman, M H AU - Pickle, L W AU - Fontham, E AU - Zahm, S H AU - Falk, R AU - Mele, J AU - Correa, P AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/05/15/ PY - 1988 DA - 1988 May 15 SP - 2911 EP - 2915 VL - 48 IS - 10 SN - 0008-5472, 0008-5472 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Vegetables KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Adult KW - Asbestos -- adverse effects KW - Aged KW - Middle Aged KW - Louisiana KW - Occupations KW - Male KW - Female KW - Peritoneal Neoplasms -- etiology KW - Mesothelioma -- etiology KW - Diet KW - Pleural Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78173803?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Case-control+study+of+diet+and+mesothelioma+in+Louisiana.&rft.au=Schiffman%2C+M+H%3BPickle%2C+L+W%3BFontham%2C+E%3BZahm%2C+S+H%3BFalk%2C+R%3BMele%2C+J%3BCorrea%2C+P%3BFraumeni%2C+J+F&rft.aulast=Schiffman&rft.aufirst=M&rft.date=1988-05-15&rft.volume=48&rft.issue=10&rft.spage=2911&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 - 1988-06-03 N1 - Date created - 1988-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fluorodeoxyuridine modulation of the incorporation of iododeoxyuridine into DNA of granulocytes: a phase I and clinical pharmacological study. AN - 78168986; 2965970 AB - The amount of iododeoxyuridine (IdUrd) incorporated into DNA determines the degree of radiosensitization. Fluorodeoxyuridine (FdUrd) has been shown to biochemically modulate IdUrd incorporation into DNA in vitro and in vivo. In this Phase I study, these drugs were coadministered to patients during 14-day continuous i.v. infusion periods in order to investigate whether the incorporation of IdUrd into DNA in vivo could be increased without increasing the dose of IdUrd. IdUrd plasma concentrations and incorporation of IdUrd into DNA of granulocytes were measured by high-performance liquid chromatography. Up to 8.8% substitution of thymidine by IdUrd was observed. Even at 3.5 mg/m2/day FdUrd for 14 days (78% of the maximum-tolerated dose as a single agent), no clinically relevant enhancement of incorporation of IdUrd into DNA of granulocytes was observed. Also, no changes in plasma levels of IdUrd were observed with escalating doses of FdUrd. Toxicity patterns (stomatitis, diarrhea, and bone marrow depression) and isobologram analysis suggested that IdUrd and FdUrd had additive, rather than synergistic, effects. JF - Cancer research AU - Speth, P A AU - Kinsella, T J AU - Belanger, K AU - Klecker, R W AU - Smith, R AU - Rowland, J B AU - Collins, J M AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/05/15/ PY - 1988 DA - 1988 May 15 SP - 2933 EP - 2937 VL - 48 IS - 10 SN - 0008-5472, 0008-5472 KW - Floxuridine KW - 039LU44I5M KW - DNA KW - 9007-49-2 KW - Idoxuridine KW - LGP81V5245 KW - Index Medicus KW - Neoplasms -- drug therapy KW - Humans KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Bone Marrow -- drug effects KW - Male KW - Female KW - Floxuridine -- administration & dosage KW - Floxuridine -- pharmacology KW - Idoxuridine -- metabolism KW - Granulocytes -- metabolism KW - DNA -- metabolism KW - Idoxuridine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78168986?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fluorodeoxyuridine+modulation+of+the+incorporation+of+iododeoxyuridine+into+DNA+of+granulocytes%3A+a+phase+I+and+clinical+pharmacological+study.&rft.au=Speth%2C+P+A%3BKinsella%2C+T+J%3BBelanger%2C+K%3BKlecker%2C+R+W%3BSmith%2C+R%3BRowland%2C+J+B%3BCollins%2C+J+M&rft.aulast=Speth&rft.aufirst=P&rft.date=1988-05-15&rft.volume=48&rft.issue=10&rft.spage=2933&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 - 1988-06-03 N1 - Date created - 1988-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Angiotensin II and guanine nucleotides stimulate formation of inositol 1,4,5-trisphosphate and its metabolites in permeabilized adrenal glomerulosa cells. AN - 78185733; 3283118 AB - Angiotensin II (AII) interacts with specific receptors in the adrenal glomerulosa cell and stimulates the hydrolysis of plasma membrane phosphoinositides by phospholipase C, with production of inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and subsequent mobilization of intracellular Ca2+. In electrically permeabilized, [3H]inositol-labeled glomerulosa cells, AII stimulated Ins-1,4,5-P3 production within 15 s with half-maximal potency of 10(-9) M. The nonhydrolyzable GTP analog, guanosine 5'-O-thiotriphosphate (GTP gamma S), stimulated Ins-1,4,5-P3 formation in a dose-dependent manner with half-maximal effect at 10(-7) M. AII-activated Ins-1,4,5-P3 production was further increased by guanine nucleotides. The rate at which GTP gamma S-stimulated inositol polyphosphate production was consistently slower than that of AII. In adrenal membrane preparations, GTP gamma S-stimulated polyphosphoinositide hydrolysis was enhanced by Ca2+, with half-maximal activity at 300 nM free Ca2+. Ins-1,4,5-P3 formation was also increased by NaF, further indicating the involvement of a guanine nucleotide regulatory protein. In addition to Ins-1,4,5-P3 and its metabolites formed during degradation via the 4-monophosphate pathway, AII and GTP gamma S stimulated the formation of the phosphorylated metabolite inositol 1,3,4,5-tetrakisphosphate and inositol 1,3,4-trisphosphate in permeabilized cells. The absence of a significant rise in inositol 1-monophosphate indicated that phosphatidylinositol hydrolysis was not stimulated by AII or GTP gamma S. Pretreatment of glomerulosa cells with pertussis toxin for 12 h before permeabilization did not inhibit AII- or GTP gamma S-stimulated inositol polyphosphate formation. However, treatment with cholera toxin, forskolin, or 8-Br-cAMP for 12 h enhanced both basal and ligand-stimulated Ins-1,4,5-P3 production. These observations suggest that agonist binding to the AII receptor activates a polyphosphoinositide-specific phospholipase C in the adrenal glomerulosa cell, and that a distinctive guanine regulatory protein is involved in this mechanism. JF - The Journal of biological chemistry AU - Baukal, A J AU - Balla, T AU - Hunyady, L AU - Hausdorff, W AU - Guillemette, G AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/05/05/ PY - 1988 DA - 1988 May 05 SP - 6087 EP - 6092 VL - 263 IS - 13 SN - 0021-9258, 0021-9258 KW - Guanine Nucleotides KW - 0 KW - Inositol Phosphates KW - Sugar Phosphates KW - Thionucleotides KW - Virulence Factors, Bordetella KW - Angiotensin II KW - 11128-99-7 KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - Guanosine Triphosphate KW - 86-01-1 KW - Sodium Fluoride KW - 8ZYQ1474W7 KW - Cholera Toxin KW - 9012-63-9 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 - Dose-Response Relationship, Drug KW - Cholera Toxin -- pharmacology KW - Calcium -- pharmacology KW - Electric Stimulation KW - Guanosine Triphosphate -- pharmacology KW - Type C Phospholipases -- metabolism KW - Guanosine Triphosphate -- analogs & derivatives KW - Virulence Factors, Bordetella -- pharmacology KW - Thionucleotides -- pharmacology KW - Cattle KW - Sodium Fluoride -- pharmacology KW - Cell Membrane Permeability KW - Time Factors KW - Sugar Phosphates -- metabolism KW - Inositol Phosphates -- metabolism KW - Guanine Nucleotides -- pharmacology KW - Angiotensin II -- pharmacology KW - Adrenal Cortex -- metabolism KW - Adrenal Cortex -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78185733?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Angiotensin+II+and+guanine+nucleotides+stimulate+formation+of+inositol+1%2C4%2C5-trisphosphate+and+its+metabolites+in+permeabilized+adrenal+glomerulosa+cells.&rft.au=Baukal%2C+A+J%3BBalla%2C+T%3BHunyady%2C+L%3BHausdorff%2C+W%3BGuillemette%2C+G%3BCatt%2C+K+J&rft.aulast=Baukal&rft.aufirst=A&rft.date=1988-05-05&rft.volume=263&rft.issue=13&rft.spage=6087&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 - 1988-06-06 N1 - Date created - 1988-06-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protein kinase C and its substrates in tumor promoter-sensitive and -resistant cells. AN - 78183782; 3360787 AB - Calcium- and phospholipid-dependent protein kinase C activity and substrates were characterized in cell lysates of preneoplastic JB6 cells, a model system of genetic variants for sensitivity to tumor promoter-induced neoplastic transformation. Protein kinase C activity was similar for sensitive and resistant variants, as measured by calcium- and phospholipid-dependent phosphorylation of an exogenous substrate (histone HIII). Of 13 endogenous protein kinase C substrates, identified by labeling proteins with [gamma-32P] ATP, at least two (80 and 23 kDa) are potential candidates for mediating events on the pathway for promotion of transformation. 32P incorporation into the 80-kDa protein kinase C substrate was stimulated by tetradecanoylphorbol acetate and correlated with phenotype: the highest incorporation was found in promotion-insensitive cells, an intermediate level in promotion-sensitive cells and the lowest in the transformed cells. The phosphorylation of an 80-kDa protein, found by labeling intact cells in monolayer growth with [32P]orthophosphate, was also stimulated by tetradecanoylphorbol acetate and correlated inversely with phenotype. The 80 kDa protein kinase C substrate from cell lysates and the 80-kDa phosphoprotein from intact cells appear to be identical, as indicated by peptide mapping with protease V8 from Staphylococcus aureus. This finding suggests that the 80-kDa substrate is relevant to promoter-induced signal transduction in the intact cell. The 23-kDa protein kinase C substrate exhibited a band shift in sodium dodecyl sulfate gels in response to another transformation promoter in JB6 cells, the calcium analog, lanthanum (Smith, B. M., Gindhart, T. D., and Colburn, N. H. (1986) Carcinogenesis 7, 1949-1956). In summary, there are no unique substrates that distinguish the variants. Quantitative differences in certain substrates or their phosphorylation may, however, account for the difference in promotion sensitivity among the variants. JF - The Journal of biological chemistry AU - Smith, B M AU - Colburn, N H AD - National Cancer Institute, Frederick Cancer Institute Facility, Maryland 21701. Y1 - 1988/05/05/ PY - 1988 DA - 1988 May 05 SP - 6424 EP - 6431 VL - 263 IS - 13 SN - 0021-9258, 0021-9258 KW - Carcinogens KW - 0 KW - Phospholipids KW - Phosphoproteins KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Calcium -- metabolism KW - Animals KW - Epidermis -- drug effects KW - Phosphorylation KW - Peptide Mapping KW - Electrophoresis, Polyacrylamide Gel KW - Phosphoproteins -- analysis KW - Phospholipids -- metabolism KW - Drug Resistance KW - Mice KW - Cell Line KW - Protein Kinase C -- metabolism KW - Carcinogens -- pharmacology KW - Cell Transformation, Neoplastic -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78183782?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Protein+kinase+C+and+its+substrates+in+tumor+promoter-sensitive+and+-resistant+cells.&rft.au=Smith%2C+B+M%3BColburn%2C+N+H&rft.aulast=Smith&rft.aufirst=B&rft.date=1988-05-05&rft.volume=263&rft.issue=13&rft.spage=6424&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 - 1988-06-06 N1 - Date created - 1988-06-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rat neuropeptide Y precursor gene expression. mRNA structure, tissue distribution, and regulation by glucocorticoids, cyclic AMP, and phorbol ester. AN - 78182293; 2834371 AB - Rat brain neuropeptide Y precursor (prepro-NPY) cDNA clones were isolated and sequenced in order to study regulation of the prepro-NPY gene. Rat prepro-NPY (98 amino acid residues) contains a 36-residue NPY sequence, followed by a proteolysis/amidation site Gly-Lys-Arg, followed by a 30-residue COOH-terminal sequence. The strong evolutionary conservation of rat and human sequences of NPY (100%) and COOH-terminal peptide (93%) suggests that both peptides have important biological functions. In the rat central nervous system, prepro-NPY mRNA (800 bases) is most abundant in the striatum and cortex and moderately abundant in the hippocampus, hypothalamus, and spinal cord. The rat adrenal, spleen, heart, and lung have significant levels of prepro-NPY mRNA. Regulation of the prepro-NPY mRNA abundance was studied in several rodent neural cell lines. PC12 rat pheochromocytoma and N18TG-2 mouse neuroblastoma cells possess low basal levels of prepro-NPY mRNA, while NG108-15 hybrid cells possess high levels. Treatment of PC12 cells with a glucocorticoid such as dexamethasone or elevation of cAMP by forskolin increased the prepro-NPY mRNA level 2-3-fold or 3-10-fold, respectively. In N18TG-2 cells dexamethasone and forskolin synergistically increased prepro-NPY mRNA 7-fold. Treatment of PC12 cells with the protein kinase C activator phorbol 12-myristate 13-acetate alone elevated prepro-NPY mRNA marginally, but the phorbol ester plus forskolin elicited 20-70-fold increases, which were further enhanced to over 200-fold by dexamethasone and the calcium ionophore A23187. These results indicate that NPY gene expression can be positively regulated by synergistic actions of glucocorticoids, cAMP elevation, and protein kinase C activation. JF - The Journal of biological chemistry AU - Higuchi, H AU - Yang, H Y AU - Sabol, S L AD - Laboratory of Biochemical Genetics, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/05/05/ PY - 1988 DA - 1988 May 05 SP - 6288 EP - 6295 VL - 263 IS - 13 SN - 0021-9258, 0021-9258 KW - Glucocorticoids KW - 0 KW - Neuropeptide Y KW - Phorbol Esters KW - Protein Precursors KW - RNA, Messenger KW - Colforsin KW - 1F7A44V6OU KW - Calcimycin KW - 37H9VM9WZL KW - Dexamethasone KW - 7S5I7G3JQL KW - preproneuropeptide Y KW - 92307-59-0 KW - Cyclic AMP KW - E0399OZS9N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Brain Chemistry KW - Dexamethasone -- pharmacology KW - Humans KW - Tissue Distribution KW - Calcimycin -- pharmacology KW - Chromatography, High Pressure Liquid KW - Rats KW - Base Sequence KW - Colforsin -- pharmacology KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Line KW - Phorbol Esters -- pharmacology KW - Cyclic AMP -- pharmacology KW - RNA, Messenger -- analysis KW - Protein Precursors -- genetics KW - Gene Expression Regulation KW - Glucocorticoids -- pharmacology KW - Neuropeptide Y -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78182293?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Rat+neuropeptide+Y+precursor+gene+expression.+mRNA+structure%2C+tissue+distribution%2C+and+regulation+by+glucocorticoids%2C+cyclic+AMP%2C+and+phorbol+ester.&rft.au=Higuchi%2C+H%3BYang%2C+H+Y%3BSabol%2C+S+L&rft.aulast=Higuchi&rft.aufirst=H&rft.date=1988-05-05&rft.volume=263&rft.issue=13&rft.spage=6288&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 - 1988-06-06 N1 - Date created - 1988-06-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Annual dose of noise absorbed by machine drivers in wine and cereal growing. AN - 78816456; 3154753 AB - We calculated the annual noise dose absorbed by machine drivers engaged in wine and cereal growing. In order to do that it has been measured the average daily noise dose in the various mechanized operations and then calculated in respect of its duration in a working year. The days spent in manual works were also taken in account. The annual dose of noise became somewhat higher than 90 dB(A) in wine growing, while in cereal growing it was a bit higher than 95 dB(A). The reliability of these data was confirmed by an epidemiological study of hearing damage. In 106 tractor-drivers, employed in farms where wine and cereal growings are done, it was found that the hearing threshold shift due to noise (average 1000-2000-4000 Hz) in relation to the years of employment, had a similar course to that forecasted by the Normative ISO-DIS 1999 in those exposed to a noise dose of 95 dB(A). JF - Giornale italiano di medicina del lavoro AU - Franzinelli, A AU - Maiorano, M AU - De Capua, B AU - Masini, M AU - Vieri, M AU - Cipolla, G AD - Servizio di Prevenzione Igiene e Sicurezza nei Luoghi di Lavoro-U.S.L. 30 Area Senese. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 131 EP - 134 VL - 10 IS - 3 SN - 0391-9889, 0391-9889 KW - Index Medicus KW - Age Factors KW - Hearing Loss, Noise-Induced -- etiology KW - Humans KW - Adult KW - Occupational Diseases -- etiology KW - Middle Aged KW - Edible Grain KW - Fruit KW - Time Factors KW - Italy KW - Agriculture KW - Noise, Occupational KW - Automobile Driving UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78816456?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Giornale+italiano+di+medicina+del+lavoro&rft.atitle=Annual+dose+of+noise+absorbed+by+machine+drivers+in+wine+and+cereal+growing.&rft.au=Franzinelli%2C+A%3BMaiorano%2C+M%3BDe+Capua%2C+B%3BMasini%2C+M%3BVieri%2C+M%3BCipolla%2C+G&rft.aulast=Franzinelli&rft.aufirst=A&rft.date=1988-05-01&rft.volume=10&rft.issue=3&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Giornale+italiano+di+medicina+del+lavoro&rft.issn=03919889&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 - Progress in understanding the relationship between the pharmacological effects of nicotine and human tobacco dependence. AN - 78470435; 3051046 AB - The present paper is intended to serve as an introduction to the series of eight papers which follow in this issue of Pharmacology Biochemistry and Behavior. A brief historical review of research that is at the root of much recent progress is provided in the present paper. In addition, we provide some data which illustrates the scope of tobacco-related research, world wide, in an effort to provide a perspective as to the vast amount of research activity that is currently in progress. Seven of the papers which follow were presented at a symposium held under the auspices of the American Society for Pharmacology and Therapeutics in 1986. Taken together, these papers are intended to provide new data and to review major areas of pharmacologic research relevant to the understanding and treatment of tobacco dependence. The topics include the behavioral and physiologic mechanisms by which the effects of nicotine are mediated, metabolic aspects of nicotine kinetics, and genetic determinants of responses to nicotine. The final paper is a discussion of the implications of these recent data for the pharmacologic treatment of tobacco dependence. JF - Pharmacology, biochemistry, and behavior AU - Henningfield, J E AU - Goldberg, S R AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 217 EP - 220 VL - 30 IS - 1 SN - 0091-3057, 0091-3057 KW - Nicotine KW - 6M3C89ZY6R KW - Index Medicus KW - History of medicine KW - History, 20th Century KW - Humans KW - History, 19th Century KW - Research KW - Nicotine -- pharmacology KW - Tobacco Use Disorder -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78470435?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Progress+in+understanding+the+relationship+between+the+pharmacological+effects+of+nicotine+and+human+tobacco+dependence.&rft.au=Henningfield%2C+J+E%3BGoldberg%2C+S+R&rft.aulast=Henningfield&rft.aufirst=J&rft.date=1988-05-01&rft.volume=30&rft.issue=1&rft.spage=217&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 - 1988-10-31 N1 - Date created - 1988-10-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anatomical analysis of frontal cortex sites at which carbachol induces motor seizures in the rat. AN - 78470386; 3174734 AB - High amplitude spiking representative of seizures, accompanied by an unusual motor behavior pattern of rearing and forelimbic clonus resembling "boxing," was elicited by microinjection of the cholinergic agonist, carbachol, 4 micrograms, into the medial prefrontal cortex of the rat. A rating scale devised to score the behavior revealed a motor pattern elicited by carbachol from the medial anterior cortex which was similar to that described by Racine for electrical stimulation of the amygdala. Topographical analysis of the areas surrounding the medial anterior cortex region revealed that the motor manifestations of seizures were elicited over a wide region of the anterior cortex, with scores significantly lower at carbachol microinjection sites greater than 1 mm rostral, 2 and 3 mm caudal, and 2 mm lateral to the standard medial prefrontal cortex site. Unilateral microinjection of carbachol yielded motor seizures primarily from the contralateral forepaw, suggesting involvement of a crossed pathway. Retrograde tracing with fast blue dye, combined with immunostaining for choline acetyltransferase and NADPH-diaphorase, found that the cholinergic neurons innervating the standard microinjection site were the dorsolateral tegmental cells, as previously reported, which have been shown to also contain substance P and corticotropin releasing factor. In addition, cholinergic neurons of the nucleus basalis of Meynert region were found to innervate the standard microinjection site. These findings implicate cholinergic innervation of the rostral cortex in classical limbic seizures. JF - Pharmacology, biochemistry, and behavior AU - Stivers, J A AU - Skirboll, L R AU - Long, R AU - Crawley, J N AD - Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 129 EP - 136 VL - 30 IS - 1 SN - 0091-3057, 0091-3057 KW - Carbachol KW - 8Y164V895Y KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Motor Activity -- physiology KW - Motor Activity -- drug effects KW - Microinjections KW - Male KW - Seizures -- chemically induced KW - Carbachol -- administration & dosage KW - Seizures -- physiopathology KW - Frontal Lobe -- drug effects KW - Frontal Lobe -- physiology KW - Frontal Lobe -- anatomy & histology KW - Carbachol -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78470386?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Anatomical+analysis+of+frontal+cortex+sites+at+which+carbachol+induces+motor+seizures+in+the+rat.&rft.au=Stivers%2C+J+A%3BSkirboll%2C+L+R%3BLong%2C+R%3BCrawley%2C+J+N&rft.aulast=Stivers&rft.aufirst=J&rft.date=1988-05-01&rft.volume=30&rft.issue=1&rft.spage=129&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 - 1988-10-31 N1 - Date created - 1988-10-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Models for the analysis of radon-exposed populations. AN - 78469421; 3051700 AB - Radon-222 is a radioactive decay product of radium-226 and uranium-238, which are found throughout the crust of the earth. Studies of underground miners clearly show that exposure to radon and its decay products increases the risk of developing lung cancer. Data on standardized mortality ratios from eight cohort studies indicate that the radon-lung cancer relationship is statistically homogeneous, even though cohorts are from different types of mines and from different countries. Regression methods for cohort data based on a Poisson probability model permit a thorough consideration of risk patterns. In this report, we review these methods, wherein the disease rate in each cell of a multi-way table is modeled as a function of the cross-classifying variables. The National Academy of Sciences' Committee on the Biological Effects of Ionizing Radiation uses the Poisson regression approach to develop a model for age-specific lung cancer risk which depends on cumulative exposure, age at risk, and time since exposure. This model is reviewed and its implications discussed. The most important determinant of lung cancer is cigarette smoking. This paper discusses relative risk models for analysis of joint exposure to radon and tobacco products. The review of available studies suggests that the joint relationship of radon and smoking with lung cancer is consistent with a multiplicative model, but a submultiplicative relationship is most likely. An additive model is rejected. JF - The Yale journal of biology and medicine AU - Lubin, J H AD - Epidemiology Methods Section, National Cancer Institute, Bethesda, Maryland 20892. PY - 1988 SP - 195 EP - 214 VL - 61 IS - 3 SN - 0044-0086, 0044-0086 KW - Radon KW - Q74S4N8N1G KW - Index Medicus KW - Risk Factors KW - Humans KW - Models, Statistical KW - Follow-Up Studies KW - Dose-Response Relationship, Radiation KW - Models, Biological KW - Neoplasms, Radiation-Induced -- mortality KW - Lung Neoplasms -- mortality KW - Mining KW - Radon -- adverse effects KW - Occupational Diseases -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78469421?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Yale+journal+of+biology+and+medicine&rft.atitle=Models+for+the+analysis+of+radon-exposed+populations.&rft.au=Lubin%2C+J+H&rft.aulast=Lubin&rft.aufirst=J&rft.date=1988-05-01&rft.volume=61&rft.issue=3&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=The+Yale+journal+of+biology+and+medicine&rft.issn=00440086&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-22 N1 - Date created - 1988-11-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Ind Med. 1988;13(1):131-47 [3344752] Am J Ind Med. 1988;13(1):149-67 [3344753] Occup Health Rev. 1971;22(1):1-15 [5158833] J Occup Med. 1973 Mar;15(3):204-11 [4693163] Am J Epidemiol. 1977 Nov;106(5):418-32 [920729] Health Phys. 1978 Oct;35(4):579-80 [748269] Health Phys. 1979 Jun;36(6):699-706 [224006] Cancer. 1980 Mar 15;45(6):1273-7 [7357519] Environ Health Perspect. 1979 Oct;32:181-92 [396152] J Natl Cancer Inst. 1980 Apr;64(4):977-89 [6929006] Biometrics. 1980 Jun;36(2):299-305 [7407317] Health Phys. 1981 Mar;40(3):307-16 [7228679] J Natl Cancer Inst. 1981 Jun;66(6):1037-52 [6941039] Biometrics. 1983 Mar;39(1):173-84 [6871346] Environ Health Perspect. 1983 Apr;50:293-308 [6873020] J Natl Cancer Inst. 1983 Sep;71(3):489-99 [6577225] Scand J Work Environ Health. 1983 Aug;9(4):353-66 [6635614] Biometrics. 1983 Sep;39(3):665-74 [6652201] Z Erkr Atmungsorgane. 1983;161(3):232-9 [6322461] N Engl J Med. 1984 Jun 7;310(23):1485-94 [6325913] Scand J Work Environ Health. 1984 Feb;10(1):25-34 [6740274] J Natl Cancer Inst. 1985 Jun;74(6):1207-13 [3858594] Am J Epidemiol. 1985 Feb;121(2):309-23 [3839345] Am J Epidemiol. 1985 Jul;122(1):149-62 [4014192] Environ Health Perspect. 1985 Nov;63:195-201 [3908088] Health Phys. 1986 May;50(5):605-18 [3700112] J Natl Cancer Inst. 1986 Aug;77(2):357-62 [3461198] Int J Epidemiol. 1987 Mar;16(1):7-12 [3570624] Health Phys. 1987 Apr;52(4):417-30 [3032855] Am J Epidemiol. 1987 Nov;126(5):949-61 [3661542] J Chronic Dis. 1987;40 Suppl 2:171S-179S [3667864] J Natl Cancer Inst. 1987 Dec;79(6):1255-60 [3480377] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Screening for current drug use disorders in alcoholics: an application of receiver operating characteristic analysis. AN - 78400688; 3416730 AB - The major objectives of the present study were 2-fold: (1) to demonstrate the superiority of receiver operating characteristic (ROC) methodology in the comparison of screening tests that yield continuous values; and (2) to identify the best screening indicator of current drug use disorders in alcoholics. We evaluated the ability of the screening tests to detect drug use disorder (DUD) according to the research diagnostic criteria. Results showed that the language of addiction - drug version and the reasons for drug use (RDU) screening tests offered excellent detectability for current DUD. The accuracy of both tests was reduced as the result of broadening the clinical spectrum in the comparative group. Implications of these findings to the neglected topic of clinical and co-morbid spectrums in screening test evaluation is presented. Issues surrounding the use of psychiatric diagnoses as standards, assessment of efficacy, the role of screening in defining subthreshold disorder, and the use of biochemical screening as an adjunct to the questionnaire approach are also discussed. JF - Drug and alcohol dependence AU - Grant, B F AU - Hasin, D S AU - Harford, T C AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 113 EP - 125 VL - 21 IS - 2 SN - 0376-8716, 0376-8716 KW - Index Medicus KW - Humans KW - Adult KW - Psychometrics KW - Alcoholism -- rehabilitation KW - Mass Screening KW - ROC Curve KW - Substance-Related Disorders -- psychology KW - Alcoholism -- psychology KW - Substance-Related Disorders -- prevention & control KW - Psychological Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78400688?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Screening+for+current+drug+use+disorders+in+alcoholics%3A+an+application+of+receiver+operating+characteristic+analysis.&rft.au=Grant%2C+B+F%3BHasin%2C+D+S%3BHarford%2C+T+C&rft.aulast=Grant&rft.aufirst=B&rft.date=1988-05-01&rft.volume=21&rft.issue=2&rft.spage=113&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 - 1988-10-20 N1 - Date created - 1988-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Haloperidol and metabolite concentrations in the rat after concurrent isotretinoin administration: a preliminary report. AN - 78398038; 3166137 AB - Blood and tissue haloperidol concentrations can be altered by the concurrent administration of a number of other drugs. Here we describe effects of concurrent administration of the vitamin A metabolite, isotretinoin, on haloperidol and reduced haloperidol concentrations in the rat. Isotretinoin increased the concentrations of both haloperidol and reduced haloperidol in serum, red blood cells, and brain. However, the dose dependence and degree of the effect varied significantly across tissues. Further study is called for to elucidate the interaction of neuroleptics such as haloperidol with the vitamin A acids such as isotretinoin. JF - Pharmacology & toxicology AU - Straw, G AU - Kirch, D AU - Freed, W J AD - Neuropsychiatry Branch, National Institute of Mental Health, Saint Elizabeth's Hospital, Washington, D.C. 20032. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 326 EP - 328 VL - 62 IS - 5 SN - 0901-9928, 0901-9928 KW - Teratogens KW - 0 KW - Tretinoin KW - 5688UTC01R KW - Isotretinoin KW - EH28UP18IF KW - Haloperidol KW - J6292F8L3D KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Interactions KW - Brain -- metabolism KW - Female KW - Tretinoin -- administration & dosage KW - Haloperidol -- blood KW - Tretinoin -- toxicity KW - Haloperidol -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78398038?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Haloperidol+and+metabolite+concentrations+in+the+rat+after+concurrent+isotretinoin+administration%3A+a+preliminary+report.&rft.au=Straw%2C+G%3BKirch%2C+D%3BFreed%2C+W+J&rft.aulast=Straw&rft.aufirst=G&rft.date=1988-05-01&rft.volume=62&rft.issue=5&rft.spage=326&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 - 1988-10-06 N1 - Date created - 1988-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methyl carbamate. Species-dependent variations in metabolism and clearance in rats and mice. AN - 78382383; 2900737 AB - Studies of the chronic toxicity and carcinogenicity of methyl carbamate (MC) in F344 rats and B6C3F1 mice indicate that this compound is more toxic to rats than mice. MC was also a carcinogen for rats but not a carcinogen for mice even when administered at a higher dose. The present study of the comparative metabolism and disposition of MC in these two species was conducted to determine possible sources of these varying responses. Results of this study indicate that, although the initial distribution of MC in the two species is similar, the mouse metabolizes and clears MC much more rapidly than does the rat. In the mouse, clearance was primarily by metabolism to CO2 and elimination in exhaled air, which accounted for approximately 70% of the dose in 48 hr. On the other hand, the rat eliminated approximately 18% of the dose as CO2 in 48 hr and a similar amount in urine. The parent compound accounted for approximately 90% of the material excreted in urine of both rats and mice. Only the parent compound was detected in tissues of either species. Less than 4% of the dose was excreted in feces of either species. The lesser ability of the rat to metabolize and eliminate MC as CO2 results in bioaccumulation of this compound on repeat exposure. Therefore, bioaccumulation of MC by the rat on chronic exposure probably results in both greater total exposure and higher peak exposure of most rat tissues vs. those of mice and may thus account for the greater toxicity and possibly carcinogenicity of MC to rats. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Ioannou, Y M AU - Sanders, J M AU - Matthews, H B AD - Toxicology Research and Testing Program, National Institute of Environmental Health Sciences Research, Triangle, NC 27709. PY - 1988 SP - 435 EP - 440 VL - 16 IS - 3 SN - 0090-9556, 0090-9556 KW - Carbamates KW - 0 KW - Carbon Dioxide KW - 142M471B3J KW - methyl carbamate KW - 9WFX634X2T KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Biotransformation KW - In Vitro Techniques KW - Mice KW - Tissue Distribution KW - Carbon Dioxide -- metabolism KW - Species Specificity KW - Male KW - Carbamates -- metabolism KW - Carbamates -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78382383?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Methyl+carbamate.+Species-dependent+variations+in+metabolism+and+clearance+in+rats+and+mice.&rft.au=Ioannou%2C+Y+M%3BSanders%2C+J+M%3BMatthews%2C+H+B&rft.aulast=Ioannou&rft.aufirst=Y&rft.date=1988-05-01&rft.volume=16&rft.issue=3&rft.spage=435&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 - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolism of 1-chloro-2-methylpropene. Evidence for reactive chloroaldehyde intermediates. AN - 78381226; 2900739 AB - Recent metabolism and disposition studies of 1-chloro-2-methylpropene (dimethylvinyl chloride) revealed cysteine and N-acetylcysteine conjugates of 3-chloro-2-methylpropenoic acid as the major metabolites. In the present studies we have investigated various steps in the metabolic pathway to determine which step was responsible for the observed trans (E)-stereochemistry of these metabolites. In vitro incubation studies of dimethylvinyl chloride with rat liver microsomes indicated cytochrome P-450-catalyzed aliphatic hydroxylation to be only stereoselective. Both (E)- and (Z)-3-chloro-2-methylpropenols formed in an identical ratio of 2:1 in incubations with microsomes from untreated male and female rats and phenobarbital-treated male rats. No alcohol formation was observed in incubations using microsomes from beta-naphthoflavone-treated male rats. Investigation of the subsequent conjugation reactions of sulfur nucleophiles with haloenoic carbonyl compounds showed that both (E)- and (Z)-3-chloro-2-methylpropenals reacted rapidly with N-acetylcysteine, the E-adduct being the sole product in either case. In contrast, the Michael reaction of the corresponding acids with N-acetylcysteine was very sluggish. Also, whereas the E-acid yielded exclusively the corresponding E-adduct, the Z-isomer afforded both Z- and E-conjugates in the ratio of 3:4. Glutathione S-transferases had poor activity towards conjugation of glutathione with these acids. Formation of only an E-glutathione conjugate could be observed from either the E- or Z-acid in these enzymatic reactions. Direct Michael reaction of glutathione with (E)-3-bromo-2-methylpropenoic acid, used in chemical synthesis of the conjugates, yielded both the E- and Z-adducts in the ratio of 95:5.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Drug metabolism and disposition: the biological fate of chemicals AU - Srinivas, P AU - Burka, L T AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1988 SP - 449 EP - 454 VL - 16 IS - 3 SN - 0090-9556, 0090-9556 KW - Carcinogens KW - 0 KW - Vinyl Compounds KW - 1-chloro-2-methylpropene KW - 513-37-1 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Glutathione KW - GAN16C9B8O KW - Vinyl Chloride KW - WD06X94M2D KW - Index Medicus KW - Rats KW - Mass Spectrometry KW - Animals KW - Chromatography, Gas KW - Glutathione -- metabolism KW - In Vitro Techniques KW - Glutathione Transferase -- metabolism KW - Spectrophotometry, Ultraviolet KW - Male KW - Chromatography, High Pressure Liquid KW - Magnetic Resonance Spectroscopy KW - Carcinogens -- metabolism KW - Microsomes, Liver -- metabolism KW - Vinyl Compounds -- metabolism KW - Vinyl Chloride -- metabolism KW - Vinyl Chloride -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78381226?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+1-chloro-2-methylpropene.+Evidence+for+reactive+chloroaldehyde+intermediates.&rft.au=Srinivas%2C+P%3BBurka%2C+L+T&rft.aulast=Srinivas&rft.aufirst=P&rft.date=1988-05-01&rft.volume=16&rft.issue=3&rft.spage=449&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 - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetic procedures for the estimation of organ clearances for the formation of short-lived metabolites. Acetaminophen-induced glutathione depletion in hamster liver. AN - 78375136; 2900728 AB - Several approaches have been developed to estimate in vivo the intrinsic clearances of enzymes that catalyze the formation of chemically reactive metabolites that do not escape the organs in which they are formed. Two basic models are considered. Model 1 is a general model in which the chemically reactive metabolite is inactivated by a combination of a pseudo-first order reaction, such as a reaction with large pools of protein, and a second order reaction with a depletable endogenous substance, such as glutathione or an enzyme. Model 2 is a special case, in which at low doses of the parent compound the reactive metabolite preferentially reacts with a depletable endogenous substance, such as glutathione. In developing both models we have assumed that the rate of formation of reactive metabolite follows first order kinetics and that the concentration of reactive metabolite in liver reaches a steady state almost instantaneously. In developing Model 2 we also have assumed that the depletion of hepatic reduced glutathione is due solely to the formation of glutathione conjugates. The uses of the approaches based on Model 2 were illustrated by studying the effects of a marginally toxic dose of acetaminophen on the depletion and subsequent repletion of hepatic glutathione in hamsters. From the calculated rate of synthesis of glutathione in liver, the fraction of the dose of acetaminophen converted to the glutathione conjugate in liver, and the clearance for the formation of glutathione conjugate in vivo was estimated and was found to be similar to that obtained with hepatic 9,000 g supernatant preparations. Other uses of the models are described. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Chen, R AU - Gillette, J R AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. PY - 1988 SP - 373 EP - 385 VL - 16 IS - 3 SN - 0090-9556, 0090-9556 KW - Acetaminophen KW - 362O9ITL9D KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Aspartate Aminotransferases -- blood KW - Animals KW - Mesocricetus KW - Models, Biological KW - Male KW - Chromatography, High Pressure Liquid KW - Cricetinae KW - Acetaminophen -- pharmacokinetics KW - Liver -- drug effects KW - Glutathione -- metabolism KW - Liver -- metabolism KW - Acetaminophen -- toxicity KW - Acetaminophen -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78375136?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pharmacokinetic+procedures+for+the+estimation+of+organ+clearances+for+the+formation+of+short-lived+metabolites.+Acetaminophen-induced+glutathione+depletion+in+hamster+liver.&rft.au=Chen%2C+R%3BGillette%2C+J+R&rft.aulast=Chen&rft.aufirst=R&rft.date=1988-05-01&rft.volume=16&rft.issue=3&rft.spage=373&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 - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Absolute and relative configuration of erythroskyrin. AN - 78367076; 3404152 AB - We have reisolated erythroskyrin from Penicillium islandicum and have determined the relative stereochemistry of the compound through extensive 1H- and 13C-nmr studies. The absolute stereochemistry was determined by nmr studies of the O-methylmandelate esters. JF - Journal of natural products AU - Beutler, J A AU - Hilton, B D AU - Clark, P AU - Tempesta, M S AU - Corley, D G AD - Program Resources, Inc., National Cancer Institute-Frederick Cancer Research Facility, Maryland. PY - 1988 SP - 562 EP - 566 VL - 51 IS - 3 SN - 0163-3864, 0163-3864 KW - Mycotoxins KW - 0 KW - Polyenes KW - erythroskyrine KW - 4987-27-3 KW - Index Medicus KW - Stereoisomerism KW - Chemistry KW - Esterification KW - Chemical Phenomena KW - Penicillium -- analysis KW - Circular Dichroism KW - Polyenes -- isolation & purification KW - Magnetic Resonance Spectroscopy KW - Mycotoxins -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78367076?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Absolute+and+relative+configuration+of+erythroskyrin.&rft.au=Beutler%2C+J+A%3BHilton%2C+B+D%3BClark%2C+P%3BTempesta%2C+M+S%3BCorley%2C+D+G&rft.aulast=Beutler&rft.aufirst=J&rft.date=1988-05-01&rft.volume=51&rft.issue=3&rft.spage=562&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 - 1988-09-13 N1 - Date created - 1988-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Time-dose response of human tumors and normal tissues during and after fractionated radiation treatment. A new model. AN - 78361673; 3406453 AB - This paper presents the background and some results of initial applications of a new model of time-dose response of tumors as well as fast-renewing normal tissues, to fractionated radiation therapy. Both the linear-quadratic and the single-hit/single-target, single-hit/multi-target model may be used for the single-dose survival of both the viable stem cells and the clonogenic tumor cells. Normal tissue tolerance is expressed as a minimum acceptable level of normal tissue functionality, due to insufficient production of replacement cells, which in turn is caused by radiation-induced depletion of the viable stem cell population. A logistic function describes the homeostatically controlled inter-fraction and post-treatment normal tissue stem cell repopulation. The onset of stem cell repopulation may be delayed, and the doubling rate of clonogenic tumor cells may increase, upon the onset of treatment. Criteria for the selection of acceptable parameter values for normal tissue as well as tumors are described. An interactive Fortran 77 program has been developed to assist in the search for acceptable parameter values, the simulation of the time-dose response of normal tissues and tumors to conventional clinical fractionation schemes and the exploration of alternative schedules, including hyperfractionation. Some provisional results are presented. JF - Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology AU - van de Geijn, J AD - Radiation Oncology Branch, NCI, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 57 EP - 78 VL - 12 IS - 1 SN - 0167-8140, 0167-8140 KW - Index Medicus KW - Radiotherapy Dosage KW - Neoplastic Stem Cells -- pathology KW - Humans KW - Dose-Response Relationship, Radiation KW - Cell Survival -- radiation effects KW - Cell Cycle -- radiation effects KW - Time Factors KW - Radiation, Ionizing KW - Neoplastic Stem Cells -- radiation effects KW - Neoplasms -- pathology KW - Computer Simulation KW - Neoplasms -- radiotherapy KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78361673?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiotherapy+and+oncology+%3A+journal+of+the+European+Society+for+Therapeutic+Radiology+and+Oncology&rft.atitle=Time-dose+response+of+human+tumors+and+normal+tissues+during+and+after+fractionated+radiation+treatment.+A+new+model.&rft.au=van+de+Geijn%2C+J&rft.aulast=van+de+Geijn&rft.aufirst=J&rft.date=1988-05-01&rft.volume=12&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Radiotherapy+and+oncology+%3A+journal+of+the+European+Society+for+Therapeutic+Radiology+and+Oncology&rft.issn=01678140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-15 N1 - Date created - 1988-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acute ethanol poisoning and the ethanol withdrawal syndrome. AN - 78357445; 3041244 AB - Ethanol, a highly lipid-soluble compound, appears to exert its effects through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the gamma-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolised at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Medical toxicology and adverse drug experience AU - Adinoff, B AU - Bone, G H AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda. PY - 1988 SP - 172 EP - 196 VL - 3 IS - 3 SN - 0113-5244, 0113-5244 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Humans KW - Alcohol Withdrawal Delirium KW - Ethanol -- blood KW - Ethanol -- adverse effects KW - Substance Withdrawal Syndrome -- complications KW - Substance Withdrawal Syndrome -- physiopathology KW - Alcoholic Intoxication -- physiopathology KW - Alcoholic Intoxication -- therapy KW - Substance Withdrawal Syndrome -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78357445?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicology+and+adverse+drug+experience&rft.atitle=Acute+ethanol+poisoning+and+the+ethanol+withdrawal+syndrome.&rft.au=Adinoff%2C+B%3BBone%2C+G+H%3BLinnoila%2C+M&rft.aulast=Adinoff&rft.aufirst=B&rft.date=1988-05-01&rft.volume=3&rft.issue=3&rft.spage=172&rft.isbn=&rft.btitle=&rft.title=Medical+toxicology+and+adverse+drug+experience&rft.issn=01135244&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-29 N1 - Date created - 1988-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of allyl isovalerate on the hematopoietic and immunologic systems in rodents. AN - 78340590; 3135219 AB - Female B6C3F1 mice plus male and female Fischer 344/N rats were gavaged with allyl isovalerate (AIV) in corn oil at 0, 31, 62, or 125 (mice) and 0, 31, 62, 125, or 250 (rats) mg/kg body weight for five daily exposures per week for a 2-week period. Hematologic, immunologic, and histopathologic studies were performed 48 to 72 hr following the final treatment. AIV exposure had no effect on hematology or bone marrow cellularity in mice or rats. AIV exposure at 250 mg/kg was toxic to rats causing reduced weight gain and hepatotoxicity. In vivo and in vitro studies revealed that pluripotent hematopoietic stem cells (CFU-S) and granulocyte-macrophage progenitors (CFU-GM) in the bone marrow were decreased in the treated mice. Hematopoietic suppression was correlated with the reduction in the hexose monophosphate shunt metabolism of bone marrow cells but the Embden-Meyerhof pathway and tricarboxylic acid pathway enzymes did not appear to be affected. Examination of host resistance following Plasmodium and Listeria challenge did not demonstrate significant differences between treated and control mice, nor were there other effects on the immune system. This suggests that the myelotoxic effects were minimal and of a degree that would not alter host resistance. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Hong, H L AU - Huff, J E AU - Luster, M I AU - Maronpot, R R AU - Dieter, M P AU - Hayes, H T AU - Boorman, G A AD - Chemical Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 655 EP - 663 VL - 10 IS - 4 SN - 0272-0590, 0272-0590 KW - Flavoring Agents KW - 0 KW - Perfume KW - Valerates KW - allyl isovalerate KW - 3551Z86V7T KW - Index Medicus KW - Animals KW - Body Weight -- drug effects KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Granulocytes -- drug effects KW - Mice KW - Macrophages -- drug effects KW - Lymphocytes -- drug effects KW - Female KW - Organ Size -- drug effects KW - Listeria monocytogenes -- immunology KW - Valerates -- toxicity KW - Flavoring Agents -- toxicity KW - Hematopoiesis -- drug effects KW - Perfume -- toxicity KW - Immunity -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78340590?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+allyl+isovalerate+on+the+hematopoietic+and+immunologic+systems+in+rodents.&rft.au=Hong%2C+H+L%3BHuff%2C+J+E%3BLuster%2C+M+I%3BMaronpot%2C+R+R%3BDieter%2C+M+P%3BHayes%2C+H+T%3BBoorman%2C+G+A&rft.aulast=Hong&rft.aufirst=H&rft.date=1988-05-01&rft.volume=10&rft.issue=4&rft.spage=655&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 - 1988-09-08 N1 - Date created - 1988-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cadmium-induced ovarian toxicity in hamsters, mice, and rats. AN - 78340525; 3396791 AB - The effects of cadmium on the female genital tract of Syrian hamsters (Cr:RGH), of four mouse strains (BALB/cAnNCr, DBA/2NCr, C57BL/6NCr, NFS/NCr), and two rat strains (F344/NCr and WF/NCr) were studied by light microscopy after a single sc injection of cadmium chloride (CdCl2). Experiments involved animals prior to and after sexual maturity, and employed CdCl2 doses ranging from 20 to 47.5 mumol/kg. Animals were examined at intervals from 24 hr to 8 weeks following treatment. Syrian hamsters were most susceptible to CdCl2-induced ovarian hemorrhagic necrosis at all ages tested. Most severe ovarian lesions occurred in immature hamsters, in mature hamsters at high doses, and shortly before ovulation at all doses. The small arteries of the developing follicles and interstitial stroma seemed selectively susceptible to CdCl2 toxicity while the corpora lutea, mesothelium, primordial oocytes, and the rete ovarii appeared resistant. Pretreatment with zinc acetate markedly reduced the extent of ovarian lesions in hamsters. Although reduced in weight by 45%, the hamster ovaries recovered morphologically within 2 months after severe acute hemorrhagic necrosis. Uterine and cervical stromal hemorrhages were seen only in immature hamsters at doses of greater than or equal to 30 mumol CdCl2/kg. Of the mice, only the DBA/2NCr strain showed significant CdCl2-induced ovarian hemorrhages, and these hemorrhages occurred at doses also producing lethal liver toxicity. Lesions of the uterus were rare. Rats showed dose- and age-dependent toxicity in the ovaries, uterus, cervix, and liver. CdCl2 exposure in mature rats induced uterine lesions only in F344 rats, while acute ovarian and hepatic toxicity was less severe in mature animals of both strains. No lesions were noted after 7 days in mature WF rats. In both rats and mice, no cycle dependency of the ovarian lesions was evident. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Rehm, S AU - Waalkes, M P AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick Cancer Research Facility, Maryland 21701-1013. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 635 EP - 647 VL - 10 IS - 4 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Mice, Inbred C57BL KW - Mesocricetus KW - Mice KW - Mice, Inbred BALB C KW - Species Specificity KW - Female KW - Mice, Inbred DBA KW - Cricetinae KW - Ovarian Diseases -- pathology KW - Ovarian Diseases -- chemically induced KW - Cadmium Poisoning -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78340525?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cadmium-induced+ovarian+toxicity+in+hamsters%2C+mice%2C+and+rats.&rft.au=Rehm%2C+S%3BWaalkes%2C+M+P&rft.aulast=Rehm&rft.aufirst=S&rft.date=1988-05-01&rft.volume=10&rft.issue=4&rft.spage=635&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 - 1988-09-08 N1 - Date created - 1988-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Post-translational alterations of the tyrosine kinase p56lck in response to activators of protein kinase C. AN - 78334953; 3041347 AB - We have found in different human cells of lymphoid and non-lymphoid origin that the 56 kilodalton (kDa) lck protein is rapidly converted to a product migrating at approximately 60 kDa (designated p60lck) in response to the phorbol ester 4 alpha-phorbol 12 beta-myristate (PMA) as well as the diacylglycerol analogue 1,2-dioctanoyl-sn-glycerol (diC8). This conversion is associated with an increase in serine phosphorylation within the amino-terminal 18 kDa portion of the lck protein. The serine phosphorylation modification and diminished electrophoretic mobility of the lck protein appear to be completely reversible within 60 min following treatment with diC8. The changes in p56lck phosphorylation and gel mobility in response to activators of protein kinase C are also associated with a small but reproducible decrease in the ability of the lck protein to be phosphorylated in immune complex kinase assays. While these alterations of the lck gene product may play an important role in antigen-mediated activation of T-lymphocytes, we demonstrated that they can also be induced independently of T-cell activation suggesting that they are not necessarily implicative of this process. JF - Oncogene research AU - Veillette, A AU - Horak, I D AU - Bolen, J B AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 385 EP - 401 VL - 2 IS - 4 SN - 0890-6467, 0890-6467 KW - Diglycerides KW - 0 KW - Membrane Proteins KW - Phorbol Esters KW - Phosphoproteins KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Lymphocyte Activation KW - Phorbol Esters -- pharmacology KW - Diglycerides -- pharmacology KW - Peptide Mapping KW - Enzyme Activation KW - Humans KW - Protein Processing, Post-Translational KW - Immunosorbent Techniques KW - Molecular Weight KW - Phosphoproteins -- physiology KW - Protein Kinase C -- physiology KW - Lymphocytes -- physiology KW - Protein-Tyrosine Kinases -- physiology KW - Membrane Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78334953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+research&rft.atitle=Post-translational+alterations+of+the+tyrosine+kinase+p56lck+in+response+to+activators+of+protein+kinase+C.&rft.au=Veillette%2C+A%3BHorak%2C+I+D%3BBolen%2C+J+B&rft.aulast=Veillette&rft.aufirst=A&rft.date=1988-05-01&rft.volume=2&rft.issue=4&rft.spage=385&rft.isbn=&rft.btitle=&rft.title=Oncogene+research&rft.issn=08906467&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-09-07 N1 - Date created - 1988-09-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dealing with spills of hazardous chemicals: some nitrosamides. AN - 78305801; 3391473 AB - Spills of N-methyl-N-nitrosourea, N-ethyl-N-nitrosourea, N-methyl-N-nitrosourethane and N-ethyl-N-nitrosourethane can be decontaminated using a mixture of ethanol and saturated aqueous sodium bicarbonate solution. Spills of N-methyl-N-nitroso-p-toluenesulphonamide, N-methyl-N'-nitro-N-nitrosoguanidine and N-ethyl-N'-nitro-N-nitrosoguanidine can be decontaminated with a solution of sulphamic acid in 2 M-hydrochloric acid. In all cases the nitrosamides are completely destroyed and only non-mutagenic reaction mixtures are produced. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Lunn, G AU - Sansone, E B AD - Environmental Control and Research Program, National Cancer Institute-Frederick Cancer Research Facility, MD 21701-1013. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 481 EP - 484 VL - 26 IS - 5 SN - 0278-6915, 0278-6915 KW - Hazardous Waste KW - 0 KW - Nitroso Compounds KW - Sewage KW - nitrosamides KW - N-ethyl-N-nitrosourethane KW - 0ROQ23IJ4F KW - Nitrosomethylurethane KW - 615-53-2 KW - Methylnitrosourea KW - 684-93-5 KW - Ethylnitrosourea KW - P8M1T4190R KW - Index Medicus KW - Nitrosomethylurethane -- analogs & derivatives KW - Decontamination KW - Chromatography, High Pressure Liquid KW - Waste Disposal, Fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78305801?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dealing+with+spills+of+hazardous+chemicals%3A+some+nitrosamides.&rft.au=Lunn%2C+G%3BSansone%2C+E+B&rft.aulast=Lunn&rft.aufirst=G&rft.date=1988-05-01&rft.volume=26&rft.issue=5&rft.spage=481&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 - 1988-08-18 N1 - Date created - 1988-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Photodynamic therapy of cancer. AN - 78300243; 2968898 AB - PDT represents another modality for the treatment of human malignancy. Photoactivated hematoporphyrins have definite antitumor activity in both in vitro and in vivo experimental systems. Much of the early clinical work involved treatment of patients with advanced, recurrent disease who had not responded to conventional therapy. Because good responses with acceptable toxicity have been obtained in these patients, active investigation continued and is aimed at defining the most appropriate sites and applications for the technique. Because of the limited depth of light penetration in tissue, the most promising sites may be those where there is limited thickness of tumor, such as in superficial skin lesions or carcinomas in situ involving the aerodigestive tract, bronchial tree, or genitourinary tract. Other potential uses include those where PDT could be combined with surgical or chemotherapeutic debulking, such as pleural mesothelioma or advanced stage ovarian cancer. Whether PDT can be of benefit in surgical cases where the margins of resection are close is an interesting but speculative notion at the present time. Clinical trials with hematoporphyrin derivative PDT in the sites mentioned are in progress. Laboratory work to better understand HpD also continues, as well as investigations into alternative photosensitizers with improved tumor localization, less cutaneous photosensitivity, and absorption peaks at deeper penetrating wavelengths of light. Attempts at measuring singlet oxygen, if successful, will permit the development of more meaningful dosimetry in order to correlate response with actual tissue levels of the purported cytotoxic agent. Hopefully, these and other developments in the field of PDT will improve the treatment for patients with cancer. JF - Comprehensive therapy AU - Delaney, T F AU - Glatstein, E AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 43 EP - 55 VL - 14 IS - 5 SN - 0098-8243, 0098-8243 KW - Antineoplastic Agents KW - 0 KW - Hematoporphyrins KW - Hematoporphyrin Derivative KW - 68335-15-9 KW - Index Medicus KW - Photochemistry KW - Animals KW - Humans KW - Hematoporphyrins -- therapeutic use KW - Mice KW - Tissue Distribution KW - Neoplasms, Experimental -- drug therapy KW - Phototherapy KW - Antineoplastic Agents -- therapeutic use KW - Male KW - Female KW - Neoplasms -- drug therapy KW - Photochemotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78300243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Comprehensive+therapy&rft.atitle=Photodynamic+therapy+of+cancer.&rft.au=Delaney%2C+T+F%3BGlatstein%2C+E&rft.aulast=Delaney&rft.aufirst=T&rft.date=1988-05-01&rft.volume=14&rft.issue=5&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Comprehensive+therapy&rft.issn=00988243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-19 N1 - Date created - 1988-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Constitutive expression of c-fos antisense RNA blocks c-fos gene induction by interferon and by phorbol ester and reduces c-myc expression in F9 embryonal carcinoma cells. AN - 78272428; 2454869 AB - To address the role of c-fos proto-oncogene we constructed a plasmid that allows constitutive expression of RNA complementary to c-fos mRNA, and stably introduced this plasmid into F9 embryonal carcinoma cells. Some F9 clones expressing c-fos antisense RNA had a reduced basal level of c-fos mRNA, and were unable to induce a c-fos mRNA as well as its protein when stimulated with phorbol ester or with interferon (IFN). Nevertheless, the ability to induce major histocompatibility class I genes following IFN treatment was not impaired in these clones. Clones expressing c-fos antisense RNA grew as rapidly as control F9 cells, and underwent differentiation after retinoic acid treatment. Unexpectedly, constitutive expression of c-myc mRNA was reduced on average by 10-fold in clones expressing c-fos antisense RNA. However, expression of the p53 gene and heat shock gene hsp 70 was not affected in these clones, indicating the existence of a specific regulatory linkage between c-fos and c-myc genes. Cycloheximide treatment led to induction of a large amount of c-fos mRNA in clones expressing c-fos antisense RNA as well as in control F9 clones. The amount of c-fos antisense RNA was also increased by cycloheximide treatment. We postulate that c-fos antisense RNA blocks expression of the endogenous c-fos gene by accelerating the degradation of c-fos mRNA and that cycloheximide treatment interferes with this degradation. JF - Genes & development AU - Levi, B Z AU - Ozato, K AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 554 EP - 566 VL - 2 IS - 5 SN - 0890-9369, 0890-9369 KW - Fluoresceins KW - 0 KW - Phorbol Esters KW - RNA, Messenger KW - Tretinoin KW - 5688UTC01R KW - Interferons KW - 9008-11-1 KW - Cycloheximide KW - 98600C0908 KW - Index Medicus KW - Clone Cells KW - Tretinoin -- pharmacology KW - Humans KW - Cycloheximide -- pharmacology KW - Cell Differentiation KW - Gene Expression Regulation KW - Nucleic Acid Hybridization KW - Cell Line, Transformed KW - Plasmids KW - Fluorescent Antibody Technique KW - Transcriptional Activation KW - Phorbol Esters -- pharmacology KW - Interferons -- pharmacology KW - RNA, Messenger -- genetics KW - Proto-Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78272428?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Constitutive+expression+of+c-fos+antisense+RNA+blocks+c-fos+gene+induction+by+interferon+and+by+phorbol+ester+and+reduces+c-myc+expression+in+F9+embryonal+carcinoma+cells.&rft.au=Levi%2C+B+Z%3BOzato%2C+K&rft.aulast=Levi&rft.aufirst=B&rft.date=1988-05-01&rft.volume=2&rft.issue=5&rft.spage=554&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 - 1988-08-01 N1 - Date created - 1988-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intravenous drug use and AIDS prevention. AN - 78247884; 3131815 AB - Research programs of the National Institute on Drug Abuse take a broad approach to investigating the problems of intervention in intravenous drug use and its relation to the AIDS epidemic. Current prevention strategies are directed to reducing the rates of infection and the progression among the infected to clinical symptoms. Programs test alternative prevention models and focus on the epidemiology of the problem and on basic studies of specific high-risk behaviors. Ultimately, the problem requires community involvement to encourage behaviors which will reduce exposure on the part of drug users, their sexual partners, and their children. JF - Public health reports (Washington, D.C. : 1974) AU - Schuster, C R AD - National Institute on Drug Abuse, Rockville, MD 20857. PY - 1988 SP - 261 EP - 266 VL - 103 IS - 3 SN - 0033-3549, 0033-3549 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - United States KW - Sexual Behavior KW - United States Public Health Service KW - Injections, Intravenous KW - Risk Factors KW - Humans KW - Research KW - Health Promotion KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - Substance-Related Disorders -- therapy KW - Acquired Immunodeficiency Syndrome -- transmission KW - Substance-Related Disorders -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78247884?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intravenous+drug+use+and+AIDS+prevention.&rft.au=Schuster%2C+C+R&rft.aulast=Schuster&rft.aufirst=C&rft.date=1988-05-01&rft.volume=103&rft.issue=3&rft.spage=261&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 - 1988-06-30 N1 - Date created - 1988-06-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Public Health. 1984 Jul;74(7):660-6 [6611092] Health Educ Q. 1986 Winter;13(4):373-82 [3781861] Health Educ Q. 1986 Winter;13(4):383-93 [3781862] Rev Infect Dis. 1988 Jan-Feb;10(1):151-8 [3281219] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stability of alcohol consumption among youth: a National Longitudinal Survey. AN - 78236273; 3374139 AB - The present study draws upon the National Longitudinal Survey (NLS) of Labor Market Experience in Youth (ages 17-24) to describe alcohol use patterns over a 2-year period during the transition years between adolescence and young adulthood. Specifically, turnover in current (using any amount of alcohol in any frequency during the past month) and heavier (drinking six or more drinks on at least 2-3 occasions during the past month) drinking levels among panel members was examined by charting incidence, remission, chronicity, and abstinence between 1982 and 1983. The prevalence of each consumption level increased between the ages of 17 and 22 but declined thereafter for each sex until the age of 24. Changes in prevalence from 1982 to 1983 were shown to be a function of changes in drinking level status. The analysis of turnover in current and heavier drinking levels indicated that there was continuity in drinking behavior over time. Sex differences observed in these trends were examined and their implications to internal and external age- and sex-appropriate constraints and paradigmatic development were explicated. JF - Journal of studies on alcohol AU - Grant, B F AU - Harford, T C AU - Grigson, M B AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 253 EP - 260 VL - 49 IS - 3 SN - 0096-882X, 0096-882X KW - Index Medicus KW - United States KW - Age Factors KW - Sex Factors KW - Humans KW - Adult KW - Temperance KW - Longitudinal Studies KW - Adolescent KW - Male KW - Female KW - Alcoholism -- epidemiology KW - Alcohol Drinking -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78236273?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Stability+of+alcohol+consumption+among+youth%3A+a+National+Longitudinal+Survey.&rft.au=Grant%2C+B+F%3BHarford%2C+T+C%3BGrigson%2C+M+B&rft.aulast=Grant&rft.aufirst=B&rft.date=1988-05-01&rft.volume=49&rft.issue=3&rft.spage=253&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 - 1988-07-14 N1 - Date created - 1988-07-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A national comparison of public- and private-sector alcoholism treatment delivery system characteristics. AN - 78235691; 3374137 AB - The primary purpose of this study was to investigate the question of the existence, nationally, of separate public- and private-sector alcoholism treatment delivery systems in regard to the economic status of clients served, types of care provided and treatment setting. The analysis was based on data from the 1982 National Federal Census Survey of Treatment units. Public- and private-sector profiles based on the aforementioned delivery system characteristics were constructed and compared. Each of the profiles was also compared to a hypothesized profile, based on perceptions drawn from the literature, of the characteristics of treatment delivery in the private sector, generally, or the private-for-profit sector, specifically. The results of the analysis support the conclusion that two separate systems of treatment delivery existed, nationally, during the study period. The distribution of the nation's alcoholism treatment units among the public and private ownership sectors and ownership trends were also investigated using data from national federal census surveys conducted in 1979, 1980, 1982 and 1984. The implications of the study findings for the future are discussed. JF - Journal of studies on alcohol AU - Yahr, H T AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 233 EP - 239 VL - 49 IS - 3 SN - 0096-882X, 0096-882X KW - Index Medicus KW - United States KW - Socioeconomic Factors KW - Humans KW - Health Surveys KW - Hospitals, Special -- supply & distribution KW - Health Facilities -- supply & distribution KW - Alcoholism -- therapy KW - Delivery of Health Care KW - Alcoholism -- economics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78235691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+national+comparison+of+public-+and+private-sector+alcoholism+treatment+delivery+system+characteristics.&rft.au=Yahr%2C+H+T&rft.aulast=Yahr&rft.aufirst=H&rft.date=1988-05-01&rft.volume=49&rft.issue=3&rft.spage=233&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 - 1988-07-14 N1 - Date created - 1988-07-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - De novo deposition of laminin-positive basement membrane in vitro by normal hepatocytes and during hepatocarcinogenesis. AN - 78229119; 2453431 AB - De novo formation of laminin-positive basement membranes was found to be a distinct morphologic feature of diethylnitrosamine/phenobarbital-induced hepatocellular carcinomas of the rat. The first appearance of extracellularly located laminin occurred in the preneoplastic liver lesions (corresponding to neoplastic nodules), and this feature became successively more prominent during the course of hepatocellular carcinoma development. Most groups of tumor cells were surrounded by laminin-positive basement membrane material. The laminin-positive material was also deposited along the sinusoids, a location where no laminin was seen in normal rat liver. The amount of extractable laminin from hepatocellular carcinomas was significantly higher (approximately 100 ng per mg tissue) than that of normal liver tissue (less than 20 ng per mg). In vitro experiments demonstrated that normal and preneoplastic rat hepatocytes had the capacity to lay down basement membrane-like material. This occurred, however, only when the hepatocytes were cocultured with certain feeder cells or when grown in the presence of their conditioned media. These results indicate that during experimental hepatocarcinogenesis in the rat some as yet undefined humoral factor(s) might influence the hepatocytes to turn on genes encoding the basement membrane components and further stimulate the assembly and deposition of basement membranes. JF - Hepatology (Baltimore, Md.) AU - Albrechtsen, R AU - Wewer, U M AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. PY - 1988 SP - 538 EP - 546 VL - 8 IS - 3 SN - 0270-9139, 0270-9139 KW - Laminin KW - 0 KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - RNA KW - 63231-63-0 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Extracellular Matrix -- metabolism KW - Tumor Cells, Cultured KW - Basement Membrane -- metabolism KW - Nucleic Acid Hybridization KW - Immunohistochemistry KW - Male KW - Extracellular Matrix -- analysis KW - RNA -- genetics KW - Liver Neoplasms, Experimental -- analysis KW - Liver Neoplasms, Experimental -- metabolism KW - Precancerous Conditions -- chemically induced KW - Laminin -- biosynthesis KW - Laminin -- analysis KW - Precancerous Conditions -- analysis KW - Liver Neoplasms, Experimental -- chemically induced KW - Liver -- metabolism KW - Precancerous Conditions -- metabolism KW - Liver -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78229119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=De+novo+deposition+of+laminin-positive+basement+membrane+in+vitro+by+normal+hepatocytes+and+during+hepatocarcinogenesis.&rft.au=Albrechtsen%2C+R%3BWewer%2C+U+M%3BThorgeirsson%2C+S+S&rft.aulast=Albrechtsen&rft.aufirst=R&rft.date=1988-05-01&rft.volume=8&rft.issue=3&rft.spage=538&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=02709139&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-06-30 N1 - Date created - 1988-06-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fecapentaenes and their precursors throughout the bowel--results of an autopsy study. AN - 78218169; 3367931 AB - The fecapentaenes are potent mutagens found in the stool of some humans and pigs. These compounds are produced by Bacteroides species in the gut from an uncharacterized family of precursor compounds, and have been postulated to pose a risk of human colorectal cancer. To better understand fecapentaene production in vivo, and to determine if excreted levels measured in epidemiologic studies are representative of the entire colon, fecapentaenes were assayed from multiple sites in the bowel in an autopsy study of 16 humans and 2 pigs. An indirect measurement of fecapentaene precursors was also made. Colonic concentrations of fecapentaenes and precursors varied widely between individuals, but were consistent for each individual throughout the colon. In addition, the measurements of rectal contents, assumed to approximate values in excreted stool, were equivalent to measurements from the colon. JF - Mutation research AU - Schiffman, M H AU - Bitterman, P AU - Viciana, A L AU - Schairer, C AU - Russell, L AU - Van Tassell, R L AU - Wilkins, T D AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 9 EP - 15 VL - 208 IS - 1 SN - 0027-5107, 0027-5107 KW - Mutagens KW - 0 KW - Polyenes KW - Index Medicus KW - Swine KW - Animals KW - Autopsy KW - Colon -- pathology KW - Duodenum -- analysis KW - Humans KW - Rectum -- analysis KW - Aged KW - Swine, Miniature KW - Rectum -- pathology KW - Cecum -- pathology KW - Ileum -- analysis KW - Adult KW - Middle Aged KW - Cecum -- analysis KW - Female KW - Male KW - Feces -- analysis KW - Mutagens -- analysis KW - Polyenes -- analysis KW - Gastrointestinal Contents -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78218169?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fecapentaenes+and+their+precursors+throughout+the+bowel--results+of+an+autopsy+study.&rft.au=Schiffman%2C+M+H%3BBitterman%2C+P%3BViciana%2C+A+L%3BSchairer%2C+C%3BRussell%2C+L%3BVan+Tassell%2C+R+L%3BWilkins%2C+T+D&rft.aulast=Schiffman&rft.aufirst=M&rft.date=1988-05-01&rft.volume=208&rft.issue=1&rft.spage=9&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 - 1988-06-14 N1 - Date created - 1988-06-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Further properties of random walks on diagrams (graphs) with and without cycles. AN - 78217798; 3368439 AB - Three problems are considered. The first is the relation between ensemble-averaged state probabilities in a random walk with absorption and time-averaged state probabilities in the corresponding closed diagram. The second problem is concerned with random walks on diagrams with cycles in which the cycle completion rates and probabilities may depend on the "remainder" after the previously completed cycle. The final topic is a study of cycle completions prior to absorption for diagrams that involve both cycles and absorption (e.g., a cycling enzyme that binds a dead-end inhibitor or poison in one of its states). JF - Proceedings of the National Academy of Sciences of the United States of America AU - Hill, T L AD - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 3271 EP - 3275 VL - 85 IS - 10 SN - 0027-8424, 0027-8424 KW - Index Medicus KW - Probability KW - Biometry KW - Models, Theoretical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78217798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Further+properties+of+random+walks+on+diagrams+%28graphs%29+with+and+without+cycles.&rft.au=Hill%2C+T+L&rft.aulast=Hill&rft.aufirst=T&rft.date=1988-05-01&rft.volume=85&rft.issue=10&rft.spage=3271&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 - 1988-06-22 N1 - Date created - 1988-06-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1988 May;85(9):2879-83 [3362853] Proc Natl Acad Sci U S A. 1975 Apr;72(4):1291-5 [1055403] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunodetection of estrogen receptor in epithelial and stromal tissues of neonatal mouse uterus. AN - 78215964; 3368444 AB - The tissue distribution and levels of estrogen receptor in neonatal mouse uterine tissue were determined in epithelial and stromal fractions separated by mild enzymatic treatment. Proteins of the isolated fractions were separated by gel electrophoresis and receptor was detected on immunoblots with monoclonal antibody H-222. Estrogen receptor protein was detectable in samples of reproductive tract tissue from 5- and 10-day-old mice. The level of receptor in 5-day-old animals was lower per unit DNA in epithelial cells than in stroma. Receptor levels were increased in both tissue types after treatment with diethylstilbestrol, but not with progesterone. Receptor protein present in these neonatal tissues was able to bind steroid as evidenced by affinity labeling with tamoxifen aziridine. Immunohistochemistry on sections of uteri from 4- and 10-day-old mice confirmed the biochemical results and indicated lower nuclear straining in epithelial cells than in stromal cells of uteri of 4-day-old mice. These results demonstrated that estrogen receptor protein is present in both epithelium and stroma of the neonatal mouse uterus, but at a higher level in stromal cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Korach, K S AU - Horigome, T AU - Tomooka, Y AU - Yamashita, S AU - Newbold, R R AU - McLachlan, J A AD - Receptor Biology, Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 3334 EP - 3337 VL - 85 IS - 10 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Antigen-Antibody Complex KW - Receptors, Estrogen KW - Receptors, Progesterone KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Animals, Newborn KW - Animals KW - Diethylstilbestrol -- pharmacology KW - Mice KW - Epithelium -- metabolism KW - Antigen-Antibody Complex -- analysis KW - Immunohistochemistry KW - Receptors, Progesterone -- pharmacology KW - Female KW - Uterus -- metabolism KW - Receptors, Estrogen -- drug effects KW - Receptors, Estrogen -- immunology KW - Receptors, Estrogen -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78215964?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immunodetection+of+estrogen+receptor+in+epithelial+and+stromal+tissues+of+neonatal+mouse+uterus.&rft.au=Korach%2C+K+S%3BHorigome%2C+T%3BTomooka%2C+Y%3BYamashita%2C+S%3BNewbold%2C+R+R%3BMcLachlan%2C+J+A&rft.aulast=Korach&rft.aufirst=K&rft.date=1988-05-01&rft.volume=85&rft.issue=10&rft.spage=3334&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 - 1988-06-22 N1 - Date created - 1988-06-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Endocrinology. 1974 Jul;95(1):174-8 [4365623] Cell Tissue Res. 1975;156(4):551-5 [1120338] Anal Biochem. 1976 May 7;72:248-54 [942051] Endocrinology. 1979 May;104(5):1324-32 [436778] Proc Natl Acad Sci U S A. 1980 Sep;77(9):5115-9 [7001472] Cancer Res. 1980 Nov;40(11):3988-99 [7193511] Am J Pathol. 1983 Oct;113(1):50-66 [6312803] J Histochem Cytochem. 1982 May;30(5):491-3 [6176617] Endocrinology. 1984 Mar;114(3):694-702 [6697957] Endocrinology. 1986 Mar;118(3):1011-8 [3004888] Endocrinology. 1986 Jul;119(1):390-6 [3720669] Endocrinology. 1987 Dec;121(6):2099-111 [3678140] Endocrinology. 1981 Jul;109(1):76-82 [7238415] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-methylformamide: cytotoxic, radiosensitizer, or chemosensitizer. AN - 78212998; 3284976 AB - N-methylformamide (NMF), a polar solvent, is currently being evaluated by the National Cancer Institute (NCI) as an antineoplastic agent because of its activity against colon, mammary, and lung tumor xenografts. Results from preclinical studies suggest that it has radiosensitizing, chemosensitizing, and differentiating activity. Its mechanism of action remains unknown, but may involve cellular depletion of glutathione, cell membrane changes, or modulation of proto-oncogene expression. Preclinical toxicology studies conducted in mice, rats, and beagle dogs showed reversible hepatotoxicity to be dose-limiting. Clinically, NMF is administered both orally and by intravenous (IV) injection. The bioavailability with oral administration is 90% to 95%. The highest reported plasma concentration of NMF is approximately 4 mmol/L in a patient who received a dose of 2,000 mg/m2 of IV NMF. Biphasic elimination with IV NMF is seen on both the daily for five days and weekly for 3 weeks schedule. Approximately 5% to 7% of the total administered IV dose is excreted in the urine. In phase I studies, dose-limiting toxicities included reversible hepatotoxicity, a generalized malaise syndrome, and nausea and vomiting. One partial response has been reported in the 111 patients treated on phase II trials in colorectal, head and neck, and renal carcinomas. Suggestions for the future development of this drug are presented. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Clagett-Carr, K AU - Sarosy, G AU - Plowman, J AU - Hoth, D F AU - Leyland-Jones, B AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 906 EP - 918 VL - 6 IS - 5 SN - 0732-183X, 0732-183X KW - Antineoplastic Agents KW - 0 KW - Formamides KW - Radiation-Sensitizing Agents KW - methylformamide KW - XPE4G7Y986 KW - Index Medicus KW - Drug Evaluation KW - Animals KW - Humans KW - Drug Evaluation, Preclinical KW - Formamides -- pharmacokinetics KW - Formamides -- pharmacology KW - Radiation-Sensitizing Agents -- pharmacology KW - Antineoplastic Agents -- pharmacokinetics KW - Antineoplastic Agents -- toxicity KW - Radiation-Sensitizing Agents -- pharmacokinetics KW - Radiation-Sensitizing Agents -- toxicity KW - Formamides -- toxicity KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78212998?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=N-methylformamide%3A+cytotoxic%2C+radiosensitizer%2C+or+chemosensitizer.&rft.au=Clagett-Carr%2C+K%3BSarosy%2C+G%3BPlowman%2C+J%3BHoth%2C+D+F%3BLeyland-Jones%2C+B&rft.aulast=Clagett-Carr&rft.aufirst=K&rft.date=1988-05-01&rft.volume=6&rft.issue=5&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 - 1988-06-10 N1 - Date created - 1988-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacology and phase I/II study of continuous intravenous infusions of iododeoxyuridine and hyperfractionated radiotherapy in patients with glioblastoma multiforme. AN - 78208810; 2835444 AB - Forty-seven adult patients with glioblastoma multiforme (GBM) were treated in a phase I/II study combining continuous intravenous (IV) infusions of iododeoxyuridine (IdUrd) and hyperfractionated radiation therapy. IdUrd was administered as a continuous infusion (24 h/d) for two separate 14-day infusion periods. The dose of IdUrd was escalated from 500 to 1,200 mg/m2/d. The initial wide-field tumor volume was treated to 45 Gy at 1.5 Gy fractions twice daily over 3 weeks. Following a planned 2-week break, a reduced-field boost of 25 Gy was delivered using 1.25 Gy fractions twice daily over 2 weeks (total dose, 70 Gy over 9 weeks). The IdUrd infusion preceded both the wide-field and reduced-field irradiation by 1 week. All treatment was performed on an outpatient basis. Dose-limiting systemic toxicity to the bone marrow (primarily thrombocytopenia) and gastrointestinal (GI) tract (both stomatitis and diarrhea) established the maximum tolerable dose (MTD) at 1,000 mg/m2/d for a 14-day infusion. Significant local toxicity (within the radiation field) was not seen. The kinetics of IdUrd were linear with dose escalation and reached steady-state plasma concentrations of 1.3 to 3.4 mumol/L. The total body clearance of IdUrd was .82 L/min/m2. The primary metabolite, 5-iodouracil (IUra) approached steady state by day 6 of the infusion when plasma levels were 60 times higher than IdUrd. Plasma levels of uracil and thymine, but not thymidine, were elevated throughout the infusion. With a minimum follow-up of 1 year, ten patients remain alive, while 33 patients died of progressive disease, and four patients died of other causes (including one treatment-related death). The median survival for all 47 patient and for the 40 patients receiving the MTD was 45 and 47 weeks, respectively, with 12% and 14% survivals at 24 months. Using a Cox regression analysis, age (less than or equal to 50 years v greater than 50 years) and pretreatment performance status (PS) (Eastern Cooperative Oncology Group [ECOG]-PS 0 to 1 v PS 2 to 3) were independent, statistically significant (P2 less than .05) predictors of survival, with the ECOG status being a better predictor. Patients with a PS 0 to 1 (28 patients) had a median survival of 64 weeks with 21% survival at 24 months, compared with a median survival of 29 weeks and 0% survival at 12 months in the 19 patients with PS 2 to 3. The overall and subgroup survival data are at least comparable to other combined modality treatment approaches in patients with GBM. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Kinsella, T J AU - Collins, J AU - Rowland, J AU - Klecker, R AU - Wright, D AU - Katz, D AU - Steinberg, S M AU - Glastein, E AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 871 EP - 879 VL - 6 IS - 5 SN - 0732-183X, 0732-183X KW - Idoxuridine KW - LGP81V5245 KW - Index Medicus KW - Drug Evaluation KW - Thrombophlebitis -- etiology KW - Combined Modality Therapy KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Radiation Tolerance -- drug effects KW - Male KW - Female KW - Radiotherapy -- adverse effects KW - Glioblastoma -- mortality KW - Idoxuridine -- pharmacokinetics KW - Idoxuridine -- therapeutic use KW - Idoxuridine -- adverse effects KW - Glioblastoma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78208810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pharmacology+and+phase+I%2FII+study+of+continuous+intravenous+infusions+of+iododeoxyuridine+and+hyperfractionated+radiotherapy+in+patients+with+glioblastoma+multiforme.&rft.au=Kinsella%2C+T+J%3BCollins%2C+J%3BRowland%2C+J%3BKlecker%2C+R%3BWright%2C+D%3BKatz%2C+D%3BSteinberg%2C+S+M%3BGlastein%2C+E&rft.aulast=Kinsella&rft.aufirst=T&rft.date=1988-05-01&rft.volume=6&rft.issue=5&rft.spage=871&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 - 1988-06-10 N1 - Date created - 1988-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunotherapy of patients with advanced cancer using tumor-infiltrating lymphocytes and recombinant interleukin-2: a pilot study. AN - 78208554; 3259261 AB - Clinical investigations using the adoptive transfer of lymphokine-activated killer (LAK) cells and recombinant interleukin-2 (rIL-2) to treat patients with advanced cancer have yielded encouraging results. We have thus sought ways to enhance the effectiveness of adoptive immunotherapy while minimizing its toxic side effects. Murine experiments have identified tumor-infiltrating lymphocytes (TIL) as killer cells more effective than LAK cells and less dependent on adjunctive systemically administered IL-2 to mediate antitumor effects. Accordingly, we performed a pilot protocol to investigate the feasibility and practicality of administering IL-2-expanded TIL to humans with metastatic cancers. Twelve patients, including six with melanoma, four with renal cell carcinoma, one with breast carcinoma, and one with colon carcinoma, were treated with varying doses and combinations of TIL (8.0 X 10(9) to 2.3 X 10(11) cells per patient), IL-2 (10,000 to 100,000 U/kg three times daily to dose-limiting toxicity), and cyclophosphamide (CPM) (up to 50 mg/kg). Two partial responses (PR) to therapy were observed: pulmonary and mediastinal masses regressed in a patient with melanoma, and a lymph node mass regressed in a patient with renal cell carcinoma. One additional patient with breast cancer experienced a partial regression of disease in lymph nodal and cutaneous sites with complete elimination of malignant cells from a pleural effusion, although cutaneous disease recurred at 4 weeks. The toxicities of therapy were similar to those ascribed to IL-2; no toxic effects were directly attributable to TIL infusions. In five of six melanoma patients, TIL demonstrated lytic activity specific for the autologous tumor target in short-term chromium-release assays, distinct from the nonspecific lytic activity characteristic of LAK cells. This study represents an initial attempt to identify and use lymphocyte subsets with enhanced tumoricidal capacity in the adoptive immunotherapy of human malignancies. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Topalian, S L AU - Solomon, D AU - Avis, F P AU - Chang, A E AU - Freerksen, D L AU - Linehan, W M AU - Lotze, M T AU - Robertson, C N AU - Seipp, C A AU - Simon, P AD - Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 839 EP - 853 VL - 6 IS - 5 SN - 0732-183X, 0732-183X KW - Interleukin-2 KW - 0 KW - Recombinant Proteins KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Phenotype KW - Cytotoxicity, Immunologic KW - Cyclophosphamide -- therapeutic use KW - Cells, Cultured KW - Humans KW - Adult KW - Pilot Projects KW - Middle Aged KW - Recombinant Proteins -- therapeutic use KW - Male KW - Female KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- therapeutic use KW - Immunization, Passive KW - Neoplasms -- therapy KW - Killer Cells, Natural -- immunology KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78208554?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immunotherapy+of+patients+with+advanced+cancer+using+tumor-infiltrating+lymphocytes+and+recombinant+interleukin-2%3A+a+pilot+study.&rft.au=Topalian%2C+S+L%3BSolomon%2C+D%3BAvis%2C+F+P%3BChang%2C+A+E%3BFreerksen%2C+D+L%3BLinehan%2C+W+M%3BLotze%2C+M+T%3BRobertson%2C+C+N%3BSeipp%2C+C+A%3BSimon%2C+P&rft.aulast=Topalian&rft.aufirst=S&rft.date=1988-05-01&rft.volume=6&rft.issue=5&rft.spage=839&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 - 1988-06-10 N1 - Date created - 1988-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bioavailability of low-dose vs high-dose 6-mercaptopurine. AN - 78205257; 3365920 AB - The bioavailability of oral 6-mercaptopurine (6MP) at standard doses is very low, largely as a result of extensive first-pass metabolism by xanthine oxidase. Fewer than one third of patients achieve 6MP plasma concentrations known to be cytocidal in vitro (greater than 1 mumol/L). Studies in vitro have suggested that first-pass metabolism can be saturated at higher doses of 6MP. To determine whether saturation occurs in vivo at clinically used doses and whether bioavailability can be enhanced by increasing the dose, the bioavailability of different doses of 6MP was studied first in rhesus monkeys and then in children with acute lymphoblastic leukemia in remission. In monkeys a higher dose of 6MP resulted in enhanced bioavailability, whereas in patients the mean relative bioavailability at the higher dose was significantly less. However, all patients achieved cytocidal (greater than 1 to 10 mumol/L) plasma concentrations at the higher dose without manifesting significant clinical toxicity. Therefore cytocidal levels of 6MP can be achieved in patients with oral 6MP without the risk of unexpectedly high levels caused by saturation of first-pass metabolism. JF - Clinical pharmacology and therapeutics AU - Arndt, C A AU - Balis, F M AU - McCully, C L AU - Jeffries, S L AU - Doherty, K AU - Murphy, R AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 588 EP - 591 VL - 43 IS - 5 SN - 0009-9236, 0009-9236 KW - 6-Mercaptopurine KW - E7WED276I5 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Humans KW - Adult KW - Macaca mulatta KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Biological Availability KW - 6-Mercaptopurine -- pharmacokinetics KW - 6-Mercaptopurine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78205257?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Bioavailability+of+low-dose+vs+high-dose+6-mercaptopurine.&rft.au=Arndt%2C+C+A%3BBalis%2C+F+M%3BMcCully%2C+C+L%3BJeffries%2C+S+L%3BDoherty%2C+K%3BMurphy%2C+R%3BPoplack%2C+D+G&rft.aulast=Arndt&rft.aufirst=C&rft.date=1988-05-01&rft.volume=43&rft.issue=5&rft.spage=588&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 - 1988-06-16 N1 - Date created - 1988-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Flavone-8-acetic acid augments systemic natural killer cell activity and synergizes with IL-2 for treatment of murine renal cancer. AN - 78196055; 3258894 AB - The investigational drug flavone-8-acetic acid (FAA) potently augments NK activity in the spleen, liver, lungs, and peritoneum in a dose-dependent manner after i.v. or i.p. administration. Augmented NK activity peaks by 24 h after FAA injection and returns to normal after 6 days. Combined treatment of established murine renal cancer with FAA and rIL-2 results in up to 80% long term survival whereas FAA or rIL-2 alone were unable to induce any long term survivors. The optimal dose of rIL-2 required for use with FAA was in the range of 10,000 to 30,000 U/day. Further studies demonstrated that the regimen of FAA plus rIL-2 administration that was effective in treating established murine renal cancer also induced a more potent augmentation of NK activity than did either FAA or rIL-2 alone. Subsequent studies revealed that the therapeutic effectiveness of FAA plus rIL-2 was significantly reduced when tumor-bearing mice were treated with anti-asialo GM1 serum. These results are consistent with a role for augmented NK activity in the therapeutic effects of FAA plus rIL-2 murine renal cancer. In addition, these studies demonstrate that FAA and rIL-2 is a useful approach for cancer treatment in that subtoxic doses of rIL-2 can be used and significant anti-tumor efficacy occurs even without accompanying adoptive immunotherapy. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Wiltrout, R H AU - Boyd, M R AU - Back, T C AU - Salup, R R AU - Arthur, J A AU - Hornung, R L AD - Laboratory of Experimental Immunology, National Cancer Institute-Frederick Cancer Research Facility. Y1 - 1988/05/01/ PY - 1988 DA - 1988 May 01 SP - 3261 EP - 3265 VL - 140 IS - 9 SN - 0022-1767, 0022-1767 KW - Antineoplastic Agents KW - 0 KW - Flavonoids KW - Glycosphingolipids KW - Interleukin-2 KW - G(M1) Ganglioside KW - 37758-47-7 KW - asialo GM1 ganglioside KW - 71012-19-6 KW - flavone acetic acid KW - 87626-55-9 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Glycosphingolipids -- physiology KW - Immunity, Innate -- drug effects KW - Immunotherapy KW - Mice KW - Drug Synergism KW - Kidney Neoplasms -- therapy KW - Interleukin-2 -- administration & dosage KW - Antineoplastic Agents -- administration & dosage KW - Cytotoxicity, Immunologic -- drug effects KW - Killer Cells, Natural -- immunology KW - Flavonoids -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78196055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Flavone-8-acetic+acid+augments+systemic+natural+killer+cell+activity+and+synergizes+with+IL-2+for+treatment+of+murine+renal+cancer.&rft.au=Wiltrout%2C+R+H%3BBoyd%2C+M+R%3BBack%2C+T+C%3BSalup%2C+R+R%3BArthur%2C+J+A%3BHornung%2C+R+L&rft.aulast=Wiltrout&rft.aufirst=R&rft.date=1988-05-01&rft.volume=140&rft.issue=9&rft.spage=3261&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 - 1988-06-03 N1 - Date created - 1988-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose-response relationship between thyroid hormone and growth velocity in cynomolgus monkeys. AN - 78190923; 3360894 AB - To investigate the dose-response relationship between thyroid hormone and linear growth, we studied 10 castrated prepubertal cynomolgus monkeys. Hypothyroidism was induced by administration of methimazole (0.0125% in drinking water) and was confirmed by high serum TSH levels (greater than 40 mU/L) in all animals. Subsequently, each animal received 1, 2, 4, or 8 micrograms/kg.day T4, im, for 9 weeks. The sequence of T4 doses was random, and 6 weeks elapsed between successive T4 doses. Serum T4, T3, TSH, and insulin-like growth factor I (IGF-I) levels and lower leg length were measured every 3 weeks. Methimazole administration decreased thyroid hormone and IGF-I levels and lower leg growth rate. With increasing doses of exogenous T4, serum T4, T3, and IGF-I as well as lower leg growth rate increased significantly. Animals not given T4 had a 65% decrease in lower leg growth rate (P less than 0.01). Animals given 4 and 8 micrograms/kg.day T4 had 56% and 73% increases, respectively, in lower leg growth rate compared to baseline (P less than 0.05 and P less than 0.01, respectively). Lower leg growth rate correlated better with serum T3 (r = 0.50; P less than 0.001) than with serum T4 (r = 0.29; P less than 0.05). Lower leg growth rate also correlated with serum IGF-I levels (r = 0.53; P less than 0.001). Serum IGF-I correlated with serum T3 (r = 0.47; P less than 0.001), but not with serum T4. We conclude that increased serum T4 and T3 levels cause progressive increases in growth velocity and IGF-I levels over a range from moderate hypothyroidism to moderate hyperthyroidism. Growth velocity and IGF-I levels correlated more strongly with the serum T3 than with the serum T4 level. JF - The Journal of clinical endocrinology and metabolism AU - Ren, S G AU - Malozowski, S AU - Simoni, C AU - Garcia, H AU - Caruso-Nicoletti, M AU - Cutler, G B AU - Cassorla, F AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 1010 EP - 1013 VL - 66 IS - 5 SN - 0021-972X, 0021-972X KW - Somatomedins KW - 0 KW - Thyroid Hormones KW - Triiodothyronine KW - 06LU7C9H1V KW - Methimazole KW - 554Z48XN5E KW - Thyroxine KW - Q51BO43MG4 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Triiodothyronine -- administration & dosage KW - Macaca fascicularis KW - Hypothyroidism -- blood KW - Dose-Response Relationship, Drug KW - Hypothyroidism -- chemically induced KW - Somatomedins -- blood KW - Castration KW - Hyperthyroidism -- blood KW - Thyroxine -- administration & dosage KW - Female KW - Male KW - Methimazole -- administration & dosage KW - Thyroid Hormones -- administration & dosage KW - Growth -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78190923?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dose-response+relationship+between+thyroid+hormone+and+growth+velocity+in+cynomolgus+monkeys.&rft.au=Ren%2C+S+G%3BMalozowski%2C+S%3BSimoni%2C+C%3BGarcia%2C+H%3BCaruso-Nicoletti%2C+M%3BCutler%2C+G+B%3BCassorla%2C+F&rft.aulast=Ren&rft.aufirst=S&rft.date=1988-05-01&rft.volume=66&rft.issue=5&rft.spage=1010&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 - 1988-06-03 N1 - Date created - 1988-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tolerance of the canine bladder to intraoperative radiation therapy: an experimental study. AN - 78182878; 3129384 AB - An experimental study of bladder tolerance to intraoperative radiotherapy (IORT) was designed using a large animal model (adult American Foxhounds, weight 25-30 kg) to access acute and late radiation effects. Dogs were subjected to laparotomy where the bladder was mobilized and IORT was delivered using a 5 cm circular cone through a cystotomy incision with 12 MeV electrons. The bladder trigone including both ureteral orifices and the proximal urethra was irradiated in groups of 3 dogs with doses of 0, 20, 25, 30, 35, and 40 Gy. Dogs were followed clinically with repeat urinalysis, intravenous pyelogram (IVP), and cystometrogram at 1 month and then Q6 months for up to 4 years. One dog from each dose group was sacrificed electively at 1 and 2 years, whereas the other dog is being followed clinically for a minimum of 4 years. Complete autopsies were performed with particular attention to genitourinary and pelvic structures. No clinically detectable acute toxicity resulted from IORT to the bladder. Three of 15 IORT dogs (1 each at 25, 35, and 40 Gy) showed obstruction of a ureteral orifice with 2 dogs dying of renal failure secondary to bilateral hydronephrosis within 1-2 years of treatment. The remaining 12 IORT dogs and 3 control dogs have normal repeat IVP's and renal function with up to 4 years of follow-up. Serial cystometry demonstrates no major loss of bladder contractility or volume. At autopsy, histological changes of mucosal thinning and telangiectasia with submucosal fibrosis were confined to the IORT field and appeared dose-related. However, the bladder epithelium remained intact at all doses. The ureterovesical junction in animals receiving 20 Gy showed mild fibrosis of the lamina propria and moderate chronic inflammation. Above 20 Gy, these histological changes at the U-V junction were more pronounced with gross stenosis in 3 animals as predicted by the IVP. We conclude that the bladder trigone will tolerate IORT to 20 Gy without major clinical sequellae. Above 20 Gy, progressive inflammation and fibrosis of the U-V junction resulted in obstructive hydronephrosis in three animals within 1-2 years of IORT. The bladder mucosa remained intact with doses to 40 Gy, although submucosal fibrosis and chronic inflammation were evident and appeared dose-related. However, bladder function as measured by cystometry showed essentially no change with follow-up to 4 years. From this large animal study, IORT for early-stage bladder carcinoma is technically feasible and deserves a careful clinical study. JF - International journal of radiation oncology, biology, physics AU - Kinsella, T J AU - Sindelar, W F AU - DeLuca, A M AU - Barnes, M AU - Tochner, Z AU - Mixon, A AU - Glatstein, E AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 939 EP - 946 VL - 14 IS - 5 SN - 0360-3016, 0360-3016 KW - Index Medicus KW - Animals KW - Radiotherapy, High-Energy -- adverse effects KW - Hydronephrosis -- etiology KW - Dogs KW - Radiation Tolerance KW - Follow-Up Studies KW - Intraoperative Period KW - Dose-Response Relationship, Radiation KW - Ureter -- radiation effects KW - Urinary Bladder -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78182878?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tolerance+of+the+canine+bladder+to+intraoperative+radiation+therapy%3A+an+experimental+study.&rft.au=Kinsella%2C+T+J%3BSindelar%2C+W+F%3BDeLuca%2C+A+M%3BBarnes%2C+M%3BTochner%2C+Z%3BMixon%2C+A%3BGlatstein%2C+E&rft.aulast=Kinsella&rft.aufirst=T&rft.date=1988-05-01&rft.volume=14&rft.issue=5&rft.spage=939&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 - 1988-06-03 N1 - Date created - 1988-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of t-[35S]butylbicyclophosphorothionate and [3H]strychnine binding by monovalent anions reveals similarities between gamma-aminobutyric acid- and glycine-gated chloride channels. AN - 78180225; 2452238 AB - The characteristics of [3H]strychnine and t-[35S]-butylbicyclophosphorothionate ([35S]TBPS) binding to sites associated with glycine- and gamma-aminobutyric acid (GABA)-gated chloride channels were compared in the presence of a series of anions with known permeabilities through these channels. Good correlations were found between (a) the potencies (EC50) of these anions to stimulate radioligand binding and their permeabilities relative to chloride; (b) the affinities (KD) of these radioligands in the presence of fixed concentrations of these anions and their relative permeabilities; (c) the potencies (EC50) of these anions to stimulate [35S]TBPS and [3H]strychnine binding; and (d) the affinities (KD) of [3H]strychnine and [35S]TBPS measured at a fixed concentration of these anions. These studies support electrophysiological and biochemical observations demonstrating similarities between glycine- and GABA-gated chloride channels, and suggest that anions enhance [3H]strychnine and [35S]TBPS binding through specific anion binding sites located at the channels. JF - Journal of neurochemistry AU - Marvizón, J C AU - Skolnick, P AD - National Institutes of Health, Laboratory of Neuroscience, Bethesda, Maryland 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 1632 EP - 1639 VL - 50 IS - 5 SN - 0022-3042, 0022-3042 KW - Anions KW - 0 KW - Bridged Bicyclo Compounds KW - Bridged Bicyclo Compounds, Heterocyclic KW - Bridged-Ring Compounds KW - Chlorides KW - Ion Channels KW - Sulfur Radioisotopes KW - Tritium KW - 10028-17-8 KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - tert-butylbicyclophosphorothionate KW - 70636-86-1 KW - Strychnine KW - H9Y79VD43J KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Spinal Cord -- metabolism KW - Cell Membrane Permeability KW - Cell Membrane -- metabolism KW - Medulla Oblongata -- metabolism KW - Male KW - Glycine -- physiology KW - Bridged-Ring Compounds -- metabolism KW - Strychnine -- metabolism KW - Ion Channels -- drug effects KW - Anions -- pharmacology KW - gamma-Aminobutyric Acid -- physiology KW - Chlorides -- metabolism KW - Bridged Bicyclo Compounds -- metabolism KW - Ion Channels -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78180225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhancement+of+t-%5B35S%5Dbutylbicyclophosphorothionate+and+%5B3H%5Dstrychnine+binding+by+monovalent+anions+reveals+similarities+between+gamma-aminobutyric+acid-+and+glycine-gated+chloride+channels.&rft.au=Marviz%C3%B3n%2C+J+C%3BSkolnick%2C+P&rft.aulast=Marviz%C3%B3n&rft.aufirst=J&rft.date=1988-05-01&rft.volume=50&rft.issue=5&rft.spage=1632&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 - 1988-06-02 N1 - Date created - 1988-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - From the National Institutes of Health. Summary of the International Symposium and Workshop on Infections due to Verocytotoxin (Shiga-like toxin)-producing Escherichia coli. AN - 78173002; 3283259 JF - The Journal of infectious diseases AU - Edelman, R AU - Karmali, M A AU - Fleming, P A AD - National iInstitute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 1102 EP - 1104 VL - 157 IS - 5 SN - 0022-1899, 0022-1899 KW - Bacterial Toxins KW - 0 KW - Cytotoxins KW - Shiga Toxin 1 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Humans KW - Diarrhea -- microbiology KW - Escherichia coli Infections -- microbiology KW - Escherichia coli -- metabolism KW - Escherichia coli Infections -- veterinary KW - Cytotoxins -- toxicity KW - Escherichia coli Infections -- epidemiology KW - Bacterial Toxins -- toxicity KW - Bacterial Toxins -- biosynthesis KW - Cytotoxins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78173002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=From+the+National+Institutes+of+Health.+Summary+of+the+International+Symposium+and+Workshop+on+Infections+due+to+Verocytotoxin+%28Shiga-like+toxin%29-producing+Escherichia+coli.&rft.au=Edelman%2C+R%3BKarmali%2C+M+A%3BFleming%2C+P+A&rft.aulast=Edelman&rft.aufirst=R&rft.date=1988-05-01&rft.volume=157&rft.issue=5&rft.spage=1102&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 - 1988-06-01 N1 - Date created - 1988-06-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hair dye use and risk of leukemia and lymphoma. AN - 78168758; 3354743 AB - Data from a population-based case-control study of incident leukemia and non-Hodgkin's lymphoma among adult men in Iowa and Minnesota were used to evaluate risk associated with hair dye use. The relative risk for ever using hair dyes was 1.8 (95% confidence interval [CI] = 1.1-2.7) among leukemia patients, and 2.0 (CI = 1.3-3.0) among cases with non-Hodgkin's lymphoma. There was a suggestion of increased risk with extent of hair dye use. Given the widespread use of hair coloring products, these observations deserve more detailed evaluation in populations where the exposure is relatively common. JF - American journal of public health AU - Cantor, K P AU - Blair, A AU - Everett, G AU - VanLier, S AU - Burmeister, L AU - Dick, F R AU - Gibson, R W AU - Schuman, L AD - National Cancer Institute, Environmental Epidemiology Branch, Bethesda, MD 20892. Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 570 EP - 571 VL - 78 IS - 5 SN - 0090-0036, 0090-0036 KW - Hair Dyes KW - 0 KW - Hair Preparations KW - Abridged Index Medicus KW - Index Medicus KW - Risk KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Sampling Studies KW - Interviews as Topic KW - Aged KW - Middle Aged KW - Male KW - Hair Preparations -- adverse effects KW - Leukemia -- chemically induced KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Hair Dyes -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78168758?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+public+health&rft.atitle=Hair+dye+use+and+risk+of+leukemia+and+lymphoma.&rft.au=Cantor%2C+K+P%3BBlair%2C+A%3BEverett%2C+G%3BVanLier%2C+S%3BBurmeister%2C+L%3BDick%2C+F+R%3BGibson%2C+R+W%3BSchuman%2C+L&rft.aulast=Cantor&rft.aufirst=K&rft.date=1988-05-01&rft.volume=78&rft.issue=5&rft.spage=570&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 - 1988-05-12 N1 - Date created - 1988-05-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1975 Jun;72(6):2423-7 [1094469] J Natl Cancer Inst. 1977 Nov;59(5):1423-5 [909104] J Natl Cancer Inst. 1981 Mar;66(3):591-602 [6937712] Am J Ind Med. 1982;3(2):169-71 [7137173] J Natl Cancer Inst. 1983 Mar;70(3):443-6 [6572734] J Natl Cancer Inst. 1984 May;72(5):1051-7 [6585583] Am J Ind Med. 1984;6(2):97-102 [6465143] Postgrad Med J. 1985 Nov;61(721):1003-5 [4070106] Int J Epidemiol. 1985 Dec;14(4):549-54 [4086141] Am J Epidemiol. 1986 Jun;123(6):1101-17 [3706280] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential growth sensitivity to 4-cis-hydroxy-L-proline of transformed rodent cell lines. AN - 78161779; 2833347 AB - The effect of 4-cis-hydroxy-L-proline (CHP), a proline analogue, on the anchorage-dependent and -independent growth of several transformed rodent cell lines was studied. Mouse NIH-3T3 fibroblasts transformed by a variety of different oncogenes (Ki-ras, mos, src, fms, fes, met, and trk) by a DNA tumor virus (SV40) or by a chemical carcinogen (N-methylnitrosourea) were all found to be more sensitive (50% inhibitory dose, 20 to 55 micrograms/ml) to the dose-dependent inhibitory effects of CHP on growth in monolayer culture than were NIH-3T3 cells (50% inhibitory dose, 120 micrograms/ml). CHP was generally found to be even more effective in inhibiting the growth of these transformed cells as colonies in soft agar than in monolayer cultures. In addition, rat embryo fibroblasts (CREF) and normal rat kidney fibroblasts (NRK) after transformation with a Ki-ras oncogene exhibit a similar increase in their sensitivity to CHP-induced growth inhibition. Treatment of NRK cells with transforming growth factor alpha (TGF-alpha) and beta (TGF-beta), which reversibly induces phenotypic transformation of these cells, increases their sensitivity to CHP to a level comparable with that observed in Ki-ras-transformed NRK cells (K-NRK). The growth inhibitory effects of CHP are reversible, since removal of CHP results in a normal resumption of cell growth. CHP uptake occurs primarily through the Na+- and energy-dependent neutral amino acid transport A system, which is 6- to 7-fold more elevated in K-NRK cells compared with NRK cells. Treatment of NRK cells with TGF-alpha and/or -beta increases the uptake of [3H]methylaminoisobutyric acid on the A system to a level that is similar to that found in K-NRK cells. The functions of the Na+/K+ and Na+/H+ exchange systems are apparently necessary for the enhanced A system activity, since ouabain and amiloride can inhibit the uptake of [3H]methylaminoisobutyric acid in K-NRK cells and in NRK cells treated with TGF-alpha and/or -beta. The activity of the A system is specifically increased in K-NRK and in TGF-alpha- and/or -beta-treated NRK cells, since the other two major neutral amino acid uptake systems, the ASC and the L systems, and the Ly+ system for basic amino acid uptake show no apparent changes in their activity in NRK cells after treatment with TGF-alpha and/or -beta or in these cells after transformation with the Ki-ras oncogene. These results suggest that the differential growth sensitivity to CHP of transformed rodent cells and of normal fibroblasts treated with TGF-alpha and/or -beta is due in part to an elevated uptake of this amino acid analogue on the neutral amino acid transport A system. JF - Cancer research AU - Ciardiello, F AU - Sanfilippo, B AU - Yanagihara, K AU - Kim, N AU - Tortora, G AU - Bassin, R H AU - Kidwell, W R AU - Salomon, D S AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/05/01/ PY - 1988 DA - 1988 May 01 SP - 2483 EP - 2491 VL - 48 IS - 9 SN - 0008-5472, 0008-5472 KW - Amino Acids KW - 0 KW - Aminoisobutyric Acids KW - Carrier Proteins KW - Culture Media KW - Growth Inhibitors KW - Peptides KW - Sodium-Hydrogen Antiporter KW - 2-(methylamino)isobutyric acid KW - 2566-34-9 KW - Ouabain KW - 5ACL011P69 KW - Transforming Growth Factors KW - 76057-06-2 KW - Amiloride KW - 7DZO8EB0Z3 KW - Hydroxyproline KW - RMB44WO89X KW - Index Medicus KW - Aminoisobutyric Acids -- metabolism KW - Animals KW - Mice KW - Carrier Proteins -- analysis KW - Amino Acids -- metabolism KW - Amiloride -- pharmacology KW - Peptides -- pharmacology KW - Ouabain -- pharmacology KW - Hydroxyproline -- pharmacology KW - Growth Inhibitors -- pharmacology KW - Cell Line, Transformed UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78161779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differential+growth+sensitivity+to+4-cis-hydroxy-L-proline+of+transformed+rodent+cell+lines.&rft.au=Ciardiello%2C+F%3BSanfilippo%2C+B%3BYanagihara%2C+K%3BKim%2C+N%3BTortora%2C+G%3BBassin%2C+R+H%3BKidwell%2C+W+R%3BSalomon%2C+D+S&rft.aulast=Ciardiello&rft.aufirst=F&rft.date=1988-05-01&rft.volume=48&rft.issue=9&rft.spage=2483&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 - 1988-05-18 N1 - Date created - 1988-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of gene expression in preneoplastic and neoplastic rat liver to adult, fetal, regenerating, and tumor-promoted liver. AN - 78154176; 2451559 AB - Computer-assisted analysis was performed on the in vitro translation products of polyadenylated RNA samples isolated from normal adult Fischer rat liver and from preneoplastic and neoplastic rat liver samples which were generated by the Solt Farber technique (Solt, D. and Farber, E., Nature 263:701-703, 1976). The vast majority of the differences in translation products observed throughout the progressive development of hepatocellular carcinoma was quantitative in nature. Importantly, this quantitative heterogeneity first became prevalent at the very early preneoplastic stage of hepatoma formation. Only 3 consistent qualitative alterations in translation products were observed to be associated with the hepatocarcinogenesis process. The appearance of two new polypeptides of molecular weight and isoelectric point of 32/5.2 and 43/5.1 appeared to be related to an early preneoplastic event in hepatoma development and the transition from a preneoplastic to a neoplastic state, respectively. Importantly, these new polypeptides were not observed in the in vitro translation products generated from fetal or regenerating liver samples or from liver samples which were chronically treated with phenobarbital or terachlorodibenzo-p-dioxin. One translation product (located at 35/6.6) of normal adult, fetal, and regenerating liver RNA samples was undetected in all preneoplastic, neoplastic, phenobarbital-, and terachlorodibenzo-p-dioxin-treated liver RNA translation products. The possibility exists that the specific loss of this gene product may promote the development of the transformed phenotype. JF - Cancer research AU - Huber, B E AU - Wirth, P J AU - Miller, M J AU - Glowinski, I B AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/05/01/ PY - 1988 DA - 1988 May 01 SP - 2382 EP - 2387 VL - 48 IS - 9 SN - 0008-5472, 0008-5472 KW - Peptides KW - 0 KW - Polychlorinated Dibenzodioxins KW - RNA, Messenger KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Phenobarbital -- pharmacology KW - Poly A -- analysis KW - Polychlorinated Dibenzodioxins -- pharmacology KW - In Vitro Techniques KW - Peptides -- analysis KW - RNA -- analysis KW - Male KW - Protein Biosynthesis KW - Liver Neoplasms, Experimental -- genetics KW - Precancerous Conditions -- genetics KW - Fetus -- analysis KW - Precancerous Conditions -- analysis KW - Liver Regeneration KW - Liver -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78154176?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+gene+expression+in+preneoplastic+and+neoplastic+rat+liver+to+adult%2C+fetal%2C+regenerating%2C+and+tumor-promoted+liver.&rft.au=Huber%2C+B+E%3BWirth%2C+P+J%3BMiller%2C+M+J%3BGlowinski%2C+I+B&rft.aulast=Huber&rft.aufirst=B&rft.date=1988-05-01&rft.volume=48&rft.issue=9&rft.spage=2382&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 - 1988-05-18 N1 - Date created - 1988-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intraoperative Ultrasound. Guidelines for the Sonographer AN - 21149687; 11625192 AB - Intraoperative ultrasound is increasingly employed in hospitals throughout the country. Involvement with this activity can result in a significant demand on the resources of an ultrasound section and can be a problem for sonographers, who must now work in the unfamiliar environment of the surgical suite. The purpose of this article is to provide sonographers with some general guidelines and suggestions about how to conduct an intraoperative examination and to discuss how ultrasound instrumentation can be operated with ease and comfort within the restricted setting of the operating room. JF - Journal of Diagnostic Medical Sonography AU - Shawker, Thomas H AU - Bradford, Mary H AU - Norton, Jeffrey A AD - Georgetown University School of Medicine, Washington, DC; Department of Radiology, National Institutes of Health, Clinical Center, Building 10, Room IC660, Bethesda, MD 20892 Y1 - 1988/05// PY - 1988 DA - May 1988 SP - 126 EP - 129 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 4 IS - 3 SN - 8756-4793, 8756-4793 KW - Biotechnology and Bioengineering Abstracts KW - ultrasonic diagnosis, surgery, operative KW - intraoperative period KW - diagnosis, surgical KW - transducers, ultrasonic KW - Ultrasound KW - Hospitals KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/21149687?accountid=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+Diagnostic+Medical+Sonography&rft.atitle=Intraoperative+Ultrasound.+Guidelines+for+the+Sonographer&rft.au=Shawker%2C+Thomas+H%3BBradford%2C+Mary+H%3BNorton%2C+Jeffrey+A&rft.aulast=Shawker&rft.aufirst=Thomas&rft.date=1988-05-01&rft.volume=4&rft.issue=3&rft.spage=126&rft.isbn=&rft.btitle=&rft.title=Journal+of+Diagnostic+Medical+Sonography&rft.issn=87564793&rft_id=info:doi/10.1177%2F875647938800400303 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-01-01 N1 - Last updated - 2015-03-31 N1 - SubjectsTermNotLitGenreText - Ultrasound; Hospitals DO - http://dx.doi.org/10.1177/875647938800400303 ER - TY - JOUR T1 - Uncoupled expression of mRNAs for alpha 1(I) and alpha 2(I) procollagen chains in chemically transformed Syrian hamster fibroblasts. AN - 78165106; 3128544 AB - Syrian hamster embryo fibroblasts transformed by 4-nitroquinoline-1-oxide (NQT-SHE cells) failed to synthesize the pro-alpha 1(I) subunit of type I procollagen but continued to synthesize altered forms of the other subunit, pro-alpha 2(I) (Peterkofsky, B., and Prather, W. (1986) J. Biol. Chem. 261, 16818-16826). This was unusual, since synthesis of the two subunits generally is coordinately regulated. Present experiments using cell-free translation and hybridization of RNA from normal and transformed Syrian hamster fibroblasts with labeled pro-alpha 1(I) DNA probes show that mRNA for pro-alpha 1(I) is absent from the transformant. In contrast, dot-blot and Southern blot hybridizations of cellular DNAs with pro-alpha 1(I) DNA probes demonstrated that the transformed cells contained pro-alpha 1(I) gene sequences and that the gross structure of the gene was unchanged by transformation. mRNA for the other type I procollagen subunit, pro-alpha 2(I), was present in transformed cells and the major collagenous polypeptide translated from this RNA migrated like the normal pro-alpha 2 subunit during sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The translated procollagen chain was cleaved to an alpha 2(I)-sized collagen chain by pepsin at 4 degrees C. These studies provide a molecular basis for the observed collagen phenotype of NQT-SHE cells. JF - The Journal of biological chemistry AU - Majmudar, G AU - Schalk, E AU - Bateman, J AU - Peterkofsky, B AD - Laboratory of Biochemistry, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04/25/ PY - 1988 DA - 1988 Apr 25 SP - 5555 EP - 5559 VL - 263 IS - 12 SN - 0021-9258, 0021-9258 KW - Procollagen KW - 0 KW - RNA, Messenger KW - 4-Nitroquinoline-1-oxide KW - 56-57-5 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Protein Biosynthesis KW - Animals KW - DNA -- genetics KW - Rabbits KW - Nucleic Acid Hybridization KW - Cell Line, Transformed KW - Cricetinae KW - Cell-Free System KW - Procollagen -- biosynthesis KW - RNA, Messenger -- metabolism KW - RNA, Messenger -- genetics KW - Procollagen -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78165106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Uncoupled+expression+of+mRNAs+for+alpha+1%28I%29+and+alpha+2%28I%29+procollagen+chains+in+chemically+transformed+Syrian+hamster+fibroblasts.&rft.au=Majmudar%2C+G%3BSchalk%2C+E%3BBateman%2C+J%3BPeterkofsky%2C+B&rft.aulast=Majmudar&rft.aufirst=G&rft.date=1988-04-25&rft.volume=263&rft.issue=12&rft.spage=5555&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 - 1988-05-18 N1 - Date created - 1988-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thermospray liquid chromatographic-mass spectrometric method for the analysis of metribuzin and its metabolites. AN - 78273646; 3384886 AB - A thermospray liquid chromatographic-mass spectrometric (TSP LC-MS) method has been developed for the analysis of the herbicide metribuzin and its three major metabolites in plant tissue. Metribuzin and its metabolites exhibited widely varying sensitivities in positive-ion TSP, with metribuzin being the most sensitive and deaminated diketo metribuzin being the least sensitive. All four compounds of interest were detected in an extract of a soybean plant which had been treated with metribuzin. JF - Journal of chromatography AU - Parker, C E AU - Geeson, A V AU - Games, D E AU - Ramsey, E D AU - Abusteit, E O AU - Corbin, F T AU - Tomer, K B AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/04/22/ PY - 1988 DA - 1988 Apr 22 SP - 359 EP - 367 VL - 438 IS - 2 KW - Herbicides KW - 0 KW - Plant Extracts KW - Triazines KW - metribuzin KW - QO836138OV KW - Index Medicus KW - Mass Spectrometry KW - Biotransformation KW - Chromatography, Liquid KW - Plant Extracts -- analysis KW - Chromatography, High Pressure Liquid KW - Triazines -- analysis KW - Herbicides -- pharmacokinetics KW - Herbicides -- analysis KW - Triazines -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78273646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography&rft.atitle=Thermospray+liquid+chromatographic-mass+spectrometric+method+for+the+analysis+of+metribuzin+and+its+metabolites.&rft.au=Parker%2C+C+E%3BGeeson%2C+A+V%3BGames%2C+D+E%3BRamsey%2C+E+D%3BAbusteit%2C+E+O%3BCorbin%2C+F+T%3BTomer%2C+K+B&rft.aulast=Parker&rft.aufirst=C&rft.date=1988-04-22&rft.volume=438&rft.issue=2&rft.spage=359&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-11 N1 - Date created - 1988-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Meeting Highlights: the biology of simian virus 40 and polyomavirus transformations. AN - 78140992; 2832617 JF - Journal of the National Cancer Institute AU - Schreier, A A AU - Gruber, J AD - Biological Carcinogenesis Branch, Division of Cancer Etiology, National Cancer Institute, Bethesda, Md. Y1 - 1988/04/20/ PY - 1988 DA - 1988 Apr 20 SP - 228 EP - 232 VL - 80 IS - 4 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - Cells, Cultured KW - Cell Transformation, Viral KW - Cell Transformation, Neoplastic KW - Simian virus 40 -- genetics KW - Polyomavirus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78140992?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Meeting+Highlights%3A+the+biology+of+simian+virus+40+and+polyomavirus+transformations.&rft.au=Schreier%2C+A+A%3BGruber%2C+J&rft.aulast=Schreier&rft.aufirst=A&rft.date=1988-04-20&rft.volume=80&rft.issue=4&rft.spage=228&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 - 1988-05-06 N1 - Date created - 1988-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of protein kinase C functional assays to clarify mechanisms of inhibitor action. AN - 78168653; 3162795 AB - The effects of inhibitors of protein kinase C on the activities of the intact enzyme, the proteolytically-generated catalytic domain, and [3H]phorbol 12,13-dibutyrate (PDBu) binding were compared in an effort to evaluate this approach for clarifying mechanisms of inhibitor action. Staurosporine, H-7 [1-(5-isoquinolinylsulfonyl)-2-methylpiperazine], and quercetin inhibited the catalytic fragment with similar potencies as for the intact enzyme while having little or no effect on binding, consistent with reports that they are competitive with ATP. Adriamycin, trifluoperazine, and tamoxifen, suggested to disrupt hydrophobic interactions between the regulatory domain of protein kinase C and phospholipid, were all most effective on the intact enzyme. They appear to possess a mixed mechanism, however, inhibiting activity of the catalytic domain with approximately 3-fold lower potencies. Gossypol inhibited intact enzyme, catalytic fragment, and PDBu binding with similar potencies. In light of multiple apparent sites of action for such protein kinase C inhibitors, comparison of their activities on the individual functional domains of the kinase may provide a useful complement to studies with the intact enzyme. JF - Biochemical pharmacology AU - Nakadate, T AU - Jeng, A Y AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04/15/ PY - 1988 DA - 1988 Apr 15 SP - 1541 EP - 1545 VL - 37 IS - 8 SN - 0006-2952, 0006-2952 KW - Histones KW - 0 KW - Phorbol Esters 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 - Phorbol Esters -- metabolism KW - Phosphorylation KW - Histones -- metabolism KW - Mice KW - Protein Binding KW - Hydrolysis KW - Catalysis KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78168653?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+protein+kinase+C+functional+assays+to+clarify+mechanisms+of+inhibitor+action.&rft.au=Nakadate%2C+T%3BJeng%2C+A+Y%3BBlumberg%2C+P+M&rft.aulast=Nakadate&rft.aufirst=T&rft.date=1988-04-15&rft.volume=37&rft.issue=8&rft.spage=1541&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 - 1988-05-17 N1 - Date created - 1988-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Survival patterns for malignant mesothelioma: the SEER experience. AN - 78168560; 3356487 AB - Statistical analyses of 1,475 histologically confirmed cases of malignant mesothelioma ascertained through the Surveillance, Epidemiology and End Results (SEER) Program of the National Cancer Institute for the years 1973-1984 showed age at diagnosis, sex, stage of disease, type of treatment, and geographic area of residence to be important predictors of patient survival, although type of treatment may be confounded with prognostic factors (patients selected for surgical treatment tended to have better performance status than other patients). Women below the age of 50 had an unusually long survival, even after adjustment for the effects of other variables in the model. A relatively large proportion of female cases had site of disease designated as peritoneum, but site was not a significant prognostic factor. These results suggest that age, gender and stage of disease should be carefully considered in designing and analyzing clinical trials for persons with mesothelioma. Survival was shorter in the 4 SEER registries which had shipbuilding as a major industry than in the others with less potential asbestos exposure, offering weak support for the hypothesis that asbestos-exposed cases of mesothelioma have worse survival experience than other cases. JF - International journal of cancer AU - Spirtas, R AU - Connelly, R R AU - Tucker, M A AD - National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04/15/ PY - 1988 DA - 1988 Apr 15 SP - 525 EP - 530 VL - 41 IS - 4 SN - 0020-7136, 0020-7136 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Age Factors KW - Sex Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Asbestos -- toxicity KW - Male KW - Female KW - Mesothelioma -- therapy KW - Mesothelioma -- etiology KW - Mesothelioma -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78168560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Survival+patterns+for+malignant+mesothelioma%3A+the+SEER+experience.&rft.au=Spirtas%2C+R%3BConnelly%2C+R+R%3BTucker%2C+M+A&rft.aulast=Spirtas&rft.aufirst=R&rft.date=1988-04-15&rft.volume=41&rft.issue=4&rft.spage=525&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 - 1988-05-17 N1 - Date created - 1988-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The lectin-like interaction between recombinant tumor necrosis factor and uromodulin. AN - 78164888; 3356692 AB - The polypeptide of uromodulin, an immunosuppressive glycoprotein isolated from human urine, has been shown to be identical to that of Tamm-Horsfall glycoprotein and is synthesized exclusively in the kidney (Hession, C., Decker, J. M., Sherblom, A. P., Kumar, S. (1987) Science 237, 1479-1484). Uromodulin binds recombinant murine interleukin 1 alpha with high affinity, and this binding can be inhibited by addition of specific saccharides (Muchmore, A. V., and Decker, J. M. (1987) J. Immunol. 138, 2541-2546). We now report that uromodulin binds recombinant human tumor necrosis factor (rTNF) with high affinity. Both diacetylchitobiose and Man(alpha 1-6)(Man(alpha 1-3]-Man-O-ethyl are effective inhibitors of the binding, whereas a wide variety of other saccharides are not inhibitory. Although Tamm-Horsfall glycoprotein contains predominantly tetraantennary N-linked chains, the binding to rTNF is unaffected by removal of terminal sialic acid, galactose, and N-acetylhexosamine residues. Fractionation of a Pronase digest of uromodulin by gel filtration yields material that inhibits the binding of uromodulin to rTNF but is of lower molecular weight than the major oligosaccharide. Uromodulin does not inhibit the cytotoxic activity of rTNF as monitored by lysis of tumor cell targets but effectively protects mice from lethal challenge with lipopolysaccharide, an event that may involve lymphokine toxicity. We have previously shown that rTNF binds to sections of human kidney and is localized in the same region as uromodulin. Thus, rTNF interacts with uromodulin via carbohydrate chains that are less processed than the major tetraantennary chain, and this interaction may be critical in promoting clearance and/or reducing toxicity of TNF and other lymphokines. JF - The Journal of biological chemistry AU - Sherblom, A P AU - Decker, J M AU - Muchmore, A V AD - Metabolism Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04/15/ PY - 1988 DA - 1988 Apr 15 SP - 5418 EP - 5424 VL - 263 IS - 11 SN - 0021-9258, 0021-9258 KW - Lectins KW - 0 KW - Lipopolysaccharides KW - Mucoproteins KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - UMOD protein, human KW - Umod protein, mouse KW - Uromodulin KW - Dactinomycin KW - 1CC1JFE158 KW - Pronase KW - EC 3.4.24.- KW - Index Medicus KW - Dactinomycin -- pharmacology KW - Animals KW - Chromatography, Gel KW - Electrophoresis, Polyacrylamide Gel KW - Lipopolysaccharides -- pharmacology KW - Kinetics KW - Humans KW - Mice KW - Pronase -- metabolism KW - Carbohydrate Conformation KW - Mucoproteins -- metabolism KW - Recombinant Proteins -- metabolism KW - Tumor Necrosis Factor-alpha -- metabolism KW - Lectins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78164888?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lectin-like+interaction+between+recombinant+tumor+necrosis+factor+and+uromodulin.&rft.au=Sherblom%2C+A+P%3BDecker%2C+J+M%3BMuchmore%2C+A+V&rft.aulast=Sherblom&rft.aufirst=A&rft.date=1988-04-15&rft.volume=263&rft.issue=11&rft.spage=5418&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 - 1988-05-23 N1 - Date created - 1988-05-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cerebrospinal fluid penetration of active metabolites of cyclophosphamide and ifosfamide in rhesus monkeys. AN - 78143668; 3349482 AB - The penetration of the active metabolites of cyclophosphamide (CP) and ifosfamide (IF) into cerebrospinal fluid (CSF) was determined in rhesus monkeys following an i.v. infusion of 1 gm/m2 of CP and IF. Active metabolites were measured using a high-performance liquid chromatography assay with fluorometric detection following derivatization with m-aminophenol. CSF to blood ratios of the active metabolites of CP and IF were found to be 0.17 and 0.13 following systemic dosing of CP and IF, respectively. The levels achieved in the CSF, however, were equivalent to levels known to be cytocidal to malignant cell lines derived from tumors which metastasize to the central nervous system. Only one animal demonstrated neurotoxicity with IF. CSF levels of active metabolite in this animal were similar to those observed in the other animals. JF - Cancer research AU - Arndt, C A AU - Balis, F M AU - McCully, C L AU - Colvin, O M AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04/15/ PY - 1988 DA - 1988 Apr 15 SP - 2113 EP - 2115 VL - 48 IS - 8 SN - 0008-5472, 0008-5472 KW - 4-hydroxycyclophosphamide KW - 1XBF4E50HS KW - 4-hydroxyifosfamide KW - 67292-64-2 KW - Cyclophosphamide KW - 8N3DW7272P KW - Ifosfamide KW - UM20QQM95Y KW - Index Medicus KW - Permeability KW - Animals KW - Macaca mulatta KW - Male KW - Cyclophosphamide -- cerebrospinal fluid KW - Cyclophosphamide -- analogs & derivatives KW - Ifosfamide -- metabolism KW - Ifosfamide -- blood KW - Cyclophosphamide -- blood KW - Ifosfamide -- cerebrospinal fluid KW - Ifosfamide -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78143668?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cerebrospinal+fluid+penetration+of+active+metabolites+of+cyclophosphamide+and+ifosfamide+in+rhesus+monkeys.&rft.au=Arndt%2C+C+A%3BBalis%2C+F+M%3BMcCully%2C+C+L%3BColvin%2C+O+M%3BPoplack%2C+D+G&rft.aulast=Arndt&rft.aufirst=C&rft.date=1988-04-15&rft.volume=48&rft.issue=8&rft.spage=2113&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 - 1988-05-12 N1 - Date created - 1988-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose-response study with N-nitrosomorpholine in drinking water of F-344 rats. AN - 78138252; 3349480 AB - A dose-response study in carcinogenesis was carried out with N-nitrosomorpholine in female F344 rats. The compound was administered in drinking water, which was supplied in controlled amounts of 20 ml per day per rat, 5 days a wk. At the two highest dose rates, 100 mg/liter and 40 mg/liter, treatment lasted 25 and 40 wk, respectively. At the other dose rates, which differed by a factor of 2.5, treatment lasted 50 or 100 wk. The average total dose received by each rat ranged from 250 mg to 0.7 mg. There were 100 animals per group at the lowest dose rates and 24 animals per group at the highest dose rates. Total doses of nitrosomorpholine above approximately 30 mg per rat caused a statistically significant decrease in survival, but at lower doses survival was similar to that of untreated controls. In nearly all of the treated groups there was a statistically significant increase in the incidence of benign or malignant hepatocellular neoplasms, with a highly significant dose-related trend. At the higher doses there was a significant incidence of hemangiosarcomas of the liver. Both hepatocellular carcinomas and hemangiosarcomas metastasized to the lungs and other organs. At the highest doses there was a significant incidence of neoplasms of the tongue and esophagus, which were rarely seen at the lower doses. The results suggest that even the lowest dose of nitrosomorpholine received by the rats, 0.7 mg or approximately 3 mg/kg body weight, was not a no-effect dose during the 2-yr lifetime of a rat. Probit analysis of the results indicate a dose estimated to cause tumors in 50% of the population of 25 mg nitrosomorpholine for liver neoplasms. JF - Cancer research AU - Lijinsky, W AU - Kovatch, R M AU - Riggs, C W AU - Walters, P T AD - National Cancer Institute-Frederick Cancer Research Facility, Biometics Research, Inc.-Basic Research Program, Maryland 21701. Y1 - 1988/04/15/ PY - 1988 DA - 1988 Apr 15 SP - 2089 EP - 2095 VL - 48 IS - 8 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - Nitrosamines KW - N-nitrosomorpholine KW - 3L25FO7FN7 KW - Index Medicus KW - Rats KW - Drinking KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Neoplasm Metastasis KW - Liver Neoplasms, Experimental -- chemically induced KW - Female KW - Nitrosamines -- toxicity KW - Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78138252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Dose-response+study+with+N-nitrosomorpholine+in+drinking+water+of+F-344+rats.&rft.au=Lijinsky%2C+W%3BKovatch%2C+R+M%3BRiggs%2C+C+W%3BWalters%2C+P+T&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1988-04-15&rft.volume=48&rft.issue=8&rft.spage=2089&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 - 1988-05-12 N1 - Date created - 1988-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A pediatric phase I and pharmacokinetic study of spirohydantoin mustard. AN - 78133450; 3349492 AB - A pediatric Phase I and pharmacokinetic study of the lipophilic alkylating agent spirohydantoin mustard (SHM) was conducted in 23 patients. The dose-limiting toxicity of SHM was neurological with disorientation, delirium, or hallucinations occurring in 9 of 23 patients. These symptoms were partially reversible and preventable with physostigmine. In 17 patients who were evaluable for response to treatment (14 of whom had central nervous system malignancies), no objective tumor responses were observed. Pharmacokinetic evaluation of SHM revealed a t1/2 alpha of 1.7 +/- 0.7 min, t1/2 beta of 16 +/- 8.3 min, and total body clearance of 2134 +/- 735 ml/min/m2. Measureable peak plasma levels were less than 40% of that which produces cytotoxicity in vitro against monolayer cultures of rat 9L brain tumor. Over 90% of SHM was protein bound, greatly limiting the free drug available for central nervous system penetration. SHM cerebrospinal fluid to plasma ratios were less than 0.047. The above suggests that in spite of its lipophilicity, SHM may not reach clinically significant levels in the central nervous system at clinically tolerable doses. JF - Cancer research AU - Heideman, R L AU - Kelley, J A AU - Packer, R J AU - Reaman, G H AU - Roth, J S AU - Balis, F AU - Ettinger, L J AU - Doherty, K M AU - Jeffries, S L AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04/15/ PY - 1988 DA - 1988 Apr 15 SP - 2292 EP - 2295 VL - 48 IS - 8 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - Hydantoins KW - Nitrogen Mustard Compounds KW - Physostigmine KW - 9U1VM840SP KW - spiromustine KW - J3HB83X76Z KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Nervous System -- drug effects KW - Adult KW - Child KW - Adolescent KW - Protein Binding KW - Physostigmine -- therapeutic use KW - Male KW - Female KW - Child, Preschool KW - Hydantoins -- adverse effects KW - Nitrogen Mustard Compounds -- adverse effects KW - Hydantoins -- pharmacokinetics KW - Antineoplastic Agents -- pharmacokinetics KW - Nitrogen Mustard Compounds -- pharmacokinetics KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78133450?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pediatric+phase+I+and+pharmacokinetic+study+of+spirohydantoin+mustard.&rft.au=Heideman%2C+R+L%3BKelley%2C+J+A%3BPacker%2C+R+J%3BReaman%2C+G+H%3BRoth%2C+J+S%3BBalis%2C+F%3BEttinger%2C+L+J%3BDoherty%2C+K+M%3BJeffries%2C+S+L%3BPoplack%2C+D+G&rft.aulast=Heideman&rft.aufirst=R&rft.date=1988-04-15&rft.volume=48&rft.issue=8&rft.spage=2292&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 - 1988-05-12 N1 - Date created - 1988-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The partial dopamine receptor agonist terguride in the MPTP-induced hemiparkinsonian monkey model. AN - 78269845; 3260191 AB - The partial dopamine agonist terguride (transdihydrolisuride) administered to four 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioned hemiparkinsonian monkeys (at a dose of 4 mg/kg orally) induced marked contralateral turning that lasted 3.5 h. The 6-n-propyl derivative of terguride (proterguride) given to two monkeys (at a dose of 0.4 mg/kg orally) caused contralateral turning which lasted for more than 24 h but produced side effects such as dyskinesia and stereotype. After terguride treatment, cerebrospinal fluid concentrations of 3-methoxy-4-hydroxy-phenylglycol (MHPG) were increased, whereas concentrations of the metabolites dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) were not significantly altered. JF - European journal of pharmacology AU - Brücke, T AU - Bankiewicz, K AU - Harvey-White, J AU - Kopin, I AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/04/13/ PY - 1988 DA - 1988 Apr 13 SP - 445 EP - 448 VL - 148 IS - 3 SN - 0014-2999, 0014-2999 KW - Ergolines KW - 0 KW - Pyridines KW - Receptors, Dopamine KW - dironyl KW - 21OJT43Q88 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Lisuride KW - E0QN3D755O KW - Index Medicus KW - Animals KW - Macaca fascicularis KW - Disease Models, Animal KW - Female KW - Parkinson Disease, Secondary -- physiopathology KW - Parkinson Disease, Secondary -- chemically induced KW - Receptors, Dopamine -- physiology KW - Lisuride -- analogs & derivatives KW - Ergolines -- pharmacology KW - Lisuride -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78269845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=The+partial+dopamine+receptor+agonist+terguride+in+the+MPTP-induced+hemiparkinsonian+monkey+model.&rft.au=Br%C3%BCcke%2C+T%3BBankiewicz%2C+K%3BHarvey-White%2C+J%3BKopin%2C+I&rft.aulast=Br%C3%BCcke&rft.aufirst=T&rft.date=1988-04-13&rft.volume=148&rft.issue=3&rft.spage=445&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 - 1988-08-11 N1 - Date created - 1988-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Measurement of cytotoxicity by target cell release and retention of the fluorescent dye bis-carboxyethyl-carboxyfluorescein (BCECF). AN - 78159245; 3258339 AB - In order to utilize a newly available scanning microfluorimeter for lymphocyte-mediated cytotoxicity assays, a number of commercially available fluorescent dyes were compared for their suitability as target cell markers. One of them, bis-carboxyethyl-carboxyfluorescein (BCEFCF), was useful for assays with about 10(4) target cells and showed substantially less spontaneous leakage than other fluorescein derivatives, while still leaking more rapidly than 51Cr. For short cytotoxicity incubations (less than 2 h) with cytotoxic T lymphocytes (CTL), the corrected percentage BCECF release into the supernatant parallels that of 51Cr. For 4 h assays cytotoxicity could be quantitated by measuring the BCECF retained by target cells. Using human CTL and natural killer (NK) cells as effectors, with a variety of lymphoid cells and fibroblasts as targets in 4 h assays, the BCECF retention technique was found to give cytotoxicity values comparable to the 51Cr release assay. Cytotoxicity assays measuring BCECF fluorescence in microtiter wells with the scanning microfluorimeter offer advantages of safety, economy, and processing time compared with the 51Cr release assay. JF - Journal of immunological methods AU - Kolber, M A AU - Quinones, R R AU - Gress, R E AU - Henkart, P A AD - Immunology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04/06/ PY - 1988 DA - 1988 Apr 06 SP - 255 EP - 264 VL - 108 IS - 1-2 SN - 0022-1759, 0022-1759 KW - Chromium Radioisotopes KW - 0 KW - Fluoresceins KW - Fluorescent Dyes KW - Receptors, Antigen, T-Cell KW - 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein KW - 85138-49-4 KW - Index Medicus KW - Animals KW - Antibody-Dependent Cell Cytotoxicity KW - Humans KW - Chromium Radioisotopes -- metabolism KW - Mice KW - Receptors, Antigen, T-Cell -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology KW - T-Lymphocytes, Cytotoxic -- metabolism KW - T-Lymphocytes, Cytotoxic -- analysis KW - Tumor Cells, Cultured KW - Killer Cells, Natural -- analysis KW - Killer Cells, Natural -- metabolism KW - Cell Line KW - Cell-Free System KW - Fluorescent Dyes -- analysis KW - Cytotoxicity Tests, Immunologic -- methods KW - Fluoresceins -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78159245?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunological+methods&rft.atitle=Measurement+of+cytotoxicity+by+target+cell+release+and+retention+of+the+fluorescent+dye+bis-carboxyethyl-carboxyfluorescein+%28BCECF%29.&rft.au=Kolber%2C+M+A%3BQuinones%2C+R+R%3BGress%2C+R+E%3BHenkart%2C+P+A&rft.aulast=Kolber&rft.aufirst=M&rft.date=1988-04-06&rft.volume=108&rft.issue=1-2&rft.spage=255&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunological+methods&rft.issn=00221759&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-05-11 N1 - Date created - 1988-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Energy requirements for diphtheria toxin translocation are coupled to the maintenance of a plasma membrane potential and a proton gradient. AN - 78156115; 3350812 AB - Translocation of diphtheria toxin (DT) or ricin to the cytosol is the rate-limiting step responsible for (pseudo) first-order decline in protein synthesis observed in intoxicated cell populations. The requirements for energy utilization in the translocation of both toxins are examined by perturbing the intoxication during this period of protein synthesis decline. Translocation of either toxin is blocked at 4 degrees C and requires energy. Ricin translocation is tightly coupled to ATP hydrolysis with no involvement of membrane potential. Cell depolarization slows the rate of DT translocation but does not block completely. Elimination of transmembrane pH gradients alone does not affect DT translocation; however, in combination with depolarization, translocation is blocked virtually completely. Energy requirements for DT intoxication are mediated by establishing a plasma membrane potential and a pH gradient across some cellular membrane. It is proposed that a postendocytotic vesicle containing processed DT fuses with the plasma membrane. Either component of the proton motive force across the plasma membrane then drives DT translocation. Ricin apparently utilizes a different energy coupling mechanism at a different intracellular site, thus demonstrating toxin specificity in the translocation mechanism. JF - The Journal of biological chemistry AU - Hudson, T H AU - Scharff, J AU - Kimak, M A AU - Neville, D M AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/04/05/ PY - 1988 DA - 1988 Apr 05 SP - 4773 EP - 4781 VL - 263 IS - 10 SN - 0021-9258, 0021-9258 KW - Azides KW - 0 KW - Diphtheria Toxin KW - Ammonium Chloride KW - 01Q9PC255D KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Deoxyglucose KW - 9G2MP84A8W KW - Potassium KW - RWP5GA015D KW - Index Medicus KW - Animals KW - Kinetics KW - Hydrogen-Ion Concentration KW - Adenosine Triphosphate -- metabolism KW - Azides -- pharmacology KW - Potassium -- pharmacology KW - Membrane Potentials KW - Vero Cells KW - Deoxyglucose -- pharmacology KW - Ammonium Chloride -- pharmacology KW - Models, Biological KW - Cell Membrane -- drug effects KW - Diphtheria Toxin -- metabolism KW - Cell Membrane -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78156115?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Energy+requirements+for+diphtheria+toxin+translocation+are+coupled+to+the+maintenance+of+a+plasma+membrane+potential+and+a+proton+gradient.&rft.au=Hudson%2C+T+H%3BScharff%2C+J%3BKimak%2C+M+A%3BNeville%2C+D+M&rft.aulast=Hudson&rft.aufirst=T&rft.date=1988-04-05&rft.volume=263&rft.issue=10&rft.spage=4773&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 - 1988-05-02 N1 - Date created - 1988-05-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol esters and diacylglycerols amplify bradykinin-stimulated prostaglandin synthesis in Swiss 3T3 fibroblasts. Possible independence from protein kinase C. AN - 78152565; 3162455 AB - When Swiss 3T3 fibroblasts were incubated with bradykinin, prostaglandin E2 (PGE2) synthesis was stimulated. Phorbol esters or the diacylglycerol analog 1-oleoyl-2-acetylglycerol (OAG), by themselves, did not acutely stimulate PGE2 synthesis. However, when cells were preincubated with phorbol esters or OAG, bradykinin-stimulated PGE2 synthesis was potentiated markedly. When phorbol esters and OAG were added together, bradykinin-stimulated PGE2 synthesis was potentiated in an additive manner. When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations. Further, the protein kinase C antagonist, H-7, only slightly inhibited phorbol ester or OAG amplification of bradykinin-stimulated PGE2 synthesis. The possibility is raised that diacylglycerol, formed in response to many receptors, may serve as a transducer of receptor-receptor interactions. Since desensitization or inhibition of protein kinase C only partially reduced the amplification of bradykinin-stimulated PGE2 synthesis by phorbol esters or OAG, the possibility is raised that diacylglycerol mimetics may have actions in addition to activation of protein kinase C. JF - The Journal of biological chemistry AU - Burch, R M AU - Ma, A L AU - Axelrod, J AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1988/04/05/ PY - 1988 DA - 1988 Apr 05 SP - 4764 EP - 4767 VL - 263 IS - 10 SN - 0021-9258, 0021-9258 KW - Diglycerides KW - 0 KW - Glycerides KW - Prostaglandins E KW - 1-oleoyl-2-acetylglycerol KW - 86390-77-4 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Dinoprostone KW - K7Q1JQR04M KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Bradykinin KW - S8TIM42R2W KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Kinetics KW - Mice KW - Protein Kinase C -- metabolism KW - Diglycerides -- pharmacology KW - Prostaglandins E -- biosynthesis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Bradykinin -- pharmacology KW - Glycerides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78152565?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phorbol+esters+and+diacylglycerols+amplify+bradykinin-stimulated+prostaglandin+synthesis+in+Swiss+3T3+fibroblasts.+Possible+independence+from+protein+kinase+C.&rft.au=Burch%2C+R+M%3BMa%2C+A+L%3BAxelrod%2C+J&rft.aulast=Burch&rft.aufirst=R&rft.date=1988-04-05&rft.volume=263&rft.issue=10&rft.spage=4764&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 - 1988-05-02 N1 - Date created - 1988-05-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The rat P450IIE1 gene: complete intron and exon sequence, chromosome mapping, and correlation of developmental expression with specific 5' cytosine demethylation. AN - 78144542; 2832413 AB - The gene coding for the ethanol-inducible, developmentally regulated P450IIE1 was isolated from an lambda EMBL 3 rat genomic library and completely sequenced. The gene spanned 10,373 base pairs and contained nine exons. Upstream and downstream DNA of 1530 and 825 base pairs, respectively, was also sequenced, and the transcription start site was identified by both S1 mapping and primer extension. A typical TATA box was found just upstream of the start site; however, no CCAAT box was apparent. Other repetitive sequences were identified including a partial R.dre.1 sequence upstream of the gene and a long stretch of 160 alternating purines in the second intron. This latter repetitive element is found in many mammalian genes. By use of a panel of mouse-hamster somatic cell hybrids, the P450IIE1 gene was localized to mouse chromosome 7. The hepatic P450IIE1 gene is transcriptionally activated within 1 day after birth and reaches a maximal level of expression at 6 days of age. Using restriction endonuclease sites generated from the gene sequence data and the cytosine methylation-sensitive enzymes HhaI and HpaII, we found that this transcriptional activation during early development is coincident with specific demethylation only at the 5' end of the P450IIE1 gene. Interestingly, other cytosine residues in the middle of the gene became demethylated as rats aged from 1 to 10 weeks, at which time no changes in gene expression occur. JF - The Journal of biological chemistry AU - Umeno, M AU - Song, B J AU - Kozak, C AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04/05/ PY - 1988 DA - 1988 Apr 05 SP - 4956 EP - 4962 VL - 263 IS - 10 SN - 0021-9258, 0021-9258 KW - Cytosine KW - 8J337D1HZY KW - NADPH-Ferrihemoprotein Reductase KW - EC 1.6.2.4 KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - Index Medicus KW - Rats KW - Animals KW - Liver -- enzymology KW - Base Sequence KW - Molecular Sequence Data KW - Transcription, Genetic KW - Mice KW - Amino Acid Sequence KW - Methylation KW - Cloning, Molecular KW - NADPH-Ferrihemoprotein Reductase -- genetics KW - Genes KW - Exons KW - Introns KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78144542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+rat+P450IIE1+gene%3A+complete+intron+and+exon+sequence%2C+chromosome+mapping%2C+and+correlation+of+developmental+expression+with+specific+5%27+cytosine+demethylation.&rft.au=Umeno%2C+M%3BSong%2C+B+J%3BKozak%2C+C%3BGelboin%2C+H+V%3BGonzalez%2C+F+J&rft.aulast=Umeno&rft.aufirst=M&rft.date=1988-04-05&rft.volume=263&rft.issue=10&rft.spage=4956&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 - 1988-05-02 N1 - Date created - 1988-05-02 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M20131; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cross-sectional tongue shape during the production of vowels. AN - 85169432; pmid-3286710 AB - This study used ultrasound imaging to examine the cross-sectional shape of the tongue during the production of the ten English vowels ( see text ) in two consonant contexts--/p/ and /s/--and at two scan angles--anterior and posterior. Results were compared with models of sagittal tongue shape. A newly built transducer holder and head restraint maintained the ultrasound transducer in a fixed position inferior to the mandible at a chosen location and angle. The transducer was free to move only in a superior/inferior direction, and demonstrated reliable tracking of the jaw. Since the tongue is anisotrophic along its length, anterior and posterior scan angles were examined to identify differences in tongue shape. Similarly, the coarticulatory effects of the sibilant /s/ versus the bilabial /p/ were examined, to assess variability of intrinsic tongue shape for the vowels. Results showed that the subject's midsagittal tongue grooving was almost universal for the vowels. Posterior grooves were deeper than anterior grooves. In /s/ context, posterior tongue grooves were shallower than in /p/ context. Anteriorly, /s/ context caused deeper grooves for low vowels. Cross-sectional tongue shape varied with tongue position similarly to sagittal tongue shape. JF - The Journal of the Acoustical Society of America AU - Stone, M AU - Shawker, T H AU - Talbot, T L AU - Rich, A H AD - Department of Rehabilitation Medicine, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. PY - 1988 SP - 1586 EP - 1596 VL - 83 IS - 4 SN - 0001-4966, 0001-4966 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85169432?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+the+Acoustical+Society+of+America&rft.atitle=Cross-sectional+tongue+shape+during+the+production+of+vowels.&rft.au=Stone%2C+M%3BShawker%2C+T+H%3BTalbot%2C+T+L%3BRich%2C+A+H&rft.aulast=Stone&rft.aufirst=M&rft.date=1988-04-01&rft.volume=83&rft.issue=4&rft.spage=1586&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+the+Acoustical+Society+of+America&rft.issn=00014966&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Short-term effects of i.v. injected murine 99MTc-F(ab')2 fragments of an anti-melanoma antibody (HMW-MAA 225.28 S) on haemato-immunological parameters in patients with melanoma. AN - 78751665; 3243979 AB - To evaluate alterations induced by injected murine radiolabelled F(ab')2 fragments of the anti HMW-MAA MoAb 225.28S on the principal haemato-immunological parameters, 32 patients with advanced malignant melanoma were studied. No statistically significant change was found after MoAb administration, but monocytes (3 h after injection) and granular eosinophils (24 h after) were reduced and circulating immune complexes increased (3 h after). No toxic effect or adverse reaction was observed. Therefore, the controlled administration of purified MoAb fragments for diagnostic purposes seems to involve only a very low risk of immediate adverse reactions. JF - The International journal of biological markers AU - Castello, G AU - Mansi, L AU - Leonardi, E AU - Lastoria, S AU - Melillo, G AD - Dept. of Haematology and Immunology, National Cancer Institute, Napoli, Italy. PY - 1988 SP - 140 EP - 144 VL - 3 IS - 2 SN - 0393-6155, 0393-6155 KW - Antibodies, Monoclonal KW - 0 KW - Antigen-Antibody Complex KW - Antigens, Neoplasm KW - Biomarkers, Tumor KW - Immunoglobulin Fab Fragments KW - Melanoma-Specific Antigens KW - Neoplasm Proteins KW - Technetium KW - 7440-26-8 KW - Index Medicus KW - Animals KW - Injections, Intravenous KW - Humans KW - Aged KW - Mice KW - Blood Cell Count KW - Antibodies, Monoclonal -- immunology KW - Adult KW - Middle Aged KW - Antigen-Antibody Complex -- analysis KW - Adolescent KW - Female KW - Male KW - Immunoglobulin Fab Fragments -- administration & dosage KW - Biomarkers, Tumor -- immunology KW - Neoplasm Proteins -- immunology KW - Melanoma -- blood KW - Melanoma -- immunology KW - Melanoma -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78751665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+International+journal+of+biological+markers&rft.atitle=Short-term+effects+of+i.v.+injected+murine+99MTc-F%28ab%27%292+fragments+of+an+anti-melanoma+antibody+%28HMW-MAA+225.28+S%29+on+haemato-immunological+parameters+in+patients+with+melanoma.&rft.au=Castello%2C+G%3BMansi%2C+L%3BLeonardi%2C+E%3BLastoria%2C+S%3BMelillo%2C+G&rft.aulast=Castello&rft.aufirst=G&rft.date=1988-04-01&rft.volume=3&rft.issue=2&rft.spage=140&rft.isbn=&rft.btitle=&rft.title=The+International+journal+of+biological+markers&rft.issn=03936155&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1989-05-26 N1 - Date created - 1989-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Deficient polymerization in vitro of a point-mutated beta-actin expressed in a transformed human fibroblast cell line. AN - 78445158; 2971650 AB - HUT-14 cells, tumorigenic human fibroblasts, express a mutant beta-actin which has a single amino acid substitution at position 244 (glycine to aspartic acid), in addition to normal beta- and gamma-actin. In order to characterize the biochemical function of the mutant beta-actin, actins were extracted and purified from HUT-14 cells. The partially purified actin fraction contained beta-, gamma-, and mutant beta-actins in the ratio of 1:1:1, the same ratio as in the cells. When the actin of this fraction was purified through a polymerization step, mutant beta-actin was always less incorporated into actin filaments than beta- and gamma-actin. When the polymerization ability of purified HUT-14 actins was examined by sedimentation technique, it was lower than those of muscle and of cytoplasmic actins from another human cell line (HUT-11) which expresses only normal beta- and gamma-actin, in the ratio of 2:1. The deficient polymerization of mutant beta-actin was also observed by examining the ratio of beta-, gamma-, and mutant beta-actins incorporated into actin filaments. The ratio of mutant beta-actin in polymerized actins under all conditions examined was always less than that before polymerization. These results indicate that the single amino acid substitution at position 244 caused the reduction of incorporation of the mutant beta-actin into actin filaments in vitro. JF - Journal of biochemistry AU - Taniguchi, S AU - Sagara, J AU - Kakunaga, T AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 707 EP - 713 VL - 103 IS - 4 SN - 0021-924X, 0021-924X KW - Actins KW - 0 KW - Biopolymers KW - Adenosine Triphosphatases KW - EC 3.6.1.- KW - Index Medicus KW - Phenotype KW - Biopolymers -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Adenosine Triphosphatases -- metabolism KW - Cell Line, Transformed KW - Mutation KW - Isoelectric Focusing KW - Fibroblasts KW - Actins -- genetics KW - Actins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78445158?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biochemistry&rft.atitle=Deficient+polymerization+in+vitro+of+a+point-mutated+beta-actin+expressed+in+a+transformed+human+fibroblast+cell+line.&rft.au=Taniguchi%2C+S%3BSagara%2C+J%3BKakunaga%2C+T&rft.aulast=Taniguchi&rft.aufirst=S&rft.date=1988-04-01&rft.volume=103&rft.issue=4&rft.spage=707&rft.isbn=&rft.btitle=&rft.title=Journal+of+biochemistry&rft.issn=0021924X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-11-08 N1 - Date created - 1988-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of platinum levels in plasma, urine, and kidney on blood urea nitrogen levels after cisplatin injection in rats. AN - 78395170; 3411443 AB - To analyze the relationship between the kinetics of filterable Pt and nephrotoxicity after cisplatin injection, Sprague-Dawley rats were given 5 mg/kg of i.v. cisplatin during hypothermia (hypothermia group) or given 5 mg/kg of cisplatin preincubated with rat serum (preincubation group). Plasma Pt levels, kidney Pt contents, urinary excretion of Pt, and blood urea nitrogen (BUN) levels after cisplatin injection were then determined. These hypothermia and preincubation treatments were performed in order to change the kinetics of filterable Pt without changing the total dose of cisplatin. Plasma Pt levels were significantly changed by both hypothermia or preincubation. Urinary excretion of Pt was unaffected by hypothermia but was significantly reduced by preincubation. However, significant differences in BUN elevation were not observed either in the hypothermia group or the preincubation group relative to the control group. Kidney Pt contents were not affected by hypothermia or preincubation at 1 h, 6 h, and 24 h after cisplatin injection. When rats were injected i.v. with 5, 7, or 10 mg/kg cisplatin, dose-related increases were observed both in kidney Pt contents and in BUN levels. These results suggest that the degree of nephrotoxicity more accurately correlates with renal Pt content rather than with plasma Pt levels or urinary concentration of Pt, and that the role of filterable Pt species in producing nephrotoxicity may have to be reevaluated. JF - Journal of pharmacobio-dynamics AU - Uozumi, J AU - Litterst, C L AD - Division of Cancer Treatment National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 277 EP - 283 VL - 11 IS - 4 SN - 0386-846X, 0386-846X KW - Platinum KW - 49DFR088MY KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Kidney -- metabolism KW - Protein Binding -- drug effects KW - In Vitro Techniques KW - Hypothermia, Induced KW - Female KW - Cisplatin -- pharmacokinetics KW - Platinum -- metabolism KW - Platinum -- blood KW - Platinum -- urine KW - Blood Urea Nitrogen UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78395170?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmacobio-dynamics&rft.atitle=The+effects+of+platinum+levels+in+plasma%2C+urine%2C+and+kidney+on+blood+urea+nitrogen+levels+after+cisplatin+injection+in+rats.&rft.au=Uozumi%2C+J%3BLitterst%2C+C+L&rft.aulast=Uozumi&rft.aufirst=J&rft.date=1988-04-01&rft.volume=11&rft.issue=4&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Journal+of+pharmacobio-dynamics&rft.issn=0386846X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-11 N1 - Date created - 1988-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The treatment of indolent lymphomas: watchful waiting v aggressive combined modality treatment. AN - 78338714; 2456618 AB - Patients with advanced indolent lymphoma often have long survival (median, 4 to 8 years) in spite of frequent relapses. The inability of combination chemotherapy or radiation therapy (RT) to render patients disease free has led to radically divergent treatment approaches. Initial treatment may vary from aggressive combined modality therapy to no initial treatment. We sought to evaluate these two divergent approaches in a randomized trial of advanced indolent lymphomas (nodular, poorly differentiated lymphocytic; nodular mixed; diffuse, well-differentiated lymphocytic; diffuse, intermediately differentiated lymphocytic; and diffuse, poorly differentiated lymphocytic). A total of 104 patients were entered: 44 were randomly assigned to "watch and wait" in which only carefully defined, limited RT was administered if necessary; 45 were randomly assigned to aggressive combined modality treatment with prednisone, methotrexate, doxorubicin, cyclophosphamide, plus etoposide plus mechlorethamine, vincristine, procarbazine, prednisone (ProMACE-MOPP), followed by total nodal irradiation (TNI); and 15, with symptoms requiring initial therapy, received the identical combined treatment but were not randomly assigned. Of 41 evaluable patients on watch and wait, 23 (56%) have still not required systemic therapy, although 16 (39%) have received limited RT. Median time to crossover was 34 months. Of 18 patients crossed over, seven of the 16 who completed therapy (43%) achieved CR; two (11%) have relapsed. Histologic progression was seen in six (15%) of 41 patients on watch and wait without intervening chemotherapy. Of 45 patients randomly assigned to chemotherapy, 37 (82%) have completed induction therapy, and 29 of the 37 (78%) achieved CR. Twenty-five of those 29 patients (86%) are still in their first remission. Median duration of initial remission has not been reached but will exceed 4 years.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Seminars in hematology AU - Young, R C AU - Longo, D L AU - Glatstein, E AU - Ihde, D C AU - Jaffe, E S AU - DeVita, V T AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20894. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 11 EP - 16 VL - 25 IS - 2 Suppl 2 SN - 0037-1963, 0037-1963 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 - Leucovorin KW - Q573I9DVLP KW - Prednisone KW - VB0R961HZT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Neoplasms, Multiple Primary -- etiology KW - Cyclophosphamide -- administration & dosage KW - Mechlorethamine -- administration & dosage KW - Neoplasms, Radiation-Induced -- etiology KW - Random Allocation KW - Combined Modality Therapy KW - Humans KW - Leucovorin -- administration & dosage KW - Leukemia, Radiation-Induced -- etiology KW - Vincristine -- administration & dosage KW - Palliative Care KW - Doxorubicin -- administration & dosage KW - Evaluation Studies as Topic KW - Procarbazine -- administration & dosage KW - Etoposide -- administration & dosage KW - Lymph Nodes -- radiation effects KW - Leukemia -- etiology KW - Methotrexate -- administration & dosage KW - Prednisone -- administration & dosage KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Lymphoma, Non-Hodgkin -- therapy KW - Lymphoma, Non-Hodgkin -- radiotherapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78338714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+hematology&rft.atitle=The+treatment+of+indolent+lymphomas%3A+watchful+waiting+v+aggressive+combined+modality+treatment.&rft.au=Young%2C+R+C%3BLongo%2C+D+L%3BGlatstein%2C+E%3BIhde%2C+D+C%3BJaffe%2C+E+S%3BDeVita%2C+V+T&rft.aulast=Young&rft.aufirst=R&rft.date=1988-04-01&rft.volume=25&rft.issue=2+Suppl+2&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Seminars+in+hematology&rft.issn=00371963&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-26 N1 - Date created - 1988-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - High pressure liquid chromatography methods for separation of omega- and (omega-1)-hydroxy fatty acids: their applications to microsomal fatty acid omega-oxidation. AN - 78298696; 3133959 AB - Fatty acids (C12-C18) and their omega- and (omega-1)-hydroxy derivatives, when converted to p-bromophenacyl (PBP) esters, can be completely separated from one another by high pressure liquid chromatography (HPLC) on a silicic acid column using 0.5% (v/v) isopropanol in n-hexane. In this system, fatty acid PBP esters are eluted at the solvent front, whereas the retention times of the omega- and (omega-1)-hydroxy derivatives are 14-20 and 24-29 min, respectively. The PBP esters can also be separated by reverse phase HPLC on a muBondapak C18 column, a method which has been developed by Fan et al. (Fan, L. L., Masters, B. S. S., and Prough, R. A. (1976) Anal. Biochem. 71, 265-272) for separation of methyl esters of fatty acids and their omega- and (omega-1)-hydroxy derivatives. In the latter method, however, the retention times of omega- and (omega-1)-hydroxy derivatives are only about 2 min apart and an increase in the solvent polarity is needed for elution of the esters of unmodified fatty acids. Fatty acid PBP esters, however, can be obtained as independent peaks which are not disturbed by the solvent front. An application of the former method to measure fatty acid omega oxidation by liver microsomes and by a reconstituted monooxygenase system containing purified cytochrome P-450 is described. JF - Analytical biochemistry AU - Aoyama, T AU - Sato, R AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 73 EP - 82 VL - 170 IS - 1 SN - 0003-2697, 0003-2697 KW - Hydroxy Acids KW - 0 KW - Palmitic Acids KW - Phenols KW - Palmitic Acid KW - 2V16EO95H1 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Oxygenases KW - EC 1.13.- KW - Cytochrome P-450 CYP4A KW - EC 1.14.15.3 KW - 4-bromophenol KW - LAO4J0183I KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Mixed Function Oxygenases -- metabolism KW - Palmitic Acids -- metabolism KW - Oxygenases -- analysis KW - Cytochrome P-450 Enzyme System -- metabolism KW - Rabbits KW - Phenols -- analysis KW - Chromatography, High Pressure Liquid KW - Hydroxy Acids -- analysis KW - Microsomes, Liver -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78298696?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=High+pressure+liquid+chromatography+methods+for+separation+of+omega-+and+%28omega-1%29-hydroxy+fatty+acids%3A+their+applications+to+microsomal+fatty+acid+omega-oxidation.&rft.au=Aoyama%2C+T%3BSato%2C+R&rft.aulast=Aoyama&rft.aufirst=T&rft.date=1988-04-01&rft.volume=170&rft.issue=1&rft.spage=73&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 - 1988-07-29 N1 - Date created - 1988-07-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lesions of testis and epididymis associated with prenatal diethylstilbestrol exposure. AN - 78270544; 3289905 AB - Cryptorchidism and retention of Müllerian duct structures occur with high frequency among the male offspring of CD-1 mice treated with 100 micrograms diethylstilbestrol/kg body weight on days 9 through 16 of pregnancy. Hyperplasia of the rete testis and Müllerian duct structures were found in many of the DES-treated male mice, as was a low but significant number of reproductive tract neoplasms. JF - Environmental health perspectives AU - Bullock, B C AU - Newbold, R R AU - McLachlan, J A AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 29 EP - 31 VL - 77 SN - 0091-6765, 0091-6765 KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Animals KW - Mice KW - Testicular Neoplasms -- chemically induced KW - Male KW - Female KW - Pregnancy KW - Testis -- drug effects KW - Diethylstilbestrol -- toxicity KW - Epididymis -- drug effects KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78270544?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Lesions+of+testis+and+epididymis+associated+with+prenatal+diethylstilbestrol+exposure.&rft.au=Bullock%2C+B+C%3BNewbold%2C+R+R%3BMcLachlan%2C+J+A&rft.aulast=Bullock&rft.aufirst=B&rft.date=1988-04-01&rft.volume=77&rft.issue=&rft.spage=29&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 - 1988-08-10 N1 - Date created - 1988-08-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1975 Dec 5;190(4218):991-2 [242076] Annu Rev Physiol. 1984;46:53-65 [6324662] Endocrinology. 1984 Nov;115(5):1863-8 [6489263] Cancer Res. 1985 Oct;45(10):5145-50 [4027990] J Urol. 1987 Dec;138(6):1446-50 [3682076] Physiol Rev. 1986 Oct;66(4):1038-90 [3532142] Am J Pathol. 1986 Dec;125(3):625-8 [3799821] Teratog Carcinog Mutagen. 1987;7(4):377-89 [2888216] Physiol Rev. 1986 Jan;66(1):71-117 [3511481] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transplantation characteristics, morphologic features, and interpretation of preputial gland neoplasia in the Fischer 344 rat. AN - 78269602; 3383821 AB - Preputial gland neoplasms in the Fischer 344 rat are relatively uncommon tumors with a prevalence of approximately 3% in the National Toxicology Program data base. They occur late in life, are well differentiated, and rarely metastasize. Based on studies through 4 serial passages, 10 well-differentiated preputial gland neoplasms transplanted into the mammary fat pads of syngeneic recipients grew to 30 mm within 10 weeks. Recipients died or were sacrificed with large transplanted tumors within 6 months. The morphologic features of the transplanted neoplasms were similar to those of the primary neoplasms through the four passages. Proliferative lesions of the preputial glands comprise a morphological continuum and separation of these growths into categories of hyperplasia, adenoma, and carcinomas is based largely on cytological features and the degree of altered growth patterns. Morphologic features to assist in diagnosis of preputial gland neoplasms and recommendations for interpreting treatment-associated increases of these neoplasms are presented. JF - Environmental health perspectives AU - Maronpot, R R AU - Ulland, B AU - Mennear, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 33 EP - 36 VL - 77 SN - 0091-6765, 0091-6765 KW - Index Medicus KW - Rats KW - Neoplasm Transplantation KW - Animals KW - Male KW - Rats, Inbred Strains KW - Rats, Inbred F344 KW - Penile Neoplasms -- classification KW - Penile Neoplasms -- pathology KW - Penile Neoplasms -- veterinary KW - Rodent Diseases -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78269602?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transplantation+characteristics%2C+morphologic+features%2C+and+interpretation+of+preputial+gland+neoplasia+in+the+Fischer+344+rat.&rft.au=Maronpot%2C+R+R%3BUlland%2C+B%3BMennear%2C+J&rft.aulast=Maronpot&rft.aufirst=R&rft.date=1988-04-01&rft.volume=77&rft.issue=&rft.spage=33&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 - 1988-08-10 N1 - Date created - 1988-08-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Endocrinology. 1972 Apr;90(4):903-8 [4334700] Anat Rec. 1963 May;146:47-59 [13970013] J Endocrinol. 1972 Nov;55(2):449-50 [4673881] J Reprod Fertil. 1974 May;38(1):91-6 [4858355] Histochem J. 1974 Nov;6(6):685-92 [4448702] J Gerontol. 1977 May;32(3):258-78 [66246] J Invest Dermatol. 1979 Mar;72(3):120-7 [422875] Lab Anim Sci. 1980 Oct;30(5):845-50 [7431866] Vet Pathol. 1981 Mar;18(2):228-38 [7467083] Cancer Res. 1984 Jun;44(6):2608-15 [6722797] Lab Invest. 1985 Aug;53(2):200-8 [4021445] Cancer Res. 1985 Sep;45(9):4301-7 [4028016] J Natl Cancer Inst. 1986 Feb;76(2):283-9 [3456066] J Exp Zool. 1960 Mar;143:153-73 [13688332] Biol Reprod. 1972 Apr;6(2):219-23 [5016868] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Proliferative lesions in the male reproductive system of F344 rats and B6C3F1 mice: incidence and classification. AN - 78268288; 3289903 AB - The incidences of all primary neoplasms in the testes and accessory reproductive organs of 51,230 male Fischer 344 (F344) rats and 46,752 male B6C3F1 mice were obtained from the pathology data base of more than 300 long-term toxicity/carcinogenicity studies performed for the National Toxicology Program. The overall incidence of reproductive system neoplasms in male F344 rats was 81.5%. The most common neoplasms were interstitial cell adenoma of the testis (76.6%), adenoma/carcinoma of the preputial glands (2.9%), mesothelioma of the tunica vaginalis (1.5%), and adenoma of the prostate gland (0.3%). The combined incidence (0.1%) of 59 other rare neoplasms consisted of 18 different types that occurred with a frequency of 4 or less. In contrast to the rats, male B6C3F1 mice had a low overall incidence (0.6%) of neoplasms in reproductive organs. The most common neoplasm was the interstitial cell adenoma (0.4%). Thirty additional types of neoplasms were identified. Each of these uncommon neoplasms occurred at a frequency of 12 or less with an overall combined incidence of 0.2%. Morphological features are described for neoplasms in the rat and mouse, and criteria are presented for differentiation of testicular interstitial cell adenoma, prostatic adenoma, and mesothelioma from hyperplastic changes. JF - Environmental health perspectives AU - Mitsumori, K AU - Elwell, M R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 11 EP - 21 VL - 77 SN - 0091-6765, 0091-6765 KW - Index Medicus KW - Rats KW - Animals KW - Adenoma -- veterinary KW - Hyperplasia KW - Adenoma -- epidemiology KW - Mice KW - Male KW - Adenoma -- classification KW - Rats, Inbred Strains KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Prostatic Neoplasms -- epidemiology KW - Rodent Diseases -- epidemiology KW - Prostatic Neoplasms -- veterinary KW - Testicular Neoplasms -- veterinary KW - Rodent Diseases -- classification KW - Prostatic Neoplasms -- classification KW - Testicular Neoplasms -- classification KW - Testicular Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78268288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Proliferative+lesions+in+the+male+reproductive+system+of+F344+rats+and+B6C3F1+mice%3A+incidence+and+classification.&rft.au=Mitsumori%2C+K%3BElwell%2C+M+R&rft.aulast=Mitsumori&rft.aufirst=K&rft.date=1988-04-01&rft.volume=77&rft.issue=&rft.spage=11&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 - 1988-08-10 N1 - Date created - 1988-08-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Pathol. 1980 Feb;98(2):569-72 [6986787] Prostate. 1981;2(3):261-8 [6170967] Environ Health Perspect. 1988 Apr;77:33-6 [3383821] Toxicol Pathol. 1985;13(3):215-21 [4070932] J Comp Pathol. 1983 Apr;93(2):339-42 [6863616] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Unit-length line-1 transcripts in human teratocarcinoma cells. AN - 78264843; 2454389 AB - We have characterized the approximately 6.5-kilobase cytoplasmic poly(A)+ Line-1 (L1) RNA present in a human teratocarcinoma cell line, NTera2D1, by primer extension and by analysis of cloned cDNAs. The bulk of the RNA begins (5' end) at the residue previously identified as the 5' terminus of the longest known primate genomic L1 elements, presumed to represent "unit" length. Several of the cDNA clones are close to 6 kilobase pairs, that is, close to full length. The partial sequences of 18 cDNA clones and full sequence of one (5,975 base pairs) indicate that many different genomic L1 elements contribute transcripts to the 6.5-kilobase cytoplasmic poly(A)+ RNA in NTera2D1 cells because no 2 of the 19 cDNAs analyzed had identical sequences. The transcribed elements appear to represent a subset of the total genomic L1s, a subset that has a characteristic consensus sequence in the 3' noncoding region and a high degree of sequence conservation throughout. Two open reading frames (ORFs) of 1,122 (ORF1) and 3,852 (ORF2) bases, flanked by about 800 and 200 bases of sequence at the 5' and 3' ends, respectively, can be identified in the cDNAs. Both ORFs are in the same frame, and they are separated by 33 bases bracketed by two conserved in-frame stop codons. ORF 2 is interrupted by at least one randomly positioned stop codon in the majority of the cDNAs. The data support proposals suggesting that the human L1 family includes one or more functional genes as well as an extraordinarily large number of pseudogenes whose ORFs are broken by stop codons. The cDNA structures suggest that both genes and pseudogenes are transcribed. At least one of the cDNAs (cD11), which was sequenced in its entirety, could, in principle, represent an mRNA for production of the ORF1 polypeptide. The similarity of mammalian L1s to several recently described invertebrate movable elements defines a new widely distributed class of elements which we term class II retrotransposons. JF - Molecular and cellular biology AU - Skowronski, J AU - Fanning, T G AU - Singer, M F AD - Laboratory of Biochemistry, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 1385 EP - 1397 VL - 8 IS - 4 SN - 0270-7306, 0270-7306 KW - DNA, Neoplasm KW - 0 KW - RNA, Messenger KW - RNA, Neoplasm KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Pseudogenes KW - Humans KW - Amino Acid Sequence KW - RNA, Neoplasm -- genetics KW - Cloning, Molecular KW - Base Sequence KW - RNA, Neoplasm -- isolation & purification KW - Genes KW - Molecular Sequence Data KW - Poly A -- genetics KW - Teratoma KW - Cell Line KW - RNA -- genetics KW - DNA, Neoplasm -- genetics KW - Transcription, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78264843?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Unit-length+line-1+transcripts+in+human+teratocarcinoma+cells.&rft.au=Skowronski%2C+J%3BFanning%2C+T+G%3BSinger%2C+M+F&rft.aulast=Skowronski&rft.aufirst=J&rft.date=1988-04-01&rft.volume=8&rft.issue=4&rft.spage=1385&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 - 1988-07-25 N1 - Date created - 1988-07-25 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M19503; GENBANK N1 - SuppNotes - Cited By: Science. 1984 Jun 29;224(4656):1436-8 [6729461] J Biol Chem. 1984 Aug 25;259(16):10481-92 [6206054] Annu Rev Biochem. 1984;53:447-91 [6383198] EMBO J. 1984 Aug;3(8):1753-9 [6090124] J Mol Biol. 1984 Oct 5;178(4):795-813 [6492166] Mol Cell Biol. 1984 Nov;4(11):2518-28 [6513928] Mol Cell Biol. 1985 Jan;5(1):46-51 [2984554] Nature. 1985 Apr 4-10;314(6010):467-9 [2984578] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1618-22 [3885215] Cell. 1985 Jun;41(2):349-59 [2580642] Gene. 1985;33(1):103-19 [2985470] Nucleic Acids Res. 1985 May 10;13(9):3389-403 [4000975] Int Rev Cytol. 1985;93:187-279 [2409043] Cell. 1985 Aug;42(1):297-308 [2410139] Nucleic Acids Res. 1985 Jul 25;13(14):5071-84 [2991851] Proc Natl Acad Sci U S A. 1985 Sep;82(18):6050-4 [2412228] J Mol Evol. 1985;22(2):117-33 [2999412] Nucleic Acids Res. 1985 Nov 11;13(21):7813-27 [2999705] Science. 1985 Dec 13;230(4731):1237-42 [2416054] Nucleic Acids Res. 1986 Mar 25;14(6):2511-22 [3515319] Nucleic Acids Res. 1986 Apr 11;14(7):3119-36 [3008107] Anal Biochem. 1986 Feb 1;152(2):232-8 [3516005] J Mol Biol. 1986 Jan 20;187(2):291-304 [3009828] Biochem Biophys Res Commun. 1986 Apr 14;136(1):341-7 [2423078] Nature. 1986 May 15-21;321(6067):209-13 [2423876] Nature. 1986 Jun 5-11;321(6070):625-8 [2423883] Nucleic Acids Res. 1986 May 12;14(9):3859-70 [3012483] Mol Cell Biol. 1985 Sep;5(9):2159-71 [3837185] Mol Cell Biol. 1985 Sep;5(9):2197-203 [3016521] Annu Rev Biochem. 1986;55:631-61 [2427017] Cell. 1986 Nov 7;47(3):451-60 [3768961] Cell. 1986 Nov 21;47(4):481-3 [3779834] Cell. 1986 Dec 26;47(6):1007-15 [2430722] Mol Cell Biol. 1986 Jan;6(1):168-82 [3023821] Mol Cell Biol. 1986 Feb;6(2):411-24 [3023845] Mol Cell Biol. 1986 Jul;6(7):2695-703 [3023945] Mol Cell Biol. 1986 Jul;6(7):2704-11 [3023946] J Mol Biol. 1986 Nov 20;192(2):221-33 [2435915] Nucleic Acids Res. 1987 Mar 11;15(5):2251-60 [3562227] Nucleic Acids Res. 1987 Mar 25;15(6):2581-92 [2436147] Cold Spring Harb Symp Quant Biol. 1986;51 Pt 1:457-64 [3472735] Cold Spring Harb Symp Quant Biol. 1986;51 Pt 1:465-9 [2438081] Mol Cell Biol. 1987 Apr;7(4):1465-75 [3037321] Mol Cell Biol. 1987 Jun;7(6):2221-30 [2439905] Mol Biol Evol. 1986 May;3(3):179-90 [3444399] Mol Biol Evol. 1985 Nov;2(6):455-68 [2835576] Science. 1977 Apr 8;196(4286):180-2 [322279] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Mol Biol. 1978 Nov 25;126(1):23-36 [739542] Methods Enzymol. 1980;65(1):499-560 [6246368] Nucleic Acids Res. 1980 Dec 20;8(24):6113-28 [6258162] Nature. 1982 Mar 25;296(5855):321-5 [6801526] J Mol Biol. 1983 Apr 5;165(2):257-86 [6188844] Nature. 1983 Jul 21-27;304(5923):277-80 [6306481] Proc Natl Acad Sci U S A. 1983 Jul;80(13):3966-70 [6306655] Nucleic Acids Res. 1983 Aug 11;11(15):5073-91 [6308571] J Mol Biol. 1983 Aug 25;168(4):715-27 [6310126] Annu Rev Biochem. 1983;52:93-124 [6311083] Nucleic Acids Res. 1983 Oct 11;11(19):6837-46 [6314260] Proc Natl Acad Sci U S A. 1983 Nov;80(21):6533-7 [6195659] J Biol Chem. 1984 Jan 25;259(2):1218-25 [6198321] Lab Invest. 1984 Feb;50(2):147-62 [6694356] Proc Natl Acad Sci U S A. 1984 Feb;81(4):1012-6 [6322182] Gene. 1983 Dec;26(1):101-6 [6323249] Nucleic Acids Res. 1984 Mar 26;12(6):2669-90 [6546796] EMBO J. 1984 Feb;3(2):467-72 [6714224] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2308-12 [6326120] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene. AN - 78257363; 3380102 AB - Transfection of a functional major histocompatibility complex class I gene into certain tumor cells, induced by oncogenic viruses or chemical carcinogens, can effectively abrogate their tumorigenic activity. Since experimentally induced tumors possess strong tumor-specific transplantation antigens, expression of cell surface class I antigens may present the tumor cells to appropriate immune effector cells. Most spontaneously arising tumors do not possess tumor-specific transplantation antigens, and their tumorigenicity may not be affected by the expression of a transfected class I gene. We demonstrate that the poorly immunogenic B16-BL6 melanoma can be rendered nontumorigenic in syngeneic mice by the expression of the class I H-2K antigen but not the class II I-A antigen. Furthermore, the poorly tumorigenic, class I-expressing B16-BL6-transfected cells can effectively immunize syngeneic C57BL/6 mice against the highly tumorigenic, class I-deficient B16-BL6 parental cells. Our success in experimentally manipulating the tumorigenicity of a spontaneously derived neoplasm offers hope for a potential modality for the effective treatment of human cancer. JF - Molecular and cellular biology AU - Tanaka, K AU - Gorelik, E AU - Watanabe, M AU - Hozumi, N AU - Jay, G AD - Laboratory of Molecular Virology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 1857 EP - 1861 VL - 8 IS - 4 SN - 0270-7306, 0270-7306 KW - Index Medicus KW - Neoplasm Transplantation KW - Mice, Inbred Strains KW - Animals KW - Graft Rejection KW - Transfection KW - Transplantation, Isogeneic KW - Mice, Inbred C57BL KW - Mice KW - Transcription, Genetic KW - Melanoma, Experimental -- immunology KW - Genes, MHC Class I UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78257363?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Rejection+of+B16+melanoma+induced+by+expression+of+a+transfected+major+histocompatibility+complex+class+I+gene.&rft.au=Tanaka%2C+K%3BGorelik%2C+E%3BWatanabe%2C+M%3BHozumi%2C+N%3BJay%2C+G&rft.aulast=Tanaka&rft.aufirst=K&rft.date=1988-04-01&rft.volume=8&rft.issue=4&rft.spage=1857&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 - 1988-07-25 N1 - Date created - 1988-07-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Cancer. 1976 Mar;33(3):241-59 [773395] Annu Rev Immunol. 1988;6:359-80 [3289570] Adv Cancer Res. 1978;28:149-250 [360795] Am J Pathol. 1979 Dec;97(3):587-600 [507192] Nature. 1980 Nov 13;288(5787):179-81 [7432518] Immunol Rev. 1981;60:85-127 [6171505] Immunogenetics. 1981 Dec;14(6):481-95 [6976317] J Immunol. 1982 Sep;129(3):1306-12 [6286762] Proc Natl Acad Sci U S A. 1982 Aug;79(16):4947-51 [6956903] J Immunol. 1983 May;130(5):2418-22 [6300246] Nature. 1983 Oct 27-Nov 2;305(5937):771-5 [6355856] J Biol Chem. 1983 Nov 25;258(22):13929-36 [6315713] Nature. 1984 Aug 23-29;310(5979):650-5 [6088985] Nature. 1984 Oct 25-31;311(5988):750-2 [6333639] Adv Cancer Res. 1984;42:1-65 [6395653] Science. 1985 Apr 5;228(4695):26-30 [3975631] Nature. 1985 May 23-29;315(6017):301-5 [3873616] Cell. 1985 Jul;41(3):987-97 [3924414] Cancer Res. 1985 Nov;45(11 Pt 1):5341-7 [2413992] J Virol. 1985 Dec;56(3):757-66 [2999432] Cell. 1985 Nov;43(1):215-22 [2934137] Cell. 1985 Nov;43(1):263-7 [4075396] EMBO J. 1986 Feb;5(2):335-41 [3011403] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4504-8 [3012570] Immunol Lett. 1986 Oct 15;13(5):237-44 [3021618] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8723-7 [3464979] Cell. 1986 Dec 5;47(5):667-74 [3096575] Science. 1987 Mar 20;235(4795):1486-8 [3823900] J Exp Med. 1987 Dec 1;166(6):1716-33 [3500265] Curr Top Microbiol Immunol. 1978;81:115-20 [567555] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occupational risks for male breast cancer in Sweden. AN - 78252501; 3378005 JF - British journal of industrial medicine AU - McLaughlin, J K AU - Malker, H S AU - Blot, W J AU - Weiner, J A AU - Ericsson, J L AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 275 EP - 276 VL - 45 IS - 4 SN - 0007-1072, 0007-1072 KW - Perfume KW - 0 KW - Soaps KW - Index Medicus KW - Printing KW - Risk Factors KW - Humans KW - Medical Staff, Hospital KW - Metallurgy KW - Male KW - Hospitals, Psychiatric KW - Chemical Industry KW - Sweden KW - Adenocarcinoma -- etiology KW - Occupational Diseases -- etiology KW - Breast Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78252501?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Occupational+risks+for+male+breast+cancer+in+Sweden.&rft.au=McLaughlin%2C+J+K%3BMalker%2C+H+S%3BBlot%2C+W+J%3BWeiner%2C+J+A%3BEricsson%2C+J+L%3BFraumeni%2C+J+F&rft.aulast=McLaughlin&rft.aufirst=J&rft.date=1988-04-01&rft.volume=45&rft.issue=4&rft.spage=275&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 - 1988-07-15 N1 - Date created - 1988-07-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br Med J. 1968 Apr 13;2(5597):83-5 [5689553] Lancet. 1975 Jan 4;1(7897):9-10 [46384] Br J Ind Med. 1986 Apr;43(4):257-62 [3964574] J Natl Cancer Inst. 1985 Feb;74(2):371-5 [3856050] Br J Ind Med. 1985 Apr;42(4):240-5 [3978043] Cancer Invest. 1983;1(5):379-86 [6199096] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of long-term ethanol inhalation on the immune and hematopoietic systems of the rat. AN - 78250512; 3287983 AB - An inhalation method of ethanol administration was used to study the effects of 14 days of ethanol administration on the immune and hematopoietic systems of the rat. A decrease in cellularity was found in the spleen, thymus, and bone marrow of ethanol-treated rats. Although the red blood cell count, white blood cell count, and hemoglobin concentration were not significantly different between treatment and control groups, treatment with ethanol altered the relative proportion of lymphocytes and polymorphonuclear leukocytes in the peripheral blood. The granulocyte-macrophage progenitor cells in the bone marrow were unaffected by ethanol treatment, but a significant decline in the number of erythroid progenitor cells was noted in ethanol-treated rats. Splenic lymphocytes, although fewer in number in the ethanol-treated rats, showed no significant difference in ability to proliferate when stimulated by nonspecific mitogens. JF - Alcoholism, clinical and experimental research AU - Marietta, C A AU - Jerrells, T R AU - Meagher, R C AU - Karanian, J W AU - Weight, F F AU - Eckardt, M J AD - Laboratory of Physiologic, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 211 EP - 214 VL - 12 IS - 2 SN - 0145-6008, 0145-6008 KW - Hemoglobins KW - 0 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Animals KW - Cell Count KW - Erythrocyte Count KW - Thymus Gland -- pathology KW - Spleen -- pathology KW - Thymus Gland -- drug effects KW - Leukocyte Count KW - Lymphocyte Activation -- drug effects KW - Rats KW - Rats, Inbred Strains KW - Hemoglobins -- analysis KW - Administration, Inhalation KW - Colony-Forming Units Assay KW - Spleen -- drug effects KW - Male KW - Ethanol -- administration & dosage KW - Ethanol -- toxicity KW - Hematopoietic System -- drug effects KW - Lymphoid Tissue -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78250512?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+long-term+ethanol+inhalation+on+the+immune+and+hematopoietic+systems+of+the+rat.&rft.au=Marietta%2C+C+A%3BJerrells%2C+T+R%3BMeagher%2C+R+C%3BKaranian%2C+J+W%3BWeight%2C+F+F%3BEckardt%2C+M+J&rft.aulast=Marietta&rft.aufirst=C&rft.date=1988-04-01&rft.volume=12&rft.issue=2&rft.spage=211&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 - 1988-07-11 N1 - Date created - 1988-07-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mouse strains for chemical carcinogenicity studies: overview of a workshop. AN - 78231197; 3286346 JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Rao, G N AU - Birnbaum, L S AU - Collins, J J AU - Tennant, R W AU - Skow, L C AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 385 EP - 394 VL - 10 IS - 3 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Mice KW - Mice, Inbred Strains KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78231197?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mouse+strains+for+chemical+carcinogenicity+studies%3A+overview+of+a+workshop.&rft.au=Rao%2C+G+N%3BBirnbaum%2C+L+S%3BCollins%2C+J+J%3BTennant%2C+R+W%3BSkow%2C+L+C&rft.aulast=Rao&rft.aufirst=G&rft.date=1988-04-01&rft.volume=10&rft.issue=3&rft.spage=385&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 - 1988-07-14 N1 - Date created - 1988-07-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Aspergillus rhinitis in Wistar (Crl:(WI)BR) rats. AN - 78230107; 3374092 AB - In two separate 24 month studies on the carcinogenic effect of single cadmium chloride injections in male Wistar (CRl:(WI)BR) rats, a total of 22% (129/597) of animals studied histologically were found to have chronic suppurative rhinitis caused by Aspergillus fumigatus. The diagnosis was based on characteristic conidial heads present in the sections, and positive methenamine-Grocott (GMS) staining of septate hyphae with dichotomous branching at angles of 45 degrees. Fungal hyphae balls, surrounded by a wall of neutrophilic granulocytes, were found in areas of the naso- and maxilloturbinates and occasionally caused complete blockage of the nasal passages. The underlying tissue showed an inflammatory response. In sections from 32 of the 129 cases (25% of the cases), epithelial necrosis and hemorrhage were indicative of fungal tissue invasion, but without dissemination to other organs. The infection rate was unaffected by the cadmium treatment or the location of rats in different cages. Positive antibody titers to Sendai and sialodacryoadenitis viruses suggested that transient inflammation of the upper respiratory tract rendered the mucosa susceptible to the fungal infection. The infection appeared to be sustained by growth around foreign bodies (hairs and plant material). Although focal squamous cell metaplasia of the respiratory epithelium with hyperplasia and hyperkeratosis occurred more frequently in rats with Aspergillus rhinitis, the incidence of tumors of the nasal cavities was not affected. JF - Laboratory animal science AU - Rehm, S AU - Waalkes, M P AU - Ward, J M AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD 21701. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 162 EP - 166 VL - 38 IS - 2 SN - 0023-6764, 0023-6764 KW - Cadmium KW - 00BH33GNGH KW - Index Medicus KW - Rats KW - Animals KW - Male KW - Aspergillosis -- veterinary KW - Rhinitis -- etiology KW - Rhinitis -- pathology KW - Rats, Inbred Strains -- microbiology KW - Aspergillosis -- etiology KW - Rhinitis -- veterinary KW - Aspergillosis -- pathology KW - Aspergillosis -- epidemiology KW - Rhinitis -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78230107?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Aspergillus+rhinitis+in+Wistar+%28Crl%3A%28WI%29BR%29+rats.&rft.au=Rehm%2C+S%3BWaalkes%2C+M+P%3BWard%2C+J+M&rft.aulast=Rehm&rft.aufirst=S&rft.date=1988-04-01&rft.volume=38&rft.issue=2&rft.spage=162&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 - 1988-07-08 N1 - Date created - 1988-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reproductive effects of theophylline in mice and rats. AN - 78225218; 3371590 AB - Theophylline was administered by gavage in 13-week studies to B6C3F1 mice (0, 75, 150, 300 mg/kg/day) and F344 rats (0, 37.5, 75, 150 mg/kg/day) with significant reductions in male mouse terminal body and testicular weights. Male rats also displayed reduced testicular weight, as well as nonsignificant but dose-related decreases in body weight. There was a significant but non-dose-related decrease in female mouse body weight. In parallel studies of B6C3F1 mice and F344 rats, theophylline administered in the diet (0, 0.1, 0.2, 0.4%) produced significantly decreased terminal body weights in male and female mice, but not rats. In rats, cauda epididymis weight was reduced at the high dose compared to the control group, and there was an increase in abnormal sperm. These studies were followed by continuous breeding reproductive assays in CD-1 mice in which theophylline was administered in feed (0.0, 0.075, 0.15, and 0.30%; calculated doses of 0, 125, 265, and 530 mg/kg/day, respectively) to breeding pairs for 14 weeks. There was a dose-dependent decrease in the number of live pups produced per litter, a significant decrease in the number of litters produced per pair (0.30%) and in the adjusted live pup weight (0.30%), a decrease in the percentage of pups born alive (0.15 and 0.30%), and an increase in the number of days needed to produce each litter (0.30%). After 19 weeks of continuous treatment at 0.30%, a crossover mating trial indicated that females and males were adversely affected by theophylline, as judged by the decreased percentage of pups born alive, the decreased live pup weight, and the decreased number of live pups per litter relative to matings within the control group, but the effects in females were more extensive. Based on other studies, there is a suggestion that the observed changes in fertility may be partially attributed to embryotoxicity. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Morrissey, R E AU - Collins, J J AU - Lamb, J C AU - Manus, A G AU - Gulati, D K AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 525 EP - 536 VL - 10 IS - 3 SN - 0272-0590, 0272-0590 KW - Theophylline KW - C137DTR5RG KW - Index Medicus KW - Animals KW - Sex Factors KW - Mice KW - Estrus -- drug effects KW - Pregnancy KW - Rats KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Testis -- drug effects KW - Spermatozoa -- drug effects KW - In Vitro Techniques KW - Species Specificity KW - Female KW - Male KW - Organ Size -- drug effects KW - Reproduction -- drug effects KW - Theophylline -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78225218?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Reproductive+effects+of+theophylline+in+mice+and+rats.&rft.au=Morrissey%2C+R+E%3BCollins%2C+J+J%3BLamb%2C+J+C%3BManus%2C+A+G%3BGulati%2C+D+K&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1988-04-01&rft.volume=10&rft.issue=3&rft.spage=525&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 - 1988-07-14 N1 - Date created - 1988-07-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of Pneumocystis carinii pneumonia with trimetrexate in acquired immunodeficiency syndrome (AIDS). AN - 78221492; 2966985 AB - In vitro studies have shown that trimetrexate, a lipid-soluble analogue of methotrexate, is 1500 times more potent than trimethoprim as an inhibitor of dihydrofolate reductase from Pneumocystis carinii. Furthermore, trimetrexate is readily taken up by P carinii, while performed folates such as leucovorin are not. These observations suggest that the combination of trimetrexate plus leucovorin, which can specifically protect mammalian host tissues from the toxic effects of the antifolate, may be useful in the treatment of pneumocystis pneumonia. This concept was tested in a clinical study of 49 patients with acquired immunodeficiency syndrome (AIDS) and P carinii pneumonia who were treated for 21 days with trimetrexate and leucovorin. Patients were divided into three groups: 16 patients who were unable to tolerate or had failed both pentamidine isethionate and trimethoprim-sulfamethoxazole therapy were treated with trimetrexate plus leucovorin (Group I); 16 patients who were unable to tolerate sulfonamide therapy were treated with trimetrexate with leucovorin as initial therapy (Group II); and 17 patients in whom trimetrexate with leucovorin plus sulfadiazine was used as initial therapy (Group III). Response and survival rates were 69% and 69% in Group I; 63% and 88%, respectively, in Group II; and 71% and 76%, respectively, in Group III. Toxicity was minimal. The results indicate that trimetrexate with leucovorin is safe and effective for initial therapy in AIDS patients with P carinii pneumonia and in those intolerant or unresponsive to standard therapies. JF - Seminars in oncology AU - Allegra, C J AU - Chabner, B A AU - Tuazon, C U AU - Ogata-Arakaki, D AU - Baird, B AU - Drake, J C AU - Masur, H AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 46 EP - 49 VL - 15 IS - 2 Suppl 2 SN - 0093-7754, 0093-7754 KW - Antineoplastic Agents KW - 0 KW - Quinazolines KW - Trimetrexate KW - UPN4ITI8T4 KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Acquired Immunodeficiency Syndrome -- complications KW - Pneumonia, Pneumocystis -- drug therapy KW - Quinazolines -- therapeutic use KW - Quinazolines -- adverse effects KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78221492?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Treatment+of+Pneumocystis+carinii+pneumonia+with+trimetrexate+in+acquired+immunodeficiency+syndrome+%28AIDS%29.&rft.au=Allegra%2C+C+J%3BChabner%2C+B+A%3BTuazon%2C+C+U%3BOgata-Arakaki%2C+D%3BBaird%2C+B%3BDrake%2C+J+C%3BMasur%2C+H&rft.aulast=Allegra&rft.aufirst=C&rft.date=1988-04-01&rft.volume=15&rft.issue=2+Suppl+2&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 - 1988-06-17 N1 - Date created - 1988-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Application of optical properties of the Vi capsular polysaccharide for quantitation of the Vi antigen in vaccines for typhoid fever. AN - 78217579; 3366868 AB - The capsular polysaccharide of Salmonella typhi and of Citrobacter freundii (Vi) is a linear homopolymer of alpha 1,4-linked N-acetylgalactosaminuronic acid, variably O-acetylated at the C-3 position. Vaccines composed of Vi confer protection against typhoid fever with an efficacy of about 70%; Vi has recently been conjugated to proteins to increase its immunogenicity and effectiveness (I.L. Acharya, R. Tapa, V.L. Gurubacharya, M.B. Shrestha, C.U. Lowe, D.D. Bryla, R. Schneerson, J.B. Robbins, T. Crampton, B. Trollfors, M. Cadoz, D. Schulz, and J. Armand, N. Engl. J. Med. 317:1101-1104, 1987; K.P. Klugman, I. Gilbertson, H.J. Kornhof, J.B. Robbins, R. Schneerson, D. Schulz, M. Cadoz, and J. Armand, Lancet ii:1165-1169, 1987; S.C. Szu, A.L. Stone, J.D. Robbins, R. Schneerson, and J.B. Robbins, J. Exp. Med. 166:1510-1524, 1987). Vi, however, cannot be measured by conventional colorimetric methods. Two optical techniques were adapted to quantitate Vi in vaccines. The first, Fourier-transformed infrared spectroscopy, was performed on salt-free, freeze-dried samples. The intensities of the absorbance peaks of Vi were proportional to the amount of Vi within the range of 0.25 to 2.0 mg. The amount of Vi was determined from integrated absorptions at the 1,235- or 1,417-cm-1 band. The second technique, spectrophotometric titration, was more sensitive than the Fourier-transformed infrared spectroscopy and could be performed on dilute solutions. The metachromatic effect of the reaction between the aromatic cationic dye acridine orange and the carboxyl groups of Vi was quantitative within +/- 2% in the range of 20 to 700 micrograms of Vi per ml. The accuracy of the titration of Vi in the vaccines was within +/- 8%. These two methods may be applicable to measure other capsular polysaccharides in vaccines. JF - Journal of clinical microbiology AU - Stone, A L AU - Szu, S C AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 719 EP - 725 VL - 26 IS - 4 SN - 0095-1137, 0095-1137 KW - Antigens, Bacterial KW - 0 KW - Polysaccharides, Bacterial KW - Typhoid-Paratyphoid Vaccines KW - Acridine Orange KW - F30N4O6XVV KW - Index Medicus KW - Spectrophotometry, Infrared KW - Citrobacter -- immunology KW - Chemistry KW - Chemical Phenomena KW - Typhoid-Paratyphoid Vaccines -- immunology KW - Polysaccharides, Bacterial -- analysis KW - Antigens, Bacterial -- analysis KW - Salmonella typhi -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78217579?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+microbiology&rft.atitle=Application+of+optical+properties+of+the+Vi+capsular+polysaccharide+for+quantitation+of+the+Vi+antigen+in+vaccines+for+typhoid+fever.&rft.au=Stone%2C+A+L%3BSzu%2C+S+C&rft.aulast=Stone&rft.aufirst=A&rft.date=1988-04-01&rft.volume=26&rft.issue=4&rft.spage=719&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 completed - 1988-06-16 N1 - Date created - 1988-06-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochim Biophys Acta. 1967 Oct 9;148(1):172-92 [4229557] J Biol Chem. 1963 Jul;238:2255-8 [14000946] J Biol Chem. 1968 Oct 10;243(19):5139-44 [5692878] Biopolymers. 1971;10(4):739-51 [4251709] J Immunol. 1971 Oct;107(4):1081-9 [5315273] Prog Immunobiol Stand. 1971;5:485-91 [4633975] Biopolymers. 1973;12(8):1879-87 [4733713] J Bacteriol. 1974 Sep;119(3):913-22 [4854538] Pediatrics. 1977 Nov;60(5):730-7 [335348] Immunochemistry. 1978 Nov;15(10-11):839-54 [372096] J Exp Med. 1980 Aug 1;152(2):361-76 [6967514] Prog Allergy. 1983;33:144-58 [6600843] Carbohydr Res. 1983 Apr 1;114(2):257-66 [6850674] Carbohydr Res. 1983 Jun 16;117:113-23 [6883366] Adv Carbohydr Chem Biochem. 1983;41:155-208 [6195893] J Infect Dis. 1983 Dec;148(6):1136-59 [6361173] J Infect Dis. 1984 Sep;150(3):436-49 [6207249] Pediatrics. 1984 Nov;74(5):857-65 [6387614] J Biol Stand. 1986 Jan;14(1):25-33 [2420803] N Engl J Med. 1987 Sep 17;317(12):717-22 [3306379] N Engl J Med. 1987 Oct 29;317(18):1101-4 [3657877] J Exp Med. 1987 Nov 1;166(5):1510-24 [3681191] Lancet. 1987 Nov 21;2(8569):1165-9 [2890805] Arch Biochem Biophys. 1954 May;50(1):223-4 [13159320] J Immunol. 1954 Jul;73(1):16-22 [13184128] J Biol Chem. 1958 Jan;230(1):81-9 [13502376] J Immunol. 1961 May;86:538-42 [13784897] Biochim Biophys Acta. 1967 Oct 9;148(1):193-206 [6077037] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Influence of retinoids and EGF on growth of embryonic mouse palatal epithelia in culture. AN - 78205016; 3259227 AB - Retinoids and growth factors seem to be important for normal mammalian reproduction and development. High levels of retinoic acid are teratogenic and induce cleft palate in the mouse. Little is known concerning the mechanisms through which retinoids induce cleft palate. Palatal epithelia from CD-1 embryonic mice on Day 12 of gestation were isolated from the mesenchyme and cultured in serum-free media, with all-trans retinoic acid or 13-cis retinoic acid, with or without epidermal growth factor (EGF). The epithelia attached and grew, and the cells differentiated over a 72-h culture period. Binding of [125I]EGF was observed in all cultures in a pattern that correlated with thymidine (TdR) uptake by the epithelia. EGF enhanced growth and [3H]TdR incorporation of the oral cells, but nasal cells generally did not proliferate. In this culture system, both retinoids suppressed [3H]TdR incorporation in a concentration-dependent manner for epithelia cultured with or without EGF. Medial cells are important to normal palatogenesis as they play a role in fusion of opposing shelves and subsequently many of these cells undergo programmed cell death. Death of medial cells in vitro is prevented by EGF and by the retinoids, either with or without EGF. This response occurs in the absence of a mesenchymal interaction, suggesting that the medial cell response to EGF and retinoids is not mediated by or dependent on the mesenchymal tissues. The survival of medial cells may be responsible for the failure of opposing shelves to fuse. JF - In vitro cellular & developmental biology : journal of the Tissue Culture Association AU - Abbott, B D AU - Pratt, R M AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 343 EP - 352 VL - 24 IS - 4 SN - 0883-8364, 0883-8364 KW - Retinoids KW - 0 KW - Epidermal Growth Factor KW - 62229-50-9 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Epithelial Cells KW - Cell Survival -- drug effects KW - Extracellular Matrix KW - Cell Division -- drug effects KW - Mice KW - DNA -- biosynthesis KW - Microscopy, Electron, Scanning KW - Palate -- cytology KW - Retinoids -- pharmacology KW - Epidermal Growth Factor -- pharmacology KW - Palate -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78205016?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Influence+of+retinoids+and+EGF+on+growth+of+embryonic+mouse+palatal+epithelia+in+culture.&rft.au=Abbott%2C+B+D%3BPratt%2C+R+M&rft.aulast=Abbott&rft.aufirst=B&rft.date=1988-04-01&rft.volume=24&rft.issue=4&rft.spage=343&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 - 1988-06-14 N1 - Date created - 1988-06-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity and disposition of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF) in the rhesus monkey (Macaca mulatta). AN - 78175026; 3358261 AB - The toxicity and disposition of 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF), a ubiquitous and acutely toxic environmental contaminant, was examined in three adult male Rhesus monkeys administered a single iv dose of 34 micrograms (0.1 mumol)/kg. Within 20 min, 4PeCDF was eliminated from the blood and was distributed to the liver, skin, adipose, and muscle tissues. Excretion occurred primarily via the feces with a minimum whole body half-life approximately 38 days. Within 7-14 days after administration, the packed cell volume and serum triglyceride and bile acid concentrations were significantly increased while serum cholesterol, protein, and albumin concentrations were decreased relative to pretreatment levels. Thyroid hormone levels were also altered with an increase in TSH and a decrease in T3 and T4 concentrations. After 28 days, two monkeys began exhibiting alopecia, hyperkeratinization of the toe and finger nails, facial chloracne-like lesions, and loss of body weight. They subsequently died 40 and 48 days after treatment. Similar symptoms of toxicity were observed in the third animal 58 days after 4PeCDF administration, but this animal appeared to fully recover and was administered 4PeCDF orally and [3H]1,2,3,7,8-pentachloro-dibenzofuran (1PeCDF) dermally 238 days after the initial iv dose. In this animal, approximately 2% of an oral dose of [14C]-4PeCDF was absorbed from the stomach and small intestine in 6 hr and was distributed mainly to the muscle and skin and less than 99% of a dermal dose of 1PeCDF remained at the site of application. Pathological findings in the monkeys that died indicated hyperplastic and metaplastic changes in the gastric mucosa, the Meibomian glands of the eyelid, and the ceruminous glands of the ear. Regression of these lesions was present in the surviving animal. Therefore, 4PeCDF produces dioxin-like toxicity in the monkey similar to that reported for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and in the same dose range. JF - Toxicology and applied pharmacology AU - Brewster, D W AU - Elwell, M R AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27707. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 231 EP - 246 VL - 93 IS - 2 SN - 0041-008X, 0041-008X KW - Benzofurans KW - 0 KW - Carbon Radioisotopes KW - Environmental Pollutants KW - Polychlorinated Dibenzodioxins KW - Thyroid Hormones KW - 2,3,4,7,8-pentachlorodibenzofuran KW - U4C2RV3124 KW - Index Medicus KW - Animals KW - Half-Life KW - Muscles -- metabolism KW - Body Weight -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity KW - Absorption KW - Macaca mulatta KW - Tissue Distribution KW - Thyroid Hormones -- blood KW - Gastric Mucosa -- pathology KW - Male KW - Environmental Pollutants -- toxicity KW - Benzofurans -- pharmacokinetics KW - Environmental Pollutants -- pharmacokinetics KW - Benzofurans -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78175026?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Toxicity+and+disposition+of+2%2C3%2C4%2C7%2C8-pentachlorodibenzofuran+%284PeCDF%29+in+the+rhesus+monkey+%28Macaca+mulatta%29.&rft.au=Brewster%2C+D+W%3BElwell%2C+M+R%3BBirnbaum%2C+L+S&rft.aulast=Brewster&rft.aufirst=D&rft.date=1988-04-01&rft.volume=93&rft.issue=2&rft.spage=231&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 - 1988-05-16 N1 - Date created - 1988-05-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Heparin-induced thrombocytopenia and thromboembolism in the postoperative period. AN - 78170398; 3353858 AB - The heparin-induced thrombocytopenia and thrombosis (HITT) syndrome is associated with hemorrhage as well as development of systemic thrombosis. A case is presented in which a posthepatectomy patient had probable heparin-induced thrombocytopenia complicated by venous thrombosis and pulmonary emboli after receiving low doses of heparin as line flushes. HITT is reviewed and factors related to its successful management in this postoperative patient are analyzed in detail. JF - Surgery AU - Rizzoni, W E AU - Miller, K AU - Rick, M AU - Lotze, M T AD - Tumor Immunology Section, Surgery Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 470 EP - 476 VL - 103 IS - 4 SN - 0039-6060, 0039-6060 KW - Heparin KW - 9005-49-6 KW - Abridged Index Medicus KW - Index Medicus KW - Thrombosis -- chemically induced KW - Platelet Aggregation KW - Renal Veins KW - Humans KW - Pulmonary Embolism -- chemically induced KW - Hepatectomy KW - Middle Aged KW - Liver Neoplasms -- surgery KW - Iliac Vein KW - Time Factors KW - Adenocarcinoma -- surgery KW - Female KW - Postoperative Complications -- chemically induced KW - Heparin -- administration & dosage KW - Thrombocytopenia -- chemically induced KW - Thromboembolism -- chemically induced KW - Thrombocytopenia -- blood KW - Heparin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78170398?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Heparin-induced+thrombocytopenia+and+thromboembolism+in+the+postoperative+period.&rft.au=Rizzoni%2C+W+E%3BMiller%2C+K%3BRick%2C+M%3BLotze%2C+M+T&rft.aulast=Rizzoni&rft.aufirst=W&rft.date=1988-04-01&rft.volume=103&rft.issue=4&rft.spage=470&rft.isbn=&rft.btitle=&rft.title=Surgery&rft.issn=00396060&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-05-12 N1 - Date created - 1988-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Potentiation of cytotoxicity by 3-aminobenzamide in DNA repair-deficient human tumor cell lines following exposure to methylating agents or anti-neoplastic drugs. AN - 78163360; 3356063 AB - We studied the potentiation by 3-aminobenzamide (3AB) of killing of nine human cell lines exposed to alkylating agents. Cell lines included normal, transformed and DNA repair-proficient and -deficient phenotypes. 3AB potentiated cell killing by the methylating agents methylmethanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in all lines tested. The degree of potentiation ranged from 1.7- to 3.8-fold, based on the LD99. The average potentiation observed with MMS (2.7-fold) was greater than with MNNG (2.2-fold). On average the potentiation of MMS and MNNG killing of repair-deficient Mer- lines (2.4-fold) was similar to that of repair-proficient Mer+ lines. The degree of 3AB potentiation of MNNG killing (2.0-fold) was similar in Mer+ Rem- lines and in Mer+ Rem+ lines. Mer+ Rem+, Mer+ Rem-, Mer- Rem+, and Mer- Rem- strains all appeared proficient in a 3AB-sensitive DNA repair pathway. Within experimental error, 20 mM 3AB did not inhibit the removal of the MNNG-induced methylpurines 7-methylguanine, O6-methylguanine and 3-methyladenine from the DNA of repair-proficient Mer+ Rem+ HT29 cells, consistent with evidence that 3AB inhibits the ligation step of excision repair. 3AB potentiated cell killing by the bifunctional alkylating agents 1-(2-chlorethyl)-1-nitrosourea or busulfan, two anti-neoplastic drugs, by only 0.9- to 1.5-fold. These drugs therefore produce DNA damage which is not efficiently repaired by the pathways that repair methylated bases. JF - Carcinogenesis AU - Babich, M A AU - Day, R S AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 541 EP - 546 VL - 9 IS - 4 SN - 0143-3334, 0143-3334 KW - Antineoplastic Agents KW - 0 KW - Benzamides KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - 1-(2-chloroethyl)-1-nitrosourea KW - 2365-30-2 KW - 3-aminobenzamide KW - 8J365YF1YH KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Busulfan KW - G1LN9045DK KW - Ethylnitrosourea KW - P8M1T4190R KW - Index Medicus KW - Kinetics KW - Humans KW - Drug Synergism KW - Tumor Stem Cell Assay KW - Methylation KW - Cell Line KW - DNA Repair KW - Busulfan -- pharmacology KW - Cell Survival -- drug effects KW - Benzamides -- pharmacology KW - Tumor Cells, Cultured -- drug effects KW - Ethylnitrosourea -- analogs & derivatives KW - Methylnitronitrosoguanidine -- pharmacology KW - Antineoplastic Agents -- pharmacology KW - Ethylnitrosourea -- pharmacology KW - Methyl Methanesulfonate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78163360?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Potentiation+of+cytotoxicity+by+3-aminobenzamide+in+DNA+repair-deficient+human+tumor+cell+lines+following+exposure+to+methylating+agents+or+anti-neoplastic+drugs.&rft.au=Babich%2C+M+A%3BDay%2C+R+S&rft.aulast=Babich&rft.aufirst=M&rft.date=1988-04-01&rft.volume=9&rft.issue=4&rft.spage=541&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-05-20 N1 - Date created - 1988-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of 32P-postlabeling and high pressure liquid chromatographic analyses for 7,12-dimethylbenz[a]anthracene--DNA adducts. AN - 78162652; 3128408 AB - [3H]7,12-Dimethylbenz[a]anthracene-modified DNA obtained from mouse cells in culture was enzymatically hydrolyzed to nucleoside 3'-phosphates, postlabeled with [32P]phosphate, and the carcinogen-modified nucleoside bisphosphates were separated by thin layer chromatography. Each adduct spot was eluted, dephosphorylated and the resulting [3H]nucleoside adducts were analyzed by high pressure liquid chromatography so that the structural information available for the liquid chromatographic peaks could be applied to the spots obtained from the postlabeling procedure. After this cross referencing, specific dihydrodiol epoxide-nucleotide adducts can now be monitored by the postlabeling technique. JF - Carcinogenesis AU - Schmeiser, H AU - Dipple, A AU - Schurdak, M E AU - Randerath, E AU - Randerath, K AD - BRI-Basic Research Program, NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 633 EP - 638 VL - 9 IS - 4 SN - 0143-3334, 0143-3334 KW - Phosphorus Radioisotopes KW - 0 KW - Tritium KW - 10028-17-8 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Fetus KW - Animals KW - Cells, Cultured KW - Kinetics KW - Chromatography, High Pressure Liquid -- methods KW - Mice KW - DNA -- metabolism KW - 9,10-Dimethyl-1,2-benzanthracene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78162652?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+of+32P-postlabeling+and+high+pressure+liquid+chromatographic+analyses+for+7%2C12-dimethylbenz%5Ba%5Danthracene--DNA+adducts.&rft.au=Schmeiser%2C+H%3BDipple%2C+A%3BSchurdak%2C+M+E%3BRanderath%2C+E%3BRanderath%2C+K&rft.aulast=Schmeiser&rft.aufirst=H&rft.date=1988-04-01&rft.volume=9&rft.issue=4&rft.spage=633&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-05-20 N1 - Date created - 1988-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA sequence specificity of guanine N7-alkylations for a series of structurally related triazenes. AN - 78157002; 2833369 AB - The base sequence selectivity for reaction at the guanine-N7 position was examined for a series of structurally related triazenes by a modification of a standard DNA sequencing method. The monomethyl and monochloroethyl triazenes alkylate guanines extensively at the N7 position with a general preference for runs of contiguous guanines, similar to, but not as striking as that observed previously for the chloroethylnitrosoureas. In contrast to the nitrosoureas, the triazenes had patterns of base sequence selectivity that differed somewhat from agent to agent, with the monochloro-ethylphenyltriazene having the pattern most different from the others in the series. Thus, the nature of the nonalkylating portion of the molecule can influence the ultimate alkylation preference. The monoethylating analogues alkylated weakly with little sequence preference, and the dimethyl analogues were essentially unreactive in this system. JF - Carcinogenesis AU - Hartley, J A AU - Mattes, W B AU - Vaughan, K AU - Gibson, N W AD - Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 669 EP - 674 VL - 9 IS - 4 SN - 0143-3334, 0143-3334 KW - Triazenes KW - 0 KW - Guanine KW - 5Z93L87A1R KW - DNA KW - 9007-49-2 KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - Index Medicus KW - Genes, ras KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Structure-Activity Relationship KW - Alkylation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78157002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=DNA+sequence+specificity+of+guanine+N7-alkylations+for+a+series+of+structurally+related+triazenes.&rft.au=Hartley%2C+J+A%3BMattes%2C+W+B%3BVaughan%2C+K%3BGibson%2C+N+W&rft.aulast=Hartley&rft.aufirst=J&rft.date=1988-04-01&rft.volume=9&rft.issue=4&rft.spage=669&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-05-20 N1 - Date created - 1988-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic heterogeneity in type 1 Gaucher disease: multiple genotypes in Ashkenazic and non-Ashkenazic individuals. AN - 78152859; 3353383 AB - Nucleotide sequence analysis of a genomic clone from an Ashkenazic Jewish patient with type 1 Gaucher disease revealed a single-base mutation (adenosine to guanosine transition) in exon 9 of the glucocerebrosidase gene. This change results in the amino acid substitution of serine for asparagine. Transient expression studies following oligonucleotide-directed mutagenesis of the normal cDNA confirmed that the mutation results in loss of glucocerebrosidase activity. Allele-specific hybridization with oligonucleotide probes demonstrated that this mutation was found exclusively in the type 1 phenotype. None of the 6 type 2 patients, 11 type 3 patients, or 12 normal controls had this allele. In contrast, 15 of 24 type 1 patients had one allele with this mutation, and 3 others were homozygous for the mutation. Furthermore, some of the Ashkenazic Jewish type 1 patients had only one allele with this mutation, suggesting that even in this population there is allelic heterozygosity. These findings indicate that there are multiple allelic mutations responsible for type 1 Gaucher disease in both the Jewish and non-Jewish populations. Allelic-specific hybridization demonstrating this mutation in exon 9, used in conjunction with the Nci I restriction fragment length polymorphism described as a marker for neuronopathic Gaucher disease, provides a tool for diagnosis and genetic counseling that is approximately equal to 80% informative in all Gaucher patients studied. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Tsuji, S AU - Martin, B M AU - Barranger, J A AU - Stubblefield, B K AU - LaMarca, M E AU - Ginns, E I AD - Molecular Neurogenetics Unit, National Institute of Mental Health, ADAMHA, Bethesda, MD 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 2349 EP - 2352 VL - 85 IS - 7 SN - 0027-8424, 0027-8424 KW - Glucosidases KW - EC 3.2.1.- KW - Glucosylceramidase KW - EC 3.2.1.45 KW - Index Medicus KW - Infant KW - Genotype KW - Risk KW - Base Sequence KW - Alleles KW - Humans KW - Adult KW - Molecular Sequence Data KW - Middle Aged KW - Child KW - Amino Acid Sequence KW - Adolescent KW - Mutation KW - Child, Preschool KW - Glucosylceramidase -- deficiency KW - Gaucher Disease -- genetics KW - Gaucher Disease -- classification KW - Glucosylceramidase -- genetics KW - Glucosidases -- genetics KW - Gaucher Disease -- enzymology KW - Jews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78152859?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+heterogeneity+in+type+1+Gaucher+disease%3A+multiple+genotypes+in+Ashkenazic+and+non-Ashkenazic+individuals.&rft.au=Tsuji%2C+S%3BMartin%2C+B+M%3BBarranger%2C+J+A%3BStubblefield%2C+B+K%3BLaMarca%2C+M+E%3BGinns%2C+E+I&rft.aulast=Tsuji&rft.aufirst=S&rft.date=1988-04-01&rft.volume=85&rft.issue=7&rft.spage=2349&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 - 1988-05-12 N1 - Date created - 1988-05-12 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M20282; GENBANK N1 - SuppNotes - Cited By: J Natl Cancer Inst. 1968 Aug;41(2):351-7 [4299537] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Proc Natl Acad Sci U S A. 1982 Sep;79(18):5607-10 [6957882] Mol Cell Biol. 1983 Feb;3(2):280-9 [6300662] Pediatr Res. 1983 May;17(5):344-8 [6856396] Proc Natl Acad Sci U S A. 1983 Jul;80(13):3963-5 [6575390] Clin Chim Acta. 1983 Jul 15;131(3):283-7 [6883722] Methods Enzymol. 1983;100:468-500 [6225933] Hum Genet. 1983;65(2):112-6 [6418635] Cell. 1984 Jan;36(1):131-8 [6198090] DNA. 1984;3(1):7-15 [6365493] Proc Natl Acad Sci U S A. 1984 Oct;81(20):6506-10 [6593712] DNA. 1985 Apr;4(2):165-70 [3996185] Proc Natl Acad Sci U S A. 1985 Aug;82(16):5442-5 [2991926] J Biol Chem. 1985 Nov 15;260(26):14319-24 [3932353] J Clin Invest. 1986 Feb;77(2):528-37 [3484754] N Engl J Med. 1987 Mar 5;316(10):570-5 [2880291] Eur J Biochem. 1987 Apr 1;164(1):171-9 [3549301] Biochem Biophys Res Commun. 1965 Jan 18;18:221-5 [14282020] Erratum In: Proc Natl Acad Sci U S A 1988 Aug;85(15):5708 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lamin B is rapidly phosphorylated in lymphocytes after activation of protein kinase C. AN - 78148330; 3353377 AB - Lamin B was shown to be a major substrate of cellular phosphorylation in the response of lymphocytes to phorbol esters. Lamins A and C, which were not observed in lymphocytes, were also substrates of phorbol-stimulated phosphorylation in those cell types that express them. Lamin B phosphopeptides labeled with 32P in intact cells treated with phorbol 12-myristate 13-acetate were compared to those produced by in vitro phosphorylation with protein kinase M, cAMP-dependent protein kinase, and Ca2+/calmodulin-dependent protein kinase II. The phosphopeptides labeled by in vivo stimulation with phorbol esters are very similar to those phosphorylated in vitro by protein kinase M, a catalytic domain of protein kinase C. Phorbol treatment of interphase cells significantly reduces the amount of detergent-insoluble lamin B, suggesting that phosphorylation of lamin may alter the architecture of the nuclear lamina. In addition, we have shown that treatment of a B-cell line with antibodies to IgM induces a modest increase in lamin B phosphorylation. These results strongly suggest that ligands that are known to activate protein kinase C at the cell surface or in the cytosol also lead to the activation of a nuclear kinase activity with a protein kinase C-type specificity. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Hornbeck, P AU - Huang, K P AU - Paul, W E AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 2279 EP - 2283 VL - 85 IS - 7 SN - 0027-8424, 0027-8424 KW - Lamin Type B KW - 0 KW - Lamins KW - Neoplasm Proteins KW - Nuclear Proteins KW - Protein Kinases KW - EC 2.7.- KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured -- metabolism KW - Humans KW - Mice KW - Rats KW - Protein Kinases -- metabolism KW - Phosphorylation KW - Enzyme Activation -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Neoplasm Proteins -- metabolism KW - Cricetinae KW - Protein Kinase C -- metabolism KW - Lymphocytes -- metabolism KW - Nuclear Proteins -- metabolism KW - Lymphocytes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78148330?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Lamin+B+is+rapidly+phosphorylated+in+lymphocytes+after+activation+of+protein+kinase+C.&rft.au=Hornbeck%2C+P%3BHuang%2C+K+P%3BPaul%2C+W+E&rft.aulast=Hornbeck&rft.aufirst=P&rft.date=1988-04-01&rft.volume=85&rft.issue=7&rft.spage=2279&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 - 1988-05-12 N1 - Date created - 1988-05-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1975 May 25;250(10):4007-21 [236308] J Biol Chem. 1987 Mar 15;262(8):3432-5 [3818650] J Biol Chem. 1980 Mar 25;255(6):2273-6 [7358670] Mol Cell Biochem. 1980 Aug 16;31(3):165-75 [6934372] J Immunol. 1981 Dec;127(6):2488-95 [6170707] J Exp Med. 1982 May 1;155(5):1523-36 [6802927] J Biol Chem. 1983 Jan 25;258(2):1156-64 [6296071] Methods Enzymol. 1983;91:227-36 [6855576] J Biol Chem. 1983 Oct 10;258(19):11442-5 [6311812] J Immunol. 1984 Mar;132(3):1472-8 [6229582] J Biol Chem. 1985 Jan 10;260(1):624-32 [3965465] J Cell Sci Suppl. 1984;1:137-60 [6597817] Proc Natl Acad Sci U S A. 1985 Apr;82(7):1941-5 [3157191] Adv Cyclic Nucleotide Protein Phosphorylation Res. 1985;19:287-306 [2988301] Eur J Biochem. 1985 Sep 2;151(2):419-23 [3161728] Nature. 1985 Oct 10-16;317(6037):546-9 [3862969] Biochem Biophys Res Commun. 1985 Sep 16;131(2):920-7 [3863618] Cell. 1985 Nov;43(1):243-51 [3000601] Proc Natl Acad Sci U S A. 1986 Jan;83(2):357-60 [3455773] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1603-7 [3006058] Science. 1986 Jul 18;233(4761):305-12 [3014651] Nature. 1986 Oct 9-15;323(6088):555-8 [3020435] Nature. 1986 Oct 9-15;323(6088):560-4 [3762708] Biochem Biophys Res Commun. 1986 Aug 29;139(1):320-6 [3464276] J Biol Chem. 1986 Nov 5;261(31):14817-24 [3021753] J Cell Biol. 1978 Nov;79(2 Pt 1):546-66 [102651] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A direct in vivo comparison of the inflammatory properties of human C5a and C5a des Arg in human skin. AN - 78139213; 3351304 AB - C5a is an 11,000-Da complement-derived inflammatory glycoprotein that has been shown to mediate inflammatory reactions in vitro as well as in vivo in human skin. The C5a degradation product, C5a des Arg, is rapidly formed after exposure of C5a to serum carboxypeptidase N and may represent the relevant C5-derived inflammatory peptide in vivo. To examine the biologic activity of human C5a des Arg in vivo and to compare it with that seen with human C5a, we purified and characterized homogeneous preparations of human C5a and C5a des Arg and injected them intradermally into seven normal volunteers. C5a des Arg exhibited biochemical and biologic properties in vitro that were different from those of C5a. When injected into human skin, C5a des Arg was less potent than C5a, in respect to both minimal dose eliciting wheal and flare reactions and maximal wheal and flare elicited at a given dose, but C5a des Arg still elicited cutaneous wheal and flare reactions at physiologically relevant concentrations. Histologically, C5a des Arg skin test sites showed dense polymorphonuclear neutrophil-rich infiltrates associated with leukocytoclasis, dermal mast cell degranulation, and endothelial cell swelling. These were virtually indistinguishable from reactions elicited by C5a and occurred with concentrations attainable in vivo. Cutaneous wheal and flare reactions elicited by either C5a or C5a des Arg were partially inhibited by H1 antihistamines but were unaffected by selected nonsteroidal anti-inflammatory agents. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Swerlick, R A AU - Yancey, K B AU - Lawley, T J AD - Dermatology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/04/01/ PY - 1988 DA - 1988 Apr 01 SP - 2376 EP - 2381 VL - 140 IS - 7 SN - 0022-1767, 0022-1767 KW - Complement C5 KW - 0 KW - Complement C5a, des-Arginine KW - Piroxicam KW - 13T4O6VMAM KW - Complement C5a KW - 80295-54-1 KW - Aspirin KW - R16CO5Y76E KW - Indomethacin KW - XXE1CET956 KW - Abridged Index Medicus KW - Index Medicus KW - Skin -- ultrastructure KW - Skin Tests KW - Humans KW - Piroxicam -- pharmacology KW - Biopsy, Needle KW - Aspirin -- pharmacology KW - Indomethacin -- pharmacology KW - Dermatitis -- immunology KW - Dermatitis -- pathology KW - Complement C5 -- administration & dosage KW - Complement C5 -- physiology KW - Complement C5 -- analogs & derivatives KW - Dermatitis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78139213?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+direct+in+vivo+comparison+of+the+inflammatory+properties+of+human+C5a+and+C5a+des+Arg+in+human+skin.&rft.au=Swerlick%2C+R+A%3BYancey%2C+K+B%3BLawley%2C+T+J&rft.aulast=Swerlick&rft.aufirst=R&rft.date=1988-04-01&rft.volume=140&rft.issue=7&rft.spage=2376&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 - 1988-04-26 N1 - Date created - 1988-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occupational risk factors for laryngeal cancer on the Texas Gulf Coast. AN - 78137439; 3349470 AB - Analyses are reported from a case-control interview study of incident laryngeal cancer on the Gulf Coast of Texas. Study subjects were 183 white men with squamous cell carcinoma of the larynx and 250 frequency matched controls. Occupational exposures were examined controlling for potential confounding by cigarette smoking and alcohol consumption. Significantly elevated risks were seen for men employed in the public services industry [transportation, communication, utilities, sanitary service; relative risk (RR), 1.6]; in metal fabricating (RR, 2.1), construction (RR, 1.7), and maintenance (RR, 2.7) occupations; and for workers potentially exposed to paint (RR, 1.8) and diesel or gasoline fumes (RR, 1.5). Elevated risks of border-line significance were seen for men employed as woodworkers/furniture makers (RR, 8.1) and for those with occupational exposure to asbestos (RR, 1.5). When asbestos was categorized by intensity of exposure, a significant positive gradient was found. JF - Cancer research AU - Brown, L M AU - Mason, T J AU - Pickle, L W AU - Stewart, P A AU - Buffler, P A AU - Burau, K AU - Ziegler, R G AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04/01/ PY - 1988 DA - 1988 Apr 01 SP - 1960 EP - 1964 VL - 48 IS - 7 SN - 0008-5472, 0008-5472 KW - Fuel Oils KW - 0 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Risk Factors KW - Paint KW - Smoking -- adverse effects KW - Texas KW - Alcohol Drinking KW - Time Factors KW - Diet -- adverse effects KW - Occupational Diseases -- etiology KW - Laryngeal Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78137439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Occupational+risk+factors+for+laryngeal+cancer+on+the+Texas+Gulf+Coast.&rft.au=Brown%2C+L+M%3BMason%2C+T+J%3BPickle%2C+L+W%3BStewart%2C+P+A%3BBuffler%2C+P+A%3BBurau%2C+K%3BZiegler%2C+R+G%3BFraumeni%2C+J+F&rft.aulast=Brown&rft.aufirst=L&rft.date=1988-04-01&rft.volume=48&rft.issue=7&rft.spage=1960&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 - 1988-04-22 N1 - Date created - 1988-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transformation of human bronchial epithelial cells by infection with SV40 or adenovirus-12 SV40 hybrid virus, or transfection via strontium phosphate coprecipitation with a plasmid containing SV40 early region genes. AN - 78136528; 2450641 AB - Normal human bronchial epithelial cells were infected with SV40 virus or an adenovirus 12-SV40 hybrid virus, or transfected via strontium phosphate coprecipitation with plasmids containing the SV40 early region genes. Colonies of morphologically altered cells were isolated and cultured; these cells had extended culture lifespans compared to normal human bronchial epithelial cells. All cultures eventually underwent senescence, with the exception of one which appears to have unlimited proliferative potential. Colonies arising after viral infection were screened for virus production by cocultivation with Vero cells; only viral nonproducer cultures were analyzed further. The cells retained electron microscopic features of epithelial cells, and keratin and SV40 T-antigen were detected by indirect immunofluorescence. All of the cultures were aneuploid with karyotypic abnormalities characteristic of SV40-transformed cells. No tumors formed after s.c. injection of the cells in nude mice. These cells should be useful for studies of multistage bronchial epithelial carcinogenesis. JF - Cancer research AU - Reddel, R R AU - Ke, Y AU - Gerwin, B I AU - McMenamin, M G AU - Lechner, J F AU - Su, R T AU - Brash, D E AU - Park, J B AU - Rhim, J S AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04/01/ PY - 1988 DA - 1988 Apr 01 SP - 1904 EP - 1909 VL - 48 IS - 7 SN - 0008-5472, 0008-5472 KW - Antigens, Viral, Tumor KW - 0 KW - DNA, Viral KW - Phosphates KW - strontium phosphate KW - 14414-90-5 KW - Keratins KW - 68238-35-7 KW - Strontium KW - YZS2RPE8LE KW - Index Medicus KW - Virus Replication KW - Karyotyping KW - Keratins -- metabolism KW - Humans KW - Adenoviruses, Human KW - Antigens, Viral, Tumor -- analysis KW - Epithelial Cells KW - Transfection KW - Genes, Viral KW - Cell Division KW - Bronchi -- cytology KW - Simian virus 40 -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78136528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transformation+of+human+bronchial+epithelial+cells+by+infection+with+SV40+or+adenovirus-12+SV40+hybrid+virus%2C+or+transfection+via+strontium+phosphate+coprecipitation+with+a+plasmid+containing+SV40+early+region+genes.&rft.au=Reddel%2C+R+R%3BKe%2C+Y%3BGerwin%2C+B+I%3BMcMenamin%2C+M+G%3BLechner%2C+J+F%3BSu%2C+R+T%3BBrash%2C+D+E%3BPark%2C+J+B%3BRhim%2C+J+S%3BHarris%2C+C+C&rft.aulast=Reddel&rft.aufirst=R&rft.date=1988-04-01&rft.volume=48&rft.issue=7&rft.spage=1904&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 - 1988-04-22 N1 - Date created - 1988-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of the acquired immunodeficiency syndrome (AIDS) and AIDS-related complex with a regimen of 3'-azido-2',3'-dideoxythymidine (azidothymidine or zidovudine) and acyclovir. A pilot study. AN - 78133303; 2964805 AB - On the basis of observation that acyclovir potentiates the in-vitro antiviral activity of 3-azido-2',3'-dideoxythymidine (also known as azidothymidine or zidovudine) against human immunodeficiency virus (HIV), we administered a regimen of azidothymidine and acyclovir to eight patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex. An oral regimen of 100 mg of azidothymidine and 800 mg of acyclovir every 4 hours was in general well tolerated, with the principal toxicity being megaloblastic erythroid changes. The pharmacokinetics of the two drugs were independent of each other. Six patients received the drug combination for at least 10 weeks; all had increased numbers of T4+ lymphocytes (P = 0.028), and two of three assessable patients had reversal of anergy. Two patients tested positive for serum HIV p24 antigen at entry, but became negative with treatment. Data for this small group suggest that this drug combination can be tolerated in patients with severe HIV infections; this study can be used as a basis for larger studies of this drug combination. JF - Annals of internal medicine AU - Surbone, A AU - Yarchoan, R AU - McAtee, N AU - Blum, M R AU - Maha, M AU - Allain, J P AU - Thomas, R V AU - Mitsuya, H AU - Lehrman, S N AU - Leuther, M AD - Clinical Oncology Program, National Cancer Institute, Bethesda, Maryland. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 534 EP - 540 VL - 108 IS - 4 SN - 0003-4819, 0003-4819 KW - Antiviral Agents KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Thymidine KW - VC2W18DGKR KW - Acyclovir KW - X4HES1O11F KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Drug Therapy, Combination KW - Hematologic Diseases -- chemically induced KW - Drug Interactions KW - Humans KW - Adult KW - T-Lymphocytes, Helper-Inducer -- drug effects KW - Pilot Projects KW - Middle Aged KW - Nervous System Diseases -- chemically induced KW - Male KW - Antiviral Agents -- therapeutic use KW - AIDS-Related Complex -- immunology KW - Acyclovir -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Thymidine -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- microbiology KW - Acyclovir -- adverse effects KW - AIDS-Related Complex -- microbiology KW - Thymidine -- adverse effects KW - Antiviral Agents -- blood KW - Acyclovir -- blood KW - AIDS-Related Complex -- drug therapy KW - Acquired Immunodeficiency Syndrome -- immunology KW - Antiviral Agents -- adverse effects KW - Thymidine -- blood KW - Thymidine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78133303?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Treatment+of+the+acquired+immunodeficiency+syndrome+%28AIDS%29+and+AIDS-related+complex+with+a+regimen+of+3%27-azido-2%27%2C3%27-dideoxythymidine+%28azidothymidine+or+zidovudine%29+and+acyclovir.+A+pilot+study.&rft.au=Surbone%2C+A%3BYarchoan%2C+R%3BMcAtee%2C+N%3BBlum%2C+M+R%3BMaha%2C+M%3BAllain%2C+J+P%3BThomas%2C+R+V%3BMitsuya%2C+H%3BLehrman%2C+S+N%3BLeuther%2C+M&rft.aulast=Surbone&rft.aufirst=A&rft.date=1988-04-01&rft.volume=108&rft.issue=4&rft.spage=534&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 - 1988-04-21 N1 - Date created - 1988-04-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol ester-mediated association of protein kinase C to the nuclear fraction in NIH 3T3 cells. AN - 78131088; 3127041 AB - Treatment of intact NIH 3T3 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) causes a rapid redistribution (stabilization) of protein kinase C to the particulate fraction. Part of the enzyme activity stabilized to the membrane fraction in response to TPA can be recovered associated with nuclear-cytoskeletal components. An apparently pure nuclear fraction prepared from NIH 3T3 cells was found to contain 25-30% of the total membrane-associated protein kinase C activity when isolated in the presence of Ca2+. In untreated control cells, most of this activity found with the nuclear fraction can be extracted by chelators. Phorbol ester (TPA) treatment of NIH 3T3 cells induces the tight association of protein kinase C to the nucleus; this tightly bound activity is not dissociable by chelators and can be recovered only by solubilization with detergent. Nuclei purified from untreated human promyelocytic leukemic HL-60 cells contain higher amounts of chelator-stable, detergent-extractable protein kinase C activity compared with control NIH 3T3 cells. However, TPA treatment of HL-60 cells does not enhance the amount of protein kinase C found tightly associated with the nuclear fraction. Immunohistochemical studies with polyclonal antibodies directed against protein kinase C further indicate that TPA treatment of NIH 3T3 cells does significantly enhance the amount of protein kinase C found tightly associated with the nucleus and cytoskeleton, whereas exposure of HL-60 cells to TPA does not appreciably alter the amount of protein kinase C observed to be associated with the nuclear fraction. The TPA-mediated association (activation) of protein kinase C to the nuclear and cytoskeletal fractions with NIH 3T3 cells is further supported by the enhanced phosphorylation of specific endogenous proteins noted when purified nuclei and cytoskeletal preparations are incubated with [gamma-32P]ATP. These results suggest that tumor promoters may induce association (activation) of protein kinase C with different subcellular components to alter the availability of endogenous substrates. This may result in differential responses by different cell types during exposure to tumor promoters. JF - Cancer research AU - Thomas, T P AU - Talwar, H S AU - Anderson, W B AD - Division of Cancer Biology and Diagnosis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/04/01/ PY - 1988 DA - 1988 Apr 01 SP - 1910 EP - 1919 VL - 48 IS - 7 SN - 0008-5472, 0008-5472 KW - Nuclear Proteins KW - 0 KW - Phosphoproteins KW - Egtazic Acid KW - 526U7A2651 KW - Edetic Acid KW - 9G34HU7RV0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Cytoskeleton -- metabolism KW - Humans KW - Mice KW - Tumor Cells, Cultured KW - Cell Compartmentation -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Nuclear Proteins -- metabolism KW - Egtazic Acid -- pharmacology KW - Cell Line KW - Edetic Acid -- pharmacology KW - Immunoenzyme Techniques KW - Phosphoproteins -- metabolism KW - Protein Kinase C -- metabolism KW - Cell Nucleus -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78131088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phorbol+ester-mediated+association+of+protein+kinase+C+to+the+nuclear+fraction+in+NIH+3T3+cells.&rft.au=Thomas%2C+T+P%3BTalwar%2C+H+S%3BAnderson%2C+W+B&rft.aulast=Thomas&rft.aufirst=T&rft.date=1988-04-01&rft.volume=48&rft.issue=7&rft.spage=1910&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 - 1988-04-22 N1 - Date created - 1988-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Geographic distribution of human immunodeficiency virus markers in parenteral drug abusers. AN - 78129788; 3348473 AB - Drug abuse treatment programs in six regions of the United States collaborated in a study aimed at monitoring trends in the seroprevalence of human immunodeficiency virus (HIV) antibodies. The wide disparities in HIV seroprevalence in the face of similarities in drug using behavior have important implications for prevention. In the New York City area (Harlem, Brooklyn), 61 per cent of samples (N = 280) obtained in late 1986 were positive, up from 50 per cent of samples (N = 585) in early 1985. In Baltimore, Maryland, 29 per cent of samples (N = 184) representing 11 programs were positive. In contrast, samples from programs distant from the Northeast corridor had far lower rates: Denver, Colorado 5 per cent (N = 100); San Antonio, Texas 2 per cent (N = 106); Southern California, 1.5 per cent (N = 413); and Tampa, Florida, 0 per cent (N = 102). Contrary to expectations, there was no corresponding difference in reported lifetime needle sharing experiences, which ranged from 70 per cent in New York to 99 per cent in San Antonio. HIV seropositivity was associated only with geographic location and ethnicity; however, because needle sharing is practiced by parenteral drug abusers in areas where seroprevalence is still relatively low, these areas are potentially vulnerable to the same catastrophic spread seen in the Northeast. A window of opportunity exists where prompt, vigorous, and aggressive efforts at prevention could have major impact. JF - American journal of public health AU - Lange, W R AU - Snyder, F R AU - Lozovsky, D AU - Kaistha, V AU - Kaczaniuk, M A AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 443 EP - 446 VL - 78 IS - 4 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - United States KW - Needles KW - Behavior KW - Humans KW - Adult KW - Geography KW - Male KW - Female KW - HIV Seropositivity -- ethnology KW - Substance-Related Disorders -- complications KW - HIV Seropositivity -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78129788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Geographic+distribution+of+human+immunodeficiency+virus+markers+in+parenteral+drug+abusers.&rft.au=Lange%2C+W+R%3BSnyder%2C+F+R%3BLozovsky%2C+D%3BKaistha%2C+V%3BKaczaniuk%2C+M+A%3BJaffe%2C+J+H&rft.aulast=Lange&rft.aufirst=W&rft.date=1988-04-01&rft.volume=78&rft.issue=4&rft.spage=443&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 - 1988-04-21 N1 - Date created - 1988-04-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Subst Abuse Treat. 1984;1(4):237-47 [6100315] Arch Intern Med. 1985 Sep;145(9):1607-12 [3875329] N Engl J Med. 1986 Feb 13;314(7):446 [3456077] N Engl J Med. 1986 Feb 13;314(7):446-7 [3945272] JAMA. 1986 Jun 13;255(22):3133-7 [3009910] N Engl J Med. 1986 Jul 17;315(3):191-2 [3724808] Am J Drug Alcohol Abuse. 1986;12(1-2):165-81 [3641524] Am J Public Health. 1987 Feb;77(2):169-72 [3467596] Transfusion. 1986 May-Jun;26(3):299-301 [3010516] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dual receptor regulation of cyclic nucleotides: alpha 1-adrenergic potentiation of vasoactive intestinal peptide stimulation of pinealocyte adenosine 3',5'-monophosphate. AN - 78117754; 2831037 AB - The purpose of this investigation was to determine if alpha 1-adrenergic receptor activation would potentiate the vasoactive intestinal peptide (VIP)-stimulated increase in cAMP accumulation in the rat pinealocyte. Treatment with VIP alone increased cAMP accumulation less than 5-fold, and treatment with phenylephrine increased cAMP accumulation less than 2-fold. However, combined treatment with VIP and phenylephrine increased cAMP accumulation more than 20-fold. This is the first report that alpha 1-adrenergic and VIP receptors can interact to regulate cAMP in a cell of neural tube origin. The demonstration of such an integrated mechanism in pinealocytes is of special interest because VIP innervation of the pineal gland is of central origin, and adrenergic innervation is of peripheral origin. The magnitude of response makes the pinealocyte an attractive model for the study of such dual receptor regulation. JF - Endocrinology AU - Chik, C L AU - Ho, A K AU - Klein, D C AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/04// PY - 1988 DA - April 1988 SP - 1646 EP - 1651 VL - 122 IS - 4 SN - 0013-7227, 0013-7227 KW - Receptors, Adrenergic, alpha KW - 0 KW - Phenylephrine KW - 1WS297W6MV KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Cyclic AMP KW - E0399OZS9N KW - Isoproterenol KW - L628TT009W KW - Norepinephrine KW - X4W3ENH1CV KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Norepinephrine -- pharmacology KW - Drug Synergism KW - Time Factors KW - Isoproterenol -- pharmacology KW - Female KW - Phenylephrine -- pharmacology KW - Vasoactive Intestinal Peptide -- pharmacology KW - Pineal Gland -- metabolism KW - Cyclic AMP -- metabolism KW - Receptors, Adrenergic, alpha -- metabolism KW - Pineal Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78117754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dual+receptor+regulation+of+cyclic+nucleotides%3A+alpha+1-adrenergic+potentiation+of+vasoactive+intestinal+peptide+stimulation+of+pinealocyte+adenosine+3%27%2C5%27-monophosphate.&rft.au=Chik%2C+C+L%3BHo%2C+A+K%3BKlein%2C+D+C&rft.aulast=Chik&rft.aufirst=C&rft.date=1988-04-01&rft.volume=122&rft.issue=4&rft.spage=1646&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-04-21 N1 - Date created - 1988-04-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pulmonary toxicity of doxorubicin administered by in situ isolated lung perfusion in dogs. AN - 78115659; 2830958 AB - The possibility of in situ isolated lung perfusion as a means of treating nonresectable pulmonary cancers unresponsive to conventional chemotherapy has been investigated. The present study has examined the biochemical and morphological effects of in situ isolated lung perfusion in dogs with doxorubicin (DOX). A dose related complication was seen in the animals following lung perfusion. Lactate dehydrogenase (LDH) activity in the perfusate increased as dose was increased, indicating tissue damage during the perfusion. Up to 7 days postperfusion, marked changes were seen in the serum protein concentrations although these were independent of doxorubicin concentrations. Serum lactate dehydrogenase showed a dose dependent increase 2 hour and 1 day after the lung perfusion. Plasma angiotensin converting enzyme activities up to 14 days postperfusion suggested that DOX produced pulmonary endothelial cell injury at higher drug doses. Histopathologic examination of the lungs from dogs receiving the highest concentrations of drug indicated that necrosis of arterial endothelia and alveolar epithelia accompanied by periarterial edema, subplural edema and emphysema of the lungs were the probable causes of acute animal mortality. The study has demonstrated that doxorubicin produces dose-dependent damage to the pulmonary tissue. However, the observed injury only appeared life-threatening at perfusate drug concentrations in excess of 20 nmol/ml. In situ lung perfusion for the treatment of unresectable pulmonary tumors may be clinically applicable. JF - Cancer AU - Minchin, R F AU - Johnston, M R AU - Schuller, H M AU - Aiken, M A AU - Boyd, M R AD - Developmental Therapeutics Program, National Cancer Institute, Bethesda, Maryland. Y1 - 1988/04/01/ PY - 1988 DA - 1988 Apr 01 SP - 1320 EP - 1325 VL - 61 IS - 7 SN - 0008-543X, 0008-543X KW - Doxorubicin KW - 80168379AG KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Peptidyl-Dipeptidase A KW - EC 3.4.15.1 KW - Abridged Index Medicus KW - Index Medicus KW - Aspartate Aminotransferases -- blood KW - Animals KW - Peptidyl-Dipeptidase A -- blood KW - Alanine Transaminase -- blood KW - Pneumonectomy KW - Dose-Response Relationship, Drug KW - Lung Neoplasms -- drug therapy KW - L-Lactate Dehydrogenase -- blood KW - Dogs KW - Lung Neoplasms -- mortality KW - Chemotherapy, Cancer, Regional Perfusion -- methods KW - Time Factors KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism KW - Doxorubicin -- pharmacokinetics KW - Lung -- drug effects KW - Doxorubicin -- toxicity KW - Doxorubicin -- administration & dosage KW - Lung -- pathology KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78115659?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pulmonary+toxicity+of+doxorubicin+administered+by+in+situ+isolated+lung+perfusion+in+dogs.&rft.au=Minchin%2C+R+F%3BJohnston%2C+M+R%3BSchuller%2C+H+M%3BAiken%2C+M+A%3BBoyd%2C+M+R&rft.aulast=Minchin&rft.aufirst=R&rft.date=1988-04-01&rft.volume=61&rft.issue=7&rft.spage=1320&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-04-13 N1 - Date created - 1988-04-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dioxin-like effects observed in male rats following exposure to octachlorodibenzo-p-dioxin (OCDD) during a 13-week study. AN - 78157010; 3354000 AB - Octachlorodibenzo-p-dioxin (OCDD) is a ubiquitous environmental pollutant which has been reported to be nontoxic following acute exposure but has recently been shown to accumulate upon repeated exposure. To determine if this accumulation results in toxic effects, male Fischer 344 rats were treated with 50 micrograms/kg [14C]OCDD by gavage for 10, 20, 40, or 65 times (once a day, 5 days/week) and terminated 3 days postexposure. OCDD accumulated linearly with increasing number of doses and the liver was the major depot, while the adipose served as a secondary sink. Hepatic accumulation resulted in alteration of several biochemical parameters. In animals given 65 doses of OCDD, 7-ethoxyresorufin-O-deethylase activity was elevated 40-fold over controls. Total cytochrome P-450 content doubled and exhibited a 2-nm blue-shift in the Soret maximum for the CO-reduced complex. Treatment-related cytoplasmic fatty vacuolization in the liver was observed concomitant with the biochemical alterations. Thus, subchronic exposure to OCDD appears to cause effects similar to those observed following exposure to low levels of TCDD, but is only 1/100-1/1000 as potent. Such a potency, given the persistent environmental levels to which man may be exposed during a lifetime, suggests that OCDD may pose a potential risk to human health. JF - Toxicology and applied pharmacology AU - Couture, L A AU - Elwell, M R AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/03/30/ PY - 1988 DA - 1988 Mar 30 SP - 31 EP - 46 VL - 93 IS - 1 SN - 0041-008X, 0041-008X KW - Bile Acids and Salts KW - 0 KW - Dioxins KW - Glucosephosphates KW - Polychlorinated Dibenzodioxins KW - Glucose-6-Phosphate KW - 56-73-5 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 - Animals KW - Liver -- pathology KW - Spleen -- pathology KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Liver -- metabolism KW - Tissue Distribution KW - Bile Acids and Salts -- analysis KW - Glucosephosphates -- analysis KW - Rats KW - Cytochrome P-450 Enzyme System -- analysis KW - Rats, Inbred F344 KW - Liver -- drug effects KW - Blood Cells -- drug effects KW - Male KW - Oxidoreductases -- biosynthesis KW - Polychlorinated Dibenzodioxins -- analogs & derivatives KW - Polychlorinated Dibenzodioxins -- analysis KW - Polychlorinated Dibenzodioxins -- pharmacokinetics KW - Polychlorinated Dibenzodioxins -- toxicity KW - Dioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78157010?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dioxin-like+effects+observed+in+male+rats+following+exposure+to+octachlorodibenzo-p-dioxin+%28OCDD%29+during+a+13-week+study.&rft.au=Couture%2C+L+A%3BElwell%2C+M+R%3BBirnbaum%2C+L+S&rft.aulast=Couture&rft.aufirst=L&rft.date=1988-03-30&rft.volume=93&rft.issue=1&rft.spage=31&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 - 1988-05-03 N1 - Date created - 1988-05-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Strain dependence in mice of resistance and susceptibility to the testicular effects of cadmium: assessment of the role of testicular cadmium-binding proteins. AN - 78151625; 3354001 AB - The nature of the cadmium (Cd)-binding proteins in the mouse testes is unknown, although some studies have implied metallothionein (MT) is responsible for the marked strain dependence of Cd-induced testicular necrosis in mice. This study attempted to define the role of MT in strain-dependent Cd resistance using NFS (susceptible) and BALB/c (resistant) mice. In all cases, testicular proteins were compared to hepatic MT isolated after treatment with zinc (Zn). A low-molecular-weight (Mr) Zn-, Cd-binding protein was detected in testicular and hepatic cytosol from both strains after gel filtration. These proteins were extractable by heat treatment and sequential acetone precipitation. When such extracts were further purified with reverse-phase HPLC, two forms of authentic MT were shown by amino acid analysis from both NFS and BALB/c livers. However, of two testicular forms separated by HPLC from NFS and BALB/c mice, neither could be classified as MT based on amino acid composition. Methylation of the MT-I gene was also studied in testicular and hepatic DNAs isolated from control mice or from mice made resistant to Cd-induced testicular necrosis by Zn treatment. Major differences in methylation between tissues were seen, as the testicular gene of both NFS and BALB/c mice was highly methylated, a condition often linked to genetic quiescence. Zn treatment had no effect on MT-I gene methylation in testes of either strain, although rendering the NFS strain resistant to Cd. Zn treatment did not alter levels of this testicular protein in either strain while causing a marked induction of hepatic MT in both. These results indicate the low-Mr Cd-, Zn-binding proteins present in the testes of both resistant and susceptible mice are not MTs and further that the MT gene may not be expressed in either strain. JF - Toxicology and applied pharmacology AU - Waalkes, M P AU - Perantoni, A AU - Bhave, M R AU - Rehm, S AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/03/30/ PY - 1988 DA - 1988 Mar 30 SP - 47 EP - 61 VL - 93 IS - 1 SN - 0041-008X, 0041-008X KW - Amino Acids KW - 0 KW - cadmium-binding protein KW - Cadmium KW - 00BH33GNGH KW - Metallothionein KW - 9038-94-2 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Animals KW - Zinc -- pharmacology KW - Amino Acids -- analysis KW - Drug Resistance KW - Mice KW - Mice, Inbred BALB C KW - Species Specificity KW - Methylation KW - Male KW - Chromatography, High Pressure Liquid KW - Testis -- drug effects KW - Metallothionein -- analysis KW - Cadmium -- toxicity KW - Metallothionein -- genetics KW - Testis -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78151625?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Strain+dependence+in+mice+of+resistance+and+susceptibility+to+the+testicular+effects+of+cadmium%3A+assessment+of+the+role+of+testicular+cadmium-binding+proteins.&rft.au=Waalkes%2C+M+P%3BPerantoni%2C+A%3BBhave%2C+M+R%3BRehm%2C+S&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1988-03-30&rft.volume=93&rft.issue=1&rft.spage=47&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 - 1988-05-03 N1 - Date created - 1988-05-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lack of relation of increased malformation rates in infants of diabetic mothers to glycemic control during organogenesis. AN - 78115612; 3344018 AB - To determine how much insulin-dependent diabetes increases a woman's risk of giving birth to a malformed infant and how that risk is influenced by metabolic control, we followed 347 diabetic and 389 control women who enrolled in the study within 21 days of conception (the early-entry group) and 279 diabetic women who entered later (the late-entry group). We detected major malformations in the infants of 4.9 percent of the early-entry diabetic women, 2.1 percent of the controls, and 9.0 percent of the late-entry diabetic women. Malformation rates were significantly higher among offspring of early-entry diabetic women than among those of controls (odds ratio, 2.45; lower one-sided 95 percent confidence limit, 1.12; P = 0.027), and higher among late-entry than among early-entry diabetic women (odds ratio, 1.91; lower one-sided 95 percent confidence limit, 1.07; P = 0.032). Mean blood glucose and glycosylated hemoglobin levels during organogenesis were not significantly higher in women whose infants were malformed. Hypoglycemia (glucose, less than or equal to 50 mg per deciliter [2.8 mmol per liter]) was not significantly more common in the same group. Hyperglycemia and glycosylated hemoglobin were not correlated with malformation. The data suggest that more sensitive measures are needed to identify the teratogenic mechanisms, or that not all malformation can be prevented by good glycemic control. Despite the increased malformation rate among infants of the early-entry diabetic women, as compared with the controls, the more favorable outcome seen in the former group as compared with the late-entry group justifies the attempt to achieve good metabolic control around the time of conception. JF - The New England journal of medicine AU - Mills, J L AU - Knopp, R H AU - Simpson, J L AU - Jovanovic-Peterson, L AU - Metzger, B E AU - Holmes, L B AU - Aarons, J H AU - Brown, Z AU - Reed, G F AU - Bieber, F R AD - Epidemiology Branch, National Institute of Child Health and Human Development, Bethesda, Md 20892. Y1 - 1988/03/17/ PY - 1988 DA - 1988 Mar 17 SP - 671 EP - 676 VL - 318 IS - 11 SN - 0028-4793, 0028-4793 KW - Blood Glucose KW - 0 KW - Hemoglobin, Sickle KW - hemoglobin S, glycosylated KW - Abridged Index Medicus KW - Index Medicus KW - Hemoglobin, Sickle -- analogs & derivatives KW - Humans KW - Morphogenesis KW - Hemoglobin, Sickle -- analysis KW - Female KW - Pregnancy KW - Embryonic and Fetal Development KW - Diabetes Mellitus, Type 1 KW - Blood Glucose -- metabolism KW - Congenital Abnormalities -- epidemiology KW - Congenital Abnormalities -- etiology KW - Pregnancy in Diabetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78115612?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Lack+of+relation+of+increased+malformation+rates+in+infants+of+diabetic+mothers+to+glycemic+control+during+organogenesis.&rft.au=Mills%2C+J+L%3BKnopp%2C+R+H%3BSimpson%2C+J+L%3BJovanovic-Peterson%2C+L%3BMetzger%2C+B+E%3BHolmes%2C+L+B%3BAarons%2C+J+H%3BBrown%2C+Z%3BReed%2C+G+F%3BBieber%2C+F+R&rft.aulast=Mills&rft.aufirst=J&rft.date=1988-03-17&rft.volume=318&rft.issue=11&rft.spage=671&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-04-07 N1 - Date created - 1988-04-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of age on the glucuronidation and toxicity of 4,4'-thiobis(6-t-butyl-m-cresol). AN - 78157763; 3127943 AB - Age-related changes in glucuronidation may potentially lead to a decrease in excretion of reactive compounds, resulting in enhanced toxic effects. 4,4'-Thiobis(6-t-butyl-m-cresol) (TBBC), a major antioxidant in the rubber industry, was selected as a model compound to evaluate glucuronidation as a function of age because it is directly conjugated to UDP-glucuronic acid (UDPGA) without requiring oxidative metabolism. To assess glucuronidation changes in vivo, male F344 rats, 2.5, 16, and 26 months of age, were administered 5 mg [14C]-TBBC/kg (10 microCi/kg) iv and urine and feces were collected for 3 days. Bile was also collected for 6 hr from animals of the same age groups after iv doses of 5 and 25 mg/kg [14C]TBBC. Total radioactivity was determined in all samples and the profile of metabolites in bile analyzed by HPLC. Along with a decrease in the older animal's ability to excrete TBBC-derived radioactivity in bile, feces, and urine, there was a decrease in the percentage of the dose eliminated in bile as glucuronide. In vitro, the microsomal glucuronyltransferase activity using TBBC as a substrate decreased in the senescent animals. The hepatic concentration of the cofactor UDPGA also decreased from 2.5 to 28 months of age. The apparent Vmax for the enzyme decreased as a function of age while the apparent Km decreased for the substrate (TBBC) but not for the cofactor (UDPGA) in the 26-month-old rats. These data suggest that with the decrease in the activity of the enzyme as well as a decrease in the available UDPGA, the ability of the senescent rats to conjugate and excrete TBBC may be altered. Thus, the in vitro decline in TBBC glucuronidation is compatible with the decreased excretion of TBBC-derived radioactivity observed in vivo in old rats. When toxicity was evaluated in 2.5-, 16-, and 26-month-old rats exposed to 0.25% TBBC in their diet for 14 days, no age-related change in the toxicity of TBBC was observed. However, there appeared to be an increase in leukemia in the treated senescent rats. JF - Toxicology and applied pharmacology AU - Borghoff, S J AU - Stefanski, S A AU - Birnbaum, L S AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 453 EP - 466 VL - 92 IS - 3 SN - 0041-008X, 0041-008X KW - Antioxidants KW - 0 KW - Cresols KW - Glucuronates KW - Uridine Diphosphate Glucuronic Acid KW - 2616-64-0 KW - 4,4'-thiobis(6-tert-butyl-3-cresol) KW - 96-69-5 KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Age Factors KW - Uridine Diphosphate Glucuronic Acid -- analysis KW - Glucuronosyltransferase -- analysis KW - Bile -- metabolism KW - Leukemia, Experimental -- chemically induced KW - Male KW - Antioxidants -- metabolism KW - Cresols -- toxicity KW - Cresols -- metabolism KW - Glucuronates -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78157763?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+effect+of+age+on+the+glucuronidation+and+toxicity+of+4%2C4%27-thiobis%286-t-butyl-m-cresol%29.&rft.au=Borghoff%2C+S+J%3BStefanski%2C+S+A%3BBirnbaum%2C+L+S&rft.aulast=Borghoff&rft.aufirst=S&rft.date=1988-03-15&rft.volume=92&rft.issue=3&rft.spage=453&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 - 1988-04-26 N1 - Date created - 1988-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of the alpha subunit of tryptophan synthase from Salmonella typhimurium. AN - 78150725; 3126743 AB - Site-specific mutagenesis has been used to prepare two mutant forms of the alpha subunit of tryptophan synthase from Salmonella typhimurium in which either cysteine-81 or cysteine-118 is replaced by a serine residue. These mutant proteins are potentially useful for x-ray crystallographic studies since a heavy metal binding site is specifically eliminated in each mutant. The purified mutant proteins are fully active in four reactions catalyzed by the wild type alpha 2 beta 2 complex of tryptophan synthase. However, the mutant alpha 2 beta 2 complexes dissociate more readily and are less heat-stable than the wild type alpha 2 beta 2 complex. Thus, cysteine-81 and cysteine-118 of the alpha subunit serve structural but not functional roles. JF - Biochemical and biophysical research communications AU - Ahmed, S A AU - Kawasaki, H AU - Bauerle, R AU - Morita, H AU - Miles, E W AD - Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 672 EP - 678 VL - 151 IS - 2 SN - 0006-291X, 0006-291X KW - Macromolecular Substances KW - 0 KW - Serine KW - 452VLY9402 KW - Cystine KW - 48TCX9A1VT KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Index Medicus KW - Base Sequence KW - X-Ray Diffraction KW - Escherichia coli -- genetics KW - Plasmids KW - Binding Sites KW - Tryptophan Synthase -- metabolism KW - Tryptophan Synthase -- genetics KW - Salmonella typhimurium -- genetics KW - Mutation KW - Salmonella typhimurium -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78150725?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Site-directed+mutagenesis+of+the+alpha+subunit+of+tryptophan+synthase+from+Salmonella+typhimurium.&rft.au=Ahmed%2C+S+A%3BKawasaki%2C+H%3BBauerle%2C+R%3BMorita%2C+H%3BMiles%2C+E+W&rft.aulast=Ahmed&rft.aufirst=S&rft.date=1988-03-15&rft.volume=151&rft.issue=2&rft.spage=672&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 - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alkylation of DNA in rats by N-nitrosomethyl-(2-hydroxyethyl)amine: dose response and persistence of the alkylated lesions in vivo. AN - 78128160; 3345527 AB - The in vivo alkylation of DNA by N-nitrosomethyl-(2-hydroxyethyl)amine (NMHEA) was examined in male and female F-344/N rats. NMHEA is a strong hepatocarcinogen in female rats when administered by gavage but a weaker hepatocarcinogen in male rats. Groups of 5 rats of each sex were treated by gavage with various doses of NMHEA dissolved in corn oil. After 4 h the animals were sacrificed and the livers, lungs, and kidneys were removed. The DNA from each liver was isolated and the neutral thermal and mild acid hydrolysates were separated by high-performance liquid chromatography. The alkylated guanines were quantified by fluorescence spectroscopy. NMHEA gives rise to four fluorescent alkylated guanines, 7- and O6-methylguanines, and 7- and O6-hydroxyethylguanines. The dose-response data revealed that all four lesions increased with dose. There was approximately 10x more methylation than hydroxyethylation at the 7 position of guanine. There was less O6 alkylation, but both methylation and hydroxyethylation were observed at all of the doses studied. The overall alkylation was the same in males and females at the 10- and 20-mg/kg doses, but at higher doses the females exhibited significantly higher levels of alkylation than males. The level of alkylation of DNA isolated from non-target tissues, lung, and kidney was low. The persistence of these lesions in vivo was studied at a dose of 25 mg/kg. Groups of five animals each were sacrificed at various times from 0 to 96 h. There was no significant difference between the sexes in persistence of any of the lesions in the liver. The 7-alkylguanines disappeared slowly over the observation period. 7-Methylguanine was present at 30% of the maximum level after 96 h, while 7-hydroxyethylguanine appeared to be more stable. The O6-alkylguanines were removed rapidly from the liver, being at base level by 48 h. The rapid removal of O6-hydroxyethylguanine suggests a repair process independent of O6-alkylguanine-DNA guanine alkyl transferase: an excision repair is postulated. In vitro alkylation of calf thymus DNA by N-nitrosomethyl-(2-tosyloxyethyl)amine, a surrogate for the putative O-sulfate conjugate of NMHEA, resulted in exclusive methylation of DNA-guanine at both the 7 and O6 positions; no hydroxyethylation was detected. In vitro alkylation of calf thymus DNA with 2-hydroxyethyl-ethylnitrosourea resulted in exclusive hydroxyethylation of DNA-guanine at the 7 and O6 positions.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Koepke, S R AU - Kroeger-Koepke, M B AU - Bosan, W AU - Thomas, B J AU - Alvord, W G AU - Michejda, C J AD - Laboratory of Chemical and Physical Carcinogenesis, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 1537 EP - 1542 VL - 48 IS - 6 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - Nitrosamines KW - N-nitrosomethyl-(2-hydroxyethyl)amine KW - 26921-68-6 KW - Guanine KW - 5Z93L87A1R KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Dose-Response Relationship, Drug KW - Time Factors KW - Methylation KW - Male KW - Guanine -- metabolism KW - Female KW - Carcinogens -- metabolism KW - DNA -- metabolism KW - Nitrosamines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78128160?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alkylation+of+DNA+in+rats+by+N-nitrosomethyl-%282-hydroxyethyl%29amine%3A+dose+response+and+persistence+of+the+alkylated+lesions+in+vivo.&rft.au=Koepke%2C+S+R%3BKroeger-Koepke%2C+M+B%3BBosan%2C+W%3BThomas%2C+B+J%3BAlvord%2C+W+G%3BMichejda%2C+C+J&rft.aulast=Koepke&rft.aufirst=S&rft.date=1988-03-15&rft.volume=48&rft.issue=6&rft.spage=1537&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 - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Single copy gene for the chicken non-histone chromosomal protein HMG-17. AN - 78123705; 2831214 AB - A chicken genomic library was screened with the human cDNA encoding the non-histone chromosomal protein HMG-17 and a 4565-base pair fragment containing the entire gene encoding this protein was isolated and characterized. Sequence analysis of the fragment revealed that from the start to end of transcription, the HMG-17 gene is 3293 base pairs long and is comprised of 6 exons ranging in size from 30 to 890 base pairs. Upstream of the putative cap site are both a CAAT box and a TATA box as well as several Sp1 binding sites. The gene has an extremely high content of G and C residues (75%) in a 1150-base pair fragment starting 500 base pairs from the putative cap site. This region satisfies the definition of an HpaII tiny fragment island. Southern analysis indicated that there is a single copy of this gene in chickens, whereas Northern analysis revealed that a single transcript is being synthesized from this gene. A comparison of the chicken and human cDNA and protein sequences and subsequent calculation of the evolutionary rates indicated that HMG-17 is a slowly evolving gene. The present article, which is the first study on the isolation and characterization of a complete gene coding for a high mobility group non-histone protein, indicates that the gene has features characteristic of housekeeping genes. JF - The Journal of biological chemistry AU - Landsman, D AU - Srikantha, T AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 3917 EP - 3923 VL - 263 IS - 8 SN - 0021-9258, 0021-9258 KW - High Mobility Group Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - Index Medicus KW - Animals KW - Chickens KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Humans KW - DNA -- genetics KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Species Specificity KW - Genes KW - High Mobility Group Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78123705?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Single+copy+gene+for+the+chicken+non-histone+chromosomal+protein+HMG-17.&rft.au=Landsman%2C+D%3BSrikantha%2C+T%3BBustin%2C+M&rft.aulast=Landsman&rft.aufirst=D&rft.date=1988-03-15&rft.volume=263&rft.issue=8&rft.spage=3917&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 - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J03229; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergistic inhibition of growth of breast and colon human cancer cell lines by site-selective cyclic AMP analogues. AN - 78122041; 2830966 AB - Our past studies on the mechanism of cyclic AMP (cAMP)-mediated control of tumor growth, using the experimental rat mammary tumor models as well as human breast cancer cell lines, indicated that the action of cAMP is mediated by the RII cAMP receptor protein, the regulatory subunit of cAMP-dependent protein kinase type II (Y. S. Cho-Chung, J. Cyclic Nucleotide Res., 6: 163, 1980). We now shown that the site-selective cAMP analogues, which are manyfold more active in binding to the cAMP receptor protein than previously studied analogues, demonstrate a potent growth inhibition of seven breast and three colon human cancer cell lines. The cAMP receptor protein has two different cAMP binding sites, and cAMP analogues that selectively bind to either one of the two binding sites are known as either site 1 selective (C-8 analogues) or site 2 selective (C-6 analogues). Nineteen site-selective analogues, C-6 and C-8 monosubstituted and C-6,-8 disubstituted, were tested for their growth regulatory effect. The majority of these analogues demonstrated an appreciable growth inhibition, with no sign of toxicity in all 10 cancer lines at micromolar concentrations. The three most potent inhibitors were 8-Cl-, N6-benzyl-, and N6-phenyl-8-thio-p-chlorophenyl-cAMP, demonstrating 50% growth inhibition at 5-25 microM concentrations (IC50). Furthermore, N6-analogues, in combination with halogen or thio derivatives of C-8 analogues, demonstrated synergistic enhancement of growth inhibition. The growth inhibition paralleled a change in cell morphology, an augmentation of the RII cAMP receptor protein, and a reduction in p21 ras protein. The growth inhibition by 8-Cl-cAMP was not due to its metabolite, 8-Cl-adenosine, since: (a) the growth inhibition by 8-Cl-cAMP was released upon cessation of treatment, whereas that by 8-Cl-adenosine was not released; (b) 8-Cl-cAMP treatment did not affect cell cycle progression, whereas 8-Cl-adenosine brought about G1 synchronization; (c) 8-Cl-cAMP treatment caused reduction of p21 ras protein, whereas 8-Cl-adenosine did not affect p21 levels; and (d) 8-Cl-adenosine was not detected in either cell extracts or medium from the cells treated with 8-Cl-cAMP for 48-72 h. Site-selective cAMP analogues thus provide a new physiological means to control the growth of breast and colon human cancer cells. JF - Cancer research AU - Tagliaferri, P AU - Katsaros, D AU - Clair, T AU - Ally, S AU - Tortora, G AU - Neckers, L AU - Rubalcava, B AU - Parandoosh, Z AU - Chang, Y A AU - Revankar, G R AD - Cellular Biochemistry Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 1642 EP - 1650 VL - 48 IS - 6 SN - 0008-5472, 0008-5472 KW - Proto-Oncogene Proteins KW - 0 KW - Receptors, Cyclic AMP KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - HRAS protein, human KW - EC 3.6.5.2 KW - Proto-Oncogene Proteins p21(ras) KW - Index Medicus KW - Receptors, Cyclic AMP -- analysis KW - Tumor Cells, Cultured -- drug effects KW - Proto-Oncogene Proteins -- analysis KW - Protein Kinases -- analysis KW - Humans KW - Receptors, Cyclic AMP -- drug effects KW - Drug Synergism KW - Molecular Weight KW - Female KW - Chromatography, High Pressure Liquid KW - Breast Neoplasms -- pathology KW - Cyclic AMP -- pharmacology KW - Cyclic AMP -- analogs & derivatives KW - Colonic Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78122041?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+growth+of+breast+and+colon+human+cancer+cell+lines+by+site-selective+cyclic+AMP+analogues.&rft.au=Tagliaferri%2C+P%3BKatsaros%2C+D%3BClair%2C+T%3BAlly%2C+S%3BTortora%2C+G%3BNeckers%2C+L%3BRubalcava%2C+B%3BParandoosh%2C+Z%3BChang%2C+Y+A%3BRevankar%2C+G+R&rft.aulast=Tagliaferri&rft.aufirst=P&rft.date=1988-03-15&rft.volume=48&rft.issue=6&rft.spage=1642&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 - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Variant forms of rat epidermal growth factor present in the urine of nude rats bearing human tumors. AN - 78121500; 3257897 AB - Epidermal growth factor (EGF) receptor-binding peptides from the urine of tumor patients have been reported to differ in molecular weight and relative hydrophobicity from those of normal individuals. Nude rats bearing human large cell lung carcinomas or chondrosarcomas and non-tumor-bearing sibling control rats were used to investigate the contributions of tumor and host to urinary EGF-related peptide growth factors. Peptides were adsorbed from urine onto methyl-bonded silica and eluted according to their relative hydrophobicity by a stepwise gradient of aqueous acetonitrile. Total EGF receptor-binding activity relative to urinary creatine was elevated in the urine of only one group of tumor-bearing rats. However, the proportion of relatively hydrophilic activity was increased markedly in all three groups of tumor-bearing rats. Rats bearing a large cell lung cancer excreted unusually hydrophilic Mr 6000 peptides that were chromatographically similar to transforming growth factor alpha on reverse phase high performance liquid chromatography but proved to be rat EGF by radioimmunoassay (RIA). EGF receptor-binding activity that was common to the urine of tumor-bearing animals regardless of tumor type, but more hydrophilic than that from control rats, had Mr 60,000, 30,000, 12,000, and 4,000 to 7,000 components. All reacted fully in the rat EGF RIA and were negative for human EGF and transforming growth factor alpha by RIA. A more hydrophobic fraction of EGF receptor-binding activity, common to control and tumor-bearing animals, contained Mr 33,000, 5,000 to 7,000, and 2,000 to 5,000 components. High performance liquid chromatography and gel electrophoresis of the Mr 33,000 activity revealed a high molecular weight rat EGF comparable to that reported in human urine. No human EGF or transforming growth factor alpha was detected by RIA in any of the active fractions from tumor-bearing rat urine. Thus, all EGF receptor-binding activity appeared to derive from rat EGF produced by the rat host and not by the xenografted tumors. JF - Cancer research AU - Hudgins, W R AU - Orth, D N AU - Stromberg, K AD - Laboratory of Viral Carcinogenesis, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 1428 EP - 1434 VL - 48 IS - 6 SN - 0008-5472, 0008-5472 KW - Peptides KW - 0 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Transforming Growth Factors KW - 76057-06-2 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Rats KW - Neoplasm Transplantation KW - Animals KW - Receptor, Epidermal Growth Factor -- metabolism KW - Humans KW - Transplantation, Heterologous KW - Mice, Nude KW - Mice KW - Radioimmunoassay KW - Molecular Weight KW - Chromatography, High Pressure Liquid KW - Peptides -- urine KW - Peptides -- immunology KW - Neoplasms, Experimental -- urine KW - Epidermal Growth Factor -- urine KW - Epidermal Growth Factor -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78121500?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Variant+forms+of+rat+epidermal+growth+factor+present+in+the+urine+of+nude+rats+bearing+human+tumors.&rft.au=Hudgins%2C+W+R%3BOrth%2C+D+N%3BStromberg%2C+K&rft.aulast=Hudgins&rft.aufirst=W&rft.date=1988-03-15&rft.volume=48&rft.issue=6&rft.spage=1428&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 - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of chromosome loss in ras/myc-induced Syrian hamster tumors. AN - 78117348; 2449958 AB - It has been shown previously that normal Syrian hamster embryo cells are neoplastically transformed by transfection with two cooperating oncogenes, v-myc plus v-Ha-ras. Karyotypic analyses of the cells from the tumors revealed a nonrandom chromosome change, monosomy of chromosome 15. In order to clarify the role of chromosome loss in these tumor cells with defined oncogene alterations, molecular and cytogenetic studies were performed on hybrids between normal Syrian hamster embryo cells and ras/myc tumor cells. Following fusion of the tumor cells with the normal cells which are not immortal, the majority of the cell hybrids senesced after less than or equal to 20 population doublings indicating that immortality was recessive. Some of the hybrids escaped senescence and grew indefinitely. These immortal hybrid cells retained the expected numbers of chromosome 15 indicating that escape from senescence did not involve loss of this chromosome. The tumorigenicity and anchorage-independent growth of the nonsenescent hybrids were still suppressed significantly. In these suppressed hybrid cells, RNAs complementary to the v-Ha-ras and v-myc oncogenes were expressed. Furthermore, radioimmune precipitation with a monoclonal antibody to p21ras of [35S]methionine-labeled cell extracts followed by polyacrylamide gel electrophoresis/sodium dodecyl sulfate electrophoresis showed that the suppressed hybrid cells contained high levels of the mutated ras protein. These results indicate that tumorigenicity is suppressed in the hybrids even though the oncogenes are expressed. When the hybrid cells were passaged, anchorage-independent variants appeared in the cultures. At this time, morphological changes occurred in the cultures and the cells were tumorigenic. Karyotypic analyses of the transformed segregants versus the parental hybrid cells revealed a nonrandom loss of one copy of chromosome 15 in the transformed segregants. No other nonrandom chromosome change was observed. These results suggest that the loss of chromosome 15 results in the loss of a cellular tumor suppressor gene which effects a phenotypic change necessary for expression of neoplastic transformation. In addition, the cellular factors responsible for the senescence of the hybrids may provide another mechanism involved in suppressing tumorigenicity. JF - Cancer research AU - Oshimura, M AU - Koi, M AU - Ozawa, N AU - Sugawara, O AU - Lamb, P W AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 1623 EP - 1632 VL - 48 IS - 6 SN - 0008-5472, 0008-5472 KW - Proto-Oncogene Proteins KW - 0 KW - RNA KW - 63231-63-0 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Karyotyping KW - Proto-Oncogene Proteins -- biosynthesis KW - Animals KW - Transfection KW - Mesocricetus KW - RNA -- analysis KW - Nucleic Acid Hybridization KW - Metaphase KW - Cell Line KW - Cricetinae KW - Cell Survival KW - Oncogenes KW - Chromosome Aberrations KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78117348?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+chromosome+loss+in+ras%2Fmyc-induced+Syrian+hamster+tumors.&rft.au=Oshimura%2C+M%3BKoi%2C+M%3BOzawa%2C+N%3BSugawara%2C+O%3BLamb%2C+P+W%3BBarrett%2C+J+C&rft.aulast=Oshimura&rft.aufirst=M&rft.date=1988-03-15&rft.volume=48&rft.issue=6&rft.spage=1623&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 - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenicity of hydroxyalkylnitrosamines in F344 rats: contrasting behavior of beta- and gamma-hydroxylated nitrosamines. AN - 78116589; 3345526 AB - The carcinogenicity of N-nitrosomethyl-(2-hydroxyethyl)amine (NMHEA), N-nitrosomethyl-(3-hydroxypropyl)amine (NMHPA), and the p-toluenesulfonate (tosylate) ester of NMHEA (NMHEATs) was tested in male and female F344 rats. The chemicals (25.6 mumol per application) were administered by twice-weekly gavage in corn oil (0.2 ml) for the lifetime of the animals. NMHEA was found to be an effective carcinogen under those conditions. The median survival time for the females was 9 mo after treatment was initiated, while for the males it was 12 mo. The principal cause of death of the females was hepatocellular carcinoma (14 of 20), while only 6 of 20 male rats exhibited that tumor. A few of the male rats had squamous cell carcinomas of the nasal epithelium (4 of 20), tumors which were not observed in the females. NMHPA was a much weaker carcinogen. Many of these rats survived for 2 yr and most had many age-related cancers. Nevertheless, 10 of the NMHPA-treated males and 2 females had adenocarcinoma of the lung, which was absent in the controls and also induced a significant number of neoplastic nodules in the livers of rats of both sexes. NMHEATs was also a weak carcinogen. However, besides many age-related tumors, it induced some hepatocellular carcinomas as well as hemangiosarcomas of the liver. NMHEATs was at least partially hydrolyzed to NMHEA, which was detected in the blood plasma of treated rats. A hypothesis has been advanced that NMHEA is activated to a proximate carcinogen by sulfate conjugation of the hydroxyl group; the present data do not contradict this hypothesis. The relatively lower carcinogenic potency of NMHPA, the different tumor spectrum induced by this chemical, and particularly the differences in chemical behavior suggest that its mode of activation is not the same as that for NMHEA. JF - Cancer research AU - Koepke, S R AU - Creasia, D R AU - Knutsen, G L AU - Michejda, C J AD - Laboratory of Chemical and Physical Carcinogenesis, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 1533 EP - 1536 VL - 48 IS - 6 SN - 0008-5472, 0008-5472 KW - Nitrosamines KW - 0 KW - N-nitrosomethyl-(2-hydroxyethyl)amine KW - 26921-68-6 KW - N-nitrosomethyl-(2-hydroxyethyl)amine 4-toluenesulfonate ester KW - 66398-63-8 KW - N-nitrosomethyl-(3-hydroxypropyl)amine KW - 70415-59-7 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Biotransformation KW - Liver Neoplasms, Experimental -- chemically induced KW - Male KW - Female KW - Hydroxylation KW - Nitrosamines -- toxicity KW - Neoplasms, Experimental -- chemically induced KW - Nitrosamines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78116589?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Carcinogenicity+of+hydroxyalkylnitrosamines+in+F344+rats%3A+contrasting+behavior+of+beta-+and+gamma-hydroxylated+nitrosamines.&rft.au=Koepke%2C+S+R%3BCreasia%2C+D+R%3BKnutsen%2C+G+L%3BMichejda%2C+C+J&rft.aulast=Koepke&rft.aufirst=S&rft.date=1988-03-15&rft.volume=48&rft.issue=6&rft.spage=1533&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 - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adult stature and risk of cancer. AN - 78116337; 3345534 AB - We examined the relationship between adult stature and cancer incidence using data from the first U.S. National Health and Nutrition Examination Survey and its follow-up study. Among 12,554 participants 25-74 years old, 460 cancers occurred in men and 399 in women after an average follow-up period of approximately 10 years. The age-adjusted relative risk of cancer for the second (Q2) through fourth (Q4) quartiles of stature compared to the first quartile among men were significantly increased: 1.5, 1.4, and 1.4. After adjustment for race, cigarette smoking, income, and body mass index, the all-sites cancer relative risk increased slightly to 1.6, 1.5, and 1.6. For most cancer sites in men, and particularly colorectal cancer (relative risk = 2.1 for Q4), the lowest incidence was observed among those in the shortest quartile of stature. A weaker, positive association was evident among women, restricted primarily to cancer of the breast and colorectum (relative risk in Q4 = 2.1 and 1.6 for the two cancers, respectively). These findings indicate that short stature is associated with reduced risk of cancer, particularly in men, and suggest a role for nutrition early in life in human carcinogenesis. JF - Cancer research AU - Albanes, D AU - Jones, D Y AU - Schatzkin, A AU - Micozzi, M S AU - Taylor, P R AD - Cancer Prevention Studies Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/03/15/ PY - 1988 DA - 1988 Mar 15 SP - 1658 EP - 1662 VL - 48 IS - 6 SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Smoking KW - Risk Factors KW - Humans KW - Adult KW - Energy Intake KW - Aged KW - Middle Aged KW - Nutritional Physiological Phenomena KW - Male KW - Female KW - Body Height KW - Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78116337?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adult+stature+and+risk+of+cancer.&rft.au=Albanes%2C+D%3BJones%2C+D+Y%3BSchatzkin%2C+A%3BMicozzi%2C+M+S%3BTaylor%2C+P+R&rft.aulast=Albanes&rft.aufirst=D&rft.date=1988-03-15&rft.volume=48&rft.issue=6&rft.spage=1658&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 - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multidrug resistance. AN - 78092490; 2892943 AB - The ability of malignant cells to develop resistance to cytotoxic drugs poses a major obstacle to the ultimate success of cancer therapy. While some mechanisms of resistance allow cells to survive exposure to a single agent, the phenomenon of multidrug resistance (MDR) confers upon cells the ability to withstand exposure to lethal doses of many structurally unrelated antineoplastic agents. MDR has been strongly linked to the overexpression of a membrane-associated glycoprotein, P-glycoprotein, which appears to play a role in drug efflux. However, several lines of evidence suggest that other mechanisms of resistance are involved in MDR; biochemical similarities observed in a human breast cancer cell line after the acquisition of MDR and in carcinogen-induced rat preneoplastic hepatic nodules indicate that changes in regulation of phase I and phase II drug-metabolizing enzymes may also play a role in MDR. An atypical pattern of MDR has been characterized and related to altered topoisomerase activity. Improvement in current cancer chemotherapy may be achieved by interfering with the regulation and expression of mechanisms of MDR. JF - Journal of the National Cancer Institute AU - Moscow, J A AU - Cowan, K H AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/03/02/ PY - 1988 DA - 1988 Mar 02 SP - 14 EP - 20 VL - 80 IS - 1 SN - 0027-8874, 0027-8874 KW - Antineoplastic Agents KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Gene Expression Regulation KW - Membrane Glycoproteins -- genetics KW - Neoplasms -- drug therapy KW - Neoplasms, Experimental -- enzymology KW - Drug Resistance -- genetics KW - Neoplasms -- enzymology KW - Neoplasms, Experimental -- drug therapy KW - Antineoplastic Agents -- therapeutic use KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78092490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Multidrug+resistance.&rft.au=Moscow%2C+J+A%3BCowan%2C+K+H&rft.aulast=Moscow&rft.aufirst=J&rft.date=1988-03-02&rft.volume=80&rft.issue=1&rft.spage=14&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 - 1988-03-23 N1 - Date created - 1988-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Partial correlation coefficients approximate the real intrasubject correlation pattern in the analysis of interregional relations of cerebral metabolic activity. AN - 85270163; pmid-3258028 AB - Correlation coefficients between pairs of regional glucose metabolic rates have been used to assess patterns of functional associations among brain regions in humans and animals. Partial correlation coefficients (partialing out the global metabolic rate) or correlations between reference ratios (regional to global metabolic rate) have been used to remove the distorting influence of systematic intersubject differences in glucose utilization. Suggesting that partial correlations may not preserve the true (but unknown) intrasubject correlation structure within the brain, others have used a theoretical example to show how an artifactually large negative partial correlation coefficient might arise. Here, we show that such an example is highly unlikely when applied to resting cerebral metabolism, and can be identified in experimental data by testing for a bimodal distribution of partial correlation values. We then show that partial correlations or reference ratio correlations of experimental resting metabolic rates give values which closely approximate the intrasubject correlation coefficients. JF - Journal of Nuclear Medicine AU - Horwitz, B AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute on Aging, Bethesda, Maryland 20892. PY - 1988 SP - 392 EP - 399 VL - 29 IS - 3 SN - 0161-5505, 0161-5505 KW - Statistics KW - Aged, 80 and over KW - Fludeoxyglucose F 18 KW - Human KW - Fluorine Radioisotopes KW - Adult KW - Glucose KW - Brain KW - Tomography, Emission-Computed KW - Middle Age KW - Deoxyglucose KW - Aged KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85270163?accountid=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+Nuclear+Medicine&rft.atitle=Partial+correlation+coefficients+approximate+the+real+intrasubject+correlation+pattern+in+the+analysis+of+interregional+relations+of+cerebral+metabolic+activity.&rft.au=Horwitz%2C+B%3BRapoport%2C+S+I&rft.aulast=Horwitz&rft.aufirst=B&rft.date=1988-03-01&rft.volume=29&rft.issue=3&rft.spage=392&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nuclear+Medicine&rft.issn=01615505&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Acetylcholine release by bradykinin, inositol 1,4,5-trisphosphate and phorbol dibutyrate in rodent neuroblastoma cells. AN - 78387560; 2842493 AB - 1. The action of bradykinin (BK), inositol 1,4,5-trisphosphate (InsP3), and phorbol dibutyrate (PDBu) on the release of acetylcholine (ACh) was studied electrophysiologically on short-distance (less than 20 micron) synapses formed between cultured NG108-15 mouse neuroblastoma x rat glioma hybrid cells and rat muscle cells. Action potentials in NG108-15 cells did not usually evoke an excitatory junction potential (EJP) in the muscle cell in this system. 2. Ionophoretic application of BK onto the somatic surface of an NG108-15 cell produced an increase in frequency of miniature end-plate potentials (MEPPs) for 40-50s in the paired myotube. Some MEPPs were evoked during BK-induced hyperpolarization (10-20 s) of the hybrid cell soma. A few MEPPs were also elicited during BK-induced depolarization. 3. Ionophoretic injection of Ca2+ into an NG108-15 cell soma generated MEPPs for a very brief period (less than 3 s), coincident with somatic hyperpolarization. No increase was observed during a subsequent somatic depolarization induced by a larger current of Ca2+. 4. Ionophoretic injection of InsP3 into the cytoplasm of an NG108-15 cell soma transiently evoked MEPPs during the InsP3-induced hyperpolarizing phase. A large InsP3 injection caused sustained generation of MEPPs for 2-4 min, associated with InsP3-evoked depolarization. 5. Within 3-5 min after exposure of NG108-15-myotube pairs to 1 microM-PDBu, the MEPP frequency increased by 2-5 times and reached a plateau after 8 min. The increase continued after wash-out of the drug. The PDBu-induced increase of MEPPs was still observed when the membrane potential of the NG108-15 cell was clamped at -30 mV. 6. The data suggest that the BK-induced facilitation results from the action of two intracellular second messengers: an InsP3-dependent release of Ca2+ from the intracellular storage sites and protein phosphorylation by diacyclglycerol (DAG)-activated protein kinase C. JF - The Journal of physiology AU - Higashida, H AD - Laboratory of Biochemical Genetics, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 209 EP - 222 VL - 397 SN - 0022-3751, 0022-3751 KW - Inositol Phosphates KW - 0 KW - Phorbol Esters KW - Sugar Phosphates KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - Acetylcholine KW - N9YNS0M02X KW - Bradykinin KW - S8TIM42R2W KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Synapses -- physiology KW - Synaptic Transmission -- drug effects KW - Mice KW - Membrane Potentials -- drug effects KW - Calcium -- pharmacology KW - Action Potentials -- drug effects KW - Hybrid Cells -- drug effects KW - Time Factors KW - Muscles -- physiology KW - Phorbol Esters -- pharmacology KW - Acetylcholine -- metabolism KW - Sugar Phosphates -- pharmacology KW - Bradykinin -- pharmacology KW - Inositol Phosphates -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78387560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+physiology&rft.atitle=Acetylcholine+release+by+bradykinin%2C+inositol+1%2C4%2C5-trisphosphate+and+phorbol+dibutyrate+in+rodent+neuroblastoma+cells.&rft.au=Higashida%2C+H&rft.aulast=Higashida&rft.aufirst=H&rft.date=1988-03-01&rft.volume=397&rft.issue=&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+physiology&rft.issn=00223751&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-13 N1 - Date created - 1988-10-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Physiol. 1968 Mar;195(2):481-92 [4296699] J Physiol. 1988 Mar;397:185-207 [3261793] J Physiol. 1974 Jun;239(3):571-94 [4152807] J Physiol. 1974 Jun;239(3):553-70 [4368961] J Cell Biol. 1974 Nov;63(2 Pt 1):691-9 [4371727] Proc Natl Acad Sci U S A. 1976 Jan;73(1):123-7 [1061105] Proc Natl Acad Sci U S A. 1976 Oct;73(10):3544-8 [185619] Brain Res. 1978 May 26;147(2):245-59 [206314] Brain Res. 1978 May 26;147(2):261-76 [25697] Proc Natl Acad Sci U S A. 1978 Mar;75(3):1314-8 [206894] Proc Natl Acad Sci U S A. 1979 Mar;76(3):1135-9 [220607] Brain Res. 1981 Jun 15;214(2):287-99 [7237172] Brain Res. 1982 May 6;239(1):191-9 [7093675] Tissue Cell. 1983;15(6):903-19 [6320493] Cold Spring Harb Symp Quant Biol. 1983;48 Pt 2:707-15 [6327174] J Neurosci. 1984 Jun;4(6):1653-61 [6327939] Proc Natl Acad Sci U S A. 1984 Jul;81(14):4353-7 [6087319] J Biol Chem. 1984 Aug 25;259(16):10201-7 [6088487] Nature. 1984 Aug 23-29;310(5979):691-3 [6236373] Mol Pharmacol. 1984 Sep;26(2):261-6 [6237255] Biochem J. 1984 Sep 15;222(3):833-6 [6091624] J Physiol. 1984 Nov;356:587-99 [6520797] FEBS Lett. 1985 Feb 25;181(2):403-6 [2857660] Brain Res. 1984 Dec 24;324(2):201-10 [6529617] FEBS Lett. 1985 Apr 22;183(2):235-9 [2580737] Brain Res. 1985 Apr 29;333(1):185-7 [2986772] Pflugers Arch. 1985 Oct;405(3):260-4 [4069982] Brain Res. 1985 Dec 30;361(1-2):77-90 [4084812] Proc Natl Acad Sci U S A. 1986 Feb;83(4):942-6 [3081891] Pflugers Arch. 1986 Feb;406(2):181-3 [2870468] Nature. 1986 May 8-14;321(6066):175-7 [3010137] Science. 1986 Jul 18;233(4761):305-12 [3014651] Brain Res. 1986 Jul 30;379(1):84-9 [3742218] Eur J Pharmacol. 1986 Jul 15;126(1-2):47-51 [2428631] Nature. 1986 Sep 25-Oct 1;323(6086):333-5 [2429190] Pflugers Arch. 1986 Oct;407(4):409-13 [3774508] Nature. 1987 Jan 1-7;325(6099):58-60 [2432432] EMBO J. 1987 Jan;6(1):49-54 [2884101] J Physiol. 1988 Mar;397:167-84 [2457696] J Physiol. 1971 Sep;217(2):497-515 [4329008] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inositol 1,4,5-trisphosphate and diacylglycerol mimic bradykinin effects on mouse neuroblastoma x rat glioma hybrid cells. AN - 78386705; 3261793 AB - 1. The role of inositol 1,4,5-trisphosphate (InsP3) and diacylglycerol (DAG) as possible mediators of the membrane current responses of NG108-15 neuroblastoma x glioma hybrid cells to bradykinin (BK, Brown & Higashida, 1988b) has been tested using intracellular ionophoresis of InsP3 and external application of phorbol dibutyrate (PDBu) and 1-oleoyl-2-acetylglycerol (OAG). 2. Intracellular ionophoresis of InsP3 into cells clamped at -30 to -50 mV produced (i) a transient outward current, (ii) a transient outward current followed by an inward current, or (iii) an inward current. All currents were accompanied by an increased input conductance. 3. The transient outward current reversed at between -80 and -90 mV. The reversal potential was shifted to more positive potentials on raising extracellular [K+], suggesting that it resulted from an increased K+ conductance. 4. The outward current was inhibited by apamin (0.4 microM) or d-tubocurarine (0.2-0.5 mM); these drugs also inhibit the outward current produced by BK or by intracellular Ca2+ injections (Brown & Higashida, 1988 a, b). The outward current was also slowly reduced in 0 mM [Ca2+] or 0.5 mM [Cd2+] plus 2 mM [Co2+] solution. 5. Ionophoretic injection of inositol 1,3,4-trisphosphate and inositol 1,3,4,5-tetrakisphosphate, guanosine trisphosphate or inorganic phosphate did not evoke an outward current but produced only an inward current with an increased conductance, reversing at between -10 and -20 mV. 6. Bath application of PDBu (10 nM-1 microM) or OAG (1-10 microM) produced an inward current with a fall in input conductance. The inward current was voltage dependent and was accompanied by an inhibition of the time-dependent current relaxations associated with activation or deactivation of the voltage-dependent K+ current, IM. 7. PDBu did not clearly reduce the Ca2+ current or the Ca2+-dependent K+ current recorded in these cells. During superfusion with PDBu, the outward current produced by intracellular ionophoresis of InsP3 was greatly enhanced. 8. The results support the view that the two membrane current responses to BK might both result from accelerated membrane phosphatidylinositide hydrolysis. One product, InsP3, releases Ca2+ and activates an apamin-curare-sensitive outward K+ current; this effect is imitated by intracellular InsP3 ionophoresis. The second product, DAG; activates protein kinase C to inhibit the voltage-dependent K+ current IM and generate an inward current; this effect is imitated by external application of PDBu or OAG. JF - The Journal of physiology AU - Brown, D A AU - Higashida, H AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 185 EP - 207 VL - 397 SN - 0022-3751, 0022-3751 KW - Diglycerides KW - 0 KW - Glycerides KW - Inositol Phosphates KW - Phorbol Esters KW - Sugar Phosphates KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - 1-oleoyl-2-acetylglycerol KW - 86390-77-4 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Potassium KW - RWP5GA015D KW - Bradykinin KW - S8TIM42R2W KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Protein Kinase C -- metabolism KW - Potassium -- physiology KW - Animals KW - Enzyme Activation -- drug effects KW - Mice KW - Membrane Potentials -- drug effects KW - Calcium -- pharmacology KW - Bradykinin -- pharmacology KW - Time Factors KW - Phorbol Esters -- pharmacology KW - Diglycerides -- pharmacology KW - Sugar Phosphates -- pharmacology KW - Hybrid Cells -- drug effects KW - Inositol Phosphates -- pharmacology KW - Glycerides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78386705?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+physiology&rft.atitle=Inositol+1%2C4%2C5-trisphosphate+and+diacylglycerol+mimic+bradykinin+effects+on+mouse+neuroblastoma+x+rat+glioma+hybrid+cells.&rft.au=Brown%2C+D+A%3BHigashida%2C+H&rft.aulast=Brown&rft.aufirst=D&rft.date=1988-03-01&rft.volume=397&rft.issue=&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+physiology&rft.issn=00223751&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-10-13 N1 - Date created - 1988-10-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1985 May;82(9):3040-4 [2581262] Pflugers Arch. 1982 May;393(3):248-53 [6285269] J Membr Biol. 1985;86(2):139-44 [2411930] Proc Natl Acad Sci U S A. 1985 Sep;82(17):5651-5 [2994039] Proc Natl Acad Sci U S A. 1985 Sep;82(17):6001-5 [2994058] Pflugers Arch. 1985 Oct;405(3):260-4 [4069982] Proc Natl Acad Sci U S A. 1986 Jan;83(1):184-8 [2417236] Biochem J. 1985 Nov 15;232(1):211-5 [4084229] J Biol Chem. 1986 Jan 25;261(3):1459-69 [3080427] FEBS Lett. 1986 Feb 17;196(2):279-83 [3005034] J Biol Chem. 1986 Mar 5;261(7):3184-92 [3081502] J Neurosci. 1986 Feb;6(2):475-80 [3456434] Proc Natl Acad Sci U S A. 1986 Feb;83(4):942-6 [3081891] J Biol Chem. 1986 Apr 25;261(12):5307-13 [3082882] Biochem Biophys Res Commun. 1986 Mar 13;135(2):507-14 [3516143] J Neurochem. 1983 Feb;40(2):547-54 [6822837] Nature. 1983 Nov 3-9;306(5938):67-9 [6605482] Cell Calcium. 1983 Dec;4(5-6):421-8 [6323004] Cell Calcium. 1983 Dec;4(5-6):429-37 [6323005] J Gen Physiol. 1984 Jul;84(1):1-23 [6086805] J Biol Chem. 1984 Aug 25;259(16):10201-7 [6088487] J Gen Physiol. 1984 Aug;84(2):157-86 [6092514] Nature. 1984 Nov 22-28;312(5992):315-21 [6095092] J Biol Chem. 1985 Feb 10;260(3):1366-9 [3155734] Nature. 1985 Jan 24-30;313(6000):313-6 [2578617] FEBS Lett. 1985 Feb 25;181(2):403-6 [2857660] J Physiol. 1985 Jan;358:335-63 [2580084] FEBS Lett. 1985 Apr 22;183(2):235-9 [2580737] J Biol Chem. 1985 May 10;260(9):5236-9 [2985584] Nature. 1986 Apr 17-23;320(6063):631-4 [3010126] Biochem Biophys Res Commun. 1986 Apr 29;136(2):622-9 [3010987] Nature. 1986 Jun 12-18;321(6071):695-7 [2423884] Science. 1986 Jul 18;233(4761):305-12 [3014651] Brain Res. 1986 Jul 30;379(1):84-9 [3742218] Eur J Pharmacol. 1986 Jul 15;126(1-2):47-51 [2428631] Nature. 1986 Sep 25-Oct 1;323(6086):333-5 [2429190] Nature. 1986 Oct 23-29;323(6090):718-20 [2430185] FEBS Lett. 1986 Nov 24;208(2):283-6 [2430833] J Pharmacol Exp Ther. 1987 Feb;240(2):617-22 [2879910] Biochem J. 1986 Nov 15;240(1):301-4 [3827851] J Neurochem. 1987 May;48(5):1632-9 [3494104] EMBO J. 1987 Jan;6(1):49-54 [2884101] J Physiol. 1987 Apr;385:591-609 [2443673] J Physiol. 1988 Mar;397:149-65 [2457695] J Physiol. 1988 Mar;397:167-84 [2457696] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2538-42 [3157991] Nature. 1980 Feb 14;283(5748):673-6 [6965523] Nature. 1982 Apr 22;296(5859):746-9 [6280066] Proc Natl Acad Sci U S A. 1982 Feb;79(4):1308-12 [6122211] J Biol Chem. 1982 Jul 10;257(13):7847-51 [7085651] Brain Res. 1982 May 6;239(1):191-9 [7093675] Nature. 1985 Jun 27-Jul 3;315(6022):752-5 [3925349] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comments on primary and adjuvant treatments of breast cancer. AN - 78269756; 3383950 JF - European journal of cancer & clinical oncology AU - Cascinelli, N AU - Greco, M AU - Leo, E AD - Division of Surgical Oncology B, National Cancer Institute, Milan, Italy. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 487 EP - 491 VL - 24 IS - 3 SN - 0277-5379, 0277-5379 KW - Cyclophosphamide KW - 8N3DW7272P KW - Fluorouracil KW - U3P01618RT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Fluorouracil -- administration & dosage KW - Cyclophosphamide -- administration & dosage KW - Lymphatic Metastasis KW - Combined Modality Therapy KW - Humans KW - Prognosis KW - Lymph Node Excision KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Methotrexate -- administration & dosage KW - Recurrence KW - Female KW - Breast Neoplasms -- mortality KW - Breast Neoplasms -- therapy KW - Breast Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78269756?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%26+clinical+oncology&rft.atitle=Comments+on+primary+and+adjuvant+treatments+of+breast+cancer.&rft.au=Cascinelli%2C+N%3BGreco%2C+M%3BLeo%2C+E&rft.aulast=Cascinelli&rft.aufirst=N&rft.date=1988-03-01&rft.volume=24&rft.issue=3&rft.spage=487&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%26+clinical+oncology&rft.issn=02775379&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-05 N1 - Date created - 1988-08-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of soybean feeding on experimental carcinogenesis--III. Carcinogenecity of nitrite and dibutylamine in mice: a histopathological study. AN - 78267770; 3383943 AB - The potential carcinogenic effect of nitrosamine precursors, DBA (dibutylamine) and nitrite, was clearly demonstrated pathologically in the liver and bladder of male Swiss albino mice. Benign tumours were induced in the bladder with an incidence of 40%, and hepatomas were detected in the liver in 27% of the cases. The protective effect of soybean and ascorbic acid, added separately to the diet or to the drinking water respectively, was demonstrated by a marked reduction in dysplastic features and absence of tumour in both the liver and the urinary bladder. JF - European journal of cancer & clinical oncology AU - Mokhtar, N M AU - el-Aaser, A A AU - el-Bolkainy, M N AU - Ibrahim, H A AU - Badr El-Din, N K AU - Moharram, N Z AD - Department of Pathology, National Cancer Institute, University of Cairo, Egypt. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 403 EP - 411 VL - 24 IS - 3 SN - 0277-5379, 0277-5379 KW - Butylamines KW - 0 KW - Nitrites KW - dibutylamine KW - 2194M2LA21 KW - Sodium Nitrite KW - M0KG633D4F KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Index Medicus KW - Urinary Bladder -- pathology KW - Mice, Inbred Strains KW - Animals KW - Liver -- pathology KW - Ascorbic Acid -- therapeutic use KW - Mice KW - Male KW - Butylamines -- toxicity KW - Urinary Bladder Neoplasms -- prevention & control KW - Urinary Bladder Neoplasms -- pathology KW - Liver Neoplasms, Experimental -- pathology KW - Nitrites -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Sodium Nitrite -- toxicity KW - Liver Neoplasms, Experimental -- prevention & control KW - Urinary Bladder Neoplasms -- chemically induced KW - Soybeans UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78267770?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%26+clinical+oncology&rft.atitle=Effect+of+soybean+feeding+on+experimental+carcinogenesis--III.+Carcinogenecity+of+nitrite+and+dibutylamine+in+mice%3A+a+histopathological+study.&rft.au=Mokhtar%2C+N+M%3Bel-Aaser%2C+A+A%3Bel-Bolkainy%2C+M+N%3BIbrahim%2C+H+A%3BBadr+El-Din%2C+N+K%3BMoharram%2C+N+Z&rft.aulast=Mokhtar&rft.aufirst=N&rft.date=1988-03-01&rft.volume=24&rft.issue=3&rft.spage=403&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%26+clinical+oncology&rft.issn=02775379&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-08-05 N1 - Date created - 1988-08-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Eur J Cancer Clin Oncol. 2010 Nov;46(17):3128 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The induction of bladder tumors in F344 rats by intravesicular administration of some nitrosamines. AN - 78229171; 3131281 AB - Three nitrosamines, metabolically related and formed in vivo from the bladder carcinogen nitrosomethyl-n-octylamine, were administered to groups of 12 female F344 rats by intraurethral instillation twice a week for 30 weeks. All three compounds induced tumors in the urinary bladder. Nitrosomethyl-2-oxopropylamine at 10 mg/ml was the most potent, causing death of half of the animals with tumors at 43 weeks, following a total dose of 1.0 mmol; most of the rats also had tumors of the nasal mucosa, and there were some tumors of the kidney and kidney pelvis. Nitrosomethyl-2-hydroxypropylamine at 10 mg/ml (total dose 1.0 mmol) was much less effective, the median week of death being 83 weeks. In addition to bladder tumors, this group had tumors of the nasal mucosa, esophagus, and kidney. Nitrosomethyl-3-carboxypropylamine at 75 mg/ml and a total dose of 6.2 mmol per rat induced a high incidence of bladder tumors and tumors of the kidney pelvis, but not tumors of the nasal mucosa; the median week of death for this group was 55 weeks. It is concluded that nitrosomethyl-n-alkylamines that induce bladder tumors by oral administration to rats are metabolized to nitrosomethyl-3-carboxypropylamine, which is excreted in the urine and further metabolized to nitrosomethyl-2-oxopropylamine, the proximate bladder carcinogen. JF - Japanese journal of cancer research : Gann AU - Thomas, B J AU - Kovatch, R M AU - Lijinsky, W AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research Program, MD 21701. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 309 EP - 313 VL - 79 IS - 3 SN - 0910-5050, 0910-5050 KW - Nitrosamines KW - 0 KW - N-nitrosomethyl-2-oxopropylamine KW - 55984-51-5 KW - N-nitrosomethyl-2-hydroxypropylamine KW - 75411-83-5 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Drug Administration Schedule KW - Nose Neoplasms -- chemically induced KW - Carcinoma, Transitional Cell -- chemically induced KW - Papilloma -- chemically induced KW - Female KW - Nitrosamines -- administration & dosage KW - Neoplasms, Experimental -- chemically induced KW - Urinary Bladder Neoplasms -- mortality KW - Neoplasms, Experimental -- mortality KW - Administration, Intravesical KW - Urinary Bladder Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78229171?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Japanese+journal+of+cancer+research+%3A+Gann&rft.atitle=The+induction+of+bladder+tumors+in+F344+rats+by+intravesicular+administration+of+some+nitrosamines.&rft.au=Thomas%2C+B+J%3BKovatch%2C+R+M%3BLijinsky%2C+W&rft.aulast=Thomas&rft.aufirst=B&rft.date=1988-03-01&rft.volume=79&rft.issue=3&rft.spage=309&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 - 1988-06-24 N1 - Date created - 1988-06-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Aspirin exposure during the first 20 weeks of gestation and IQ at four years of age. AN - 78227589; 3368878 AB - The relationship between maternal aspirin use during the first 20 weeks of pregnancy and the child's IQ at 4 years of age was investigated in 19,226 pregnancies occurring from 1959 to 1966 in the Collaborative Perinatal Project. The mean IQ of children exposed to aspirin was 98.3, which was 2.1 points higher (95% confidence interval = 1.7, 2.6; P less than 0.0001) than that of unexposed children. Adjustment for multiple social, demographic, and other confounders reduced this difference to less than one point in favor of the aspirin exposed group, although statistical significance remained. Total days of exposure was used as an index of dose, and no dose-response relationship between aspirin use and IQ was found. The effect of prenatal aspirin exposure did not vary by infant sex. It is concluded that an adverse effect of aspirin exposure on IQ is unlikely. JF - Teratology AU - Klebanoff, M A AU - Berendes, H W AD - Prevention Research Program, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 249 EP - 255 VL - 37 IS - 3 SN - 0040-3709, 0040-3709 KW - Aspirin KW - R16CO5Y76E KW - Index Medicus KW - Age Factors KW - Data Collection -- methods KW - Humans KW - Male KW - Female KW - Pregnancy KW - Pregnancy Trimester, Second -- drug effects KW - Intelligence -- drug effects KW - Aspirin -- adverse effects KW - Pregnancy Trimester, First -- drug effects KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78227589?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Aspirin+exposure+during+the+first+20+weeks+of+gestation+and+IQ+at+four+years+of+age.&rft.au=Klebanoff%2C+M+A%3BBerendes%2C+H+W&rft.aulast=Klebanoff&rft.aufirst=M&rft.date=1988-03-01&rft.volume=37&rft.issue=3&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Teratology&rft.issn=00403709&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-06-13 N1 - Date created - 1988-06-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bioavailability of oral trimetrexate in patients with acquired immunodeficiency syndrome. AN - 78197607; 2966610 AB - The combination of the lipophilic antifolate trimetrexate and the rescue agent leucovorin has shown promise in the treatment of Pneumocystis carinii pneumonia in patients with acquired immunodeficiency syndrome. The pharmacokinetic behavior of trimetrexate administered either by intravenous bolus or orally was studied in six patients with acquired immunodeficiency syndrome with a reversed-phase high-pressure liquid chromatography assay. The mean clearance following bolus injection was 38 ml/min per m2, with a range of 15 to 55 ml/min per m2. The postdistributive half-life ranged from 6 to 16 h. With oral administration, the mean bioavailability was 44% (range, 19 to 67%). An oral dose of 60 mg/m2 (162 mumol/m2) resulted in concentrations in plasma that approximated those achieved with a 30-mg/m2 (81-mumol/m2) intravenous dose. The toxicity of this combination regimen was minimal. It appears that the oral route is a practical route of administration for trimetrexate in patients with acquired immunodeficiency syndrome requiring long-term outpatient treatment or prophylaxis for P. carinii pneumonia. JF - Antimicrobial agents and chemotherapy AU - Rogers, P AU - Allegra, C J AU - Murphy, R F AU - Drake, J C AU - Masur, H AU - Poplack, D G AU - Chabner, B A AU - Parrillo, J E AU - Lane, H C AU - Balis, F M AD - Department of Critical Care Medicine, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 324 EP - 326 VL - 32 IS - 3 SN - 0066-4804, 0066-4804 KW - Folic Acid Antagonists KW - 0 KW - Quinazolines KW - Trimetrexate KW - UPN4ITI8T4 KW - Index Medicus KW - AIDS/HIV KW - Administration, Oral KW - Injections, Intravenous KW - Half-Life KW - Humans KW - Adult KW - Middle Aged KW - Chromatography, High Pressure Liquid KW - Biological Availability KW - Quinazolines -- pharmacokinetics KW - Folic Acid Antagonists -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- complications KW - Quinazolines -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Folic Acid Antagonists -- pharmacokinetics KW - Acquired Immunodeficiency Syndrome -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78197607?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Bioavailability+of+oral+trimetrexate+in+patients+with+acquired+immunodeficiency+syndrome.&rft.au=Rogers%2C+P%3BAllegra%2C+C+J%3BMurphy%2C+R+F%3BDrake%2C+J+C%3BMasur%2C+H%3BPoplack%2C+D+G%3BChabner%2C+B+A%3BParrillo%2C+J+E%3BLane%2C+H+C%3BBalis%2C+F+M&rft.aulast=Rogers&rft.aufirst=P&rft.date=1988-03-01&rft.volume=32&rft.issue=3&rft.spage=324&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 - 1988-06-03 N1 - Date created - 1988-06-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Pharmacol Exp Ther. 1977 Dec;203(3):640-5 [21956] Biochem Pharmacol. 1979 Jun 15;28(12):1983-7 [454469] J Pharm Sci. 1982 Mar;71(3):372-3 [7069605] Cancer Res. 1983 May;43(5):2342-5 [6572562] Cancer Res. 1983 Nov;43(11):5286-92 [6225514] Ann Intern Med. 1984 May;100(5):663-71 [6231873] N Engl J Med. 1987 Oct 15;317(16):978-85 [2958710] Biochem Pharmacol. 1984 May 15;33(10):1697-9 [6233981] Cancer Res. 1986 Jan;46(1):169-74 [2933145] Cancer Res. 1987 Jan 15;47(2):609-16 [2947679] Cancer Res. 1987 Sep 15;47(18):4973-6 [2957048] Clin Pharmacol Ther. 1987 Sep;42(3):351-6 [2957140] N Engl J Med. 1984 Jun 21;310(25):1682-8 [6328301] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mixed Sertoli-Leydig cell tumor and rete testis adenocarcinoma in rats treated with CdCl2. AN - 78194944; 2834860 JF - Veterinary pathology AU - Rehm, S AU - Waalkes, M P AD - National Cancer Institute, Frederick, MD 21701-1013. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 163 EP - 166 VL - 25 IS - 2 SN - 0300-9858, 0300-9858 KW - Cadmium KW - 00BH33GNGH KW - Cadmium Chloride KW - J6K4F9V3BA KW - Index Medicus KW - Animals KW - Adenocarcinoma -- chemically induced KW - Dose-Response Relationship, Drug KW - Sertoli Cell Tumor -- chemically induced KW - Leydig Cell Tumor -- veterinary KW - Rats KW - Rete Testis KW - Sertoli Cell Tumor -- veterinary KW - Leydig Cell Tumor -- complications KW - Adenocarcinoma -- veterinary KW - Leydig Cell Tumor -- chemically induced KW - Sertoli Cell Tumor -- complications KW - Male KW - Rats, Inbred Strains KW - Rodent Diseases -- chemically induced KW - Testicular Neoplasms -- veterinary KW - Cadmium -- toxicity KW - Testicular Neoplasms -- chemically induced KW - Neoplasms, Glandular and Epithelial -- veterinary KW - Neoplasms, Glandular and Epithelial -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78194944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Veterinary+pathology&rft.atitle=Mixed+Sertoli-Leydig+cell+tumor+and+rete+testis+adenocarcinoma+in+rats+treated+with+CdCl2.&rft.au=Rehm%2C+S%3BWaalkes%2C+M+P&rft.aulast=Rehm&rft.aufirst=S&rft.date=1988-03-01&rft.volume=25&rft.issue=2&rft.spage=163&rft.isbn=&rft.btitle=&rft.title=Veterinary+pathology&rft.issn=03009858&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-06-02 N1 - Date created - 1988-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clonidine partially blocks the physiologic effects but not the subjective effects produced by smoking marijuana in male human subjects. AN - 78191126; 2834758 AB - Clonidine, an alpha 2-agonist, was studied in three male human subjects in a multi-dose pilot study in combination with smoking marijuana cigarettes. Marijuana alone caused increases in responses on subjective effect questionnaires and increased heart rate. Pretreatment with single oral doses of clonidine three hours prior to marijuana induced no changes in subjective effects prior to smoking marijuana and did not diminish the subjective effects produced by marijuana. Clonidine did substantially reduce but did not abolish the marijuana-induced rise in heart rate. Based on these preliminary data from three subjects, it is concluded that clonidine does not have therapeutic value in the clinical management of active marijuana abuse. JF - Pharmacology, biochemistry, and behavior AU - Cone, E J AU - Welch, P AU - Lange, W R AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 649 EP - 652 VL - 29 IS - 3 SN - 0091-3057, 0091-3057 KW - Adrenocorticotropic Hormone KW - 9002-60-2 KW - Clonidine KW - MN3L5RMN02 KW - Index Medicus KW - Drug Evaluation KW - Heart Rate -- drug effects KW - Adrenocorticotropic Hormone -- secretion KW - Humans KW - Marijuana Abuse -- drug therapy KW - Blood Pressure -- drug effects KW - Male KW - Marijuana Smoking -- psychology KW - Marijuana Smoking -- drug therapy KW - Clonidine -- pharmacology KW - Marijuana Smoking -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78191126?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Clonidine+partially+blocks+the+physiologic+effects+but+not+the+subjective+effects+produced+by+smoking+marijuana+in+male+human+subjects.&rft.au=Cone%2C+E+J%3BWelch%2C+P%3BLange%2C+W+R&rft.aulast=Cone&rft.aufirst=E&rft.date=1988-03-01&rft.volume=29&rft.issue=3&rft.spage=649&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 - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human P450PCN1: sequence, chromosome localization, and direct evidence through cDNA expression that P450PCN1 is nifedipine oxidase. AN - 78184319; 3267210 AB - P450PCN protein levels and nifedipine oxidase activities were quantitated in 12 human livers and were shown to be highly correlated. Antibody against rat P450PCN1 completely inhibited all nifedipine oxidase activity in three human liver samples. These results suggest that a human P450 related to rat P450PCN1 is the major form of P450 catalyzing nifedipine oxidation. The cDNA for a human P450, designated phPCN1, was isolated from a human liver lambda gt11 cDNA library, and sequenced completely. The deduced amino acid sequence is 77% similar to rat P450PCN1. By use of the adenovirus- and SV40-based expression vecotr p91023(B), the phP450PCN1 cDNA was expressed in COS cells and had high nifedipine oxidase activity, providing conclusive evidence that this P450 is the primary enzyme associated with metabolism and inactivation of this important drug. Using somatic cell hybrids, the P450PCN gene was localized to human chromosome 7. JF - DNA (Mary Ann Liebert, Inc.) AU - Gonzalez, F J AU - Schmid, B J AU - Umeno, M AU - Mcbride, O W AU - Hardwick, J P AU - Meyer, U A AU - Gelboin, H V AU - Idle, J R AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 79 EP - 86 VL - 7 IS - 2 SN - 0198-0238, 0198-0238 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - CYP3A protein, human KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP3A KW - Nifedipine KW - I9ZF7L6G2L KW - Index Medicus KW - Oxidation-Reduction KW - Sequence Homology, Nucleic Acid KW - Multigene Family KW - Humans KW - Microsomes, Liver -- enzymology KW - Molecular Sequence Data KW - Gene Expression Regulation KW - Amino Acid Sequence KW - Chromosomes, Human, Pair 7 KW - Chromosome Mapping KW - Cytochrome P-450 Enzyme System -- genetics KW - Nifedipine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78184319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+%28Mary+Ann+Liebert%2C+Inc.%29&rft.atitle=Human+P450PCN1%3A+sequence%2C+chromosome+localization%2C+and+direct+evidence+through+cDNA+expression+that+P450PCN1+is+nifedipine+oxidase.&rft.au=Gonzalez%2C+F+J%3BSchmid%2C+B+J%3BUmeno%2C+M%3BMcbride%2C+O+W%3BHardwick%2C+J+P%3BMeyer%2C+U+A%3BGelboin%2C+H+V%3BIdle%2C+J+R&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1988-03-01&rft.volume=7&rft.issue=2&rft.spage=79&rft.isbn=&rft.btitle=&rft.title=DNA+%28Mary+Ann+Liebert%2C+Inc.%29&rft.issn=01980238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M18907; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sample size and power for case-control studies when exposures are continuous. AN - 78174322; 3358016 AB - In estimating the sample size for a case-control study, epidemiologic texts present formulae that require a binary exposure of interest. Frequently, however, important exposures are continuous and dichotomization may result in a 'not exposed' category that has little practical meaning. In addition, if risks vary monotonically with exposure, then dichotomization will obscure risk effects and require a greater number of subjects to detect differences in the exposure distributions among cases and controls. Starting from the usual score statistic to detect differences in exposure, this paper develops sample size formulae for case-control studies with arbitrary exposure distributions; this includes both continuous and dichotomous exposure measurements as special cases. The score statistic is appropriate for general differentiable models for the relative odds, and, in particular, for the two forms commonly used in prospective disease occurrence models: (1) the odds of disease increase linearly with exposure; or (2) the odds increase exponentially with exposure. Under these two models we illustrate calculation of sample sizes for a hypothetical case-control study of lung cancer among non-smokers who are exposed to radon decay products at home. JF - Statistics in medicine AU - Lubin, J H AU - Gail, M H AU - Ershow, A G AD - Biostatistics Branch, National Cancer Institute, Bethesda, Maryland 20205. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 363 EP - 376 VL - 7 IS - 3 SN - 0277-6715, 0277-6715 KW - Radioactive Pollutants KW - 0 KW - Radon KW - Q74S4N8N1G KW - Index Medicus KW - Risk KW - Radiation Dosage KW - Lung Neoplasms -- etiology KW - Neoplasms, Radiation-Induced -- etiology KW - Radioactive Pollutants -- adverse effects KW - Humans KW - Sampling Studies KW - Retrospective Studies KW - Environmental Exposure KW - Radon -- adverse effects KW - Time Factors KW - Models, Theoretical KW - Probability KW - Epidemiologic Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78174322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sample+size+and+power+for+case-control+studies+when+exposures+are+continuous.&rft.au=Lubin%2C+J+H%3BGail%2C+M+H%3BErshow%2C+A+G&rft.aulast=Lubin&rft.aufirst=J&rft.date=1988-03-01&rft.volume=7&rft.issue=3&rft.spage=363&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 - 1988-05-16 N1 - Date created - 1988-05-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytotoxic activity of an interleukin 2-Pseudomonas exotoxin chimeric protein produced in Escherichia coli. AN - 78148874; 3126499 AB - A cDNA clone for human interleukin 2 (IL-2) has been fused to the 5' end of a modified Pseudomonas exotoxin (PE) gene that lacks the sequences encoding the cell recognition domain. The chimeric protein IL-2-PE40 was produced in Escherichia coli. It was extremely toxic to IL-2 receptor-positive cells but had no measurable effect on cells lacking the IL-2 receptor. IL-2-PE40 might be a useful cytotoxic agent in the treatment of diseases involving IL-2 receptor-positive cells and in the treatment of allograft rejection. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Lorberboum-Galski, H AU - FitzGerald, D AU - Chaudhary, V AU - Adhya, S AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 1922 EP - 1926 VL - 85 IS - 6 SN - 0027-8424, 0027-8424 KW - Exotoxins KW - 0 KW - IL-2-PE40 chimeric protein, recombinant KW - Immunotoxins KW - Interleukin-2 KW - Receptors, Immunologic KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins KW - Recombinant Proteins KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Graft Rejection KW - Receptors, Immunologic -- metabolism KW - Humans KW - DNA -- analysis KW - Transplantation, Homologous KW - Plasmids KW - Cell Line KW - Cloning, Molecular KW - Interleukin-2 -- pharmacology KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Recombinant Fusion Proteins -- pharmacology KW - Escherichia coli -- genetics KW - Interleukin-2 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78148874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytotoxic+activity+of+an+interleukin+2-Pseudomonas+exotoxin+chimeric+protein+produced+in+Escherichia+coli.&rft.au=Lorberboum-Galski%2C+H%3BFitzGerald%2C+D%3BChaudhary%2C+V%3BAdhya%2C+S%3BPastan%2C+I&rft.aulast=Lorberboum-Galski&rft.aufirst=H&rft.date=1988-03-01&rft.volume=85&rft.issue=6&rft.spage=1922&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 - 1988-04-19 N1 - Date created - 1988-04-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1983 Feb 10;258(3):1565-70 [6296105] Nature. 1982 Nov 18;300(5889):267-9 [6815536] Gut. 1984 Jan;25(1):32-40 [6228498] Science. 1984 Jun 22;224(4655):1312-6 [6427923] J Exp Med. 1985 Jul 1;162(1):358-62 [3925068] N Engl J Med. 1985 Aug 8;313(6):353-60 [3159965] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2624-7 [2939456] Clin Exp Immunol. 1986 Apr;64(1):71-9 [3089651] Science. 1986 Nov 14;234(4778):859-63 [3095922] Cell. 1986 Dec 5;47(5):641-8 [3536124] J Mol Biol. 1986 May 5;189(1):113-30 [3537305] Cell. 1987 Jan 16;48(1):129-36 [3098436] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9694-8 [3099289] Transplant Proc. 1987 Feb;19(1 Pt 1):594-8 [3103282] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2474-8 [3104916] Diabetologia. 1987 Jan;30(1):44-6 [3106125] J Biol Chem. 1987 Apr 25;262(12):5723-31 [3106342] Nature. 1987 Jun 11-17;327(6122):518-22 [3108674] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4538-42 [3299371] J Mol Biol. 1969 May 14;41(3):459-72 [4896022] Nature. 1970 Aug 15;227(5259):680-5 [5432063] J Biol Chem. 1971 Mar 10;246(5):1496-503 [5545092] J Biol Chem. 1977 Feb 25;252(4):1515-22 [190237] Proc Natl Acad Sci U S A. 1978 Nov;75(11):5319-23 [281682] J Biol Chem. 1979 Feb 25;254(4):1022-7 [762110] J Natl Cancer Inst. 1979 Jun;62(6):1387-95 [286111] Immunol Rev. 1980;51:337-57 [7000676] J Immunol. 1981 Jul;127(1):347-51 [6787129] J Exp Med. 1981 Nov 1;154(5):1455-74 [6975347] J Clin Endocrinol Metab. 1983 Jan;56(1):164-9 [6600169] Science. 1983 Feb 11;219(4585):644-50 [6218613] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA binding and mutagenicity of ethyl methanesulfonate in wild-type and uvrB cells of Salmonella typhimurium. AN - 78147177; 3280980 AB - The extent of DNA ethylation and the influence of excision repair on ethyl methanesulfonate (EMS) mutagenesis of Salmonella typhimurium were examined. The relationship between the dose to DNA and the exposure concentration of EMS was linear. EMS induction of his+ revertants followed exponential kinetics and did not parallel the increase in total DNA ethylation. Mutant induction was influenced by the cells' nucleotide excision repair ability. Although mutagenized to a larger extent than the wild-type (uvr+) strain at high doses, the uvrB strain was more resistant to the mutagenic effect of low doses of EMS. JF - Mutation research AU - Matijasević, Z AU - Zeiger, E AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 1 EP - 8 VL - 198 IS - 1 SN - 0027-5107, 0027-5107 KW - Bacterial Proteins KW - 0 KW - DNA, Bacterial KW - Escherichia coli Proteins KW - Ethyl Methanesulfonate KW - 9H154DI0UP KW - Endodeoxyribonucleases KW - EC 3.1.- KW - endodeoxyribonuclease uvrABC KW - EC 3.1.25.- KW - Index Medicus KW - DNA Repair KW - Dose-Response Relationship, Drug KW - DNA Damage KW - Drug Resistance, Microbial KW - Mutation KW - Alkylation KW - Salmonella typhimurium -- metabolism KW - Bacterial Proteins -- genetics KW - Ethyl Methanesulfonate -- pharmacology KW - Endodeoxyribonucleases -- genetics KW - Salmonella typhimurium -- drug effects KW - Ethyl Methanesulfonate -- metabolism KW - DNA, Bacterial -- metabolism KW - Salmonella typhimurium -- genetics KW - Endodeoxyribonucleases -- physiology KW - DNA, Bacterial -- drug effects KW - Bacterial Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78147177?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+binding+and+mutagenicity+of+ethyl+methanesulfonate+in+wild-type+and+uvrB+cells+of+Salmonella+typhimurium.&rft.au=Matijasevi%C4%87%2C+Z%3BZeiger%2C+E&rft.aulast=Matijasevi%C4%87&rft.aufirst=Z&rft.date=1988-03-01&rft.volume=198&rft.issue=1&rft.spage=1&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 - 1988-04-26 N1 - Date created - 1988-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational specificity of benzo[a]pyrene diolepoxide in monkey cells. AN - 78146986; 3127698 AB - Benzo[a]pyrene diolepoxide (BPDE) is thought to be the major mutagenic and carcinogenic intermediate in benzo[a]pyrene metabolism in mammalian cells. In order to test the mutagenic specificity of this compound in mammalian cells, we have used the pZ189 shuttle vector system to identify and analyze point mutations induced when DNA treated in vitro with BPDE is replicated in monkey cells. We find that point mutations occur almost exclusively at G.C base pairs; G.C----T.A and G.C----C.G transversions and single base pair deletions occur most frequently. This pattern is consistent with the known preferential covalent binding of BPDE to G residues. JF - Mutation research AU - Roilides, E AU - Gielen, J E AU - Tuteja, N AU - Levine, A S AU - Dixon, K AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 199 EP - 206 VL - 198 IS - 1 SN - 0027-5107, 0027-5107 KW - Dihydroxydihydrobenzopyrenes KW - 0 KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - Guanine KW - 5Z93L87A1R KW - Index Medicus KW - Base Composition -- drug effects KW - Genetic Vectors -- drug effects KW - Animals KW - Base Sequence KW - Cercopithecus aethiops KW - Molecular Sequence Data KW - Kidney KW - Cell Line KW - Fibroblasts -- drug effects KW - DNA Damage KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- pharmacology KW - Mutation KW - Dihydroxydihydrobenzopyrenes -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78146986?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutational+specificity+of+benzo%5Ba%5Dpyrene+diolepoxide+in+monkey+cells.&rft.au=Roilides%2C+E%3BGielen%2C+J+E%3BTuteja%2C+N%3BLevine%2C+A+S%3BDixon%2C+K&rft.aulast=Roilides&rft.aufirst=E&rft.date=1988-03-01&rft.volume=198&rft.issue=1&rft.spage=199&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 - 1988-04-26 N1 - Date created - 1988-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preliminary results of treatment of Ewing's sarcoma of bone in children and young adults: six months of intensive combined modality therapy without maintenance. AN - 78145846; 3280743 AB - Thirty-one previously untreated patients with Ewing's sarcoma were treated with an intensive chemotherapy program of vincristine, Adriamycin (doxorubicin; Adria Laboratories, Columbus, OH), and cyclosphosphamide (VADRIAC) in combination with radiation therapy to the primary site (greater than 50 Gy) and bone metastases (45 to 50 Gy). An intensified regimen with one further cycle of chemotherapy (VADRIAC), total body irradiation (TBI), and autologous bone marrow transplantation was given to patients with primary tumors of the pelvis, humerus, femur, and chest wall without metastases and to all patients with metastases at diagnosis. Patients with primary tumors of the distal extremity and other sites without metastases at diagnosis were treated on a less intensive chemotherapy regimen of VADRIAC without the intensification. Therapy was completed within 6 to 7 months in all patients. Thirteen patients had metastatic disease at diagnosis; only two of these had the lung as the sole site of metastatic disease. Eighteen patients had no evidence of metastatic disease at diagnosis: ten of these patients had tumors that arose in central axis and proximal extremity sites, and eight had tumors that arose in distal extremity and other sites. Thirty of the 31 patients achieved a complete remission, although two patients underwent amputation: one before chemotherapy and radiation and one after chemotherapy and radiation because of persistent local disease. Seventeen remain in their first complete remission at a median time on study of 30 months and a median time after completion of therapy of 24 months. Fourteen patients have relapsed (13) or progressed (1): ten in metastatic sites and four in the primary site. One patient had persistent local disease after radiation requiring amputation. Nine of the 13 patients with metastatic disease at diagnosis have relapsed compared with five of the 18 patients without metastatic disease. For the entire group, the actuarial survival is 78% (65% to 87%) at 30 months, and the actuarial disease-free survival is 58% (46% to 69%) at 30 months. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Miser, J S AU - Kinsella, T J AU - Triche, T J AU - Tsokos, M AU - Forquer, R AU - Wesley, R AU - Horvath, K AU - Belasco, J AU - Longo, D L AU - Steis, R AD - Pediatric Branch, National Cancer Institute, Bethesda, MD. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 484 EP - 490 VL - 6 IS - 3 SN - 0732-183X, 0732-183X KW - Index Medicus KW - Whole-Body Irradiation KW - Combined Modality Therapy KW - Humans KW - Adult KW - Follow-Up Studies KW - Child KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Adolescent KW - Male KW - Female KW - Bone Marrow Transplantation KW - Child, Preschool KW - Bone Neoplasms -- therapy KW - Sarcoma, Ewing -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78145846?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preliminary+results+of+treatment+of+Ewing%27s+sarcoma+of+bone+in+children+and+young+adults%3A+six+months+of+intensive+combined+modality+therapy+without+maintenance.&rft.au=Miser%2C+J+S%3BKinsella%2C+T+J%3BTriche%2C+T+J%3BTsokos%2C+M%3BForquer%2C+R%3BWesley%2C+R%3BHorvath%2C+K%3BBelasco%2C+J%3BLongo%2C+D+L%3BSteis%2C+R&rft.aulast=Miser&rft.aufirst=J&rft.date=1988-03-01&rft.volume=6&rft.issue=3&rft.spage=484&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 - 1988-05-03 N1 - Date created - 1988-05-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antihypertensive drug side effects in the Hypertension Detection and Follow-up Program. AN - 78137548; 3350594 AB - The 5485 participants in the Hypertension Detection and Follow-up Program, Stepped-Care group form one of the largest groups to date on which detailed surveillance of long-term antihypertensive therapy and drug side effects has been reported. During a 5-year period, among all hypertensive persons (mild, moderate, and severe combined) who were not taking antihypertensive medications at the beginning of the study and who attended the clinic at least once during the 5-year trial, a total of 9.3% had definite or probable side effects severe enough to cause discontinuation of the drug treatment in question. Less than 1% of active participants required hospitalization for side effects. No death that could be attributed to side effects was detected. Thus, the Hypertension Detection and Follow-up Program data, which have previously demonstrated the beneficial effects of antihypertensive therapy, confirm the relative safety of such therapy. JF - Hypertension (Dallas, Tex. : 1979) AU - Curb, J D AU - Schneider, K AU - Taylor, J O AU - Maxwell, M AU - Shulman, N AD - National Institute on Aging, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - II51 EP - II55 VL - 11 IS - 3 Pt 2 SN - 0194-911X, 0194-911X KW - Antihypertensive Agents KW - 0 KW - Cholesterol KW - 97C5T2UQ7J KW - Index Medicus KW - Cholesterol -- blood KW - Humans KW - Adult KW - Sexual Dysfunction, Physiological -- chemically induced KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Male KW - Female KW - Hypertension -- blood KW - Antihypertensive Agents -- adverse effects KW - Hypertension -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78137548?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antihypertensive+drug+side+effects+in+the+Hypertension+Detection+and+Follow-up+Program.&rft.au=Curb%2C+J+D%3BSchneider%2C+K%3BTaylor%2C+J+O%3BMaxwell%2C+M%3BShulman%2C+N&rft.aulast=Curb&rft.aufirst=J&rft.date=1988-03-01&rft.volume=11&rft.issue=3+Pt+2&rft.spage=II51&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 - 1988-05-06 N1 - Date created - 1988-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Health hazards of nitrite inhalants. AN - 78132147; 2894765 JF - The American journal of medicine AU - Haverkos, H W AU - Dougherty, J AD - Clinical Medicine Branch, National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 479 EP - 482 VL - 84 IS - 3 Pt 1 SN - 0002-9343, 0002-9343 KW - Nitrites KW - 0 KW - Nitrosamines KW - n-butyl nitrite KW - 44P8QG0F3T KW - Amyl Nitrite KW - 8017-89-8 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Acquired Immunodeficiency Syndrome -- complications KW - Humans KW - Nitrosamines -- metabolism KW - Substance-Related Disorders -- complications KW - Administration, Inhalation KW - Immune System -- drug effects KW - Amyl Nitrite -- adverse effects KW - Sarcoma, Kaposi -- chemically induced KW - Nitrites -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78132147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Health+hazards+of+nitrite+inhalants.&rft.au=Haverkos%2C+H+W%3BDougherty%2C+J&rft.aulast=Haverkos&rft.aufirst=H&rft.date=1988-03-01&rft.volume=84&rft.issue=3+Pt+1&rft.spage=479&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 - 1988-04-12 N1 - Date created - 1988-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ultraviolet light-induced chromosomal aberrations in cultured cells from Cockayne syndrome and complementation group C xeroderma pigmentosum patients: lack of correlation with cancer susceptibility. AN - 78131111; 3348214 AB - Both Cockayne syndrome (CS) and xeroderma pigmentosum (XP) are inherited diseases with defective repair of damage induced in DNA by UV. Patients with XP, but not those with CS, have an increased susceptibility to formation of sunlight-induced skin tumors. We determined the frequency of UV-induced chromosomal aberrations in cultured lymphoblastoid cell lines from five CS patients and three complementation-group-C XP patients to determine whether such aberrations were abnormally increased only in the XP cells. We found that CS cells had the same abnormally increased number of induced aberrations as the XP cells, indicating that the number of UV-induced aberrations in XP group C cells does not account for the susceptibility of these XP patients to sunlight-induced skin cancer. JF - American journal of human genetics AU - Seguin, L R AU - Tarone, R E AU - Liao, K H AU - Robbins, J H AD - Dermatology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 468 EP - 475 VL - 42 IS - 3 SN - 0002-9297, 0002-9297 KW - Index Medicus KW - Disease Susceptibility KW - Cells, Cultured KW - Humans KW - Lymphocytes -- radiation effects KW - Lymphocytes -- ultrastructure KW - Ultraviolet Rays KW - Cockayne Syndrome -- genetics KW - Dwarfism -- genetics KW - Chromosome Aberrations KW - Xeroderma Pigmentosum -- genetics KW - Neoplasms, Radiation-Induced -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78131111?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ultraviolet+light-induced+chromosomal+aberrations+in+cultured+cells+from+Cockayne+syndrome+and+complementation+group+C+xeroderma+pigmentosum+patients%3A+lack+of+correlation+with+cancer+susceptibility.&rft.au=Seguin%2C+L+R%3BTarone%2C+R+E%3BLiao%2C+K+H%3BRobbins%2C+J+H&rft.aulast=Seguin&rft.aufirst=L&rft.date=1988-03-01&rft.volume=42&rft.issue=3&rft.spage=468&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 - 1988-04-13 N1 - Date created - 1988-04-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1968 May 18;218(5142):652-6 [5655953] Am J Dermatopathol. 1985 Aug;7(4):387-92 [3842793] Acta Paediatr Scand. 1969 Mar;58(2):121-4 [5385496] Nature. 1970 Oct 24;228(5269):359-61 [4319741] J Lab Clin Med. 1971 May;77(5):759-67 [5557662] Ann Hum Genet. 1971 Oct;35(2):149-60 [4334062] Nat New Biol. 1972 Jul 19;238(81):80-3 [4505415] Ann Intern Med. 1974 Feb;80(2):221-48 [4811796] Cancer Res. 1974 Aug;34(8):1965-70 [4842250] Proc Natl Acad Sci U S A. 1975 Jan;72(1):219-23 [1054497] Nature. 1976 Jun 17;261(5561):593-5 [934300] Cancer Res. 1977 Mar;37(3):904-10 [837385] Hum Genet. 1977 Apr 15;36(2):213-8 [858627] Mutat Res. 1977 Mar;42(3):433-42 [854043] Pediatrics. 1977 Aug;60(2):135-9 [887325] Mutat Res. 1977 Nov;45(2):253-61 [593287] J Invest Dermatol. 1978 May;70(5):237-9 [641373] Proc Natl Acad Sci U S A. 1978 Apr;75(4):1984-8 [273925] Cancer Res. 1978 Jun;38(6):1601-9 [647673] Arch Neurol. 1978 Jun;35(6):337-45 [655905] Cancer Res. 1979 Oct;39(10):4237-41 [157803] Mutat Res. 1979 Aug;62(1):159-71 [492196] Biochim Biophys Acta. 1979 Aug 29;564(1):122-31 [534635] Mutat Res. 1980 Jan;69(1):107-12 [7360141] Photochem Photobiol. 1979 May;29(5):971-5 [538093] Cancer Res. 1980 Aug;40(8 Pt 1):2736-9 [7388823] J Invest Dermatol. 1981 Jan;76(1):59-62 [7462668] Nature. 1981 Jan 29;289(5796):353-7 [6258076] Basic Life Sci. 1980;15:285-313 [7011308] Br J Dermatol. 1981 Jul;105(1):1-12 [7259973] Photochem Photobiol. 1981 Nov;34(5):603-7 [7301938] Mutat Res. 1982 Mar;93(1):235-47 [7062933] Mutat Res. 1982 Dec;106(2):347-56 [6185841] Photochem Photobiol. 1983 May;37(5):503-8 [6878443] Proc Natl Acad Sci U S A. 1983 Sep;80(18):5612-6 [6577447] Cancer Genet Cytogenet. 1985 Jan 1;14(1-2):163-8 [3965121] J Invest Dermatol. 1984 May;82(5):480-4 [6096450] Proc Natl Acad Sci U S A. 1985 Oct;82(19):6622-6 [2995975] Cancer Res. 1986 Feb;46(2):489-92 [3940626] Eur J Cell Biol. 1986 Jan;39(2):346-51 [3956512] Photodermatol. 1986 Jun;3(3):125-32 [3748852] Eur J Cell Biol. 1986 Aug;41(2):352-5 [3758088] Pediatr Res. 1987 Jan;21(1):34-7 [2432457] Proc Soc Exp Biol Med. 1969 Nov;132(2):802-6 [4311214] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A simple technique for quantitation of low levels of DNA damage in individual cells. AN - 78130350; 3345800 AB - Human lymphocytes were either exposed to X-irradiation (25 to 200 rads) or treated with H2O2 (9.1 to 291 microM) at 4 degrees C and the extent of DNA migration was measured using a single-cell microgel electrophoresis technique under alkaline conditions. Both agents induced a significant increase in DNA migration, beginning at the lowest dose evaluated. Migration patterns were relatively homogeneous among cells exposed to X-rays but heterogeneous among cells treated with H2O2. An analysis of repair kinetics following exposure to 200 rads X-rays was conducted with lymphocytes obtained from three individuals. The bulk of the DNA repair occurred within the first 15 min, while all of the repair was essentially complete by 120 min after exposure. However, some cells demonstrated no repair during this incubation period while other cells demonstrated DNA migration patterns indicative of more damage than that induced by the initial irradiation with X-rays. This technique appears to be sensitive and useful for detecting damage and repair in single cells. JF - Experimental cell research AU - Singh, N P AU - McCoy, M T AU - Tice, R R AU - Schneider, E L AD - Laboratory of Molecular Genetics, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 184 EP - 191 VL - 175 IS - 1 SN - 0014-4827, 0014-4827 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Electrophoresis, Agar Gel -- methods KW - X-Rays KW - Humans KW - In Vitro Techniques KW - Dose-Response Relationship, Radiation KW - Male KW - DNA Damage KW - Lymphocytes -- radiation effects KW - Lymphocytes -- analysis KW - DNA -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78130350?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+simple+technique+for+quantitation+of+low+levels+of+DNA+damage+in+individual+cells.&rft.au=Singh%2C+N+P%3BMcCoy%2C+M+T%3BTice%2C+R+R%3BSchneider%2C+E+L&rft.aulast=Singh&rft.aufirst=N&rft.date=1988-03-01&rft.volume=175&rft.issue=1&rft.spage=184&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 - 1988-04-19 N1 - Date created - 1988-04-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - c-H-ras and c-K-ras gene hypomethylation in the livers and hepatomas of rats fed methyl-deficient, amino acid-defined diets. AN - 78125733; 3345576 AB - The extent of methylation of the c-H-ras and c-K-ras oncogenes was compared in neoplastic and preneoplastic livers of rats fed one of several methyl-deficient, amino acid-defined diets for 18 months, with or without a preceding initiating dose of diethylnitrosamine (DEN). The restriction endonucleases MspI, HpaII, HhaI, PaeR71 and XhoI were used for studying the extent and pattern of DNA methylation. The results indicated that both c-H-ras and c-K-ras oncogenes were hypomethylated in all DNA samples derived from both neoplastic and preneoplastic livers of rats fed any of the methyl-deficient diets used, regardless of whether or not the rats had received an initiating dose of DEN. It thus appears that dietary methyl deficiency does indeed lead to hypomethylation of ras genes in the DNAs of the resulting tumors. However, the significance of this hypomethylation in the tumorigenic process is not clearly understood. JF - Carcinogenesis AU - Bhave, M R AU - Wilson, M J AU - Poirier, L A AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, MD 21701. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 343 EP - 348 VL - 9 IS - 3 SN - 0143-3334, 0143-3334 KW - Amino Acids KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Base Sequence KW - Diet KW - Mutation KW - Methylation KW - Male KW - Liver Neoplasms, Experimental -- etiology KW - Liver Neoplasms, Experimental -- metabolism KW - DNA -- metabolism KW - Liver -- metabolism KW - Amino Acids -- metabolism KW - Precancerous Conditions -- metabolism KW - Proto-Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78125733?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=c-H-ras+and+c-K-ras+gene+hypomethylation+in+the+livers+and+hepatomas+of+rats+fed+methyl-deficient%2C+amino+acid-defined+diets.&rft.au=Bhave%2C+M+R%3BWilson%2C+M+J%3BPoirier%2C+L+A&rft.aulast=Bhave&rft.aufirst=M&rft.date=1988-03-01&rft.volume=9&rft.issue=3&rft.spage=343&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenicity and in vitro covalent DNA binding of 2-hydroxyamino-3-methylimidazolo[4,5-f]quinoline. AN - 78117814; 3162208 AB - The 2-hydroxyamino-3-methylimidazolo[4,5-f]quinoline (N-hydroxy-IQ), a metabolite of the food mutagen--carcinogen IQ, was mutagenic to Salmonella TA98 (nitroreductase deficient). When either rat hepatic cytosol, NADPH (1 mM) or ascorbate (0.5 mM) was added to the mutagenicity assay, mutagenicity increased up to 15-, 10- and 50-fold respectively. In light of the effects of ascorbate and NADPH, it appears likely that hepatic cytosol may contain factors that protect N-hydroxy-IQ from oxidative decomposition. In contrast, hepatic monooxygenase metabolism of N-hydroxy-IQ decreased mutagenicity. When pentachlorophenol, an inhibitor of O-acetyltransferase and sulfotransferase, was added to the mutagenicity assay, a dose-dependent inhibition of N-hydroxy-IQ mutagenicity was observed. 2,6-Dichloro-4-nitrophenol, a more specific inhibitor of sulfotransferase than O- acetyltransferase, did not inhibit the mutagenicity of N-hydroxy-IQ at concentrations which appear to selectively inhibit only bacterial sulfotransferase. The data suggest that bacterial O-acetyltransferase rather than sulfotransferase mutagenically activates N-hydroxy-IQ. N-hydroxy-IQ covalently bound to calf thymus DNA in vitro under non-enzymatic conditions at pH 7.4. Rat hepatic cytosolic O-acetyltransferase and sulfotransferase enhanced the covalent binding of N-hydroxy-IQ to DNA 30- and 5-fold respectively. The data suggest that the mutagenicity of N-hydroxy-IQ is due to the reactivity of N-hydroxy-IQ with DNA and the ability of N-hydroxy-IQ to be further activated by bacterial O-acetyltransferase. JF - Carcinogenesis AU - Snyderwine, E G AU - Wirth, P J AU - Roller, P P AU - Adamson, R H AU - Sato, S AU - Thorgeirsson, S S AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 411 EP - 418 VL - 9 IS - 3 SN - 0143-3334, 0143-3334 KW - Imidazoles KW - 0 KW - Mutagens KW - Nitrophenols KW - Quinolines KW - 2,6-dichloro-4-nitrophenol KW - 618-80-4 KW - 2-hydroxyamino-3-methylimidazolo(4,5-f)quinoline KW - 77314-23-9 KW - DNA KW - 9007-49-2 KW - Pentachlorophenol KW - D9BSU0SE4T KW - Acetyltransferases KW - EC 2.3.1.- KW - Sulfurtransferases KW - EC 2.8.1.- KW - Index Medicus KW - Rats KW - Cytosol -- metabolism KW - Animals KW - Rats, Inbred F344 KW - Mutagenicity Tests KW - Nitrophenols -- pharmacology KW - Acetyltransferases -- physiology KW - Liver -- metabolism KW - Sulfurtransferases -- physiology KW - Pentachlorophenol -- pharmacology KW - Male KW - Mutagens -- metabolism KW - Imidazoles -- metabolism KW - DNA -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78117814?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutagenicity+and+in+vitro+covalent+DNA+binding+of+2-hydroxyamino-3-methylimidazolo%5B4%2C5-f%5Dquinoline.&rft.au=Snyderwine%2C+E+G%3BWirth%2C+P+J%3BRoller%2C+P+P%3BAdamson%2C+R+H%3BSato%2C+S%3BThorgeirsson%2C+S+S&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1988-03-01&rft.volume=9&rft.issue=3&rft.spage=411&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-04-14 N1 - Date created - 1988-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mitogenic activation of EL-4 cells does not require surface Thy-1 expression. AN - 78117042; 2449976 AB - The ability of monoclonal anti-Thy-1 antibodies to stimulate IL-2 production and T-cell proliferation has raised the possibility that Thy-1 may play an important role in T-cell activation. To examine this postulated role we have produced Thy-1-negative variants of the murine T lymphoma EL-4 by mutagenesis with ethyl methanesulfonate (EMS) and subsequent negative selection with anti-Thy-1 monoclonal antibodies (mAbs) and complement. Although the parental EL-4 cell line produced interleukin-2 (IL-2) in response to concanavalin A (Con A), phytohemagglutinin, anti-Thy-1 mAbs, and an anti-T3 mAb, as well as after exposure to phorbol myristate acetate (PMA), only PMA was capable of inducing IL-2 production by several Thy-1-negative cell lines. The loss of responsiveness to cell surface stimulatory ligands appeared to be correlated with loss of Thy-1 expression because mutagenized cells selected for high levels of Thy-1 expression all responded normally to Con A. However, when Thy-1 expression was reconstituted in the "nonresponder" (Thy-1-negative) cell lines either by transfection of a Thy-1.2 gene or by 5-azadeoxycytidine treatment, the revertant cell lines were still unable to produce IL-2 when stimulated with Con A, anti-Thy-1, or anti-T3. Furthermore, several other independently derived Thy-1-negative EL-4 cell lines responded normally to mitogens and mitogenic mAbs. Taken together, these results suggest that Thy-1 expression is not required for the T-cell activation process and that the EMS mutagenesis procedure resulted in an additional mutation(s) responsible for the inability of certain Thy-1-negative cell lines to be triggered by mitogens and mitogenic mAbs. These cell lines may prove to be valuable tools for further biochemical and molecular studies of the sequence of events associated with T-cell activation. JF - Cellular immunology AU - Gunter, K C AU - Germain, R N AU - Leo, O AU - Chan, C AU - Shevach, E M AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 135 EP - 146 VL - 112 IS - 1 SN - 0008-8749, 0008-8749 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation, T-Lymphocyte KW - Antigens, Surface KW - Antigens, Thy-1 KW - Mitogens KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Phenotype KW - Animals KW - Azacitidine -- pharmacology KW - Transfection KW - Mice KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Mutation KW - Antibodies, Monoclonal -- physiology KW - Cell Line KW - T-Lymphocytes -- classification KW - Mitogens -- pharmacology KW - Lymphocyte Activation -- drug effects KW - Lymphoma -- genetics KW - Lymphoma -- immunology KW - T-Lymphocytes -- immunology KW - Antigens, Surface -- genetics KW - Antigens, Surface -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78117042?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mitogenic+activation+of+EL-4+cells+does+not+require+surface+Thy-1+expression.&rft.au=Gunter%2C+K+C%3BGermain%2C+R+N%3BLeo%2C+O%3BChan%2C+C%3BShevach%2C+E+M&rft.aulast=Gunter&rft.aufirst=K&rft.date=1988-03-01&rft.volume=112&rft.issue=1&rft.spage=135&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 - 1988-04-12 N1 - Date created - 1988-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of the glycosaminoglycan-attachment site of mouse invariant-chain proteoglycan core protein by site-directed mutagenesis. AN - 78114604; 3422739 AB - The invariant chain (Ii), a nonpolymorphic glycoprotein that associates with the immunoregulatory Ia proteins encoded by the major histocompatibility complex, has a proteoglycan form (Ii-CS) that bears a chondroitin sulfate glycosaminoglycan. In this proteoglycan form, Ii may remain associated with Ia at the cell surface. Inhibitors that prevent the addition of glycosaminoglycan to Ii have been found to depress antigen-presenting function. Ii does not have multiple candidate glycosaminoglycan-attachment sites, and we used site-directed mutagenesis to replace a candidate serine glycosaminoglycan-acceptor site with alanine at position 201 in the murine Ii protein. Transfection of the normal or altered gene into Ii-negative COS-7 cells showed that equivalent amounts of core Ii protein and its acidic, terminally glycosylated forms were synthesized, but the Ala-201 mutant Ii did not give rise to Ii-CS. The mutant protein had apparently normal transport through the Golgi compartment and associated stably with Ia molecules. Thus, this mutation directly identifies the site of glycosaminoglycan addition and shows that it can be eliminated without adversely affecting the overall biosynthesis of Ii. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Miller, J AU - Hatch, J A AU - Simonis, S AU - Cullen, S E AD - Laboratory of Immunology, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 1359 EP - 1363 VL - 85 IS - 5 SN - 0027-8424, 0027-8424 KW - Antigens, Differentiation, B-Lymphocyte KW - 0 KW - Chondroitin Sulfate Proteoglycans KW - Histocompatibility Antigens Class II KW - Proteoglycans KW - invariant chain KW - Index Medicus KW - DNA Mutational Analysis KW - Structure-Activity Relationship KW - Histocompatibility Antigens Class II -- genetics KW - Proteoglycans -- metabolism KW - Histocompatibility Antigens Class II -- metabolism KW - Chondroitin Sulfate Proteoglycans -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78114604?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Identification+of+the+glycosaminoglycan-attachment+site+of+mouse+invariant-chain+proteoglycan+core+protein+by+site-directed+mutagenesis.&rft.au=Miller%2C+J%3BHatch%2C+J+A%3BSimonis%2C+S%3BCullen%2C+S+E&rft.aulast=Miller&rft.aufirst=J&rft.date=1988-03-01&rft.volume=85&rft.issue=5&rft.spage=1359&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 - 1988-04-01 N1 - Date created - 1988-04-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Cell. 1977 Dec;12(4):1133-41 [23215] Proc Natl Acad Sci U S A. 1979 Mar;76(3):1373-6 [286319] Mol Immunol. 1979 Jan;16(1):51-60 [376435] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Nucleic Acids Res. 1981 Jan 24;9(2):309-21 [6259625] J Exp Med. 1981 May 1;153(5):1198-214 [6166712] Nature. 1982 Oct 14;299(5884):644-5 [6181417] J Immunol. 1982 Dec;129(6):2564-9 [6982931] J Immunol. 1983 Jul;131(1):352-8 [6408179] Arch Biochem Biophys. 1983 Aug;225(1):370-83 [6614928] Methods Enzymol. 1983;100:468-500 [6225933] J Exp Med. 1983 Dec 1;158(6):1979-92 [6580373] Proc Natl Acad Sci U S A. 1984 Mar;81(5):1534-8 [6424118] EMBO J. 1984 Apr;3(4):869-72 [6586420] EMBO J. 1984 Apr;3(4):873-7 [6327293] Anal Biochem. 1984 Mar;137(2):505-16 [6731831] Nucleic Acids Res. 1984 Jul 25;12(14):5707-17 [6589587] Proc Natl Acad Sci U S A. 1984 Sep;81(18):5657-61 [6091101] Hybridoma. 1982;1(2):125-31 [6821397] J Biol Chem. 1984 Dec 10;259(23):14762-72 [6094573] Fed Proc. 1985 Feb;44(2):373-80 [3917944] Immunogenetics. 1985;21(1):83-90 [2981770] Proc Natl Acad Sci U S A. 1985 Mar;82(5):1321-5 [3919394] J Immunol. 1985 Jun;134(6):4212-7 [3921620] J Immunol. 1985 Jul;135(1):399-407 [3873494] J Immunol. 1985 Jul;135(1):416-22 [3858382] Surv Immunol Res. 1985;4(1):27-34 [3890055] Immunogenetics. 1985;22(2):193-9 [2993162] Nature. 1985 Sep 26-Oct 2;317(6035):359-61 [3876513] J Biol Chem. 1985 Nov 25;260(27):14722-6 [2932448] J Exp Med. 1985 Dec 1;162(6):1916-34 [3864916] Biochem J. 1985 Nov 15;232(1):277-9 [3936484] J Cell Biol. 1986 Jun;102(6):2169-75 [3458708] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3968-71 [3487084] Biochem J. 1986 Jun 1;236(2):313-25 [2944511] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7683-7 [3484330] J Exp Med. 1986 Nov 1;164(5):1478-89 [3464691] J Exp Med. 1986 Nov 1;164(5):1490-504 [2430042] Cell. 1986 Nov 21;47(4):619-25 [3779839] Cell. 1986 Dec 26;47(6):1071-7 [3490919] Nature. 1986 Nov 20-26;324(6094):260-2 [2946957] Proc Natl Acad Sci U S A. 1986 Dec;83(23):9207-10 [2947243] Biochem J. 1986 May 15;236(1):1-14 [3539097] J Immunol. 1987 Mar 1;138(5):1319-21 [3468174] EMBO J. 1986 Dec 20;5(13):3483-8 [3104027] Proc Natl Acad Sci U S A. 1987 May;84(10):3194-8 [3472204] Proc Natl Acad Sci U S A. 1987 May;84(9):2901-5 [3106979] EMBO J. 1987 Jun;6(6):1677-83 [3038530] J Immunol. 1987 Sep 15;139(6):1946-51 [3497984] Cell. 1982 May;29(1):61-9 [6955026] J Biol Chem. 1977 Sep 25;252(18):6316-21 [561070] J Biol Chem. 1978 Oct 10;253(19):6687-93 [690122] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anemia and erythropoiesis in patients with the acquired immunodeficiency syndrome (AIDS) and Kaposi sarcoma treated with zidovudine. AN - 78107983; 3422548 AB - We evaluated the development of anemia as part of a trial of zidovudine therapy in patients with the acquired immunodeficiency syndrome (AIDS) with Kaposi sarcoma. Patients were randomized to one of three treatment groups or a placebo group. Transfusion-requiring anemia (hemoglobin less than 100 g/L) developed in 6 of 15 patients on zidovudine therapy at a mean of 6 weeks after starting treatment. A fall in the reticulocyte count was the earliest peripheral blood indicator of toxicity. Mean corpuscular volume increased markedly in patients on zidovudine therapy not developing anemia yet remained stable or only slightly increased in those who became anemic. Bone marrow examination showed pure red cell aplasia in 2 patients, erythroid maturation arrest in 1, and erythroid hypoplasia in 3. Megaloblastic erythropoiesis was present in 2 of the 6 anemic patients. Erythropoietin levels measured at the time of first transfusion were increased. Thus, the anemia associated with zidovudine therapy is due to red cell hypoplasia or aplasia. JF - Annals of internal medicine AU - Walker, R E AU - Parker, R I AU - Kovacs, J A AU - Masur, H AU - Lane, H C AU - Carleton, S AU - Kirk, L E AU - Gralnick, H R AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 372 EP - 376 VL - 108 IS - 3 SN - 0003-4819, 0003-4819 KW - Antiviral Agents KW - 0 KW - Hemoglobins KW - Zidovudine KW - 4B9XT59T7S KW - Thymidine KW - VC2W18DGKR KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Hemoglobins -- drug effects KW - Erythropoiesis -- drug effects KW - Drug Evaluation KW - Prospective Studies KW - Random Allocation KW - Humans KW - Erythrocyte Indices -- drug effects KW - Adult KW - Middle Aged KW - Male KW - Antiviral Agents -- therapeutic use KW - Sarcoma, Kaposi -- drug therapy KW - Acquired Immunodeficiency Syndrome -- complications KW - Acquired Immunodeficiency Syndrome -- blood KW - Anemia -- chemically induced KW - Sarcoma, Kaposi -- blood KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Antiviral Agents -- adverse effects KW - Thymidine -- therapeutic use KW - Thymidine -- analogs & derivatives KW - Thymidine -- adverse effects KW - Sarcoma, Kaposi -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78107983?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Anemia+and+erythropoiesis+in+patients+with+the+acquired+immunodeficiency+syndrome+%28AIDS%29+and+Kaposi+sarcoma+treated+with+zidovudine.&rft.au=Walker%2C+R+E%3BParker%2C+R+I%3BKovacs%2C+J+A%3BMasur%2C+H%3BLane%2C+H+C%3BCarleton%2C+S%3BKirk%2C+L+E%3BGralnick%2C+H+R%3BFauci%2C+A+S&rft.aulast=Walker&rft.aufirst=R&rft.date=1988-03-01&rft.volume=108&rft.issue=3&rft.spage=372&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 - 1988-03-23 N1 - Date created - 1988-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of gonadotropin secretion rate on the radiosensitivity of the rat luteinizing hormone-releasing hormone neuron and gonadotroph. AN - 78106939; 3125043 AB - To test the hypothesis that the functional state of hypothalamic LHRH neurons and pituitary gonadotrophs might alter their radiosensitivity, we determined the experimental conditions under which the gonadotropin response to castration could be impaired by a single dose of cranial irradiation. Single doses of cranial irradiation greater than 2000 rads were lethal to unshielded rats. Shielding of the oropharynx and esophagus allowed the animals to survive doses up to 5000 rads. Doses between 2000 and 5000 rads had no effect on basal gonadotropin levels for as long as 3 months after irradiation. Irradiation caused a dose- and time-dependent impairment, however, in the gonadotropin response to castration. Impairment of the gonadotropin levels of castrate animals occurred in animals that were irradiated either before or after castration. However, rats irradiated in the castrate state showed a decreased susceptibility to irradiation damage. Additionally, stimulation of the pituitary by LHRH agonist (LHRHa) 3 h before irradiation significantly reduced the impairment of gonadotropin secretion 12-20 weeks after irradiation (P less than 0.05). Thus, increased functional activity of the rat hypothalamus or pituitary at the time of irradiation, induced by either castration or acute LHRHa administration, was associated with some protection against the gonadotropin-lowering effect of irradiation. Based upon these data, we hypothesize that stimulation of gonadotropin secretion at the time of therapeutic cranial irradiation in humans might protect against subsequent impairment of gonadotropin secretion. JF - Endocrinology AU - Winterer, J AU - Barnes, K M AU - Lichter, A S AU - Deluca, A M AU - Loriaux, D L AU - Cutler, G B AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 884 EP - 890 VL - 122 IS - 3 SN - 0013-7227, 0013-7227 KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Testosterone KW - 3XMK78S47O KW - Triptorelin Pamoate KW - 57773-63-4 KW - Tryptal KW - 57773-65-6 KW - Luteinizing Hormone KW - 9002-67-9 KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Thyroxine KW - Q51BO43MG4 KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Thyroid Gland -- physiology KW - Testosterone -- pharmacology KW - Body Weight -- radiation effects KW - Thyroxine -- blood KW - Dose-Response Relationship, Radiation KW - Thyroid Gland -- radiation effects KW - Male KW - Orchiectomy KW - Luteinizing Hormone -- secretion KW - Hypothalamus -- radiation effects KW - Hypothalamus -- physiology KW - Pituitary Gland -- physiology KW - Hypothalamus -- drug effects KW - Triptorelin Pamoate -- analogs & derivatives KW - Gonadotropin-Releasing Hormone -- pharmacology KW - Gonadotropin-Releasing Hormone -- analogs & derivatives KW - Follicle Stimulating Hormone -- secretion KW - Pituitary Gland -- radiation effects KW - Pituitary Gland -- drug effects KW - Gonadotropin-Releasing Hormone -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78106939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+gonadotropin+secretion+rate+on+the+radiosensitivity+of+the+rat+luteinizing+hormone-releasing+hormone+neuron+and+gonadotroph.&rft.au=Winterer%2C+J%3BBarnes%2C+K+M%3BLichter%2C+A+S%3BDeluca%2C+A+M%3BLoriaux%2C+D+L%3BCutler%2C+G+B&rft.aulast=Winterer&rft.aufirst=J&rft.date=1988-03-01&rft.volume=122&rft.issue=3&rft.spage=884&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-04-06 N1 - Date created - 1988-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retrospective analysis of stage I and II indolent lymphomas at the National Cancer Institute. AN - 78105824; 2449414 AB - We have retrospectively reviewed the records of 54 patients with Stages I and II indolent lymphoma treated at the National Cancer Institute between January 1958 and December 1984. Patients were treated by a variety of approaches, with 48/54 patients receiving some form of radiation therapy. The median potential follow-up was 9 years (rang 1.7-23.7 years). Overall survival and disease-free survival at 10 years were 69% and 48%, respectively. There were no relapses among Stage I patients after 6.5 years, with 11 of 27 patients followed beyond that time, suggesting that some patients may be cured. Of the 38 patients who received radiation therapy alone as primary treatment, 17 ultimately relapsed. Seventy-one percent of these relapses were nodal. Our data suggest that patients with early stage indolent lymphoma can be treated with curative intent. The finding that most relapses after radiation therapy occur in untreated lymph nodes suggests that total lymphoid irradiation may prolong disease-free survival and, perhaps, overall survival as well. JF - International journal of radiation oncology, biology, physics AU - Lawrence, T S AU - Urba, W J AU - Steinberg, S M AU - Sundeen, J T AU - Cossman, J AU - Young, R C AU - Glatstein, E AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 417 EP - 424 VL - 14 IS - 3 SN - 0360-3016, 0360-3016 KW - Cytarabine KW - 04079A1RDZ KW - Bleomycin KW - 11056-06-7 KW - Procarbazine KW - 35S93Y190K 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 - Bleomycin -- administration & dosage KW - Combined Modality Therapy KW - Humans KW - Vincristine -- administration & dosage KW - Retrospective Studies KW - Prognosis KW - Aged KW - Doxorubicin -- administration & dosage KW - Cytarabine -- administration & dosage KW - Procarbazine -- administration & dosage KW - Etoposide -- administration & dosage KW - Adult KW - Middle Aged KW - Adolescent KW - Methotrexate -- administration & dosage KW - Prednisone -- administration & dosage KW - Female KW - Male KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Lymphoma, Non-Hodgkin -- therapy KW - Lymphoma, Non-Hodgkin -- radiotherapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Lymphoma, Non-Hodgkin -- pathology KW - Radiotherapy, High-Energy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78105824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Retrospective+analysis+of+stage+I+and+II+indolent+lymphomas+at+the+National+Cancer+Institute.&rft.au=Lawrence%2C+T+S%3BUrba%2C+W+J%3BSteinberg%2C+S+M%3BSundeen%2C+J+T%3BCossman%2C+J%3BYoung%2C+R+C%3BGlatstein%2C+E&rft.aulast=Lawrence&rft.aufirst=T&rft.date=1988-03-01&rft.volume=14&rft.issue=3&rft.spage=417&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 - 1988-03-29 N1 - Date created - 1988-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transfer by pro gene transfection of tumor promoter-sensitive phenotype to promotion-insensitive JB6 cells. AN - 78102940; 3342399 AB - Transfection of activated promotion sensitivity genes (pro genes) confers on insensitive (P-) cells susceptibility to induction of anchorage-independent growth by tumor-promoting phorbol esters. Promotion-sensitive (P+) JB6 cell variants, from which activated pro-1 and pro-2 were cloned, respond to 12-O-tetradecanoylphorbol-13-acetate (TPA) and various nonphorbol tumor promoters with anchorage-independent transformation that is irreversible 60-80% of the time. Anchorage-independent (Tx) clonal lines derived from these TPA-induced agar colonies were also tumorigenic in nude mice. This report has addressed the question of whether the phenotypes associated with parental P+ cells are transferred by transfection of activated pro-1 and pro-2. Clonal lines were established after transfection of JB6 P- cells with activated pro-1 or pro-2, induction of anchorage-independent colony formation by TPA, and growth of individual agar colonies to yield clonal transfectant lines. The lines so derived from transfected populations included Tx, P+, and P- lines, reflecting irreversible neoplastic transformation and greater and lesser degrees of preneoplastic progression, respectively. The anchorage-independent transfectants were found to be tumorigenic. Since untransfected P- cells subjected to the same single-cycle TPA treatment and cloning in agar yielded no anchorage-independent and few P+ transfectants, the appearance of P+ and Tx transfectants after pro-1 and pro-2 transfection is therefore likely to be due to the transfected pro genes. Indirect assay of pro gene uptake by quick-blot hybridization of transfectant cell DNA with the vectors into which pro genes had been cloned confirmed the association of transferred P+ and Tx phenotypes with the presence of the transfected DNA. Finally, assay of the sensitivity of P+ pro-1 and pro-2 transfectants to transformation by TPA at various concentrations showed that transfection with pro-1 or pro-2 conferred about equal responses that were somewhat lower than those observed with parental P+ controls. Taken together these data indicate that promotion-insensitive JB6 cells need only an activated pro gene and TPA exposure to become neoplastically transformed. JF - Cancer research AU - Colburn, N H AU - Smith, B M AU - Wendel, E J AU - Dowjat, W K AU - Shimada, T AD - Cell Biology Section, National Cancer Institute, Frederick Maryland 21701-1013. Y1 - 1988/03/01/ PY - 1988 DA - 1988 Mar 01 SP - 1195 EP - 1200 VL - 48 IS - 5 SN - 0008-5472, 0008-5472 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Phenotype KW - Animals KW - Mice KW - Mice, Inbred BALB C KW - Transfection KW - Cell Transformation, Neoplastic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78102940?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transfer+by+pro+gene+transfection+of+tumor+promoter-sensitive+phenotype+to+promotion-insensitive+JB6+cells.&rft.au=Colburn%2C+N+H%3BSmith%2C+B+M%3BWendel%2C+E+J%3BDowjat%2C+W+K%3BShimada%2C+T&rft.aulast=Colburn&rft.aufirst=N&rft.date=1988-03-01&rft.volume=48&rft.issue=5&rft.spage=1195&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 - 1988-03-28 N1 - Date created - 1988-03-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A single point mutation in the envelope gene is responsible for replication and XC fusion deficiency of the endogenous ecotropic C3H/He murine leukemia virus and for its repair in culture. AN - 78088390; 2828688 AB - The molecular basis has been determined for differences in infectivity and XC phenotype of endogenous ecotropic murine leukemia virus of the low-leukemia mouse strain C3H/He, its relative in the high-leukemia mouse strain AKR, and highly infectious, XC-positive C3H virus variants selected in vitro. Endogenous ecotropic type C virus induced by iododeoxyuridine from the nontransformed C3H/10T1/2 cell line is XC negative and replication deficient. In contrast, viruses produced late after iododeoxyuridine induction in chemically transformed C3H/10T1/2 cells (MCA5) are XC positive and infectious. XC-negative viruses can be converted to XC-positive viruses by being grown in certain transformed cell lines. We have cloned the endogenous ecotropic provirus of C3H/He from MCA5 cells, which is XC negative and replication deficient, as well as two XC-positive C3H proviruses derived by in vitro conversion. Fragment exchange between the XC-negative molecular clone p110 and the XC-positive AKR virus clone p623 revealed that the defect in p110 lies 3' of the SalI site located in the pol region. Nucleotide sequencing established that the C3H p110 provirus was integrated within the R region of an endogenous VL30 long terminal repeat (LTR) in reverse orientation and that the virus differed from the infectious AKR p623 provirus by a point mutation, substituting Lys for Arg at the potential precursor cleavage site for gp70 and p15E. In vitro-converted XC-positive C3H proviral clones 3211 and 4211 are identical to XC-negative C3H p110, except that they have Arg at this site and the normal cleavage site is thus regenerated in these clones. The XC-negative C3H p110 was blocked in processing of Pr85env, whereas clones 3211 and 4211 had normal cleavage of the env precursor into gp70. Both the XC-negative C3H provirus and the in vitro-converted XC-positive C3H proviruses had a single copy of a 99-base-pair enhancer element in the LTR, whereas two copies of this sequence are present in the AKR proviral LTR. Substitution of Arg for Lys at the envelope precursor processing site of C3H p110 by site-directed mutagenesis is sufficient by itself to convert the virus to the XC-positive replication-competent phenotype. Thus, we have established that a single point mutation at the processing site of the envelope precursor protein Pr85 is responsible for the difference in the infectivity and XC phenotype of endogenous ecotropic murine leukemia virus from C3H/He and AKR mice and that the basis for in vitro conversion is a mutation at this site. JF - Journal of virology AU - Sithanandam, G AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21701. Y1 - 1988/03// PY - 1988 DA - March 1988 SP - 932 EP - 943 VL - 62 IS - 3 SN - 0022-538X, 0022-538X KW - DNA, Recombinant KW - 0 KW - Viral Envelope Proteins KW - Index Medicus KW - Phenotype KW - Animals KW - AKR murine leukemia virus -- genetics KW - Base Sequence KW - Protein Processing, Post-Translational KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Cell Transformation, Neoplastic -- microbiology KW - Cell Line KW - Virus Replication KW - Retroviridae -- pathogenicity KW - Leukemia Virus, Murine -- physiology KW - Leukemia Virus, Murine -- genetics KW - Cell Fusion KW - Viral Envelope Proteins -- physiology KW - Viral Envelope Proteins -- biosynthesis KW - Retroviridae -- physiology KW - Mice, Inbred C3H -- microbiology KW - Leukemia Virus, Murine -- pathogenicity KW - Retroviridae -- genetics KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78088390?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=A+single+point+mutation+in+the+envelope+gene+is+responsible+for+replication+and+XC+fusion+deficiency+of+the+endogenous+ecotropic+C3H%2FHe+murine+leukemia+virus+and+for+its+repair+in+culture.&rft.au=Sithanandam%2C+G%3BRapp%2C+U+R&rft.aulast=Sithanandam&rft.aufirst=G&rft.date=1988-03-01&rft.volume=62&rft.issue=3&rft.spage=932&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 - 1988-03-18 N1 - Date created - 1988-03-18 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M21031; GENBANK; M21028; M19005; M19006 N1 - SuppNotes - Cited By: Virology. 1981 Jan 30;108(2):445-52 [6258297] J Virol. 1987 Sep;61(9):2852-6 [3039173] Cell. 1981 May;24(2):519-29 [7237558] J Virol. 1969 Feb;3(2):126-32 [4304442] Virology. 1970 Dec;42(4):1136-9 [4099080] J Exp Med. 1971 Jun 1;133(6):1219-33 [4325132] J Exp Med. 1971 Jun 1;133(6):1234-41 [4325133] Science. 1971 Oct 8;174(4005):155-6 [4330367] J Exp Med. 1972 Jul 1;136(1):175-84 [4113509] J Exp Med. 1972 Nov 1;136(5):1272-85 [4343244] J Exp Med. 1972 Nov 1;136(5):1286-301 [4343245] Adv Virus Res. 1972;17:129-86 [4348509] Virology. 1973 Apr;52(2):456-67 [4705382] Science. 1973 May 25;180(4088):865-6 [4122421] J Virol. 1974 Jan;13(1):181-5 [4359422] Proc Natl Acad Sci U S A. 1974 Sep;71(9):3555-9 [4372624] Virology. 1975 Jun;65(2):392-409 [165619] J Virol. 1975 Oct;16(4):991-9 [51938] J Mol Biol. 1975 Nov 5;98(3):503-17 [1195397] Proc Natl Acad Sci U S A. 1975 Oct;72(10):3961-5 [1105573] J Virol. 1976 May;18(2):411-7 [58071] Science. 1977 Apr 8;196(4286):175-7 [322278] Science. 1977 Apr 8;196(4286):180-2 [322279] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Int J Cancer. 1978 Mar 15;21(3):356-60 [631935] Cell. 1978 Oct;15(2):687-701 [719759] Nature. 1979 Nov 29;282(5738):471-7 [503226] Proc Natl Acad Sci U S A. 1980 Jan;77(1):614-8 [6244569] Methods Enzymol. 1979;68:281-98 [232217] Proc Natl Acad Sci U S A. 1980 Mar;77(3):1642-5 [6154937] Nature. 1980 Sep 25;287(5780):301-6 [7421990] Proc Natl Acad Sci U S A. 1980 Oct;77(10):5774-8 [6255464] Nature. 1981 Jul 23;292(5821):311-7 [6166864] Virology. 1981 Sep;113(2):725-35 [7023022] J Exp Med. 1982 Apr 1;155(4):1233-8 [6278049] Cell. 1982 Apr;28(4):881-8 [6284378] J Virol. 1982 Jun;42(3):1088-98 [6284989] J Mol Appl Genet. 1982;1(4):327-41 [6286831] J Virol. 1982 Jul;43(1):26-36 [6287001] J Virol. 1982 Oct;44(1):144-57 [6183444] J Virol. 1982 Dec;44(3):950-7 [6294342] J Virol. 1983 Feb;45(2):740-54 [6300431] J Virol. 1983 Feb;45(2):755-65 [6300432] Proc Natl Acad Sci U S A. 1983 Jul;80(13):3963-5 [6575390] J Virol. 1983 Sep;47(3):656-9 [6620466] J Virol. 1984 Feb;49(2):437-44 [6319743] J Virol. 1984 Feb;49(2):471-8 [6319746] Gene. 1983 Dec;26(2-3):171-9 [6323258] Cell. 1984 Jul;37(3):1075-89 [6430565] DNA. 1984 Dec;3(6):479-88 [6096101] J Virol. 1985 Dec;56(3):798-806 [2999434] Mol Cell Biol. 1986 Apr;6(4):1276-82 [3023879] J Virol. 1987 Mar;61(3):701-7 [3027396] Mol Cell Biol. 1987 Jun;7(6):2296-8 [3600664] J Supramol Struct. 1980;14(3):343-52 [6261043] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Equipment Considerations for Intraoperative Ultrasound AN - 21201616; 11625184 AB - For most ultrasound sections and especially for those who are just beginning intraoperative ultrasound, it will be necessary to perform these studies with scanners brought from the general ultrasound section. The purpose of this article is to familiarize sonographers with the preparation of equipment for intraoperative ultrasound: choosing and sterilizing the most appropriate transducer, and ensuring that the scanner is clean and electrically safe for operating room use. JF - Journal of Diagnostic Medical Sonography AU - Shawker, Thomas H AU - Bradford, Mary H AU - Norton, Jeffrey A AD - Department of Radiology and the Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland; Georgetown University School of Medicine, Washington, DC.; Department of Radiology, National Institutes of Health, Clinical Center, Bldg 10, Room 1C660, Bethesda, MD 20892 Y1 - 1988/03// PY - 1988 DA - Mar 1988 SP - 49 EP - 54 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 4 IS - 2 SN - 8756-4793, 8756-4793 KW - Biotechnology and Bioengineering Abstracts KW - ultrasonic diagnosis KW - surgery, operative KW - intraoperative period KW - diagnosis, surgical KW - transducers, ultrasonic KW - Ultrasound KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/21201616?accountid=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+Diagnostic+Medical+Sonography&rft.atitle=Equipment+Considerations+for+Intraoperative+Ultrasound&rft.au=Shawker%2C+Thomas+H%3BBradford%2C+Mary+H%3BNorton%2C+Jeffrey+A&rft.aulast=Shawker&rft.aufirst=Thomas&rft.date=1988-03-01&rft.volume=4&rft.issue=2&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Journal+of+Diagnostic+Medical+Sonography&rft.issn=87564793&rft_id=info:doi/10.1177%2F875647938800400201 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-01-01 N1 - Last updated - 2015-03-31 N1 - SubjectsTermNotLitGenreText - Ultrasound DO - http://dx.doi.org/10.1177/875647938800400201 ER - TY - JOUR T1 - Preparation of raf-oncogene-specific antiserum with raf protein produced in E. coli. AN - 78103288; 3277669 AB - In this report we describe the expression of v-raf protein in E. coli using a tryptophan-promoter-driven expression vector and its immunological characterization by anti-peptide sera. The purified recombinant protein was used to produce raf-specific antibodies which are suitable for studying v-raf and c-raf proteins in vitro and in vivo in a variety of species ranging from mouse to man. JF - Biochimica et biophysica acta AU - Kolch, W AU - Schultz, A M AU - Oppermann, H AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, NCI-Frederick Cancer Research Facility, MD 21701. Y1 - 1988/02/28/ PY - 1988 DA - 1988 Feb 28 SP - 233 EP - 239 VL - 949 IS - 2 SN - 0006-3002, 0006-3002 KW - Peptide Fragments KW - 0 KW - Recombinant Proteins KW - Index Medicus KW - Antibody Specificity KW - Chemical Precipitation KW - Escherichia coli -- genetics KW - Amino Acid Sequence KW - Peptide Fragments -- immunology KW - Molecular Weight KW - Structure-Activity Relationship KW - Cloning, Molecular KW - Oncogenes KW - Recombinant Proteins -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78103288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preparation+of+raf-oncogene-specific+antiserum+with+raf+protein+produced+in+E.+coli.&rft.au=Kolch%2C+W%3BSchultz%2C+A+M%3BOppermann%2C+H%3BRapp%2C+U+R&rft.aulast=Kolch&rft.aufirst=W&rft.date=1988-02-28&rft.volume=949&rft.issue=2&rft.spage=233&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 - 1988-04-01 N1 - Date created - 1988-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene transactivation mediated by the TAT gene of human immunodeficiency virus in transgenic mice. AN - 19623683; 8744427 AB - Transgenic mice were generated carrying either the long terminal repeat of Human Immunodeficiency Virus fused to the bacterial chloramphenicol acetyl transferase reporter gene or a control element of the murine alpha A crystallin gene fused to the tat gene of human immunodeficiency virus. By crossing these two strains, progeny were obtained which carried both transgenes. The bacterial reporter gene was specifically transactivated in the eyes of these animals. Images JF - Nucleic Acids Research AU - Khillan, J S AU - Deen, K C AU - Yu, S H AU - Sweet, R W AU - Rosenberg, M AU - Westphal, H AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1988/02/25/ PY - 1988 DA - 1988 Feb 25 SP - 1423 EP - 1430 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 16 IS - 4 SN - 0305-1048, 0305-1048 KW - Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - tat gene KW - Crystallin KW - Chloramphenicol KW - Human immunodeficiency virus KW - Reporter gene KW - Long terminal repeat KW - Transgenes KW - Transgenic mice KW - Genetic crosses KW - J 02310:Genetics & Taxonomy KW - W 30925:Genetic Engineering KW - V 22360:AIDS and HIV KW - N 14845:Miscellaneous KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19623683?accountid=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=Gene+transactivation+mediated+by+the+TAT+gene+of+human+immunodeficiency+virus+in+transgenic+mice.&rft.au=Khillan%2C+J+S%3BDeen%2C+K+C%3BYu%2C+S+H%3BSweet%2C+R+W%3BRosenberg%2C+M%3BWestphal%2C+H&rft.aulast=Khillan&rft.aufirst=J&rft.date=1988-02-25&rft.volume=16&rft.issue=4&rft.spage=1423&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 - tat gene; Crystallin; Chloramphenicol; Long terminal repeat; Reporter gene; Transgenes; Transgenic mice; Genetic crosses; Human immunodeficiency virus ER - TY - JOUR T1 - Immunopurification of the suppressor tRNA dependent rabbit beta-globin readthrough protein. AN - 78208160; 3365379 AB - In mammalian cells, the rabbit beta-globin readthrough protein is the only known example of a naturally occurring readthrough protein which does not involve a viral system. To provide an efficient means for its isolation, detection, and study, we elicited specific antibodies against this unique protein. The 22 amino acid peptide corresponding to the readthrough portion of this protein was synthesized, coupled to keyhole limpet hemocyanin, and injected into sheep. Specific antibodies to the peptide were produced as demonstrated by the enzyme-linked immunosorbent assay technique and by immunoblotting. The antibodies did not react with globin. The rabbit beta-globin readthrough protein was separated from globin and other reticulocyte proteins by polyacrylamide gel electrophoresis and visualized by silver staining or by labeling with [35S]methionine. Incorporation of [35S]methionine into the readthrough protein was significantly enhanced upon addition of an opal suppressor tRNA to reticulocyte lysates. Immunoblotting revealed that the readthrough protein also occurs in lysates without added suppressor tRNA. The antibodies were purified on an affi-gel column which had been coupled with the peptide antigen. The readthrough protein was then purified from reticulocytes by immunoaffinity chromatography and by high-performance liquid chromatography. The results provide conclusive evidence that the beta-globin readthrough protein is naturally occurring in rabbit reticulocytes. JF - Biochemistry AU - Hatfield, D AU - Thorgeirsson, S S AU - Copeland, T D AU - Oroszlan, S AU - Bustin, M AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/02/23/ PY - 1988 DA - 1988 Feb 23 SP - 1179 EP - 1183 VL - 27 IS - 4 SN - 0006-2960, 0006-2960 KW - Antigen-Antibody Complex KW - 0 KW - Immunoglobulin G KW - Peptides KW - RNA, Messenger KW - beta-Globins KW - beta-globin readthrough protein, Oryctolagus cuniculus KW - Globins KW - 9004-22-2 KW - RNA, Transfer KW - 9014-25-9 KW - Index Medicus KW - Animals KW - Base Sequence KW - Kinetics KW - Molecular Sequence Data KW - Rabbits KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Immunoassay KW - Chromatography, Affinity -- methods KW - Globins -- isolation & purification KW - RNA, Transfer -- genetics KW - Globins -- genetics KW - Suppression, Genetic KW - Peptides -- genetics KW - Peptides -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78208160?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immunopurification+of+the+suppressor+tRNA+dependent+rabbit+beta-globin+readthrough+protein.&rft.au=Hatfield%2C+D%3BThorgeirsson%2C+S+S%3BCopeland%2C+T+D%3BOroszlan%2C+S%3BBustin%2C+M&rft.aulast=Hatfield&rft.aufirst=D&rft.date=1988-02-23&rft.volume=27&rft.issue=4&rft.spage=1179&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-06-14 N1 - Date created - 1988-06-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of two trans-regulatory genes (tat-III,trs) of HIV-1. AN - 78101636; 3277284 AB - Point mutations were introduced into the overlapping trans-regulatory genes (tat-III and trs) of human immunodeficiency virus type 1 (HIV-1), and the mutants were evaluated for virus expression. The results showed that tat-III has a positive transacting role and is required for transcriptional activation. A chain terminating mutation early in the trs gene resulted in an increase in transcription of viral messenger RNA as measured by nuclear transcription experiments, but only one major species of viral messenger RNA (1.8 kilobases) was detected, and little or no viral structural proteins were made. Thus, the trs gene product is essential for expression of virus structural proteins but, at the same time, may have a negative trans-regulatory role in transcription. Cotransfection of the point mutant proviruses defective in tat or trs with each other or with a complementary DNA clone containing tat and trs sequences restored the normal transcription pattern and subsequent virus production. JF - Science (New York, N.Y.) AU - Sadaie, M R AU - Benter, T AU - Wong-Staal, F AD - Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1988/02/19/ PY - 1988 DA - 1988 Feb 19 SP - 910 EP - 913 VL - 239 IS - 4842 SN - 0036-8075, 0036-8075 KW - Codon KW - 0 KW - RNA, Messenger KW - RNA, Viral KW - DNA KW - 9007-49-2 KW - Acetyltransferases KW - EC 2.3.1.- KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Humans KW - Transcription, Genetic KW - Plasmids KW - RNA, Messenger -- genetics KW - Transfection KW - Acquired Immunodeficiency Syndrome -- immunology KW - DNA -- genetics KW - Acetyltransferases -- genetics KW - Immunosorbent Techniques KW - RNA, Viral -- genetics KW - Cell Line KW - Genes, Viral KW - Mutation KW - HIV -- genetics KW - Genes, Regulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78101636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Site-directed+mutagenesis+of+two+trans-regulatory+genes+%28tat-III%2Ctrs%29+of+HIV-1.&rft.au=Sadaie%2C+M+R%3BBenter%2C+T%3BWong-Staal%2C+F&rft.aulast=Sadaie&rft.aufirst=M&rft.date=1988-02-19&rft.volume=239&rft.issue=4842&rft.spage=910&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 - 1988-03-21 N1 - Date created - 1988-03-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of pumiliotoxin-B on the excitability of bullfrog sympathetic neurons. AN - 78224982; 3259508 AB - The effects of the alkaloid pumiliotoxin-B were investigated on neurons from bullfrog paravertebral ganglia using current-clamp techniques. Pumiliotoxin-B (2 microM) induced repetitive action potential discharge or bursting pacemaker activity in response to a single stimulus. The toxin had no significant effect on the mean resting potential or action potential characteristics of single action potentials evoked prior to the action potential discharge onset. During the action potential discharge, action potential threshold and afterhyperpolarization amplitude were decreased. In the presence of pumiliotoxin-B, single action potentials were followed by a depolarizing afterpotential. Pumiliotoxin-B still induced action potential discharge in Ca2+-free or Cd2+-containing solutions. Brief superfusion with a Na+-free or tetrodotoxin-containing solution abolished the pumiliotoxin-B-induced action potential discharge prior to the blockade of directly elicited single action potentials. These solutions decreased or abolished the depolarizing afterpotential. Pumiliotoxin-B increases membrane excitability and can induce a stimulation-dependent action potential discharge which appears to result from a tetrodotoxin-sensitive Na+-sensitive potential. JF - European journal of pharmacology AU - Schofield, G G AU - Weight, F F AU - Ikeda, S R AD - Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1988/02/16/ PY - 1988 DA - 1988 Feb 16 SP - 39 EP - 48 VL - 147 IS - 1 SN - 0014-2999, 0014-2999 KW - Alkaloids KW - 0 KW - Indolizines KW - Piperidines KW - Tetrodotoxin KW - 4368-28-9 KW - pumiliotoxin B KW - 67016-65-3 KW - Sodium KW - 9NEZ333N27 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Synapses -- drug effects KW - Sodium -- physiology KW - Rana catesbeiana KW - In Vitro Techniques KW - Calcium -- physiology KW - Membrane Potentials -- drug effects KW - Action Potentials -- drug effects KW - Tetrodotoxin -- pharmacology KW - Electric Stimulation KW - Microelectrodes KW - Neurons -- drug effects KW - Sympathetic Nervous System -- drug effects KW - Alkaloids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78224982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=The+effect+of+pumiliotoxin-B+on+the+excitability+of+bullfrog+sympathetic+neurons.&rft.au=Schofield%2C+G+G%3BWeight%2C+F+F%3BIkeda%2C+S+R&rft.aulast=Schofield&rft.aufirst=G&rft.date=1988-02-16&rft.volume=147&rft.issue=1&rft.spage=39&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 - 1988-06-28 N1 - Date created - 1988-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intrahippocampal injections of a specific mu-receptor ligand PL017 produce generalized convulsions in rats. AN - 78167391; 2834004 AB - The effects of a selective mu-agonist, [NMe-Phe3-D-Pro4]morphiceptin (PL017), and a selective mu-antagonist, beta-funaltrexamine (beta-FNA), on convulsions and wet dog shakes (WDS) were studied. Electroencephalogram demonstrated that a single injection of PL017 into the ventral hippocampus evoked epileptiform spiking which appeared initially in the ventral hippocampus and spread to the cortical area when the animal developed generalized convulsion. Behavioral studies showed that PL017-induced convulsions and WDS were dose-dependent, and these behavioral changes were blocked by beta-FNA pretreatment. The results indicate that mu-receptors in the hippocampus may play an important role in seizure activities evoked by opioids. JF - Brain research AU - Lee, P H AU - Obie, J AU - Hong, J S AD - Laboratory of Behavioral and Neurological Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1988/02/16/ PY - 1988 DA - 1988 Feb 16 SP - 381 EP - 385 VL - 441 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Convulsants KW - 0 KW - Endorphins KW - Receptors, Opioid KW - Receptors, Opioid, mu KW - morphiceptin, N-Me-Phe(3)- KW - 83397-56-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Cerebral Cortex -- physiology KW - Cerebral Cortex -- drug effects KW - Electroencephalography KW - Male KW - Seizures -- chemically induced KW - Endorphins -- pharmacology KW - Hippocampus -- physiology KW - Seizures -- physiopathology KW - Receptors, Opioid -- drug effects KW - Convulsants -- pharmacology KW - Receptors, Opioid -- physiology KW - Hippocampus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78167391?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intrahippocampal+injections+of+a+specific+mu-receptor+ligand+PL017+produce+generalized+convulsions+in+rats.&rft.au=Lee%2C+P+H%3BObie%2C+J%3BHong%2C+J+S&rft.aulast=Lee&rft.aufirst=P&rft.date=1988-02-16&rft.volume=441&rft.issue=1-2&rft.spage=381&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 - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Elsie 4: quantitative computer analysis of sets of two-dimensional gel electrophoretograms. AN - 78221740; 3369688 AB - We have developed and refined a system for quantitative computer analysis of two-dimensional polyacrylamide gel electrophoretograms. The system, named Elsie 4, is based on one described by Vo et al. (Anal. Biochem. 112, 258 (1981]. It is highly automated. Elsie 4 can find, and measure the intensity of, almost any spot resolvable on two-dimensional gels, including spots visible only as shoulders off larger spots and spots so close together that there is no "valley" between them. It can automatically match the spot patterns of different gels, potentially without the need for a user to provide landmark matches. The matches between paired gels let us follow the synthesis of any spot through a set of gels. Information about a group of matched spots can be obtained by referring to any spot in the group. There is generally no need for a standard or reference gel. Data for two experiments can be combined and compared by matching any gel in one experiment with any gel in the other. There are ways to automatically find possible mismatches in sets of gels. Scans and the results of the analysis can be shown on an image displayer. The programs use function libraries; this helps ensure consistency and increase portability. The programs and functions can be linked together in many ways; this lets users build custom programs for analysis of specific experiments. JF - Analytical biochemistry AU - Olson, A D AU - Miller, M J AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 49 EP - 70 VL - 169 IS - 1 SN - 0003-2697, 0003-2697 KW - Index Medicus KW - Software KW - Computer Systems KW - Electrophoresis, Polyacrylamide Gel -- methods KW - Image Processing, Computer-Assisted UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78221740?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Elsie+4%3A+quantitative+computer+analysis+of+sets+of+two-dimensional+gel+electrophoretograms.&rft.au=Olson%2C+A+D%3BMiller%2C+M+J&rft.aulast=Olson&rft.aufirst=A&rft.date=1988-02-15&rft.volume=169&rft.issue=1&rft.spage=49&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 - 1988-06-14 N1 - Date created - 1988-06-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of a promonocyte clone chronically infected with HIV and inducible by 13-phorbol-12-myristate acetate. AN - 78112892; 2449497 AB - The present study has investigated the effect of PMA, an inducer of monocyte differentiation, on HIV expression in a chronically infected promonocyte clone. After acute HIV infection of U937 cells, clones that constitutively expressed varying levels of HIV were isolated by limiting dilution. One clone (U1) produced low levels of HIV but was found to increase its production 20-fold after PMA induction, as detected by reverse transcriptase or A capture. Further characterization of U1 indicated that PMA could induce cellular differentiation and maturation in the clone similar to that in uninfected U937 cells. In addition, functional studies revealed that superoxide anion production from the U1 clone was not different from that of uninfected U937 cells. Electron microscopic studies of U1 indicated that PMA induced endocytotic vesicles containing many HIV particles. These studies provide a model at the clonal level to 1) examine latency or chronicity of HIV infection in monocytes and 2) delineate the signals required for conversion to high level viral expression. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Folks, T M AU - Justement, J AU - Kinter, A AU - Schnittman, S AU - Orenstein, J AU - Poli, G AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 1117 EP - 1122 VL - 140 IS - 4 SN - 0022-1767, 0022-1767 KW - Retroviridae Proteins KW - 0 KW - Superoxides KW - 11062-77-4 KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Clone Cells -- pathology KW - Lymphoma, Large B-Cell, Diffuse -- pathology KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Superoxides -- biosynthesis KW - Tumor Cells, Cultured -- microbiology KW - Retroviridae Proteins -- biosynthesis KW - RNA-Directed DNA Polymerase -- biosynthesis KW - Virus Replication -- drug effects KW - Kinetics KW - Tumor Cells, Cultured -- pathology KW - Cell Differentiation -- drug effects KW - Clone Cells -- drug effects KW - HIV -- physiology KW - Monocytes -- pathology KW - HIV -- isolation & purification KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Monocytes -- drug effects KW - Monocytes -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78112892?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+a+promonocyte+clone+chronically+infected+with+HIV+and+inducible+by+13-phorbol-12-myristate+acetate.&rft.au=Folks%2C+T+M%3BJustement%2C+J%3BKinter%2C+A%3BSchnittman%2C+S%3BOrenstein%2C+J%3BPoli%2C+G%3BFauci%2C+A+S&rft.aulast=Folks&rft.aufirst=T&rft.date=1988-02-15&rft.volume=140&rft.issue=4&rft.spage=1117&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 - 1988-04-05 N1 - Date created - 1988-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of oxygen radicals in 12-O-tetradecanoylphorbol-13-acetate-induced squamous differentiation of cultured normal human bronchial epithelial cells. AN - 78109214; 2827886 AB - The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibits growth and induces terminal squamous differentiation of normal human bronchial cells when added to the culture media [J. C. Willey, A. J. Saladino, C. Ozanne, J. F. Lechner, and C. C. Harris, Carcinogenesis (lond.), 5: 209-215, 1984]. We have investigated the possibility of oxygen free radicals being involved as intermediates in this process. Electron paramagnetic resonance measurements using the spin-trapping agent 5,5-dimethyl-1-pyrroline-1-oxide failed to detect oxygen free radicals in bronchial epithelial cells exposed to TPA, although oxy radicals were detected in bronchial epithelial cells after a nontoxic exposure to menadione, and in human neutrophils after exposure to TPA. Addition to the culture media of free radical scavenger, i.e., reduced glutathione, N-acetylcysteine, D-alpha-tocopherol, copper (II) (3,5-diisopropylsalicyclic acid)2, or the combination of superoxide dismutase and catalase did not affect the dose-dependent growth inhibition of TPA on the bronchial epithelial cells. Moreover, exposure of the bronchial epithelial cells to TPA did not result in increased DNA single strand breaks measured by alkaline elution, as would be expected with a free radical mediated mechanism. Thus, our results argue against the importance of oxygen free radicals in the inhibition of growth and the induction of squamous differentiation by TPA in normal human bronchial epithelial cells. JF - Cancer research AU - Gabrielson, E W AU - Rosen, G M AU - Grafstrom, R C AU - Strauss, K E AU - Miyashita, M AU - Harris, C C AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 822 EP - 825 VL - 48 IS - 4 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - Free Radicals KW - Salicylates KW - Vitamin E KW - 1406-18-4 KW - copper bis(3,5-diisopropylsalicylate) KW - 21246-18-4 KW - Catalase KW - EC 1.11.1.6 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Glutathione KW - GAN16C9B8O KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Acetylcysteine KW - WYQ7N0BPYC KW - Index Medicus KW - DNA Damage KW - Humans KW - Acetylcysteine -- pharmacology KW - Catalase -- pharmacology KW - Glutathione -- pharmacology KW - Epithelium -- drug effects KW - Salicylates -- pharmacology KW - Superoxide Dismutase -- pharmacology KW - Epithelial Cells KW - Electron Spin Resonance Spectroscopy KW - Kinetics KW - Vitamin E -- pharmacology KW - Antineoplastic Agents -- pharmacology KW - Tetradecanoylphorbol Acetate -- toxicity KW - Cell Survival -- drug effects KW - Bronchi -- drug effects KW - Bronchi -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78109214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+oxygen+radicals+in+12-O-tetradecanoylphorbol-13-acetate-induced+squamous+differentiation+of+cultured+normal+human+bronchial+epithelial+cells.&rft.au=Gabrielson%2C+E+W%3BRosen%2C+G+M%3BGrafstrom%2C+R+C%3BStrauss%2C+K+E%3BMiyashita%2C+M%3BHarris%2C+C+C&rft.aulast=Gabrielson&rft.aufirst=E&rft.date=1988-02-15&rft.volume=48&rft.issue=4&rft.spage=822&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 - 1988-03-14 N1 - Date created - 1988-03-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - B cell stimulatory factor 1 (IL-4) enhances the development of cytotoxic T cells from Lyt-2+ resting murine T lymphocytes. AN - 78102665; 3257770 AB - B cell stimulatory factor 1 (BSF-1) (IL-4) was shown to synergize with phorbol esters or with monoclonal anti-TCR antibody in stimulation of the development of CTL from small resting murine T cells. IL-2 also synergized with PMA in such differentiation but was less effective than BSF-1. The combination of these two lymphokines with PMA had the most potent effect on the development of CTL. BSF-1 plus PMA stimulated a significant increase in the intracellular content of N-benzyloxycarbonyl-L-lysine thiobenzylester esterase, a granule-associated biochemical marker, whereas IL-2 plus PMA was only marginally effective. Depletion of L3T4+ cells did not result in the abrogation of these effects. Lyt-2+ T cells that were incubated for 72 h with BSF-1 plus PMA accumulated N-benzyloxycarbonyl-L-lysine thiobenzylester esterase and secreted this intragranular marker after interaction with immobilized anti-T cell receptor mAb. These BSF-1/PMA-stimulated Lyt-2+, L3T4- T cells were also able to kill FcR positive target cells in a retargeting assay with a mAb to murine T3 Ag, providing evidence that BSF-1 plus PMA acted directly on precursors of cytotoxic T cells. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Trenn, G AU - Takayama, H AU - Hu-Li, J AU - Paul, W E AU - Sitkovsky, M V AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 1101 EP - 1106 VL - 140 IS - 4 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Ly KW - Interleukin-2 KW - Interleukins KW - Receptors, Antigen, T-Cell KW - Interleukin-4 KW - 207137-56-2 KW - Granzymes KW - EC 3.4.21.- KW - Serine Endopeptidases KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-2 -- pharmacology KW - Antigens, Ly -- analysis KW - Serine Endopeptidases -- analysis KW - Receptors, Antigen, T-Cell -- immunology KW - Mice KW - Mice, Inbred BALB C KW - Antibodies, Monoclonal -- immunology KW - Serine Endopeptidases -- secretion KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cytotoxicity, Immunologic -- drug effects KW - Cell Differentiation -- drug effects KW - Drug Synergism KW - Female KW - T-Lymphocytes -- cytology KW - Interleukins -- pharmacology KW - T-Lymphocytes, Cytotoxic -- cytology KW - T-Lymphocytes -- drug effects KW - T-Lymphocytes -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78102665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=B+cell+stimulatory+factor+1+%28IL-4%29+enhances+the+development+of+cytotoxic+T+cells+from+Lyt-2%2B+resting+murine+T+lymphocytes.&rft.au=Trenn%2C+G%3BTakayama%2C+H%3BHu-Li%2C+J%3BPaul%2C+W+E%3BSitkovsky%2C+M+V&rft.aulast=Trenn&rft.aufirst=G&rft.date=1988-02-15&rft.volume=140&rft.issue=4&rft.spage=1101&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 - 1988-04-05 N1 - Date created - 1988-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of the CD2 alternate pathway of T cell activation by CD3. Evidence for heterologous desensitization. AN - 78102549; 2893822 AB - Normal resting T cells were stimulated through the alternate CD2 pathway. A CD3 mAb VIT3 completely blocked their proliferative response. The time interval for 50% inhibition lasted for 24 h after the onset of CD2 stimulation. Mitogen-activated cloned long term cultured T cells could also be stimulated via CD2. This proliferative response was again inhibitable by VIT3, indicating that CD3 regulates the CD2 pathway not only in resting cells, but also in lymphocytes actively involved in an Ir. T cells were further loaded with Quin2 and their free cytoplasmic Ca2+ levels were monitored in response to CD3 and CD2 stimulation. Antibodies directed against both surface R triggered a rapid elevation of Ca2+ levels. Both responses were abrogated when the cells had been treated overnight with VIT3. The free cytoplasmic Ca2+ levels of VIT3-pretreated cells, however, were not higher than those of control cells. These results point to a functional interaction between CD3 and CD2 possibly at the level of signal transducing proteins. Finally, cholera toxin was found to inhibit the Ca2+ response in Jurkat T cells. Both the CD3 and CD2 stimulation were sensitive to cholera toxin, indicating that a GTP-binding protein may be involved in signal transduction for both surface structures. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Holter, W AU - Majdic, O AU - Stockinger, H AU - Howard, B H AU - Knapp, W AD - Laboratory of Molecular Biology, National Institutes of Health, Bethesda, MD. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 1043 EP - 1046 VL - 140 IS - 4 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD2 KW - Antigens, CD3 KW - Antigens, Differentiation, T-Lymphocyte KW - Carrier Proteins KW - Phytohemagglutinins KW - Receptors, Immunologic KW - Cholera Toxin KW - 9012-63-9 KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Calcium -- metabolism KW - Cells, Cultured KW - Humans KW - Cholera Toxin -- pharmacology KW - Phytohemagglutinins -- pharmacology KW - Antibodies, Monoclonal -- immunology KW - Lymphocyte Activation -- drug effects KW - T-Lymphocytes -- metabolism KW - Receptors, Immunologic -- physiology KW - Antigens, Differentiation, T-Lymphocyte -- physiology KW - Carrier Proteins -- physiology KW - T-Lymphocytes -- drug effects KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78102549?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+the+CD2+alternate+pathway+of+T+cell+activation+by+CD3.+Evidence+for+heterologous+desensitization.&rft.au=Holter%2C+W%3BMajdic%2C+O%3BStockinger%2C+H%3BHoward%2C+B+H%3BKnapp%2C+W&rft.aulast=Holter&rft.aufirst=W&rft.date=1988-02-15&rft.volume=140&rft.issue=4&rft.spage=1043&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 - 1988-04-05 N1 - Date created - 1988-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Topoisomerase II-mediated DNA damage produced by 4'-(9-acridinylamino)methanesulfon-m-anisidide and related acridines in L1210 cells and isolated nuclei: relation to cytotoxicity. AN - 78099264; 2827887 AB - 4'-(9-Acridinylamino)methanesulfon-m-anisidide (m-AMSA) is a DNA intercalating 9-aminoacridine with clinical activity in adult acute leukemia. m-AMSA has been shown to produce protein-linked DNA strand breaks in mammalian cells through an interaction with the nuclear enzyme DNA topoisomerase II. We have compared the effects of m-AMSA and several acridine analogues (9-aminoacridine; A, NSC 343499; B, SN 16507; C, NSC 140701; D, SN 13553) on DNA integrity and cell survival in L1210 leukemia in vitro. Cells (or isolated nuclei) were treated with drugs (0.1-50 microM) for 0.5-1.0 h and subsequently analyzed using the alkaline elution technique. All drugs, except Compound D, produced DNA-protein cross-links (DPC) in L1210 cells. At 1 microM, potency was in the order, C greater than m-AMSA greater than B greater than A much greater than 9-aminoacridine. In isolated nuclei, DPC and single-strand breaks were produced in essentially a 1:1 ratio, which is consistent with topoisomerase II-mediated protein-linked DNA breaks. Potency differences were less pronounced in nuclei than in cells. In isolated nuclei, Compound D produced extensive DPC not associated with single-strand breaks, which suggests a more complex activity for this compound. Colony formation assays demonstrated the cytotoxicity of most of these acridine analogues (C greater than B greater than A approximately equal to m-AMSA much greater than D = 9-aminoacridine). Correlation of DPC with cell kill gave similar curves for each compound. These results are evidence for a causal relationship between drug-induced topoisomerase II-mediated DNA breaks and cytotoxicity. JF - Cancer research AU - Covey, J M AU - Kohn, K W AU - Kerrigan, D AU - Tilchen, E J AU - Pommier, Y AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 860 EP - 865 VL - 48 IS - 4 SN - 0008-5472, 0008-5472 KW - Aminoacridines KW - 0 KW - Amsacrine KW - 00DPD30SOY KW - 4'-(9-acridinylamino)methanesulfon-o-anisidide KW - 51264-17-6 KW - DNA Topoisomerases, Type II KW - EC 5.99.1.3 KW - Index Medicus KW - Animals KW - Cell Survival -- drug effects KW - Kinetics KW - Isomerism KW - Mice KW - Structure-Activity Relationship KW - Amsacrine -- toxicity KW - Cell Nucleus -- enzymology KW - DNA Damage KW - Amsacrine -- analogs & derivatives KW - DNA Topoisomerases, Type II -- metabolism KW - Leukemia L1210 -- enzymology KW - Cell Nucleus -- drug effects KW - Leukemia L1210 -- genetics KW - Aminoacridines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78099264?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Topoisomerase+II-mediated+DNA+damage+produced+by+4%27-%289-acridinylamino%29methanesulfon-m-anisidide+and+related+acridines+in+L1210+cells+and+isolated+nuclei%3A+relation+to+cytotoxicity.&rft.au=Covey%2C+J+M%3BKohn%2C+K+W%3BKerrigan%2C+D%3BTilchen%2C+E+J%3BPommier%2C+Y&rft.aulast=Covey&rft.aufirst=J&rft.date=1988-02-15&rft.volume=48&rft.issue=4&rft.spage=860&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 - 1988-03-14 N1 - Date created - 1988-03-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Locus of inhibitory action of cAMP-dependent protein kinase in the antigen receptor-triggered cytotoxic T lymphocyte activation pathway. AN - 78089981; 2448308 AB - The mechanism of the cAMP involvement in regulation of cellular functions was studied here using a novel functional assay (antigen receptor-triggered exocytosis of granules) of cloned cytotoxic T lymphocytes (CTL). We suggest that cAMP-dependent protein kinase, protein kinase A, counteracts the protein kinase C and Ca2+-mediated stimulatory T-cell antigen receptor (TcR)-triggered biochemical pathway. This suggestion is supported by experimental results which satisfy criteria for protein kinase A involvement in cellular functions. Pretreatment of CTL with cholera toxin induces cAMP accumulation in CTL, partially inhibits TcR-triggered "lethal hit" delivery to the target cell, and almost completely blocks TcR-triggered exocytosis of granules from CTL. Other agents that raise the intracellular level of cAMP, including forskolin and isobutylmethylxanthine (IBMX) also inhibit TcR-triggered CTL activation. Involvement of cAMP-dependent protein kinase in an inhibitory pathway is suggested by the synergistic effects of cyclic nucleotide analogs 8-bromo-cAMP and N6-benzoyl-cAMP in inhibition of TcR-triggered exocytosis. Forskolin and IBMX inhibited TcR-triggered phosphoinositide turnover in CTL, suggesting that cAMP affected very early events in signal transduction that follow TcR cross-linking by a ligand. The ability of IBMX to inhibit CTL activation when the TcR cross-linking step was by-passed by the combination of phorbol myristate acetate and ionophore A23187 suggests that the locus of inhibitory effect of cAMP is at both the early and late stages of the TcR-triggered transmembrane signaling pathway. JF - The Journal of biological chemistry AU - Takayama, H AU - Trenn, G AU - Sitkovsky, M V AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 2330 EP - 2336 VL - 263 IS - 5 SN - 0021-9258, 0021-9258 KW - Receptors, Antigen, T-Cell KW - 0 KW - Colforsin KW - 1F7A44V6OU KW - Calcimycin KW - 37H9VM9WZL KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - 1,9-dideoxyforskolin KW - OAW710HWIX KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Index Medicus KW - Animals KW - Colforsin -- pharmacology KW - Exocytosis KW - Cyclic AMP -- metabolism KW - Colforsin -- analogs & derivatives KW - Cholera Toxin -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cytotoxicity, Immunologic -- drug effects KW - Calcimycin -- pharmacology KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - Lymphocyte Activation KW - Protein Kinases -- metabolism KW - Receptors, Antigen, T-Cell -- metabolism KW - T-Lymphocytes, Cytotoxic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78089981?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Locus+of+inhibitory+action+of+cAMP-dependent+protein+kinase+in+the+antigen+receptor-triggered+cytotoxic+T+lymphocyte+activation+pathway.&rft.au=Takayama%2C+H%3BTrenn%2C+G%3BSitkovsky%2C+M+V&rft.aulast=Takayama&rft.aufirst=H&rft.date=1988-02-15&rft.volume=263&rft.issue=5&rft.spage=2330&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 - 1988-03-23 N1 - Date created - 1988-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of steroid hormones and peptide growth factors on protooncogene c-fos expression in human breast cancer cells. AN - 78082666; 3257409 AB - To investigate if the estrogen control of the tumorigenic phenotype of breast cancer cells was mediated through activation of the c-fos protooncogene, we examined the expression of this oncogene in MCF-7 cells. In cells synchronized by double thymidine blockade, the peptide growth factors transforming growth factor alpha and epidermal growth factor increased c-fos mRNA levels 6-fold above controls after 30 min of treatment. The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, increased c-fos mRNA levels 4- to 5-fold above control. 17 beta-Estradiol, a growth stimulator, increased c-fos mRNA levels less than 2-fold above control levels, while progesterone, vitamin D3, dihydrotestosterone, and dexamethasone had little effect on c-fos mRNA levels. In contrast, 17 beta-estradiol treatment initially diminished the c-myc RNA level after 30 min of treatment and resulted in an elevation of c-myc by 2.5 h after initiation of treatment. We conclude that c-fos induction in these cells is growth related and accompanies stimulation by transforming growth factor alpha and epidermal growth factor. 17 beta-Estradiol, on the other hand, induced much smaller increases in c-fos mRNA levels, suggesting an alternative or more complex mechanism of cellular stimulation. JF - Cancer research AU - Wilding, G AU - Lippman, M E AU - Gelmann, E P AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20878. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 802 EP - 805 VL - 48 IS - 4 SN - 0008-5472, 0008-5472 KW - Growth Substances KW - 0 KW - Peptides KW - RNA, Messenger KW - Progesterone KW - 4G7DS2Q64Y KW - Estradiol KW - 4TI98Z838E KW - Epidermal Growth Factor KW - 62229-50-9 KW - Transforming Growth Factors KW - 76057-06-2 KW - Dexamethasone KW - 7S5I7G3JQL KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Kinetics KW - Humans KW - Cell Division -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Breast Neoplasms KW - Female KW - DNA Replication -- drug effects KW - Cell Line KW - Transcription, Genetic -- drug effects KW - Progesterone -- pharmacology KW - Growth Substances -- pharmacology KW - Dexamethasone -- pharmacology KW - RNA, Messenger -- drug effects KW - Estradiol -- pharmacology KW - Epidermal Growth Factor -- pharmacology KW - RNA, Messenger -- genetics KW - Peptides -- pharmacology KW - Proto-Oncogenes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78082666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+steroid+hormones+and+peptide+growth+factors+on+protooncogene+c-fos+expression+in+human+breast+cancer+cells.&rft.au=Wilding%2C+G%3BLippman%2C+M+E%3BGelmann%2C+E+P&rft.aulast=Wilding&rft.aufirst=G&rft.date=1988-02-15&rft.volume=48&rft.issue=4&rft.spage=802&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 - 1988-03-14 N1 - Date created - 1988-03-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - JB/MS murine melanoma: a new model for studies on the modulation of differentiation and of tumorigenic and metastatic potential. AN - 78081987; 2828247 AB - The recently obtained JB/MS melanoma (induced by DMBA in C57Bl/6 mice) has been successfully established in culture, and characterization of various parameters of these cells, as they have been serially passaged in vivo and in vitro, has begun. The culture lines were initially highly dendritic and melanotic, growing slowly in vitro and extremely slowly in vivo. During serial passage in vivo and in vitro the cell lines have gradually evolved into less melanotic, but more proliferative, tumorigenic and metastatic cells. We have been able to demonstrate that the JB/MS melanoma shares the common melanoma TSTA previously reported for B16, K1735 and JB/RH melanomas, but does not cross-react with the S91 melanoma or with other non-melanoma cell lines used as specificity controls. The JB/MS cells can be induced to differentiate in vitro by alpha-melanocyte stimulating hormone, a physiologically relevant agent, and studies have been initiated to detail the level at which this induction occurs. These sublines should prove to be excellent models for study of the progression of transformed cells from non-tumorigenic to tumorigenic phenotypes, and for progression through stages of varying metastatic potential, immunogenicity and differentiation. JF - International journal of cancer AU - Hearing, V J AU - Cannon, G B AU - Vieira, W D AU - Jiménez-Atiénzar, M AU - Kameyama, K AU - Law, L W AD - Laboratory of Cell Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/02/15/ PY - 1988 DA - 1988 Feb 15 SP - 275 EP - 282 VL - 41 IS - 2 SN - 0020-7136, 0020-7136 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - alpha-MSH KW - 581-05-5 KW - Monophenol Monooxygenase KW - EC 1.14.18.1 KW - Index Medicus KW - Pigmentation -- drug effects KW - Animals KW - Monophenol Monooxygenase -- analysis KW - Neoplasm Metastasis KW - Cell Differentiation KW - Mice KW - Flow Cytometry KW - alpha-MSH -- pharmacology KW - Cell Line KW - Cell Survival KW - Melanoma -- analysis KW - Melanoma -- pathology KW - Melanoma -- chemically induced KW - Melanoma -- physiopathology KW - Melanoma -- immunology KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78081987?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=JB%2FMS+murine+melanoma%3A+a+new+model+for+studies+on+the+modulation+of+differentiation+and+of+tumorigenic+and+metastatic+potential.&rft.au=Hearing%2C+V+J%3BCannon%2C+G+B%3BVieira%2C+W+D%3BJim%C3%A9nez-Ati%C3%A9nzar%2C+M%3BKameyama%2C+K%3BLaw%2C+L+W&rft.aulast=Hearing&rft.aufirst=V&rft.date=1988-02-15&rft.volume=41&rft.issue=2&rft.spage=275&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 - 1988-03-16 N1 - Date created - 1988-03-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biologically effective ultraviolet radiation: surface measurements in the United States, 1974 to 1985. AN - 78107183; 3340857 AB - Recent reports of stratospheric ozone depletion have prompted concerns about the levels of solar ultraviolet radiation that reach the earth's surface. Since 1974 a network of ground-level monitoring stations in the United States has tracked measurements of biologically effective ultraviolet radiation (UVB, 290 to 330 nanometers). The fact that no increases of UVB have been detected at ground levels from 1974 to 1985 suggests that meteorological, climatic, and environmental factors in the troposphere may play a greater role in attenuating UVB radiation than was previously suspected. JF - Science (New York, N.Y.) AU - Scotto, J AU - Cotton, G AU - Urbach, F AU - Berger, D AU - Fears, T AD - Biostatistics Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/02/12/ PY - 1988 DA - 1988 Feb 12 SP - 762 EP - 764 VL - 239 IS - 4841 Pt 1 SN - 0036-8075, 0036-8075 KW - Index Medicus KW - United States KW - Neoplasms, Radiation-Induced -- etiology KW - Skin Neoplasms -- etiology KW - Meteorological Concepts KW - Melanoma -- etiology KW - Humans KW - Ultraviolet Rays KW - Sunlight -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78107183?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Sleep+Medicine+Reviews&rft.atitle=The+effects+of+testosterone+on+sleep+and+sleep-disordered+breathing+in+men%3A+Its+bidirectional+interaction+with+erectile+function&rft.au=Andersen%2C+Monica+Levy%3BTufik%2C+Sergio&rft.aulast=Andersen&rft.aufirst=Monica&rft.date=2008-10-01&rft.volume=12&rft.issue=5&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Sleep+Medicine+Reviews&rft.issn=10870792&rft_id=info:doi/10.1016%2Fj.smrv.2007.12.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-03-22 N1 - Date created - 1988-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Coordinate N-ras mRNA up-regulation with mutational activation in tumorigenic guinea pig cells. AN - 78104504; 3278301 AB - Tumorigenic guinea pig cell lines with mutationally activated N-ras alleles also exhibited up-regulated N-ras mRNA. Mutational activation and mRNA up-regulation were limited to tumorigenic cells; preneoplastic progenitors were unaffected. Therefore, up-regulation occurred at a late stage of carcinogenesis closely associated with acquisition of tumorigenicity. cDNA and S1 protection analysis demonstrated that polyadenylation site of the short N-ras message and the mRNA start sites were different from that reported for human. The promoter region contained no canonical TATA or CCAAT boxes, but exhibited GGGCGG and CCGCCC SPl binding motifs characteristic of growth control genes. Moreover, both mutant and wild-type alleles were up-regulated in a guinea pig line heterozygous for N-ras codon 61. Coordinate N-ras mutational activation and up-regulation in five independent tumorigenic lines with unique chromosome constitutions suggests that both events are required for expression of the neoplastic phenotype. JF - Nucleic acids research AU - Doniger, J AU - DiPaolo, J A AD - Laboratory of Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/02/11/ PY - 1988 DA - 1988 Feb 11 SP - 969 EP - 980 VL - 16 IS - 3 SN - 0305-1048, 0305-1048 KW - DNA, Recombinant KW - 0 KW - Neoplasm Proteins KW - Proto-Oncogene Proteins KW - RNA, Messenger KW - RNA, Neoplasm KW - DNA KW - 9007-49-2 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - Promoter Regions, Genetic KW - Alleles KW - Guinea Pigs KW - DNA -- genetics KW - Gene Expression Regulation KW - Mutation KW - Cell Line KW - RNA, Neoplasm -- biosynthesis KW - Tumor Cells, Cultured -- metabolism KW - Neoplasm Proteins -- genetics KW - Proto-Oncogene Proteins -- genetics KW - RNA, Messenger -- biosynthesis KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78104504?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gedragstherapie&rft.atitle=Cognitieve+gedragstherapie+bij+seksuele+disfuncties+van+vrouwen+en+mannen%3A+Een+overzicht&rft.au=van+Lankveld%2C+Jacques%3BBoth%2C+Stephanie%3Bter+Kuile%2C+Moniek&rft.aulast=van+Lankveld&rft.aufirst=Jacques&rft.date=2012-06-01&rft.volume=45&rft.issue=2&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Gedragstherapie&rft.issn=01677454&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-03-29 N1 - Date created - 1988-03-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1972 Jun;69(6):1408-12 [4504350] Mol Cell Biol. 1987 Jul;7(7):2592-6 [3614201] Cancer Res. 1976 Apr;36(4):1404-13 [1260765] Nature. 1976 Sep 16;263(5574):211-4 [822353] Science. 1977 Jun 17;196(4296):1313-9 [325648] Biochemistry. 1977 Oct 18;16(21):4743-51 [911786] Cell. 1977 Nov;12(3):721-32 [922889] FEBS Lett. 1978 Mar 1;87(1):107-10 [631324] Nature. 1981 Mar 26;290(5804):304-10 [6259538] Annu Rev Biochem. 1981;50:349-83 [6791577] Proc Natl Acad Sci U S A. 1983 Jan;80(1):278-82 [6572002] Science. 1984 Jan 6;223(4631):63-6 [6318314] Gene. 1983 Nov;25(2-3):263-9 [6198242] Science. 1984 Mar 16;223(4641):1197-9 [6322298] Gene. 1983 Dec;26(1):101-6 [6323249] Proc Natl Acad Sci U S A. 1984 Apr;81(7):2147-51 [6326107] Cell. 1984 Aug;38(1):275-85 [6088070] Nucleic Acids Res. 1985 Jul 25;13(14):5255-68 [2991860] Proc Natl Acad Sci U S A. 1985 Aug;82(15):4920-4 [2991899] Science. 1985 Dec 20;230(4732):1378-81 [2999983] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2340-4 [3517865] Mol Cell Biol. 1985 Nov;5(11):2975-83 [3018490] EMBO J. 1986 Oct;5(10):2617-21 [3023052] J Biol Chem. 1987 Mar 15;262(8):3813-9 [3029126] Cancer Res. 1975 Apr;35(4):1035-44 [1116142] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulation of choleragen enzymatic activities by GTP and two soluble proteins purified from bovine brain. AN - 78087574; 3123477 AB - Choleragen (cholera toxin) activates adenylate cyclase by catalyzing ADP-ribosylation of Gs alpha, the stimulatory guanine nucleotide-binding protein. It was recently found (Tsai, S.-C., Noda, M., Adamik, R., Moss, J., and Vaughan, M. (1987) Proc. Natl. Acad. Sci. U. S. A. 84, 5139-5142) that a bovine brain membrane protein known as ADP-ribosylation factor or ARF, which enhances ADP-ribosylation of Gs alpha, also increases the GTP-dependent NAD:arginine and NAD:protein ADP-ribosyltransferase, NAD glycohydrolase, and auto-ADP-ribosylation activities of choleragen. We report here the purification and characterization of two soluble proteins from bovine brain that similarly enhance the Gs alpha-dependent and independent ADP-ribose transfer reactions catalyzed by toxin. Like membrane ARF, both soluble factors are 19-kDA proteins dependent on GTP or GTP analogues for activity. Maximal ARF effects were observed at a molar ratio of less than 2:1, ARF/toxin A subunit. Dimyristoyl phosphatidylcholine was necessary for optimal ADP-ribosylation of Gs alpha but inhibited auto-ADP-ribosylation of the choleragen A1 subunit and NAD:agmatine ADP-ribosyltransferase activity. It appears that the soluble factors directly activate choleragen in a GTP-dependent fashion. The relationships of the ARF proteins to the ras oncogene products and to the family of guanine nucleotide-binding regulatory proteins that includes Gs alpha remains to be determined. JF - The Journal of biological chemistry AU - Tsai, S C AU - Noda, M AU - Adamik, R AU - Chang, P P AU - Chen, H C AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1988/02/05/ PY - 1988 DA - 1988 Feb 05 SP - 1768 EP - 1772 VL - 263 IS - 4 SN - 0021-9258, 0021-9258 KW - Nerve Tissue Proteins KW - 0 KW - Thionucleotides KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Guanylyl Imidodiphosphate KW - 34273-04-6 KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - Pentosyltransferases KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Thionucleotides -- pharmacology KW - Animals KW - Cattle KW - Guanylyl Imidodiphosphate -- pharmacology KW - Chromatography, Gel KW - Enzyme Activation KW - Electrophoresis, Polyacrylamide Gel KW - GTP-Binding Proteins -- metabolism KW - Pentosyltransferases -- metabolism KW - Molecular Weight KW - Guanosine Triphosphate -- analogs & derivatives KW - Brain Chemistry KW - Adenylyl Cyclases -- metabolism KW - Adenosine Diphosphate Ribose -- metabolism KW - Nerve Tissue Proteins -- pharmacology KW - Guanosine Triphosphate -- pharmacology KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78087574?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Stimulation+of+choleragen+enzymatic+activities+by+GTP+and+two+soluble+proteins+purified+from+bovine+brain.&rft.au=Tsai%2C+S+C%3BNoda%2C+M%3BAdamik%2C+R%3BChang%2C+P+P%3BChen%2C+H+C%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Tsai&rft.aufirst=S&rft.date=1988-02-05&rft.volume=263&rft.issue=4&rft.spage=1768&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 - 1988-03-07 N1 - Date created - 1988-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of the common genetic defect in humans deficient in debrisoquine metabolism. AN - 78102858; 3123997 AB - In population studies of individuals given the antihypertensive drug debrisoquine, two distinct phenotypes have been described: extensive metabolizers excrete 10-200 times more of the urinary metabolite 4-hydroxydebrisoquine than poor metabolizers. In family studies the poor-metabolizer phenotype behaves as an autosomal recessive trait with an incidence between 5% and 10% in the white population of Europe and North America, and extends to the deficient metabolism of more than 20 commonly prescribed drugs. Clinical studies have shown that such individuals are at high risk for the development of adverse side effects from these and probably many other drugs. Here we show that poor metabolizers have negligible amounts of the cytochrome P450 enzyme P450db1. We have cloned the human P450db1 complementary DNA and expressed it in mammalian cell culture. Furthermore, by directly cloning and sequencing cDNAs from several poor-metabolizer livers, we have identified three variant messenger RNAs that are products of mutant genes producing incorrectly spliced db1 pre-mRNA, providing a molecular explanation for one of man's most commonly defective genes (frequency of mutant alleles 35-43%). JF - Nature AU - Gonzalez, F J AU - Skoda, R C AU - Kimura, S AU - Umeno, M AU - Zanger, U M AU - Nebert, D W AU - Gelboin, H V AU - Hardwick, J P AU - Meyer, U A AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1988/02/04/ PY - 1988 DA - 1988 Feb 04 SP - 442 EP - 446 VL - 331 IS - 6155 SN - 0028-0836, 0028-0836 KW - Immunoglobulin Heavy Chains KW - 0 KW - Immunoglobulin Variable Region KW - Mixed Function Oxygenases KW - EC 1.- KW - Cytochrome P-450 CYP2D6 KW - EC 1.14.14.1 KW - Index Medicus KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Mixed Function Oxygenases -- deficiency KW - Immunoglobulin Variable Region -- genetics KW - Immunoglobulin Heavy Chains -- genetics KW - Leukemia, Lymphoid -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78102858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=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=bookitem&rft.jtitle=&rft.atitle=Erectile+dysfunction%3A+Integration+of+medical+and+psychological+approaches&rft.au=Rosen%2C+Raymond+C.%3BMiner%2C+Martin+M.%3BWincze%2C+John+P.&rft.aulast=Rosen&rft.aufirst=Raymond&rft.date=2014-01-01&rft.volume=&rft.issue=&rft.spage=61&rft.isbn=978-1-4625-1367-3&rft.btitle=Principles+and+practice+of+sex+therapy+%285th+ed.%29&rft.title=Principles+and+practice+of+sex+therapy+%285th+ed.%29&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-03-11 N1 - Date created - 1988-03-11 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - Y00300; GENBANK; X08006; X07618; X07619; X07620 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of locus ceruleus and olfactory bulb stimulation on rat olfactory tubercle neuron activity. AN - 85200882; pmid-3128753 AB - The effects of electrical stimulation of the olfactory bulb and the locus ceruleus on olfactory tubercle neurons were examined in rat models. Ipsilateral stimulation of the olfactory bulb produced excitation in 31% of olfactory tubercle neurons tested and inhibition in 17%. Twenty-two percent of the olfactory tubercle neurons were excited, whereas 9% were inhibited by ipsilateral stimulation of the locus ceruleus. Contralateral stimulation of the locus ceruleus produced similar responses in the same neuron entities. A negative-positive evoked potential was recorded in the olfactory tubercle after ipsilateral and contralateral stimulation of the locus ceruleus. Thirty-three percent of the olfactory tubercle neurons that responded orthodromically or antidromically to stimulation of the olfactory bulb were excited by ipsilateral stimulation of the locus ceruleus. In contrast, only 10% responded with excitation to ipsilateral stimulation of the locus ceruleus among the olfactory tubercle neurons that were unresponsive to stimulation of the olfactory bulb. These findings suggest that olfactory tubercle neurons that receive input from or sending output to the olfactory bulb are influenced by the noradrenergic system of the locus ceruleus. A possible role of the olfactory tubercle in olfactory transduction will also be discussed. JF - Otolaryngology--Head and Neck Surgery AU - Inokuchi, A AU - Boran, T V AU - Kimmelman, C P AU - Snow, J B AD - Department of Otorhinolaryngology and Human Communication, University of Pennsylvania School of Medicine, Philadelphia 19104.; National Institute on Deafness and other Communication Disorders, Bethesda, Maryland 20892, USA. PY - 1988 SP - 116 EP - 120 VL - 98 IS - 2 SN - 0194-5998, 0194-5998 KW - Rats KW - Rats, Inbred Strains KW - Support, U.S. Gov't, P.H.S. KW - Evoked Potentials KW - Neurons KW - Animal KW - Locus Coeruleus KW - Olfactory Bulb KW - Electric Stimulation KW - Neural Inhibition UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85200882?accountid=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=Effects+of+locus+ceruleus+and+olfactory+bulb+stimulation+on+rat+olfactory+tubercle+neuron+activity.&rft.au=Inokuchi%2C+A%3BBoran%2C+T+V%3BKimmelman%2C+C+P%3BSnow%2C+J+B&rft.aulast=Inokuchi&rft.aufirst=A&rft.date=1988-02-01&rft.volume=98&rft.issue=2&rft.spage=116&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 - Is ethanol a discriminating substance? AN - 78211031; 2834827 JF - Seminars in liver disease AU - Tabakoff, B AU - Hoffman, P L AU - McLaughlin, A AD - Laboratory of Physiologic & Pharmacologic Studies, National Institutes of Health Clinical Center, Bethesda, MD 20892. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 26 EP - 35 VL - 8 IS - 1 SN - 0272-8087, 0272-8087 KW - Membrane Proteins KW - 0 KW - Ethanol KW - 3K9958V90M KW - Sodium-Potassium-Exchanging ATPase KW - EC 3.6.3.9 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Brain -- enzymology KW - Sodium-Potassium-Exchanging ATPase -- metabolism KW - Fluorescence Polarization KW - Cell Membrane -- enzymology KW - Alcoholic Intoxication -- physiopathology KW - Cell Membrane -- drug effects KW - Membrane Proteins -- metabolism KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Brain -- drug effects KW - Membrane Fluidity -- drug effects KW - Adenylyl Cyclases -- metabolism KW - Ethanol -- adverse effects KW - Ethanol -- pharmacology KW - Ethanol -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78211031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Is+ethanol+a+discriminating+substance%3F&rft.au=Tabakoff%2C+B%3BHoffman%2C+P+L%3BMcLaughlin%2C+A&rft.aulast=Tabakoff&rft.aufirst=B&rft.date=1988-02-01&rft.volume=8&rft.issue=1&rft.spage=26&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 - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiology of alcoholic liver disease. AN - 78195094; 3283941 AB - Although there exists a relationship between alcohol consumption and alcoholic liver disease at both the aggregate and individual levels, it is also well established that less than one-third of alcoholics or heavy drinkers develop serious alcohol-related liver damage. A number of factors have been proposed to account for this susceptibility. Evidence supporting the direct dose-response relationship and the role of genetic and environmental factors in influencing vulnerability are reviewed. To date, no consistent evidence attests to the significance of any one factor in the susceptibility to developing alcoholic liver disease. JF - Seminars in liver disease AU - Grant, B F AU - Dufour, M C AU - Harford, T C AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 12 EP - 25 VL - 8 IS - 1 SN - 0272-8087, 0272-8087 KW - HLA Antigens KW - 0 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Nutritional Status KW - Sex Factors KW - Humans KW - Antibody Formation KW - Ethanol -- metabolism KW - Alcohol Drinking KW - Ethanol -- adverse effects KW - Hepatitis B -- complications KW - Immunity, Cellular KW - Risk Factors KW - Liver Cirrhosis, Alcoholic -- mortality KW - Alcoholic Beverages -- adverse effects KW - HLA Antigens -- analysis KW - Liver Cirrhosis, Alcoholic -- epidemiology KW - Male KW - Female KW - Liver Diseases, Alcoholic -- mortality KW - Liver Diseases, Alcoholic -- immunology KW - Liver Diseases, Alcoholic -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78195094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epidemiology+of+alcoholic+liver+disease.&rft.au=Grant%2C+B+F%3BDufour%2C+M+C%3BHarford%2C+T+C&rft.aulast=Grant&rft.aufirst=B&rft.date=1988-02-01&rft.volume=8&rft.issue=1&rft.spage=12&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 - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - MDMA-induced neurotoxicity: parameters of degeneration and recovery of brain serotonin neurons. AN - 78192974; 2452449 AB - This study investigates a number of parameters that influence the neurotoxic effects of 3,4-methylenedioxymethamphetamine (MDMA) on serotonin (5-HT) neurons in brain. Both the dose and number of injections of MDMA affect the degree of neurotoxicity on 5-HT axons and terminals as assessed by decreases in the content of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) and the density of 5-HT uptake sites. Repeated systemic administration of various doses of MDMA (5-20 mg/kg twice daily for 4 consecutive days) results in dose-dependent decreases in 5-HT, 5-HIAA and 5-HT uptake sites. Increasing the number of injections of MDMA resulted in progressively greater reductions in 5-HT and 5-HIAA which occurred prior to decreases in 5-HT uptake sites. In contrast, no significant changes were observed in the density of norepinephrine uptake sites following single or repeated injections of 20 mg/kg MDMA. With respect to neuronal regeneration, following an initial 90% loss of 5-HT uptake sites after treatment with MDMA, the recovery of these sites occurred over a protracted period of time; a marked 25% reduction was seen at 6 months and the concentration of 5-HT uptake sites returned to control levels at 12 months following treatment with MDMA. Pretreatment with the selective 5-HT uptake blocker, citalopram, prior to each injection of MDMA prevented the neurotoxic effects of MDMA on the 5-HT parameters described above suggesting that active uptake of MDMA or a MDMA-related substance into brain 5-HT neurons was involved in the neurotoxic actions of the drug. In addition, the neurodegenerative effects of MDMA on 5-HT neurons exhibited some species specificity as comparable decreases in cerebral cortical 5-HT, 5-HIAA and 5-HT uptake sites were observed in rat and guinea pig while no significant changes in any of these serotonergic parameters were seen in mouse brain. JF - Pharmacology, biochemistry, and behavior AU - Battaglia, G AU - Yeh, S Y AU - De Souza, E B AD - Neuroscience Branch, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 269 EP - 274 VL - 29 IS - 2 SN - 0091-3057, 0091-3057 KW - Amphetamines KW - 0 KW - Serotonin KW - 333DO1RDJY KW - 3,4-Methylenedioxyamphetamine KW - 4764-17-4 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - N-Methyl-3,4-methylenedioxyamphetamine KW - KE1SEN21RM KW - Index Medicus KW - Animals KW - Nerve Degeneration -- drug effects KW - Dose-Response Relationship, Drug KW - Guinea Pigs KW - Hydroxyindoleacetic Acid -- metabolism KW - Neurons -- drug effects KW - Nerve Regeneration -- drug effects KW - Mice KW - Rats, Inbred Strains KW - Rats KW - Biological Transport, Active -- drug effects KW - Neurons -- physiology KW - Species Specificity KW - Male KW - 3,4-Methylenedioxyamphetamine -- administration & dosage KW - Brain -- drug effects KW - 3,4-Methylenedioxyamphetamine -- analogs & derivatives KW - Serotonin -- metabolism KW - Brain -- physiology KW - 3,4-Methylenedioxyamphetamine -- toxicity KW - Amphetamines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78192974?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=MDMA-induced+neurotoxicity%3A+parameters+of+degeneration+and+recovery+of+brain+serotonin+neurons.&rft.au=Battaglia%2C+G%3BYeh%2C+S+Y%3BDe+Souza%2C+E+B&rft.aulast=Battaglia&rft.aufirst=G&rft.date=1988-02-01&rft.volume=29&rft.issue=2&rft.spage=269&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 - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The iminodipropionitrile (IDPN)-induced dyskinetic syndrome in mice: antagonism by the calcium channel antagonist nifedipine. AN - 78189506; 2452450 AB - Chronic administration of IDPN leads to the development of a persistent syndrome which is characterized by lateral and vertical neck dyskinesias, random circling behaviors, and locomotor hyperactivity. Although the dihydropyridine (DHP) calcium channel antagonist nifedipine inhibited all aspects of the syndrome, lateral head dyskinesias (laterocollis) and circling abnormalities were the most significantly affected signs. Dysregulation of calcium-dependent processes might be involved in the pathogenesis of the IDPN-induced dyskinetic abnormalities and clinical disorders of movement in humans. JF - Pharmacology, biochemistry, and behavior AU - Cadet, J L AU - Taylor, E AU - Freed, W J AD - Preclinical Neurosciences Section, NIMH, St. Elizabeth's Hospital, Washington, DC 20032. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 381 EP - 385 VL - 29 IS - 2 SN - 0091-3057, 0091-3057 KW - Dihydropyridines KW - 0 KW - Ion Channels KW - Nitriles KW - 3,3'-iminodipropionitrile KW - 3XP1CVU865 KW - 1,4-dihydropyridine KW - 7M8K3P6I89 KW - Nifedipine KW - I9ZF7L6G2L KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Calcium -- metabolism KW - Animals KW - Brain -- drug effects KW - Ion Channels -- drug effects KW - Dihydropyridines -- metabolism KW - Mice KW - Brain -- metabolism KW - Female KW - Ion Channels -- metabolism KW - Binding Sites KW - Nifedipine -- pharmacology KW - Dyskinesia, Drug-Induced -- metabolism KW - Dyskinesia, Drug-Induced -- prevention & control KW - Nitriles -- antagonists & inhibitors KW - Dyskinesia, Drug-Induced -- etiology KW - Nitriles -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78189506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+iminodipropionitrile+%28IDPN%29-induced+dyskinetic+syndrome+in+mice%3A+antagonism+by+the+calcium+channel+antagonist+nifedipine.&rft.au=Cadet%2C+J+L%3BTaylor%2C+E%3BFreed%2C+W+J&rft.aulast=Cadet&rft.aufirst=J&rft.date=1988-02-01&rft.volume=29&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 - 1988-06-09 N1 - Date created - 1988-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA sequence analysis of spontaneous mutations in the SUP4-o gene of Saccharomyces cerevisiae. AN - 78146897; 3280976 AB - A collection of 196 spontaneous mutations in the SUP4-o gene of the yeast Saccharomyces cerevisiae was analyzed by DNA sequencing. The classes of mutation identified included all possible types of base-pair substitution, deletions of various lengths, complex alterations involving multiple changes, and insertions of transposable elements. Our findings demonstrate that at least several different mechanisms are responsible for spontaneous mutagenesis in S. cerevisiae. JF - Molecular and cellular biology AU - Giroux, C N AU - Mis, J R AU - Pierce, M K AU - Kohalmi, S E AU - Kunz, B A AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 978 EP - 981 VL - 8 IS - 2 SN - 0270-7306, 0270-7306 KW - DNA, Fungal KW - 0 KW - Index Medicus KW - Base Sequence KW - Base Composition KW - Molecular Sequence Data KW - Nucleic Acid Conformation KW - Saccharomyces cerevisiae -- genetics KW - Genes, Fungal KW - DNA, Fungal -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78146897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+sequence+analysis+of+spontaneous+mutations+in+the+SUP4-o+gene+of+Saccharomyces+cerevisiae.&rft.au=Giroux%2C+C+N%3BMis%2C+J+R%3BPierce%2C+M+K%3BKohalmi%2C+S+E%3BKunz%2C+B+A&rft.aulast=Giroux&rft.aufirst=C&rft.date=1988-02-01&rft.volume=8&rft.issue=2&rft.spage=978&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 - 1988-05-04 N1 - Date created - 1988-05-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cold Spring Harb Symp Quant Biol. 1966;31:157-71 [4866373] Mutat Res. 1987 Apr;182(2):65-74 [3550444] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Cell. 1978 Jun;14(2):221-36 [352537] Nature. 1980 Jul 24;286(5771):414-8 [6250065] Cell. 1980 Jul;20(3):701-9 [6998562] Cold Spring Harb Symp Quant Biol. 1981;45 Pt 2:575-80 [6266751] Adv Genet. 1982;21:173-254 [7036692] Mol Cell Biol. 1983 Jan;3(1):20-31 [6298605] Cold Spring Harb Symp Quant Biol. 1983;47 Pt 2:851-61 [6345080] Cell. 1983 Sep;34(2):655-64 [6352054] Mutat Res. 1985 Jul;154(1):1-27 [3889622] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8577-81 [3866242] Annu Rev Genet. 1985;19:29-55 [3909945] Gene. 1985;40(2-3):317-23 [3007296] EMBO J. 1986 Jun;5(6):1199-204 [3015589] Mol Cell Biol. 1987 Mar;7(3):1198-207 [3550432] Genetics. 1973 Nov;75(3):459-64 [4590686] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cholera toxin and pertussis toxin stimulate prostaglandin E2 synthesis in a murine macrophage cell line. AN - 78121364; 2831352 AB - When RAW264.7 murine macrophages were incubated with cholera toxin or pertussis toxin, prostaglandin E2 (PGE2) synthesis was enhanced markedly. Cholera toxin and pertussis toxin added together synergistically stimulated PGE2 synthesis. Cholera toxin and pertussis toxin also stimulated cyclic AMP (cAMP) accumulation. However, PGE2 synthesis was independent of increases in cAMP, as neither forskolin nor isoproterenol, which increased cAMP accumulation, nor dibutyryl-cAMP had any effect on PGE2 synthesis. In intact cells, cholera toxin and pertussis toxin stimulated phospholipase A2 to enhance metabolism of phosphatidylinositol to lysophosphatidylinositol and glycerophosphoinositol, with time courses similar to their stimulation of PGE2 synthesis. Cholera toxin catalyzed ADP-ribosylation of proteins of Mr 45,000 and 49,000 in intact cells, whereas an additional substrate of Mr 41,000 was observed in vitro. Preincubation of intact cells with pertussis toxin blocked subsequent in vitro labeling of the Mr 41,000 protein by cholera toxin, suggesting that the same protein was ADP-ribosylated by both toxins. Western blot analysis using specific antisera against Gi, Go and Gs revealed that the Mr 41,000 substrate was bound by the anti-Gi and anti-Go but not anti-Gs. The present data suggest that guanine nucleotide binding regulatory proteins are involved in the regulation of arachidonic acid metabolism to PGE2 in RAW264.7 cells. Furthermore, the possibility is raised that phospholipase A2 is regulated by both stimulatory and inhibitory guanine nucleotide binding proteins. JF - The Journal of pharmacology and experimental therapeutics AU - Burch, R M AU - Jelsema, C AU - Axelrod, J AD - Section on Pharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 765 EP - 773 VL - 244 IS - 2 SN - 0022-3565, 0022-3565 KW - Arachidonic Acids KW - 0 KW - Membrane Proteins KW - Prostaglandins E KW - Thionucleotides KW - Virulence Factors, Bordetella KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Arachidonic Acid KW - 27YG812J1I KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Phospholipases A KW - EC 3.1.1.32 KW - Phospholipases A2 KW - EC 3.1.1.4 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Dinoprostone KW - K7Q1JQR04M KW - Index Medicus KW - Phospholipases A -- analysis KW - Animals KW - Membrane Proteins -- metabolism KW - Mice KW - GTP-Binding Proteins -- analysis KW - Adenosine Diphosphate Ribose -- metabolism KW - Arachidonic Acids -- secretion KW - Molecular Weight KW - Guanosine Triphosphate -- pharmacology KW - Guanosine Triphosphate -- analogs & derivatives KW - Thionucleotides -- pharmacology KW - Cyclic AMP -- analysis KW - Cell Line KW - Virulence Factors, Bordetella -- pharmacology KW - Prostaglandins E -- biosynthesis KW - Cholera Toxin -- pharmacology KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78121364?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cholera+toxin+and+pertussis+toxin+stimulate+prostaglandin+E2+synthesis+in+a+murine+macrophage+cell+line.&rft.au=Burch%2C+R+M%3BJelsema%2C+C%3BAxelrod%2C+J&rft.aulast=Burch&rft.aufirst=R&rft.date=1988-02-01&rft.volume=244&rft.issue=2&rft.spage=765&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 - 1988-04-12 N1 - Date created - 1988-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenic activity of some coffee flavor ingredients. AN - 78115663; 3278213 AB - The mutagenicity of 4 coffee flavor ingredients (chlorogenic acid, caffeic acid, pyrazine, and trigonelline) was evaluated in the Salmonella plate incorporation assay and mouse lymphoma L5178Y TK +/- assay. Two of the compounds, pyrazine and trigonelline, were negative in both assays. The other two compounds, caffeic acid and chlorogenic acid, were positive in the mouse lymphoma assay but negative in the Salmonella assay. JF - Mutation research AU - Fung, V A AU - Cameron, T P AU - Hughes, T J AU - Kirby, P E AU - Dunkel, V C AD - National Cancer Institute, Bethesda, MD 20892. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 219 EP - 228 VL - 204 IS - 2 SN - 0027-5107, 0027-5107 KW - Alkaloids KW - 0 KW - Caffeic Acids KW - Cinnamates KW - Coffee KW - Pyrazines KW - Chlorogenic Acid KW - 318ADP12RI KW - trigonelline KW - 3NQ9N60I00 KW - caffeic acid KW - U2S3A33KVM KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Chemistry KW - Mutagenicity Tests -- methods KW - Biotransformation KW - Chemical Phenomena KW - Mesocricetus KW - Mice KW - Male KW - Leukemia L5178 -- pathology KW - Cricetinae KW - Coffee -- analysis KW - Chlorogenic Acid -- pharmacology KW - Tumor Cells, Cultured -- drug effects KW - Caffeic Acids -- pharmacology KW - Pyrazines -- pharmacology KW - Cinnamates -- pharmacology KW - Alkaloids -- pharmacology KW - Salmonella typhimurium -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78115663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutagenic+activity+of+some+coffee+flavor+ingredients.&rft.au=Fung%2C+V+A%3BCameron%2C+T+P%3BHughes%2C+T+J%3BKirby%2C+P+E%3BDunkel%2C+V+C&rft.aulast=Fung&rft.aufirst=V&rft.date=1988-02-01&rft.volume=204&rft.issue=2&rft.spage=219&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 - 1988-03-29 N1 - Date created - 1988-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rapid cycling affective disorder: contributing factors and treatment responses in 51 patients. AN - 78110406; 3341463 AB - For 51 patients with rapid cycling affective disorder, clinical and family history data indicated that the illness was phenotypically and genetically related to more typical forms of affective disorder, was characterized by a bipolar course (100%), and was more common in women (92%). Manic-depressive cycles were separate from menstrual cycles. At the time of onset of rapid cycling, 73% of the patients were taking antidepressant drugs; the continuation of rapid cycling was associated with antidepressant drug therapy in 51% of the patients. Although most patients had been referred to a research ward because they were considered to be refractory to treatment, 37% attained essentially complete remissions, usually during treatment with lithium and/or monoamine oxidase inhibitors. JF - The American journal of psychiatry AU - Wehr, T A AU - Sack, D A AU - Rosenthal, N E AU - Cowdry, R W AD - Clinical Psychobiology Branch, NIMH, Bethesda, MD 20892. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 179 EP - 184 VL - 145 IS - 2 SN - 0002-953X, 0002-953X KW - Antidepressive Agents KW - 0 KW - Monoamine Oxidase Inhibitors KW - Lithium KW - 9FN79X2M3F KW - Abridged Index Medicus KW - Index Medicus KW - Mood Disorders -- diagnosis KW - Thyroid Diseases -- complications KW - Sex Factors KW - Humans KW - Lithium -- therapeutic use KW - Antidepressive Agents -- adverse effects KW - Mood Disorders -- genetics KW - Thyroid Diseases -- genetics KW - Hospitalization KW - Adult KW - Mood Disorders -- chemically induced KW - Menstruation KW - Middle Aged KW - Female KW - Male KW - Monoamine Oxidase Inhibitors -- therapeutic use KW - Bipolar Disorder -- diagnosis KW - Bipolar Disorder -- drug therapy KW - Bipolar Disorder -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78110406?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Rapid+cycling+affective+disorder%3A+contributing+factors+and+treatment+responses+in+51+patients.&rft.au=Wehr%2C+T+A%3BSack%2C+D+A%3BRosenthal%2C+N+E%3BCowdry%2C+R+W&rft.aulast=Wehr&rft.aufirst=T&rft.date=1988-02-01&rft.volume=145&rft.issue=2&rft.spage=179&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 - 1988-03-14 N1 - Date created - 1988-03-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pumiliotoxin B binds to a site on the voltage-dependent sodium channel that is allosterically coupled to other binding sites. AN - 78107745; 2448797 AB - Pumiliotoxin B (PTX-B), an alkaloid that has cardiotonic and myotonic activity, increases sodium influx in guinea pig cerebral cortical synaptoneurosomes. In the presence of scorpion venom (Leiurus) or purified alpha-scorpion toxin, the PTX-B-induced sodium influx is enhanced severalfold. PTX-B alone has no effect on sodium flux in N18 neuroblastoma cells but, in the presence of alpha-scorpion toxin, stimulation of sodium influx by PTX-B reaches levels comparable to that attained with the sodium channel activator veratridine. In neuroblastoma LV9 cells, a variant mutant that lacks sodium channels, neither veratridine nor PTX-B induces sodium fluxes in either the presence or absence of alpha-scorpion toxin. In synaptoneurosomes and in N18 cells, the sodium influx induced by the combination of PTX-B and alpha-scorpion toxin is inhibited by tetrodotoxin and local anesthetics. PTX-B does not interact with two of the known toxin sites on the sodium channel, as evidenced by a lack of effect on binding of [3H]saxitoxin or [3H]batrachotoxinin A benzoate to brain synaptoneurosomes. Synergistic effects on sodium influx with alpha-scorpion toxin, beta-scorpion toxin, and brevetoxin indicate that PTX-B does not interact directly with three other toxin sites on the sodium channel. Thus, PTX-B appears to activate sodium influx by interacting with yet another site on the voltage-dependent sodium channel, a site that is coupled allosterically to sites for alpha-scorpion toxin, beta-scorpion toxin, and brevetoxin. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Gusovsky, F AU - Rossignol, D P AU - McNeal, E T AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 1272 EP - 1276 VL - 85 IS - 4 SN - 0027-8424, 0027-8424 KW - Alkaloids KW - 0 KW - Anesthetics, Local KW - Indolizines KW - Ion Channels KW - Piperidines KW - Toxins, Biological KW - pumiliotoxin B KW - 67016-65-3 KW - Sodium KW - 9NEZ333N27 KW - Index Medicus KW - Animals KW - Drug Interactions KW - Anesthetics, Local -- pharmacology KW - Cerebral Cortex -- metabolism KW - Guinea Pigs KW - Neuroblastoma KW - Binding Sites KW - Biological Transport -- drug effects KW - Stimulation, Chemical KW - Cells, Cultured KW - Toxins, Biological -- pharmacology KW - Allosteric Site KW - Synaptosomes -- metabolism KW - Sodium -- metabolism KW - Alkaloids -- metabolism KW - Ion Channels -- drug effects KW - Alkaloids -- pharmacology KW - Ion Channels -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78107745?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pumiliotoxin+B+binds+to+a+site+on+the+voltage-dependent+sodium+channel+that+is+allosterically+coupled+to+other+binding+sites.&rft.au=Gusovsky%2C+F%3BRossignol%2C+D+P%3BMcNeal%2C+E+T%3BDaly%2C+J+W&rft.aulast=Gusovsky&rft.aufirst=F&rft.date=1988-02-01&rft.volume=85&rft.issue=4&rft.spage=1272&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 - 1988-03-21 N1 - Date created - 1988-03-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1976 Sep 25;251(18):5528-36 [965375] Mol Pharmacol. 1987 Mar;31(3):273-8 [2436034] Anal Biochem. 1977 Dec;83(2):346-56 [603028] Toxicon. 1978;16(2):189-94 [635932] Biochim Biophys Acta. 1980 Aug 14;600(3):882-97 [6250606] Mol Pharmacol. 1981 Jan;19(1):78-86 [6259514] J Biol Chem. 1981 Sep 10;256(17):8922-7 [6114956] Mol Pharmacol. 1981 May;19(3):411-24 [6455594] Toxicon. 1982;20(1):9-16 [6281941] Mol Pharmacol. 1983 Mar;23(2):350-8 [6300644] Science. 1984 Feb 17;223(4637):653-61 [6320365] J Med Chem. 1985 Apr;28(4):482-6 [3981541] J Neurosci. 1985 Aug;5(8):2240-53 [2991484] Toxicon. 1985;23(3):497-504 [2411017] J Neurochem. 1986 Jun;46(6):1763-70 [2422324] Proc Natl Acad Sci U S A. 1986 May;83(9):3003-7 [2422664] J Biol Chem. 1977 Dec 10;252(23):8669-76 [925017] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The protein kinase C activator 1-oleoyl-2-acetylglycerol inhibits voltage-dependent Ca2+ current in the pituitary cell line AtT-20. AN - 78105952; 2449624 AB - The role of protein kinase C in regulating Ca2+ channel activity was investigated using the whole-cell patch-clamp technique in the mouse pituitary tumor cell line AtT-20. The Ca2+ current was activated by depolarizing voltage steps from a holding potential of -80 mV. Extracellular application of the protein kinase C activator 1-oleoyl-2-acetylglycerol (OAG) reduced voltage-dependent Ca2+ current. This effect was reversible and dose dependent (10-100 microM). Pertussis toxin did not block the effect of OAG on Ca2+ current, suggesting that OAG does not affect Ca2+ channels via a pertussis toxin sensitive guanosine triphosphate binding protein. Na+-free solutions did not block the effect of OAG on Ca2+ channels, suggesting that this effect of OAG does not involve the Na+/H+ antiporter. The phorbol esters 12-deoxyphorbol-13-isobutyrate (10 microM) and phorbol-12,13-diacetate (100 microM) also reduced Ca2+ current. The results suggest that protein kinase C may be an inhibitory regulator of voltage-dependent Ca2+ channels. JF - Neuroendocrinology AU - Lewis, D L AU - Weight, F F AD - Section on Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Md. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 169 EP - 175 VL - 47 IS - 2 SN - 0028-3835, 0028-3835 KW - Diglycerides KW - 0 KW - Glycerides KW - Ion Channels KW - Phorbol Esters KW - Virulence Factors, Bordetella KW - 12-deoxyphorbol 13-isobutyrate KW - 25090-74-8 KW - 1-oleoyl-2-acetylglycerol KW - 86390-77-4 KW - Sodium KW - 9NEZ333N27 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Virulence Factors, Bordetella -- pharmacology KW - Phorbol Esters -- pharmacology KW - Animals KW - Sodium -- physiology KW - Mice KW - Membrane Potentials -- drug effects KW - Electric Stimulation KW - Cell Line KW - Protein Kinase C -- metabolism KW - Diglycerides -- pharmacology KW - Pituitary Gland -- physiology KW - Ion Channels -- drug effects KW - Pituitary Gland -- cytology KW - Calcium -- physiology KW - Protein Kinase C -- physiology KW - Ion Channels -- physiology KW - Glycerides -- pharmacology KW - Pituitary Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78105952?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+protein+kinase+C+activator+1-oleoyl-2-acetylglycerol+inhibits+voltage-dependent+Ca2%2B+current+in+the+pituitary+cell+line+AtT-20.&rft.au=Lewis%2C+D+L%3BWeight%2C+F+F&rft.aulast=Lewis&rft.aufirst=D&rft.date=1988-02-01&rft.volume=47&rft.issue=2&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=Neuroendocrinology&rft.issn=00283835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1988-04-05 N1 - Date created - 1988-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Poorly expressed endogenous ecotropic provirus of DBA/2 mice encodes a mutant Pr65gag protein that is not myristylated. AN - 78026486; 2826810 AB - DBA/2 mice carry a single endogenous ecotropic murine leukemia provirus designated Emv-3. Although this provirus appears to be nondefective by genomic restriction enzyme mapping, weanling mice do not produce virus and only about one-third of adult mice ever express virus. 5-Iododeoxyuridine and 5-azacytidine, two potent inducers of ecotropic virus expression, are relatively ineffective at inducing Emv-3 expression. However, the chemical carcinogen 7,12-dimethylbenz(a)anthracene can induce ecotropic virus expression in approximately 95% of treated DBA/2 mice. Previous experiments involving DNA transfection and marker rescue analysis of molecularly cloned Emv-3 DNA suggested that Emv-3 carries a small defect(s) in the gag gene, not detectable by restriction enzyme mapping, that inhibits virus expression in vivo and in vitro. Using a combination of approaches, including DNA sequencing, peptide mapping, and metabolic labeling of cells with [3H]myristate, we have demonstrated that the defect in Emv-3 most likely results from a single nucleotide substitution within the gene for p15gag that inhibits myristylation of the Pr65gag N terminus. Myristylation of Pr65gag is thought to be required for this protein to associate with the plasma membrane and is essential for virus particle formation. These results provide a conceptual framework for understanding how Emv-3 expression is regulated during development and after chemical induction. JF - Journal of virology AU - Copeland, N G AU - Jenkins, N A AU - Nexø, B AU - Schultz, A M AU - Rein, A AU - Mikkelsen, T AU - Jørgensen, P AD - Bionetics Research, Inc., National Cancer Institute, Frederick, Maryland 21701. Y1 - 1988/02// PY - 1988 DA - February 1988 SP - 479 EP - 487 VL - 62 IS - 2 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - Gene Products, gag KW - Myristic Acids KW - Retroviridae Proteins KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - Index Medicus KW - Virus Replication KW - Animals KW - Base Sequence KW - Peptide Mapping KW - Transfection KW - Molecular Sequence Data KW - Mice KW - Gene Expression Regulation KW - Mutation KW - DNA, Viral -- genetics KW - Myristic Acids -- metabolism KW - Mice, Inbred DBA KW - Leukemia Virus, Murine -- genetics KW - Retroviridae Proteins -- metabolism KW - Retroviridae Proteins -- genetics KW - Proviruses -- genetics KW - Genes, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/78026486?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Poorly+expressed+endogenous+ecotropic+provirus+of+DBA%2F2+mice+encodes+a+mutant+Pr65gag+protein+that+is+not+myristylated.&rft.au=Copeland%2C+N+G%3BJenkins%2C+N+A%3BNex%C3%B8%2C+B%3BSchultz%2C+A+M%3BRein%2C+A%3BMikkelsen%2C+T%3BJ%C3%B8rgensen%2C+P&rft.aulast=Copeland&rft.aufirst=N&rft.date=1988-02-01&rft.volume=62&rft.issue=2&rft.spage=479&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 - 1988-02-20 N1 - Date created - 1988-02-20 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M19118; GENBANK N1 - SuppNotes - Cited By: Virology. 1987 Apr;157(2):543-7 [3029987] Nature. 1981 Oct 1;293(5831):370-4 [6268990] Mol Cell Biol. 1982 Jun;2(6):638-52 [14582159] J Virol. 1969 Feb;3(2):126-32 [4304442] J Exp Med. 1971 Jun 1;133(6):1219-33 [4325132] J Exp Med. 1971 Jun 1;133(6):1234-41 [4325133] Science. 1971 Oct 8;174(4005):155-6 [4330367] Science. 1971 Oct 8;174(4005):157-9 [5119627] J Exp Med. 1972 Nov 1;136(5):1286-301 [4343245] Proc Natl Acad Sci U S A. 1973 Jul;70(7):2055-8 [4352968] Eur J Biochem. 1975 Aug 15;56(2):335-41 [1175627] J Virol. 1979 Mar;29(3):1213-20 [221675] J Virol. 1979 Apr;30(1):255-66 [480454] Nucleic Acids Res. 1981 Jan 24;9(2):309-21 [6259625] J Mol Biol. 1980 Oct 25;143(2):161-78 [6260957] Proc Natl Acad Sci U S A. 1981 Aug;78(8):5207-11 [6272295] Anal Biochem. 1981 Aug;115(2):450-7 [7304971] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6290-4 [6171816] Cell. 1981 Oct;26(2 Pt 2):221-32 [6277495] J Exp Med. 1982 Apr 1;155(4):1233-8 [6278049] Proc Natl Acad Sci U S A. 1981 Dec;78(12):7609-13 [6950402] Proc Natl Acad Sci U S A. 1982 Feb;79(4):1230-4 [6951170] Nature. 1982 Aug 12;298(5875):623-8 [6285203] J Mol Appl Genet. 1982;1(4):327-41 [6286831] Proc Natl Acad Sci U S A. 1982 Jul;79(14):4298-302 [6956859] J Virol. 1982 Oct;44(1):144-57 [6183444] J Virol. 1983 Feb;45(2):505-13 [6834466] Proc Natl Acad Sci U S A. 1983 Jan;80(2):339-43 [6340098] Virology. 1983 Mar;125(2):454-67 [6836917] J Virol. 1983 May;46(2):355-61 [6302307] Virology. 1983 Apr 15;126(1):51-72 [6302996] Cancer Res. 1983 Sep;43(9):4132-5 [6409397] Cancer Res. 1983 Dec;43(12 Pt 1):5647-51 [6315214] J Virol. 1984 Feb;49(2):437-44 [6319743] J Virol. 1984 Feb;49(2):471-8 [6319746] Virology. 1984 Mar;133(2):431-7 [6608821] Virology. 1984 Apr 15;134(1):196-207 [6200992] J Virol. 1985 Jan;53(1):273-8 [2981347] Proc Natl Acad Sci U S A. 1985 Mar;82(5):1451-5 [2579397] J Virol. 1985 Dec;56(3):798-806 [2999434] J Virol. 1986 May;58(2):314-23 [3009848] Nature. 1986 Jul 3-9;322(6074):78-80 [3014349] Proc Natl Acad Sci U S A. 1986 Aug;83(16):6048-52 [3016738] Proc Natl Acad Sci U S A. 1986 Oct;83(19):7246-50 [3489936] Cell. 1986 Nov 7;47(3):391-9 [3768959] J Virol. 1986 Dec;60(3):980-6 [3023686] Mol Cell Biol. 1986 Nov;6(11):3999-4007 [3025623] Mol Cell Biol. 1986 Dec;6(12):4387-95 [3796606] Infect Immun. 1977 Feb;15(2):376-81 [191398] J Virol. 1977 Jun;22(3):804-15 [69041] Cancer Res. 1978 Mar;38(3):729-35 [203389] Cell. 1978 Jul;14(3):601-9 [80281] Ann N Y Acad Sci. 1980;354:410-25 [6261656] J Virol. 1981 May;38(2):581-92 [7241663] Nature. 1981 Jul 23;292(5821):311-7 [6166864] Proc Natl Acad Sci U S A. 1987 May;84(9):2708-12 [3106975] N1 - Last updated - 2017-01-17 ER -