FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Soher, BJ vanZijl, PCM Duyn, JH Barker, PB AF Soher, BJ vanZijl, PCM Duyn, JH Barker, PB TI Quantitative proton MR spectroscopic imaging of the human brain SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE proton MR spectroscopy; quantitation ID MAGNETIC-RESONANCE SPECTROSCOPY; ABSOLUTE QUANTITATION; NMR-SPECTROSCOPY; CELL COUNTS; INVIVO; METABOLITES; SPECTRA; WATER; QUANTIFICATION; SUPPRESSION AB Multislice proton MR spectroscopic images (SI) of the brain were quantitated, using the phantom replacement technique. In 16 normal volunteers, ranging in age from 5 to 74 years, average ''whole brain'' concentrations of choline (Cho), creatine (Cr), and N-acetylaspartate (NAA) were found to be 2.4 +/- 0.4, 7.9 +/- 1.3, and 11.8 +/- 1.0 (mM, mean +/- SD), respectively, These values are in good general agreement with those previously determined by single-voxel localization techniques, Cortical gray matter was found to have lower Cho and NAA levels, compared to those of white matter, corpus callosum, and basal ganglia. Cho was also found to increase significantly with age in several locations, Quantitative multislice proton SI is feasible in the clinical environment, and regional and age-dependent variations occur that must be accounted for when evaluating spectra from pathological conditions. C1 JOHNS HOPKINS UNIV,SCH MED,RUSSELL H MORGAN DEPT RADIOL & RADIOL SCI,BALTIMORE,MD. NIH,LAB DIAGNOST RADIOL RES,BALTIMORE,MD. RI van Zijl, Peter/B-8680-2008; Duyn, Jozef/F-2483-2010 FU NINDS NIH HHS [NS 32833, NS 31490] NR 40 TC 210 Z9 212 U1 1 U2 11 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD MAR PY 1996 VL 35 IS 3 BP 356 EP 363 DI 10.1002/mrm.1910350313 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TX775 UT WOS:A1996TX77500010 PM 8699947 ER PT J AU Hamel, E AF Hamel, E TI Antimitotic natural products and their interactions with tubulin SO MEDICINAL RESEARCH REVIEWS LA English DT Review ID BOVINE BRAIN TUBULIN; MACROCYCLIC LACTONE ANTIBIOTICS; MICROTUBULE-ASSOCIATED PROTEINS; ASYMMETRIC TOTAL SYNTHESIS; MARINE SPONGE; ANTINEOPLASTIC AGENTS; BETA-TUBULIN; PHOMOPSIN-A; COLCHICINE-BINDING; CELL-GROWTH RP Hamel, E (reprint author), NCI,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,DIV CANC TREATMENT,NATL INST HLTH,BLDG 37,BETHESDA,MD 20892, USA. NR 143 TC 285 Z9 288 U1 1 U2 15 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0198-6325 J9 MED RES REV JI Med. Res. Rev. PD MAR PY 1996 VL 16 IS 2 BP 207 EP 231 DI 10.1002/(SICI)1098-1128(199603)16:2<207::AID-MED4>3.0.CO;2-4 PG 25 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UK002 UT WOS:A1996UK00200004 PM 8656780 ER PT J AU Wickner, RB AF Wickner, RB TI Double-stranded RNA viruses of Saccharomyces cerevisiae SO MICROBIOLOGICAL REVIEWS LA English DT Review ID RIBOSOMAL FRAMESHIFTING SIGNAL; EUKARYOTIC MESSENGER-RNA; YEAST KILLER TOXIN; POL FUSION PROTEIN; L-A-VIRUS; N-ACETYLTRANSFERASE; CHROMOSOMAL GENES; COAT PROTEIN; ALPHA-FACTOR; VIRAL-RNA AB The L-A double-stranded RNA virus of Saccharomyces cerevisiae has a 4.6-kb single-segment genome encapsidated in an icosahedral T = 1 particle whose asymmetric element is a dimer of Gag the major coat protein. L-A encodes Gag and its RNA-dependent RNA polymerase (Pol), the latter formed as a Gag-Pol fusion protein produced by a -1 ribosomal frameshift. The efficiency of ribosomal frameshifting is important for viral propagation and is controlled by the host MOF genes. In vitro template-dependent, viral RNA-specific, RNA-binding replication and transcription systems have been wed to study the mechanisms of these reactions. The packaging site on viral plus strands and the part of the Pol domain of the Gag-Pol fusion protein that recognizes it have been defined. The viral transcripts lack both 5' cap structure and 3' poly(A). The host SKI2, SKI3, and SKI8 genes limit viral propagation by blocking the translation of non-poly(A) mRNA. The host SKI1/XRN1 gene encodes a 5' --> 3' exoribonuclease specific for uncapped mRNA and known to be involved ill mRNA turnover. Its action on the uncapped viral mRNA is limited by the cap removal activity of the viral Gag protein acting on cellular mRNAs. M double-stranded RNAs, satellites of L-A, encode secreted ''killer'' toxins as a preprotein. The processing of the preprotoxin is carried out by the Kex1p and Kex2p proteases. The discovery of these genes in this system led to the discovery of mammalian prohormone processing enzymes. Yeast genetics enables detailed dissection of host-virus interactions, most of which probably have homologs in mammalian systems. C1 NIDDKD, SECT GENET SIMPLE EUKARYOTES, BETHESDA, MD 20892 USA. NR 175 TC 187 Z9 196 U1 0 U2 8 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0146-0749 J9 MICROBIOL REV JI Microbiol. Rev. PD MAR PY 1996 VL 60 IS 1 BP 250 EP + PG 1 WC Microbiology SC Microbiology GA TZ695 UT WOS:A1996TZ69500011 PM 8852903 ER PT J AU Little, SF Novak, JM Lowe, JR Leppla, SH Singh, Y Klimpel, KR Lidgerding, BC Friedlander, AM AF Little, SF Novak, JM Lowe, JR Leppla, SH Singh, Y Klimpel, KR Lidgerding, BC Friedlander, AM TI Characterization of lethal factor binding and cell receptor binding domains of protective antigen of Bacillus anthracis using monoclonal antibodies SO MICROBIOLOGY-UK LA English DT Article DE Bacillus anthracis; protective antigen; epitope mapping ID ADENYLATE-CYCLASE; TOXIN ACTIVITY; EXPRESSION; COMPONENT; TOXICITY; GROWTH; ASSAY AB Lethal toxin from Bacillus anthracis is composed of protective antigen (PA) and lethal factor (LF). Anti-PA mAbs that neutralized lethal toxin activity, either in vivo or in vitro, identified three non-overlapping antigenic regions on PA. Two distinct antigenic regions were recognized by the four mAbs that neutralized lethal toxin activity by inhibiting the binding of I-125-LF to cell-bound PA. Mapping showed that one mAb, 1G3(PA63), recognized an epitope on a 17 kDa fragment located between amino acid residues Ser-168 and Phe-314. The three other mAbs, ZD3(PA), ZD5(PA) and 10D2(PA), recognized an epitope between amino acids IIe-581 and Asn-601. A single antigenic region was recognized by the three mAbs, 3B6(PA), 14B7(PA) and 10E10(PA63), that inhibited binding of I-125-PA to cells. This region was located between amino acids Asp-671 and IIe-721. These results confirm previously defined functional domains of PA and suggest that LF may interact with two different sites on PA to form lethal toxin. C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. RP Little, SF (reprint author), USA,MED RES INST INFECT DIS,FREDERICK,MD 21702, USA. NR 31 TC 92 Z9 95 U1 0 U2 3 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 1350-0872 J9 MICROBIOL-UK JI Microbiology-(UK) PD MAR PY 1996 VL 142 BP 707 EP 715 PN 3 PG 9 WC Microbiology SC Microbiology GA TZ852 UT WOS:A1996TZ85200028 PM 8868446 ER PT J AU Gorospe, M Liu, YS Xu, QB Chrest, FJ Holbrook, NJ AF Gorospe, M Liu, YS Xu, QB Chrest, FJ Holbrook, NJ TI Inhibition of G(1) cyclin-dependent kinase activity during growth arrest of human breast carcinoma cells by prostaglandin A(2) SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ANTINEOPLASTIC PROSTAGLANDINS; PROTEIN; SUPPRESSION; FIBROBLASTS; EXPRESSION; ACTIVATION; INDUCTION; CISPLATIN; PHASE; P21 AB Prostaglandin A(2) (PGA(2)) potently inhibits cell proliferation and Suppresses tumor growth in vivo, but little is known regarding the molecular mechanisms mediating these effects. Here we demonstrate that treatment of breast carcinoma MCF-7 cells with PGA(2) leads to G(1) arrest associated with a dramatic decrease in the levels of cyclin D1 and cyclin dependent kinase 4 (cdk4) and accompanied by an increase in the expression of p21. We further show that these effects occur independent of cellular p53 status. The decline in cyclin D and cdk4 protein levels is correlated with loss in cdk4 kinase activity. cdk2 activity is also significantly inhibited in PGA(2)-treated cells, an effect closely associated with the upregulation of p21. Immunoprecipitation experiments verified that p21 was indeed complexed with cdk2 in PGA(2)-treated cells. Additional experiments with synchronized MCF-7 cultures stimulated with serum revealed that treatment with PGA(2) prevents the progression of cells from G(1) to S. Accordingly, the kinase activity associated with cdk4, cyclin E, and cdk2 immunocomplexes, which normally increases following serum addition, was unchanged in PGA(2)-treated cells. Furthermore, the retinoblastoma protein (Rb), a substrate of cdk4 and cdk2 whose phosphorylation is necessary for cell cycle progression, remains underphosphorylated in PGA(2)-treated serum-stimulated cells. These findings indicate that PGA(2) exerts its growth-inhibitory effects through modulation of the expression and/or activity of several key G(1) regulatory proteins. Our results highlight the chemotherapeutic potential of PGA(2), particularly for suppressing growth of tumors lacking p53 function. C1 NIA,NIH,CTR GERONTOL RES,GENE EXPRESS & AGING SECT,BALTIMORE,MD 21224. NIA,NIH,CLIN IMMUNOL SECT,GENE EXPRESS & AGING SECT,BALTIMORE,MD 21224. RI Liu, Yusen/E-3527-2011 NR 56 TC 110 Z9 112 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1996 VL 16 IS 3 BP 762 EP 770 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TW172 UT WOS:A1996TW17200004 PM 8622677 ER PT J AU Sithanandam, G Latif, F Duh, FM Bernal, R Smola, U Li, H Kuzmin, I Wixler, V Geil, L Shrestha, S Lloyd, PA Bader, S Sekido, Y Tartof, KD Kashuba, VI Zabarovsky, ER Dean, M Klein, G Lerman, MI Minna, JD Rapp, UR Allikmets, R AF Sithanandam, G Latif, F Duh, FM Bernal, R Smola, U Li, H Kuzmin, I Wixler, V Geil, L Shrestha, S Lloyd, PA Bader, S Sekido, Y Tartof, KD Kashuba, VI Zabarovsky, ER Dean, M Klein, G Lerman, MI Minna, JD Rapp, UR Allikmets, R TI 3pK, a new mitogen-activated protein kinase-activated protein kinase located in the small cell lung cancer tumor suppressor gene region SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MAP KINASE; SIGNAL TRANSDUCTION; SUBSTRATE RECOGNITION; HOMOZYGOUS DELETION; SKELETAL-MUSCLE; PHOSPHORYLATION; IDENTIFICATION; TYROSINE; CARCINOMA; SEQUENCE AB NotI linking clones, localized to the human chromosome 3p21.3 region and homozygously deleted in small cell lung cancer cell lines NCI-H740 and NCI-H1450, were used to search for a putative tumor suppressor gene(s). One of these clones, NL1G210, detected a 2.5-kb mRNA in all examined human tissues, expression being especially high in the heart and skeletal muscle. Two overlapping cDNA clones containing the entire open reading frame were isolated from a human heart cDNA library and fully characterized. Computer analysis and a search of the GenBank database revealed high sequence identity of the product of this gene to serine-threonine kinases, especially to mitogen-activated protein kinase-activated protein kinase 2, a recently described substrate of mitogen-activated kinases. Sequence identity was 72% at the nucleotide level and 75% at the amino acid level, strongly suggesting that this protein is a serine-threonine kinase. Here we demonstrate that the new gene, referred to as 3pK (for chromosome 3p kinase), in fact encodes a mitogen activated protein kinase-regulated protein serine-threonine kinase with a novel substrate specificity. C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. UNIV TEXAS,HC SIMMONS COMPREHENS CANC CTR,DALLAS,TX 75235. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. KAROLINSKA INST,CTR MICROBIOL & TUMOR BIOL,STOCKHOLM,SWEDEN. RI Zabarovsky, Eugene/A-6645-2010; Bernal, Ricardo/B-2124-2010; Dean, Michael/G-8172-2012; Sekido, Yoshitaka/P-9756-2015 OI Dean, Michael/0000-0003-2234-0631; FU NCI NIH HHS [CA58220, 5 RO1 CA14054-15] NR 64 TC 85 Z9 87 U1 0 U2 7 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1996 VL 16 IS 3 BP 868 EP 876 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TW172 UT WOS:A1996TW17200015 PM 8622688 ER PT J AU Jeffers, M Rong, S VandeWoude, GF AF Jeffers, M Rong, S VandeWoude, GF TI Enhanced tumorigenicity and invasion-metastasis by hepatocyte growth factor scatter factor-met signalling in human cells concomitant with induction of the urokinase proteolysis network SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PLASMINOGEN-ACTIVATOR; EPITHELIAL-CELLS; TYROSINE KINASE; RECEPTOR; PROTOONCOGENE; EXPRESSION; IDENTIFICATION; INVASIVENESS; BINDS; GENE AB Hepatocyte growth factor/scatter factor (HGF/SF) is a pleiotropic effector of cells expressing the Met tyrosine kinase receptor. Although HGF/SF is synthesized by mesenchymal cells and acts predominantly on epithelial cells, we have recently demonstrated that human sarcoma cell lines often inappropriately express high levels of Met and respond mitogenically to HGF/SF. In the present report we show that HGF/SF-Met signalling in the human leiomyosarcoma cell line SK-LMS-1 enhances its in vivo tumorigenicity, an effect for which the mitogenicity of this signalling pathway is likely to play a role. In addition, we found that HGF/SF-Met signalling dramatically induces the in vitro invasiveness and in vivo metastatic potential of these cells. We have studied the molecular basis by which HGF/SF-Met signalling mediates the invasive phenotype. A strong correlation has previously been demonstrated between the activation of the urokinase plasminogen activator (uPA) proteolysis network and the acquisition of the invasive-metastatic phenotype, and we show here that HGF/SF-Met signalling significantly increases the protein levels of both uPA and its cellular receptor in SK-LMS-1 cells. This results in elevated levels of cell-associated uPA and enhanced plasmin generating ability by these cells. These studies couple HGF/SF-Met signalling to the activation of proteases that mediate dissolution of the extracellular matrix basement membrane, an important property for cellular invasion-metastasis. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 57 TC 276 Z9 278 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1996 VL 16 IS 3 BP 1115 EP 1125 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TW172 UT WOS:A1996TW17200042 PM 8622656 ER PT J AU Button, D Eidsath, A AF Button, D Eidsath, A TI Aequorin targeted to the endoplasmic reticulum reveals heterogeneity in luminal Ca++ concentration and reports agonist- or IP3-induced release of Ca++ SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article ID C-TERMINAL PROLINE; PHOTOPROTEIN AEQUORIN; RECOMBINANT AEQUORIN; BINDING-PROTEIN; LIVER NUCLEI; FREE CALCIUM; CA-2+; CA2+; STORES; CELLS AB A chimeric protein (ERaeq) comprised of the invariant chain (I-i) of class II major histocompatability complex (MHC-II) and aequorin was localized in the endoplasmic reticulum (ER) of transfected human embryonal kidney 293 cells. The targeted aequorin resided in the lumen of the ER membrane system, including the nuclear cistern, and following addition of the chromophore coelenterazine underwent Ca++-activated chemiluminescence. The majority of chemiluminescence produced by coelenterazine treatment of ERaeq-expressing 293 cells was consumed rapidly (within 2-4 min) upon re-addition of Ca++ to coelenterazine-loaded cells, a finding consistent with very high Ca++ concentrations (similar to 10(-5)-10(-3) M Ca++ ion) inside the ER. However, following the initial rapid consumption of ERaeq chemiluminescence, the activity that remained (10-30% of total sample luminescence of permeabilized cells or 50-70% of total sample luminescence of intact cells) was found to produce a stable baseline corresponding to a Ca++ ion concentration less than or equal to 1-2 mu M. The stable baseline of luminescence observed following rapid consumption of the majority of the sample's activity was not derived from re-binding of fresh chromophore to spent photoprotein, suggesting that a minority fraction of the ER membrane system within which the ERaeq chimera was distributed contained a relatively low Ca++ concentration. Addition of IP3 to digitonin-permeabilized cells, or agonist treatment of intact cells decreased this residual signal. Luminescence recordings from cells expressing an ER-targeted aequorin with relatively high affinity for Ca++ thus reveal heterogeneity in luminal ER Ca++ concentration and permit observation of receptor- and IP3-activated release of Ca++ from the ER membrane system. C1 NIH, NATL CTR RES RESOURCES, BIOMED ENGN & INSTRUMENTAT PROGRAM, BETHESDA, MD 20892 USA. RP Button, D (reprint author), NIMH, CELL BIOL LAB,BLDG 36,RM 3B-12,36 CONVENT DR, MSC 4090, BETHESDA, MD 20892 USA. NR 43 TC 34 Z9 35 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 EI 1939-4586 J9 MOL BIOL CELL JI Mol. Biol. Cell PD MAR PY 1996 VL 7 IS 3 BP 419 EP 434 PG 16 WC Cell Biology SC Cell Biology GA TZ761 UT WOS:A1996TZ76100007 PM 8868470 ER PT J AU Margolis, RL Li, SH Young, WS Wagster, MV Stine, OC Kidwai, AS Ashworth, RG Ross, CA AF Margolis, RL Li, SH Young, WS Wagster, MV Stine, OC Kidwai, AS Ashworth, RG Ross, CA TI DRPLA gene (Atrophin-1) sequence and mRNA expression in human brain SO MOLECULAR BRAIN RESEARCH LA English DT Article DE trinucleotide repeat; dentatorubral pallidoluysian atrophy; microsatellite; Huntington's disease ID ANDROGEN RECEPTOR GENE; HUNTINGTONS-DISEASE; REPEAT; REGION AB Dentatorubral pallidoluysian atrophy (DRPLA, Smith's disease) is one of five disorders currently known to result from expansion of a CAG trinucleotide repeat encoding glutamine. The reported full length cDNA sequence encodes a serine repeat and a region of alternating acidic and basic amino acids, as well as the glutamine repeat. We now report the nucleic acid and deduced amino acid sequences of the open reading frame of this gene, obtained from a series of independently isolated and sequenced cDNA clones. Eight nucleotide differences from the originally published sequence result in a change of 34 amino acids, most prominently in the region of alternating acidic and basic residues. Northern analysis and in situ hybridization indicate that atrophin-1 mRNA is expressed in multiple brain regions. The level of mRNA expression as determined by in situ hybridization in a DRPLA-diseased brain is indistinguishable from the level observed in a matched control brain. These results indicate that the correlation between atrophin-1 expression and regions of pathology in DRPLA is at best partial, and that the expanded allele does not cause a major loss of mRNA expression. The pathology of the disorder may therefore arise from the altered structure and function of the abnormal protein. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED GENET,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,NEUROPATHOL LAB,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,PROGRAM CELLULAR & MOL MED,BALTIMORE,MD 21205. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP Margolis, RL (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,MOLEC NEUROBIOL LAB,618 ROSS BLDG,720 RUTLAND AVE,BALTIMORE,MD 21205, USA. RI Young, W Scott/A-9333-2009; Ross, Christopher/H-8395-2013 OI Young, W Scott/0000-0001-6614-5112; NR 39 TC 23 Z9 24 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD MAR PY 1996 VL 36 IS 2 BP 219 EP 226 DI 10.1016/0169-328X(95)00241-J PG 8 WC Neurosciences SC Neurosciences & Neurology GA UD315 UT WOS:A1996UD31500003 ER PT J AU Chen, TK Smith, LM Gebhardt, DK Birrer, MJ Brown, PH AF Chen, TK Smith, LM Gebhardt, DK Birrer, MJ Brown, PH TI Activation and inhibition of the AP-1 complex in human breast cancer cells SO MOLECULAR CARCINOGENESIS LA English DT Article DE breast cancer; transcription factor; jun; fos; AP-1 ID SIGNAL TRANSDUCTION PATHWAYS; GENE FAMILY MEMBERS; C-JUN; GROWTH-FACTORS; NEGATIVE REGULATOR; FOS; EXPRESSION; PROTEINS; PHOSPHORYLATION; TRANSFORMATION AB We have studied the expression and activity of the jun and fos families of transcription factors in a panel of human breast cancer cells. Numerous breast-cancer cell lines showed variable levels of expression of jun and fos family-member RNA, activator protein-1 (AP-1) DNA binding, and transcriptional-activating activities during exponential growth. In all of the breast-cancer lines tested, c-jun RNA and AP-1 DNA-binding activity correlated. In addition, in most breast cancer cell lines AP-1 DNA-binding activity also correlates with AP-1-transactivating activity. However, some breast cancer cell lines have high c-jun RNA expression, high AP-1 DNA-binding activity, and low AP-1-transactivating activity. Such results suggest that in these breast cancer cell lines there exist AP-1 complexes that can bind DNA but cannot activate transcription. Multiple peptide growth factors as well as the tumor promoter 12-O-tetradecanoylphorbol-13-acetate induced the expression of jun and fos family-member RNAs and also increased AP-1 DNA-binding activity and functional AP-1-transcriptional activating activity in MCF7 breast cancer cells. However, treatment with estrogen, a steroid growth factor, failed to increase jun and fos RNA expression and induced minimal increases in AP-1 DNA binding and AP-1-induced transcriptional-activating activity in comparison with that seen after peptide hormone treatment. Thus, mitogenic peptide hormones and the tumor promoter 12-O-tetradecanoylphorbol-13-acetate, but not estrogen, strongly activate the AP-1 transcription factor in breast cancer cells. A dominant-negative mutant of c-jun that specifically inhibits AP-1-transactivating activity in rat fibroblasts inhibited AP-1-transactivating activity in breast-cancer cells and blocked the increase in AP-1-mediated transcription induced by serum or specific growth factors. This dominant-negative mutant also inhibited MCF7 colony formation, indicating that expression of this AP-1 inhibitor suppressed the proliferation of these breast cancer cells. Such results suggest that growth factor-induced proliferation of breast cancer cells can possibly be blocked by inhibiting AP-1-transactivating activity, (C) 1996 Wiley-Liss, Inc. C1 NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD. NR 36 TC 68 Z9 69 U1 1 U2 6 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD MAR PY 1996 VL 15 IS 3 BP 215 EP 226 DI 10.1002/(SICI)1098-2744(199603)15:3<215::AID-MC7>3.0.CO;2-G PG 12 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA UA443 UT WOS:A1996UA44300007 PM 8597534 ER PT J AU Gentry, DR Cashel, M AF Gentry, DR Cashel, M TI Mutational analysis of the Escherichia coli spoT gene identifies distinct but overlapping regions involved in ppGpp synthesis and degradation SO MOLECULAR MICROBIOLOGY LA English DT Article ID GUANOSINE TETRAPHOSPHATE; SALMONELLA-TYPHIMURIUM; RELA GENE; STRINGENT RESPONSE; OPERON EXPRESSION; PROTEIN-SYNTHESIS; RNA-POLYMERASE; GROWTH-RATE; RIBOSOME; PRODUCT AB The spoT gene of Escherichia coli encodes a guanosine 3',5'-bis(diphosphate) 3'-pyrophosphohydrolase (ppGppase) as well as an apparent guanosine 3',5'-bis(diphosphate) synthetase (designated PSII). To determine the regions of the SpoT protein that are required for these two competing activities, we analysed plasmid-borne deletion mutations for their ability to complement chromosomal mutations defective in each activity. We found that a region containing the first 203 amino acids of the 702-amino-acid SpoT protein was sufficient for ppGppase activity while an overlapping region containing residues 67-374 was sufficient for PSII activity. These data indicate that the catalytic sites involved in the two activities are separate but closely linked in the primary sequence of the SpoT protein. A ppGppase-defective Delta 1-58 deletion mutant strain failed to synthesize ppGpp in response to nutrient limitation, also supporting the notion that PSII activity from wild-type SpoT does not increase in response to nutrient limitation. Using a strain lacking PSII activity but retaining ppGppase activity, we determined the contribution of the RelA protein (ppGpp synthetase I, PSI) to ppGpp synthesis following glucose starvation. We found that the RelA protein activity accounts for the initial burst of ppGpp synthesis at the onset of glucose starvation but that this source of synthesis is absent when amino acids are present during glucose starvation. C1 NICHHD,NIH,MOLEC GENET LAB,BETHESDA,MD 20892. NR 52 TC 112 Z9 114 U1 0 U2 5 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0950-382X J9 MOL MICROBIOL JI Mol. Microbiol. PD MAR PY 1996 VL 19 IS 6 BP 1373 EP 1384 DI 10.1111/j.1365-2958.1996.tb02480.x PG 12 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA UE086 UT WOS:A1996UE08600021 PM 8730877 ER PT J AU Licinio, J AF Licinio, J TI Molecular psychiatry: The integration of molecular medicine and clinical psychiatry SO MOLECULAR PSYCHIATRY LA English DT Editorial Material RP Licinio, J (reprint author), NIMH,INTRAMURAL RES PROGRAM,CLIN NEUROENDOCRINOL BRANCH,NIH,UNIT CLIN RES,BLDG 10,RM 3S231,BETHESDA,MD 20892, USA. RI Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 0 TC 8 Z9 8 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD MAR PY 1996 VL 1 IS 1 BP 1 EP 3 PG 3 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA VG814 UT WOS:A1996VG81400001 PM 9118305 ER PT J AU Badner, JA AF Badner, JA TI DNA pooling and affected sib pair analysis SO MOLECULAR PSYCHIATRY LA English DT Article ID PEDIGREE-MEMBER METHOD; LINKAGE ANALYSIS; IDENTITY RP Badner, JA (reprint author), NIMH,NIH,CLIN NEUROGENET BRANCH,10-3N218,BETHESDA,MD 20892, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD MAR PY 1996 VL 1 IS 1 BP 15 EP 15 PG 1 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA VG814 UT WOS:A1996VG81400007 PM 9118308 ER PT J AU Hu, RJ AF Hu, RJ TI The Society for Neuroscience 1995 annual meeting SO MOLECULAR PSYCHIATRY LA English DT Editorial Material ID CORTICOTROPIN-RELEASING FACTOR; PROTEIN; DISEASE RP Hu, RJ (reprint author), NIDDKD,NEUROSCI LAB,BLDG 8,RM 105,BETHESDA,MD 20892, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD MAR PY 1996 VL 1 IS 1 BP 18 EP 20 PG 3 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA VG814 UT WOS:A1996VG81400009 PM 9118310 ER PT J AU Iwasaki, K Sunderland, T Kusiak, JW Wolozin, B AF Iwasaki, K Sunderland, T Kusiak, JW Wolozin, B TI Changes in gene transcription during a beta-mediated cell death SO MOLECULAR PSYCHIATRY LA English DT Article DE amyloid; Alzheimer's disease; neurons; apoptosis; bcl-2; jun; fos; toxicity ID AMYLOID PRECURSOR PROTEIN; FAMILIAL ALZHEIMERS-DISEASE; DNA FRAGMENTATION; IN-SITU; APOPTOSIS; BCL-2; NEURONS; EXPRESSION; MUTATION; IDENTIFICATION AB The a beta peptide induces cell death in neurons grown in cell culture, Previous studies have shown that the mechanism of a beta-mediated cell death of central nervous system neurons appears to be via apoptosis, Apoptosis is an active process that involves both gene transcription and translation, Using semi-quantitative polymerase chain reaction, we have analyzed the levels of a variety of transcripts in primary neuronal cultures treated with a beta that are likely to play important roles in apoptosis, Following addition of 10 mu M a beta(1-42) the immediate early response gene, c-fos, shows a rapid and sustained increase in transcript level while c-jun levels increase at a slower rate, Bcl-2 and its homologues, bcl-X and bar, also increase in amount with bcl-2 and bcl-X increasing more rapidly than bar. These data provide support indicating that a beta-mediated cell death in central nervous system neurons is an active process similar to that seen in apoptosis. C1 NIMH,GERIATR PSYCHIAT SERV,BETHESDA,MD 20892. NIA,MOL NEUROBIOL UNIT,BETHESDA,MD 20892. NR 29 TC 19 Z9 19 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD MAR PY 1996 VL 1 IS 1 BP 65 EP 71 PG 7 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA VG814 UT WOS:A1996VG81400015 PM 9118317 ER PT J AU Gasser, T Bove, CM Ozelius, LJ Hallett, M Charness, ME Hochberg, FH Breakefield, XO AF Gasser, T Bove, CM Ozelius, LJ Hallett, M Charness, ME Hochberg, FH Breakefield, XO TI Haplotype analysis at the DYT1 locus in Ashkenazi Jewish patients with occupational hand dystonia SO MOVEMENT DISORDERS LA English DT Article DE hand dystonia; DYT1 locus; musician's cramp; writer's cramp; genetics of dystonia ID AUTOSOMAL DOMINANT INHERITANCE; TORSION DYSTONIA; DNA POLYMORPHISMS; JEWS; GENE; FAMILY; MAP AB Genetic haplotypes at five marker loci that are closely linked to the DYT1 gene on chromosome 99 were determined in 10 Ashkenazi Jewish patients with focal hand dystonia (eight with musician's cramp, two with writer's cramp). The founder haplotype associated with >90% of cases of generalized dystonia in the Ashkenazi Jewish population could not be constructed from any of the twenty chromosomes. Potential haplotypes were determined, and no common haplotype was discerned in these patients. These findings argue against a role for the founder mutation in the DYTI gene in the etiology of occupational hand dystonia in this ethnic group. Further, if the DYTI gene is involved in these later onset dystonias, there is no evidence for a common mutation in the Ashkenazic Jewish population. It appears that excessive, repetitive use, possibly in combination with ulnar neuropathy, may serve as the inciting cause of some focal dystonias. C1 MASSACHUSETTS GEN HOSP EAST,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA. UNIV MUNICH,KLINIKUM GROSSHADERN,DEPT NEUROL,D-81377 MUNICH,GERMANY. NIH,BETHESDA,MD 20892. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. FU NINDS NIH HHS [NS28384] NR 24 TC 19 Z9 19 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PD MAR PY 1996 VL 11 IS 2 BP 163 EP 166 DI 10.1002/mds.870110208 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA TY140 UT WOS:A1996TY14000007 PM 8684386 ER PT J AU Steeg, PS AF Steeg, PS TI Granin expectations in breast cancer? SO NATURE GENETICS LA English DT Editorial Material ID AGGREGATION; CELLS RP Steeg, PS (reprint author), NCI,WOMENS CANC SECT,PATHOL LAB,BETHESDA,MD 20892, USA. NR 12 TC 13 Z9 13 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD MAR PY 1996 VL 12 IS 3 BP 223 EP 225 DI 10.1038/ng0396-223 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA TY183 UT WOS:A1996TY18300003 PM 8589705 ER PT J AU Bedell, MA Jenkins, NA Copeland, NG AF Bedell, MA Jenkins, NA Copeland, NG TI Good genes in bad neighbourhoods SO NATURE GENETICS LA English DT Editorial Material ID POSITION-EFFECT VARIEGATION; BETA-GLOBIN GENE; MURINE LEUKEMIA-VIRUS; T-CELL LYMPHOMAS; HEREDITARY PERSISTENCE; FETAL HEMOGLOBIN; C-MYC; REGION; EXPRESSION; ACTIVATION RP Bedell, MA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702, USA. NR 49 TC 76 Z9 79 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD MAR PY 1996 VL 12 IS 3 BP 229 EP 232 DI 10.1038/ng0396-229 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA TY183 UT WOS:A1996TY18300007 PM 8589709 ER PT J AU Koonin, EV AF Koonin, EV TI Human choroideremia protein contains a FAD-binding domain SO NATURE GENETICS LA English DT Letter ID RAB GERANYLGERANYL TRANSFERASE; BOVINE BRAIN CYTOSOL; SUBSEQUENT BINDING; COMPONENT-A; GENE; GTP; PURIFICATION; DISSOCIATION; CLONING; GDP RP Koonin, EV (reprint author), NATL INST HLTH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BETHESDA,MD 20894, USA. NR 19 TC 4 Z9 4 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD MAR PY 1996 VL 12 IS 3 BP 237 EP 239 DI 10.1038/ng0396-237 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA TY183 UT WOS:A1996TY18300010 PM 8589712 ER PT J AU Overturf, K AlDhalimy, M Tanguay, R Brantly, M Ou, CN Finegold, M Grompe, M AF Overturf, K AlDhalimy, M Tanguay, R Brantly, M Ou, CN Finegold, M Grompe, M TI Hepatocytes corrected by gene therapy are selected in vivo in a murine model of hereditary tyrosinaemia type I SO NATURE GENETICS LA English DT Article ID TYROSINEMIA TYPE-I; LETHAL ALBINO MICE; FUMARYLACETOACETATE HYDROLASE; LIVER; EXPRESSION; DEFICIENT; ENZYME; TRANSPLANTATION; MOUSE; CELLS AB Current strategies for hepatic gene therapy are either quantitatively inefficient or suffer from lack of permanent gene expression. We have utilized an animal model of hereditary tyrosinaemia type I (HT1), a recessive liver disease caused by deficiency of fumarylacetoacetate hydrolase (FAH), to determine whether in vivo selection of corrected hepatocytes could improve the efficiency of liver gene transfer. As few as 1,000 transplanted wild-type hepatocytes were able to repopulate mutant liver, demonstrating their strong competitive growth advantage. Mutant hepatocytes corrected in situ by retroviral gene transfer were also positively selected. In mutant animals treated by multiple retrovirus injections >90% of hepatocytes became FAH positive and liver function was restored to normal. Our results demonstrate that in vivo selection is a useful strategy for hepatic gene therapy and may lead to effective treatment of human HT1 by retroviral gene transfer. C1 OREGON HLTH SCI UNIV,DEPT MOLEC & MED GENET,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT PEDIAT,PORTLAND,OR 97201. UNIV LAVAL,LAB GENET CELLULAIRE & DEV,ST FOY,PQ G1K 7P4,CANADA. NHLBI,NIH,PULM CRIT CARE MED BRANCH,BETHESDA,MD 20892. TEXAS CHILDRENS HOSP,DEPT PATHOL,HOUSTON,TX 77030. FU NIDDK NIH HHS [DK-48252] NR 51 TC 387 Z9 395 U1 5 U2 9 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD MAR PY 1996 VL 12 IS 3 BP 266 EP 273 DI 10.1038/ng0396-266 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA TY183 UT WOS:A1996TY18300015 PM 8589717 ER PT J AU Thomas, JT Lin, KM Nandedkar, M Camargo, M Cervenka, A Luyten, FP AF Thomas, JT Lin, KM Nandedkar, M Camargo, M Cervenka, A Luyten, FP TI A human chondrodysplasia due to a mutation in a TGF-beta superfamily member SO NATURE GENETICS LA English DT Letter ID BONE-INDUCTIVE PROTEIN; FAMILY; PURIFICATION; OSTEOGENIN; MOUSE; GENE C1 UNIV ANTIOQUIA,DEPT BIOL,MEDELLIN,COLOMBIA. UNIV MINNESOTA,SCH DENT,DEPT ORAL SCI,MINNEAPOLIS,MN 55455. RP Thomas, JT (reprint author), NIDR,NIH,BONE RES BRANCH,BETHESDA,MD 20892, USA. NR 26 TC 298 Z9 314 U1 0 U2 4 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD MAR PY 1996 VL 12 IS 3 BP 315 EP 317 DI 10.1038/ng0396-315 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA TY183 UT WOS:A1996TY18300023 PM 8589725 ER PT J AU Steeg, PS AF Steeg, PS TI Cyclin E - A better prognostic marker for breast cancer than cyclin D? Reply SO NATURE MEDICINE LA English DT Letter RP Steeg, PS (reprint author), NCI,DIV CLIN SCI,PATHOL LAB,WOMENS CANC SECT,BETHESDA,MD 20892, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD MAR PY 1996 VL 2 IS 3 BP 254 EP 254 DI 10.1038/nm0396-254b PG 1 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TY640 UT WOS:A1996TY64000003 ER PT J AU Rade, JJ Schulick, AH Virmani, R Dichek, DA AF Rade, JJ Schulick, AH Virmani, R Dichek, DA TI Local adenoviral-mediated expression of recombinant hirudin reduces neointima formation after arterial injury SO NATURE MEDICINE LA English DT Article ID MUSCLE CELL-PROLIFERATION; THROMBIN; RECEPTOR; HEPARIN; ANGIOPLASTY; RESTENOSIS; INHIBITOR AB Catalytically active thrombin, acting locally, is thought to mediate neointima formation after arterial injury. We constructed an adenovirus vector, AdHV-1.2, containing a complementary DNA for the thrombin inhibitor hirudin. AdHV-1.2 directed the synthesis and secretion of biologically active hirudin from vascular cells in vitro. In vivo gene transfer of hirudin into smooth muscle cells of injured rat carotid arteries resulted in peak secretion of at least 34 +/- 23 pg hirudin per vessel per 24 hours, and resulted in a significant (P < 0.05) 35% reduction in neointima formation. Systemic partial thromboplastin times were not affected by local hirudin expression. These results support the hypothesis that local thrombin activity contributes to neointima formation after arterial injury and suggest that local delivery of a highly specific antithrombin may constitute an effective intervention for arterial proliferative disease. C1 UNIV CALIF SAN FRANCISCO,GLADSTONE INST CARDIOVASC DIS,SAN FRANCISCO,CA 94141. NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,DIV CARDIOVASC,WASHINGTON,DC 20307. JOHNS HOPKINS SCH MED,DIV CARDIOL,BALTIMORE,MD 21205. NR 38 TC 133 Z9 135 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD MAR PY 1996 VL 2 IS 3 BP 293 EP 298 DI 10.1038/nm0396-293 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TY640 UT WOS:A1996TY64000037 PM 8612227 ER PT J AU Pai, LH Wittes, R Setser, A Willingham, MC Pastan, I AF Pai, LH Wittes, R Setser, A Willingham, MC Pastan, I TI Treatment of advanced solid tumors with immunotoxin LMB-1: An antibody linked to Pseudomonas exotoxin SO NATURE MEDICINE LA English DT Article ID MONOCLONAL-ANTIBODIES; ESCHERICHIA-COLI; PHASE-I; THERAPY; CANCER AB Immunotoxin LMB-1 is composed of monoclonal antibody B3 chemically linked to PE38, a genetically engineered form of Pseudomonas exotoxin. B3 recognizes a carbohydrate antigen (Le(Y)) present on many human solid tumors(1). LMB-1 has excellent antitumor activity in nude mice bearing Le(Y)-positive tumors(2). We conducted a phase I study of 38 patients with solid tumors who failed conventional therapy and whose tumors expressed the Le(Y) antigen. Objective antitumor activity was observed in 5 patients, 18 had stable disease, 15 progressed. A complete remission was observed in a patient with metastatic breast cancer to supraclavicular nodes. A greater than 75% tumor reduction and resolution of all clinical symptoms lasting for more than six months was observed in a colon cancer patient with extensive retroperitoneal and cervical metastasis. Three patients (two colon, one breast cancer) had minor responses. The maximum tolerated dose of LMB-1 is 75 mu g/kg given intravenously three times every other day. The major toxicity is vascular leak syndrome manifested by hypoalbuminemia, fluid retention, hypotension and, in one case, pulmonary edema. Although immunotoxins have been evaluated in clinical studies for more than two decades, this is the first report of antitumor activity in epithelial tumors. C1 NCI,NIH,MED BRANCH,BETHESDA,MD 20892. MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. RP Pai, LH (reprint author), NCI,NIH,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 17 TC 177 Z9 181 U1 1 U2 5 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD MAR PY 1996 VL 2 IS 3 BP 350 EP 353 DI 10.1038/nm0396-350 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TY640 UT WOS:A1996TY64000048 PM 8612238 ER PT J AU Oliveira, AM Farina, M Ludka, IP Kachar, B AF Oliveira, AM Farina, M Ludka, IP Kachar, B TI Vaterite, calcite, and aragonite in the otoliths of three species of piranha SO NATURWISSENSCHAFTEN LA English DT Article ID FISH OTOLITHS; OTOCONIA C1 UNIV FED RIO DE JANEIRO,DEPT GEOL,BR-21949900 RIO JANEIRO,BRAZIL. NIH,LAB CELLULAR BIOL,BETHESDA,MD 20892. RP Oliveira, AM (reprint author), UNIV FED RIO DE JANEIRO,INST BIOFIS CARLOS CHAGAS FILHO,BR-21949900 RIO JANEIRO,BRAZIL. RI Farina, Marcos/I-3744-2014 NR 23 TC 26 Z9 28 U1 0 U2 9 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0028-1042 J9 NATURWISSENSCHAFTEN JI Naturwissenschaften PD MAR PY 1996 VL 83 IS 3 BP 133 EP 135 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD701 UT WOS:A1996UD70100008 ER PT J AU Brining, SK Jones, CR Chang, MCJ AF Brining, SK Jones, CR Chang, MCJ TI Effects of chronic beta-amyloid treatment on fatty acid incorporation into rat brain SO NEUROBIOLOGY OF AGING LA English DT Article DE Beta-amyloid; Alzheimer's disease; Fatty acids; phospholipid incorporation; osmotic pump; rat brain; arachidonate; docosahexaenoate; palmitate ID CEREBRAL PALMITATE INCORPORATION; ALZHEIMERS-DISEASE; UNANESTHETIZED RATS; SENILE PLAQUES; PLASMA PALMITATE; PROTEIN; PHOSPHOLIPIDS; PATHOLOGY; DEMENTIA; ENZYMES AB The present study evaluated the effects of chronic A beta administration on radio-labeled plasma fatty acid incorporation in rat brain. A beta was chronically infused intraventricularly via an osmotic minipump, for 1 week, at a concentration of 460 mu M. After the infusion, fatty acid incorporation was quantified using an in vivo method developed in this laboratory. Three radiolabeled fatty acids were separately infused IV in awake animals. Biochemical analyses of fatty acid incorporation and histology for A beta showed no differences between control (vehicle infusion only) and experimental groups. However, in vitro tests on the cytotoxicity of A beta showed that it caused significant cell death relative to controls (PC-12 cells). The lack of effect of infused A beta on radiolabeled fatty acid incorporation is discussed. RP Brining, SK (reprint author), NIA,NIH,10 CTR DR,MSC 1582,BLDG 10,ROOM 6C-103,BETHESDA,MD 20892, USA. NR 51 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD MAR-APR PY 1996 VL 17 IS 2 BP 301 EP 309 DI 10.1016/0197-4580(95)02071-3 PG 9 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA UH440 UT WOS:A1996UH44000017 PM 8744412 ER PT J AU Bertrand, N Ishii, H Spatz, M AF Bertrand, N Ishii, H Spatz, M TI Cerebral ischemia in young and adult gerbils: Effects on cholinergic metabolism SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article ID RAT-BRAIN; ACETYLCHOLINE-RELEASE; ACETYLTRANSFERASE; ONTOGENY; NEURONS AB The effect of transient cerebral ischemia on cholinergic metabolism was investigated in adult and young gerbils subjected to bilateral carotid artery occlusion (15 min) alone or with release. Ischemia decreased brain acetylcholine (ACh) and increased choline (Ch) levels, affecting the young to a lesser degree than the adult gerbils. Blood recirculation induced a rapid early restoration of brain ACh levels in young animals, whereas a tremendous rebound of. ACh was observed in the adults. After 2 h of reflow, Ch levels normalized in the adult brain, whereas a decreased choline level was seen in the young brain. This is the first study demonstrating an age-dependent susceptibility of cholinergic neurotransmission to cerebral ischemia. C1 NIH,NINDS,STROKE BRANCH,BETHESDA,MD 20892. NR 22 TC 16 Z9 16 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD MAR PY 1996 VL 28 IS 3 BP 293 EP 297 DI 10.1016/0197-0186(95)00086-0 PG 5 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA TY943 UT WOS:A1996TY94300008 PM 8813247 ER PT J AU Heldman, E Barg, J Vogel, Z Pollard, HB Zimlichman, R AF Heldman, E Barg, J Vogel, Z Pollard, HB Zimlichman, R TI Correlation between secretagogue-induced Ca2+ influx, intracellular Ca2+ levels and secretion of catecholamines in cultured adrenal chromaffin cells SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article ID EXOCYTOTIC SECRETION; MEDULLA CELLS; SYNAPTIC VESICLES; MEMBRANE-FUSION; CALCIUM-UPTAKE; CA-2+; PHOSPHOLIPASE-A2; RELEASE; PHOSPHORYLATION; CYTOSKELETON AB Catecholamine secretion induced by various secretagogues in cultured bovine chromaffin cells has been correlated with Ca2+ influx and intracellular Ca2+ concentrations. Nicotine and high K+ caused prompt secretion of catecholamines from cells. Coincidently, both secretagogues evoked (45)[Ca2+] influx with a parallel increase in free intracellular Ca2+ concentration, as determined by Quin 2 fluorescence. However, the rate of return of Ca2+ level to baseline after nicotine stimulation was more rapid than after K+ stimulation. In comparison, stimulation with veratridine produced a slow and prolonged Ca2+ influx accompanied by lower levels of intracellular Ca2+ than those observed after nicotine or K+ stimulation. Yet, during 15 min of stimulation, veratridine induced a substantial catecholamine release, which was larger than that obtained after nicotine or K+ stimulations. The Ca2+ ionophore A23187 (1 mu M) induced a pronounced increase in intracellular Ca2+ levels, but did not evoke any significant catecholamine release. Finally, addition of the Ca2+ channel blocker verapamil following stimulation, at a time when intracellular Ca2+ concentration was at its peak level, did not affect the rate of decline in intracellular free Ca2+ concentration but promptly blocked Ca2+ uptake and catecholamine secretion. These findings suggest that the rate of Ca2+ influx, rather than the absolute level of intracellular Ca2+ concentration, determines the rate and extent of catecholamine release. C1 ISRAEL INST BIOL RES,IL-74100 NESS ZIONA,ISRAEL. WEIZMANN INST SCI,DEPT NEUROBIOL,IL-76100 REHOVOT,ISRAEL. NIDDK,CELL BIOL & GENET LAB,NIH,BETHESDA,MD 20892. TEL AVIV UNIV,SCH MED,E WOLFSON MED CTR,CARDIOVASC & HYPERTENS RES LAB,HOLON,ISRAEL. FU NIDA NIH HHS [DA-6265] NR 37 TC 10 Z9 10 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD MAR PY 1996 VL 28 IS 3 BP 325 EP 334 DI 10.1016/0197-0186(96)83614-X PG 10 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA TY943 UT WOS:A1996TY94300012 PM 8813251 ER PT J AU Liberski, PP Yanagihara, R Brown, P Kordek, R Kloszewska, I Bratosiewicz, J Gajdusek, DC AF Liberski, PP Yanagihara, R Brown, P Kordek, R Kloszewska, I Bratosiewicz, J Gajdusek, DC TI Microwave treatment enhances the immunostaining of amyloid deposits in both the transmissible and non-transmissible brain amyloidoses SO NEURODEGENERATION LA English DT Article DE amyloid; immunohistochemistry; microwave ID CREUTZFELDT-JAKOB DISEASE; SCRAPIE PRION PROTEINS; ALZHEIMERS-DISEASE; PLAQUE AB The immunolocalization of amyloid deposits containing either protease-resistant prion protein (PrP) or amyloid beta protein (A beta) in the brains of patients with transmissible or non-transmissible cerebral amyloidoses has been greatly facilitated by the pretreatment of tissue sections with concentrated formic acid. We have investigated whether microwave processing of formalin-fixed tissue sections would obviate the need for formic acid pretreatment. Exposure of brain sections to microwaves, even for periods as brief as 1 sec, greatly enhanced the immunostaining of PrP and A beta amyloid deposits in both the transmissible and non-transmissible brain amyloidoses. Microwaving for 1 min yielded staining intensities similar to that following pretreatment with concentrated formic acid for 10 min. Moreover, the combination of formic acid pretreatment and microwave processing resulted in an even more intense staining of amyloid deposits. Microwave processing, which is easy to perform and comparatively inexpensive, makes exposure to the potentially toxic fumes of formic acid unnecessary. (C) 1996 Academic Press Limited. C1 NINCDS,CENT NERVOUS SYST STUDIES LAB,NIH,BETHESDA,MD 20892. MED ACAD LODZ,DEPT ONCOL,ELECTRON MICROSCOPY LAB,LODZ,POLAND. MED ACAD LODZ,DEPT PSYCHIAT 2,LODZ,POLAND. RI Kordek, Radzislaw/S-9616-2016 NR 19 TC 14 Z9 14 U1 1 U2 2 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 1055-8330 J9 NEURODEGENERATION JI Neurodegeneration PD MAR PY 1996 VL 5 IS 1 BP 95 EP 99 DI 10.1006/neur.1996.0013 PG 5 WC Neurosciences SC Neurosciences & Neurology GA UE434 UT WOS:A1996UE43400013 PM 8731388 ER PT J AU Li, SJ Scanlon, MN Jarai, Z Varga, K Gantenberg, NS LazarWesley, E Kunos, G AF Li, SJ Scanlon, MN Jarai, Z Varga, K Gantenberg, NS LazarWesley, E Kunos, G TI Alpha-2-adrenergic activation of proopiomelanocortin-containing neurons in the arcuate nucleus causes opioid-mediated hypotension and bradycardia SO NEUROENDOCRINOLOGY LA English DT Article DE beta-endorphin; blood pressure; opiate peptides; catecholamine receptors; proopiomelancortin ID GROWTH-HORMONE RELEASE; BETA-ENDORPHIN; MESSENGER-RNA; BLOOD-PRESSURE; POSSIBLE INVOLVEMENT; BRAIN-STEM; MONOSODIUM GLUTAMATE; ANESTHETIZED RATS; ALPHA-METHYLDOPA; NERVOUS-SYSTEM AB Treatment of rats for 4 days with alpha-methyldopa, 200 mg/kg/day i.p., increases steady state levels of proopiomelanocortin (POMC) mRNA in the mediobasal hypothalamus, as measured by DNA excess solution hybridization. The increase is prevented by parallel treatment with yohimbine, 2 mg/kg/day i.p., but not by naltrexone, 2 mg/kg/day i.p. Treatment with the peripheral vasodilator hydralazine, 2 mg/kg/day, does not affect POMC mRNA levels. In situ hybridization histochemistry with a cRNA probe for POMC indicates that POMC-containing cells are located within the confines of the arcuate nucleus both in control and in cr-methyldopa-treated rats, and confirms the increase in POMC mRNA in the latter. Microinjection of 2 mu g of alpha-methylnorepinephrine unilaterally into the arcuate nucleus of urethane-anesthetized rats causes hypotension and bradycardia, which can be inhibited by 200 ng of yohimbine microinjected into the same site, or by 100 ng l-naloxone microinjected into the ipsilateral nucleus tractus solitarii, but not into the arcuate nucleus. These findings are interpreted to indicate that activation of alpha(2)-adrenergic receptors located on POMC-containing neurons in the arcuate nucleus causes beta-endorphin release and stimulation of opiate receptors in the NTS, which results in hypotension and bradycardia, and that this mechanism contributes to the hypotensive action of alpha-methyldopa. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,SCH MED,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. NIAAA,BETHESDA,MD. FU NHLBI NIH HHS [HL49938] NR 57 TC 11 Z9 11 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD MAR PY 1996 VL 63 IS 3 BP 275 EP 283 DI 10.1159/000126966 PG 9 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA TZ653 UT WOS:A1996TZ65300008 PM 8677016 ER PT J AU Kim, SY Post, RM Rosen, JB AF Kim, SY Post, RM Rosen, JB TI Differential regulation of basal and kindling-induced TRH mRNA expression by thyroid hormone in the hypothalamic and limbic structures SO NEUROENDOCRINOLOGY LA English DT Article DE kindling; hybridization, in situ; thyrotropin-releasing hormone; thyroid hormone; limbic system; amygdala; hippocampus ID THYROTROPIN-RELEASING-HORMONE; PARAVENTRICULAR NUCLEUS; GENE-EXPRESSION; MESSENGER-RNA; NERVOUS-SYSTEM; RAT-BRAIN; BIOSYNTHESIS; SEIZURES AB It has previously been demonstrated that thyrotropin-releasing hormone (TRH) mRNA expression is dramatically increased in limbic structures including dentate gyrus granular layer, and pyriform, entorhinal and perirhinal cortices following amygdala kindling. Since thyroid hormone regulates TRH mRNA in the paraventricular nucleus of the hypothalamus (PVN), we investigated whether basal or kindling-induced TRH mRNA expression in limbic regions is also regulated by thyroid hormone. Hypo- and hyperthyroidism was induced by treating rats with 0.05% 6-n-propyl-2-thiouracil (PTU) (equivalent to similar to 30 mg/kg/day) or 0.9 mu M 3,5,3'-triiodo-L-thyronine (T-3) (equivalent to similar to 50 mu g/kg/day), respectively, in their drinking water for 10 days before kindling and throughout the kindling procedure. Rats were sacrificed 4 h after their first stage 5 seizure. None of the thyroid hormone manipulations altered kindling development, or behavioral and electrographic afterdischarge seizure durations. Pituitary TSH beta mRNA levels were significantly increased by PTU and suppressed by T-3, but unaffected by kindling. In addition, in situ hybridization showed that PTU administration increased and T-3 administration decreased TRH mRNA levels in the PVN, consistent with thyroid hormone's negative feedback effects. At the same time, kindling had no effect on TRH mRNA in the PVN. In contrast, kindling dramatically increased TRH mRNA in the dentate gyrus granular layer, and pyriform, entorhinal and perirhinal cortices, but thyroid hormone manipulations did not affect either basal or kindling-induced TRH mRNA expression in limbic structures. These findings demonstrate that TRH mRNA expression is differentially regulated in the hypothalamic PVN and limbic structures. C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. NR 44 TC 23 Z9 23 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD MAR PY 1996 VL 63 IS 3 BP 297 EP 304 DI 10.1159/000126969 PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA TZ653 UT WOS:A1996TZ65300011 PM 8677019 ER PT J AU Misiewicz, B Zelazowska, E Raybourne, RB Cizza, G Sternberg, EM AF Misiewicz, B Zelazowska, E Raybourne, RB Cizza, G Sternberg, EM TI Inflammatory responses to carrageenan injection in LEW/N and F344/N rats: LEW/N rats show sex- and age-dependent changes in inflammatory reactions SO NEUROIMMUNOMODULATION LA English DT Article DE corticotropin-releasing hormone; hypothalamus; carrageenan; inflammation ID CD4+ T-CELLS; TYROSINE-PHOSPHATASE; SIGNAL-TRANSDUCTION; ANIMAL-MODELS; IMMUNE; AUTOIMMUNITY; ACTIVATION; EXPRESSION; RECEPTOR; SUBSETS AB We studied the inflammatory responses of LEW/N and F344/N inbred rat strains after peripheral injection of carrageenan. The inflammatory responses were assessed in terms of volume, relative and total white blood cell counts of the exudates. Moreover, in both strains, blood CD4, CD8, CD25, naive CD4 (CD4/CD45RC) cell and B (CD45R) cell counts and plasma corticosterone levels, constituents of systemic inflammatory responses to carrageenan were evaluated. In general, LEW/N rats are highly responsive to challenge with carrageenan, whereas F344 rats are not. The strong local inflammatory responses to carrageenan are primarily exhibited by female LEW/N rats. The intensity of local inflammatory responses of LEW/N rats changes with the rat age, the highest exhibited by LEW/N rats up to 3 months of age, thereafter the carrageenan-induced inflammatory responses decline. Our results indicate that peripheral injection of carrageenan induces strong systemic immune component. After carrageenan injection, increases in CD8 and naive CD4 blood lymphocytes are seen. Although the carrageenan challenge does not change CD4 blood lymphocytes in both LEW/N and F344/N rat strains, LEW/N rats exhibit higher levels of CD4 cells than F344/N rats, Additionally, LEW/N rats demonstrated lower levels of B cells and higher naive CD4 lymphocytes. Carrageenan challenges induce significant increases in plasma corticosterone response in F344/N rats, as well as increases in LEW/N rats 1 h after injection. Our data stress the importance of rat age and gender in experiments studying inflammatory responses. C1 US FDA,LAUREL,MD. RP Misiewicz, B (reprint author), NIMH,CLIN NEUROENDOCRINOL BRANCH,SECT NEUROENDOCRINE IMMUNOL & BEHAV,BLDG 10,RM 3S 231,BETHESDA,MD 20892, USA. NR 40 TC 15 Z9 15 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1021-7401 J9 NEUROIMMUNOMODULAT JI Neuroimmunomodulation PD MAR-JUN PY 1996 VL 3 IS 2-3 BP 93 EP 101 DI 10.1159/000097233 PG 9 WC Endocrinology & Metabolism; Immunology; Neurosciences SC Endocrinology & Metabolism; Immunology; Neurosciences & Neurology GA VT878 UT WOS:A1996VT87800005 PM 8945724 ER PT J AU Myers, RH Schaefer, EJ Wilson, PWF DAgostino, R Ordovas, JM Espino, A Au, R White, RF Knoefel, JE Cobb, JL McNulty, KA Beiser, A Wolf, PA AF Myers, RH Schaefer, EJ Wilson, PWF DAgostino, R Ordovas, JM Espino, A Au, R White, RF Knoefel, JE Cobb, JL McNulty, KA Beiser, A Wolf, PA TI Apolipoprotein E epsilon 4 association with dementia in a population-based study: The Framingham study SO NEUROLOGY LA English DT Article ID FAMILIAL ALZHEIMER-DISEASE; E POLYMORPHISM; TYPE-4 ALLELE; CHROMOSOME-19; GENE; FREQUENCY; GENOTYPE; BINDING; LINKAGE AB Apolipoprotein E type 4 allele (apoE epsilon 4) is associated with Alzheimer's disease (AD) in the late-onset familial form and in sporadic cases, but the age-associated risk in a randomly sampled elderly population is not established. We examined the association of apoE epsilon 4 with AD and other dementias (mainly multi-infarct or dementia following stroke) in 1,030 persons aged 71 to 100 years in the population-based Framingham Study cohort. Kaplan-Meier survival analysis revealed that 55% of the apoE epsilon 4/epsilon 4 homozygotes developed AD by age 80, whereas 27% of apoE epsilon 3/epsilon 4 heterozygotes developed AD by age 85, and 9% of those without a 4 allele developed AD by age 85 years. In comparison with persons without a 4 allele, the risk ratio for AD was 3.7 (95% CI = 1.9 to 7.5) for apoE epsilon 3/epsilon 4 heterozygotes and 30.1 (95% CI: = 10.7 to 84.4) for apoE epsilon 4 homozygotes. ApoE epsilon 2 (2/2, 2/3, or 2/4 genotypes) was associated with an absence of AD. One-half (n = 21) of the 43 AD patients were either homozygous or heterozygous for apoE epsilon 4. We found evidence for an association of apoE epsilon 4 with other dementia, primarily multi-infarct dementia and stroke. The risk ratio is 2.3 (95% CI = 0.9 to 6.1) for non-AD dementias among persons with apoE epsilon 3/epsilon 4. Although the apoE epsilon 4 allele is a potent risk factor for AD and may be associated with other forms of dementia, most apoE epsilon 4 carriers do not develop dementia, and about one-half of AD is not apoE epsilon 4 associated. The low positive predictive value of this marker (0.10) suggests that use of apoE genotyping as a screening test for AD is not supported. C1 TUFTS UNIV,USDA,HUMAN NUTR RES CTR,LIPID METAB LAB,BOSTON,MA 02111. NHLBI,FRAMINGHAM HEART STUDY,FRAMINGHAM,MA. BOSTON UNIV,DEPT MATH,BOSTON,MA 02215. BOSTON UNIV,VET ADM MED CTR,SCH MED,DEPT NEUROL,BOSTON,MA 02215. BOSTON UNIV,SCH PUBL HLTH,DEPT BIOSTAT & EPIDEMIOL,BOSTON,MA. RP Myers, RH (reprint author), BOSTON UNIV,SCH MED,DEPT NEUROL,80 E CONCORD ST,BOSTON,MA 02118, USA. FU NHLBI NIH HHS [N01-HC-38038]; NIA NIH HHS [2R01-AG-08122-06] NR 37 TC 246 Z9 249 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR PY 1996 VL 46 IS 3 BP 673 EP 677 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA UB778 UT WOS:A1996UB77800016 PM 8618665 ER PT J AU Chapman, J Arlazoroff, A Goldfarb, LG Cervenakova, L Neufeld, MY Werber, E Herbert, M Brown, P Gajdusek, DC Korczyn, AD AF Chapman, J Arlazoroff, A Goldfarb, LG Cervenakova, L Neufeld, MY Werber, E Herbert, M Brown, P Gajdusek, DC Korczyn, AD TI Fatal insomnia in a case of familial Creutzfeldt-Jakob disease with the codon 200(Lys) mutation SO NEUROLOGY LA English DT Article ID CODON-178ASN PRNP MUTATION; AMYLOID PRECURSOR GENE; PRION PROTEIN GENE; LIBYAN ORIGIN; JEWS; POLYMORPHISM AB Fatal familial insomnia (FFI) has been exclusively associated with a pathogenic mutation at codon 178 in the PRNP gene coupled with methionine (Met) at codon 129. We now describe a subject with familial Creutzfeldt-Jakob disease, heterozygous for the pathogenic lysine (Lys) mutation at codon 200 and homozygous for Met at codon 129 of the PRNP gene, who was affected by severe insomnia. At autopsy the patient had significant involvement of the thalamus, as previously described in subjects affected by FFI with the colon 178 mutation. This case demonstrates the wide variability of the clinical expressions in patients with the codon 200 mutation, that may include insomnia and thalamic pathology. C1 ASSAF HAROFE MED CTR,TEL AVIV,ISRAEL. TEL AVIV UNIV,SACKLER FAC MED,DEPT PHYSIOL & PHARMACOL,IL-69978 TEL AVIV,ISRAEL. NINCDS,NIH,CNS STUDIES LAB,BETHESDA,MD 20892. RP Chapman, J (reprint author), TEL AVIV MED CTR & SCH MED,DEPT NEUROL,6 WEIZMAN ST,IL-64239 TEL AVIV,ISRAEL. RI Chapman, Joab/E-4598-2010; Korczyn, Amos/C-3461-2017 OI Korczyn, Amos/0000-0003-0125-2579 NR 16 TC 58 Z9 58 U1 2 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR PY 1996 VL 46 IS 3 BP 758 EP 761 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA UB778 UT WOS:A1996UB77800029 PM 8618678 ER PT J AU Floeter, MK Andermann, F Andermann, E Nigro, M Hallett, M AF Floeter, MK Andermann, F Andermann, E Nigro, M Hallett, M TI Physiological studies of spinal inhibitory pathways in patients with hereditary hyperekplexia SO NEUROLOGY LA English DT Article ID LATENCY AUTOGENIC INHIBITION; RECIPROCAL IA INHIBITION; PRESYNAPTIC INHIBITION; RECURRENT INHIBITION; STARTLE DISEASE; HUMAN FOREARM; GLYCINE-LIKE; H-REFLEX; MOTONEURONS; CAT AB Because hereditary hyperekplexia results from a defect in the glycine receptor, we studied in five patients several spinal inhibitory pathways that are thought to use either glycine or gamma-aminobutyric acid as a neurotransmitter. Three patients had a mutation in the alpha, subunit of the glycine receptor, whereas two sisters with the same clinical syndrome did not have this mutation. Compared with normal subjects, reciprocal inhibition between flexor and extensor muscles of the forearm was diminished during the first period of inhibition and preserved during the second period of inhibition in all three patients tested. Facilitation after the early period of inhibition was prominent. Recurrent inhibition of the soleus H reflex was normal in four patients, as was inhibition of the H reflex produced by Achilles' tendon vibration. There was no significant difference in nonreciprocal (Ib) inhibition between patients and normal individuals. The findings suggest that disynaptic reciprocal inhibition in humans is mediated through glycinergic interneurons, but that recurrent inhibition may have a contribution from nonglycinergic mechanisms. C1 NINCDS,NIH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. MCGILL UNIV,MONTREAL NEUROL HOSP & INST,MONTREAL,PQ,CANADA. WAYNE STATE UNIV,SCH MED,DETROIT,MI. NR 43 TC 20 Z9 21 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR PY 1996 VL 46 IS 3 BP 766 EP 772 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA UB778 UT WOS:A1996UB77800031 PM 8618680 ER PT J AU Baumann, MH Rothman, RB AF Baumann, MH Rothman, RB TI Chronic cocaine exposure potentiates prolactin and head shake responses to 5-HT2 receptor stimulation in rats SO NEUROPHARMACOLOGY LA English DT Article DE cocaine; serotonin (5-HT); 5-HT2 receptor; DOI; prolactin; head shakes ID SEROTONERGIC STIMULATION; AGONIST DOI; DOPAMINE; BRAIN; SECRETION; NEURONS; SENSITIZATION; SENSITIVITY; INVOLVEMENT; INJECTIONS AB The effect of repeated cocaine administration on serotonin(2) (5-HT2) receptor function was examined in male rats. Rats were fitted with indwelling jugular catheters and subsequently received cocaine (15 mg/kg, i.p., b.i.d.) or saline for 7 days. Rats were challenged with the 5-HT2 agonist DOI (25, 100, 400 mu g/kg, i.v.) or saline 42 hr and 8 days after cessation of chronic treatment. Serial blood samples were collected at various times after DOI challenge and analyzed for prolactin levels. DOI-induced head shakes and skin jerks were examined concurrently in the same subjects. After 42 hr of withdrawal, the stimulatory effects of DOI on prolactin release and shaking behavior were significantly enhanced in cocaine-treated rats. Conversely, the skin jerk response to DOI was not altered by prior cocaine exposure. After 8 days of withdrawal, the prolactin and head shake responses to DOI were still potentiated in cocaine-treated rats, but this effect was no longer statistically significant. The data indicate that chronic cocaine enhances the sensitivity of 5-HT2 receptor mechanisms. Our findings further suggest the possibility that altered 5-HT2 receptor function may be involved in the mood disturbances experienced by abstinent cocaine addicts. Published by Elsevier Science Ltd. RP Baumann, MH (reprint author), NIDA,CLIN PSYCHOPHARMACOL SECT,DIV INTRAMURAL RES,NIH,4940 EASTERN AVE,BLDG C,BALTIMORE,MD 21224, USA. NR 47 TC 25 Z9 25 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3908 J9 NEUROPHARMACOLOGY JI Neuropharmacology PD MAR PY 1996 VL 35 IS 3 BP 295 EP 301 DI 10.1016/0028-3908(95)00166-2 PG 7 WC Neurosciences; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA UQ415 UT WOS:A1996UQ41500008 PM 8783204 ER PT J AU Egan, MF Chrapusta, SJ Karoum, F Wyatt, RJ AF Egan, MF Chrapusta, SJ Karoum, F Wyatt, RJ TI The effects of acute and chronic haloperidol treatment on dopamine release mediated by the medial forebrain bundle in the striatum and nucleus accumbens SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE depolarization inactivation; haloperidol; neuroleptic; dopamine; 3-methoxytyramine; nigrostriatal; mesolimbic; psychosis ID FREELY MOVING RATS; DEPOLARIZATION BLOCK; EXTRACELLULAR DOPAMINE; INVIVO MICRODIALYSIS; CHRONIC CLOZAPINE; INTRACEREBRAL DIALYSIS; EXCITABLE-MEMBRANES; PREFRONTAL CORTEX; FRONTAL-CORTEX; BASAL DOPAMINE AB The delayed therapeutic effects of neuroleptics have been attributed to D-2-mediated depolarization inactivation (DI) of mesolimbic dopaminergic neurons and concomitant reduction in dopamine release. Several studies have suggested, however, that DI may not reduce dopamine release and have hypothesized that this is due to increased impulse independent release. To examine the mechanisms that modulate dopamine release during DI, tetrodotoxin (TTX) was infused into the left medial forebrain bundle (MFB) of Sprague Dawley rats. Three-methoxytyramine (3-MT) levels 10 minutes after pargyline (75 mg/kg) were used as a measure of dopamine release. A dose response study showed that infusions of 10(-5) mol/L and 10(-4) mol/L TTX reduced 3-MT levels on the infused sine by 70% in the striatum and 50% to 60% in the nucleus accumbens. In a time course study, 10(-5) mol/L TTX reduced striatal 3-MT at 30, 90, and 120 minutes: After intraperitoneal injections of haloperidol (0.4 mg/kg)for 1 or 21 days, TTX infusions again reduced 3-MT levels by approximately 70% in the striatum and 53% to 59% in the nucleus accumbens on the infused side. Acute and chronic haloperidol treatment did not alter the percent of TTX-induced reductions. These data suggest that dopaminergic neuronal impulse flow modulates similar amounts of total transmitter release after both acute and chronic haloperidol treatment. The results do not support the notion that DI ?mediates the antipsychotic effects of neuroleptics by markedly reducing total basal dopamine release or increasing impulse independent release. Alternatively, DI could reduce psychotic symptoms by changing the responsiveness of the dopamine system to external stimuli or by reducing synaptic dopamine levels that have been hypothesized to be elevated in psychotic patients. RP Egan, MF (reprint author), NIMH, NEUROSCI CTR ST ELIZABETHS, NEUROPSYCHIAT BRANCH, 2700 MARTIN LUTHER KING JR AVE SE, WASHINGTON, DC 20032 USA. NR 71 TC 6 Z9 6 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X EI 1740-634X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD MAR PY 1996 VL 14 IS 3 BP 211 EP 223 DI 10.1016/0893-133X(95)00111-P PG 13 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA TY372 UT WOS:A1996TY37200008 PM 8866705 ER PT J AU Weinberger, DR AF Weinberger, DR TI On the plausibility of ''The neurodevelopmental hypothesis'' of schizophrenia SO NEUROPSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT Symposium on A New Understanding - Neurological Basis and Long-Term Outcome of Schizophrenia, at the CINP Congress CY JUN 28, 1994 CL WASHINGTON, D.C. DE schizophrenia; brain development; neurodevelopmental hypothesis; neuropathology ID CEREBRAL BLOOD-FLOW; POTENTIAL ANIMAL-MODEL; PRENATAL EXPOSURE; PREFRONTAL CORTEX; CORTICAL DEVELOPMENT; INFLUENZA EPIDEMICS; ADULT SCHIZOPHRENIA; HUNTINGTONS-DISEASE; HIPPOCAMPAL DAMAGE; MAGNETIC-RESONANCE AB Speculation that schizophrenia is associated with abnormal brain development, the so-called neurodevelopmental hypothesis, has become so popular that it is rarely challenged in the literature. This paper critically examines the evidence for this hypothesis, taking primarily the ''devil's advocate'' position. The evidence from neuroimaging studies, from studies of prenatal and perinatal intrauterine events and of premorbid development are circumstantial with respect to brain development, many studies ave methodologically flawed, and most do not exclude alternative explanations. Evidence from postmortem studies of anomalous cytoarchitecture in limbic and prefrontal cortices is especially noteworthy, as a developmental defect is virtually certain if artifacts can be excluded. Unfortunately, the studies responsible for these findings have serious methodological limitations. The neurobiological plausibility of the hypothesis, which might have been predicted to be its weakest aspect, has proved surprisingly unshakeable in a recent series of animal studies. Ironically, the principal weakness of the neurodevelopmental hypothesis at present is the clinical database on which it rests. RP Weinberger, DR (reprint author), NIMH, INTRAMURAL RES PROGRAM, CLIN BRAIN DISORDERS BRANCH, NIH, 2700 MARTIN LUTHER KING JR AVE SE, WASHINGTON, DC 20032 USA. NR 78 TC 103 Z9 107 U1 3 U2 6 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD MAR PY 1996 VL 14 IS 3 SU S BP S1 EP S11 DI 10.1016/0893-133X(95)00199-N PG 11 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA TZ694 UT WOS:A1996TZ69400001 PM 8866738 ER PT J AU Li, YX Bertram, R Rinzel, J AF Li, YX Bertram, R Rinzel, J TI Modeling N-methyl-D-aspartate-induced bursting in dopamine neurons SO NEUROSCIENCE LA English DT Article DE basal ganglia; glutamate agonist; sodium pump; oscillations; firing patterns ID SUBSTANTIA-NIGRA; MEMBRANE-PROPERTIES; VOLTAGE DEPENDENCE; COMPACTA NEURONS; FIRING PATTERN; RAT; INVITRO; OSCILLATIONS; ELECTROPHYSIOLOGY; VASOPRESSIN AB Burst firing of dopaminergic neurons of the substantia nigra pars compacta can be induced in vitro by the glutamate agonist N-methyl-D-aspartate. It has been suggested that the interburst hyperpolarization is due to Na+ extrusion by a ouabain-sensitive pump [Johnson et al. (1992) Science 258, 665-667]. We formulate and explore a theoretical model, with a minimal number of currents, for this novel mechanism of burst generation. This minimal model is further developed into a more elaborate model based on observations of additional currents and hypotheses about their spatial distribution in dopaminergic neurons [Hounsgaard (1992) Neuroscience 50, 513-518; Llinas et al. (1984) Brain Res. 294, 127-132]. Using the minimal model, we confirm that interaction between the regenerative, inward N-methyl-D-aspartate-mediated current and the outward Nac-pump current is sufficient to generate the slow oscillation (similar to 0.5 Hz) underlying the burst. The negative-slope region of the N-methyl-D-aspartate channel's current-voltage relation is indispensable for this slow rhythm generation. The time-scale of Na+-handling determines the burst's slow frequency. Moreover, we show that, given the constraints of sodium handling, such bursting is best explained mechanistically by using at least two spatial, cable-like compartments: a soma where action potentials are produced and a dendritic compartment where the slow rhythm is generated. Our result is consistent with recent experimental evidence that burst generation originates in distal dendrites [Seutin et al. (1994) Neuroscience 58, 201-206]. Responses of the model to a number of electrophysiological and pharmacological stimuli are consistent with known responses observed under similar conditions. These include the persistence of the slow rhythm when the tetrodotoxin-sensitive Na+ channel is blocked and when the soma is voltage-clamped at -60 mV. Using our more elaborate model, we account for details of the observed frequency adaptation in N-methyl-D-aspartate-induced bursting, the origin of multiple spiking and bursting mechanisms, and the interaction between two different bursting mechanisms. Besides reproducing several well established firing patterns, this model also suggests that new firing modes, not yet recorded, might also occur in dopaminergic neurons. This model provides mechanistic insights and explanations into the origin of a variety of experimentally observed membrane potential firing patterns in dopaminergic neurons, including N-methyl-D-aspartate-induced bursting and its dendritic origin. Such a model, capable of reproducing a number of realistic behaviors of dopaminergic neurons, could be useful in further studies of the basal ganglia-thalamocortical motor circuit. It may also shed light on bursting that involves N-methyl-D-aspartate channel activity in other neuron types. C1 NIDDK,NIH,MATH RES BRANCH,BETHESDA,MD 20892. NR 44 TC 61 Z9 63 U1 0 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD MAR PY 1996 VL 71 IS 2 BP 397 EP 410 DI 10.1016/0306-4522(95)00483-1 PG 14 WC Neurosciences SC Neurosciences & Neurology GA TX743 UT WOS:A1996TX74300010 PM 9053795 ER PT J AU Abbott, LC Isaacs, KR Heckroth, JA AF Abbott, LC Isaacs, KR Heckroth, JA TI Co-localization of tyrosine hydroxylase and Zebrin II immunoreactivities in Purkinje cells of the mutant mice, tottering and tottering leaner SO NEUROSCIENCE LA English DT Article DE cerebellum; myoclonus; immunocytochemistry; hereditary ataxia; sagittal zonation; epilepsy ID CALCIUM-BINDING PROTEIN; RAT CEREBELLAR CORTEX; CLIMBING FIBER DISTRIBUTION; CENTRAL NERVOUS-SYSTEM; HAN-WISTAR RAT; CAT CEREBELLUM; SPINOCEREBELLAR PROJECTION; OLIVOCEREBELLAR PROJECTION; PARASAGITTAL ORGANIZATION; SAGITTAL ORGANIZATION AB The mutant mice tottering, leaner and the compound heterozygous tottering/leaner exhibit varying degrees of several abnormal neurological phenotypes including petit mal-like epilepsy, ataxia and an intermittent myoclonus-like movement disorder. Aberrant expression of tyrosine hydroxylase in cerebellar Purkinje cells of tottering, leaner and tottering/leaner mice has been observed previously [Austin M. C. et al. (1992) Molec. Brain Res. 15, 227-240; Hess E. J. and Wilson M. C. (1991) Neuron 6, 123-132]. In the present study, the distribution of tyrosine hydroxylase expression was compared with that of Zebrin II in Purkinje cells of adult homozygous tottering and compound heterozygous tottering/leaner mutant mice using single and double immunocytochemistry and double immunofluorescence. The pattern of Zebrin II expression in the cerebella of the mutant mice was identical to that described for normal mice [Hawkes R. et al. (1985) Brain Res. 333, 359-365; Hawkes R. and Leclerc N. (1987) J. comp. Neurol. 256, 29-41]. In addition, sections through tottering and tottering/leaner cerebella demonstrated an exact correspondence between the bands of tyrosine hydroxylase immunoreactivity and bands of Zebrin II immunoreactivity. Similarly, the compartments of the Purkinje cell layer which were negative for Zebrin II staining were also negative for tyrosine hydroxylase immunoreactivity. This study provides evidence that the cerebellar Purkinje cells of tottering and tottering/leaner mice were able to express a normal gene product, Zebrin II, in a normal spatial pattern and the same Purkinje cells can also express an aberrant gene product, tyrosine hydroxylase. This abnormal gene expression may indicate that at least some Purkinje cells in these mutant mice are not functioning normally. This possibility, taken together with the morphological changes observed in many mutant Purkinje cell axons, suggests that Purkinje cell function could be altered in tottering and totteringlleaner mice, thereby contributing to the neurological abnormalities exhibited by these mice. It is also possible that alteration in function of mutant Purkinje cells could correlate with the rostrocaudal zonation pattern described in this study. C1 UNIV ILLINOIS,COLL VET MED,DEPT VET BIOSCI,URBANA,IL 61801. NIMH,NIH,CLIN SCI LAB,BETHESDA,MD 20892. ST LOUIS UNIV,SCH MED,DEPT ANAT & NEUROBIOL,ST LOUIS,MO 63104. FU NCRR NIH HHS [S-507-RR5371]; NINDS NIH HHS [1K08NS01681-01] NR 67 TC 27 Z9 28 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD MAR PY 1996 VL 71 IS 2 BP 461 EP 475 DI 10.1016/0306-4522(95)00444-0 PG 15 WC Neurosciences SC Neurosciences & Neurology GA TX743 UT WOS:A1996TX74300015 PM 9053800 ER PT J AU BechtelBoenning, C AF BechtelBoenning, C TI State of the art - Antiviral treatment of HIV infection SO NURSING CLINICS OF NORTH AMERICA LA English DT Article ID IMMUNODEFICIENCY-VIRUS INFECTION; AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; ANTIRETROVIRAL THERAPY; ZIDOVUDINE THERAPY; CUBIC MILLIMETER; INTERFERON-ALPHA; DOUBLE-BLIND; AZT; DIDEOXYCYTIDINE AB Antiretroviral drugs have been the mainstay of treatment for HN infection. New categories of antiretrovirals and recommendations for treatment have emerged as a result of basic science research, new understandings of the infectious process, and data from clinical studies. This article summarizes the currently available drugs for nurses who act as educators and advocates in helping HIV-infected persons explore their treatment options. RP BechtelBoenning, C (reprint author), NIAID,NIH,BLDG 10,ROOM 8C401,BETHESDA,MD 20892, USA. NR 48 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD MAR PY 1996 VL 31 IS 1 BP 1 EP & PG 14 WC Nursing SC Nursing GA UA311 UT WOS:A1996UA31100002 PM 8604373 ER PT J AU Engle, J AF Engle, J TI Immune-based therapy for HIV SO NURSING CLINICS OF NORTH AMERICA LA English DT Article ID TUMOR-NECROSIS-FACTOR; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; BONE-MARROW TRANSPLANTATION; INTERFERON-ALPHA; VIRUS TYPE-1; SYNDROME AIDS; INFECTION; REPLICATION; ZIDOVUDINE; EXPRESSION AB Even if there were antiretrovirals developed that could completely eliminate HIV from the body, it is thought that immune-based therapy would still be necessary. Pervasive damage occurs in the immune system even in early stages of the disease, and this damage would not be corrected by antiretrovirals. Several different types of immune-based therapies are presented in this article; some have been successful, and some have not been successful. All have been important, however, in increasing the knowledge base of HIV pathogenesis and in narrowing the options that might rebuild the immune system and, thereby, reverse this pathology. RP Engle, J (reprint author), WARREN GRANT MAGNUSON CLIN CTR,NIH,HIV RES CLIN,4831 SEDGWICK ST NW,WASHINGTON,DC 20016, USA. NR 45 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD MAR PY 1996 VL 31 IS 1 BP 15 EP & PG 10 WC Nursing SC Nursing GA UA311 UT WOS:A1996UA31100003 PM 8604377 ER PT J AU Grady, C Kelly, G AF Grady, C Kelly, G TI State of the science - HIV vaccine development SO NURSING CLINICS OF NORTH AMERICA LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS VACCINE; CHALLENGE; ISSUES; SIV AB Developing a vaccine able to prevent HIV infection would be a great benefit to the world. Vaccines have contributed to substantially reduced morbidity and mortality fi om several important infectious diseases. However, HIV has so:me characteristics that distinguish it from many other viruses and make vaccine development challenging. This article discusses scientific strategies, obstacles, and progress to date towards the development of a preventive HIV vaccine. C1 NATL INST HLTH,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD 20892. RP Grady, C (reprint author), NINR,NIH,BLDG 31,ROOM 5B10,BETHESDA,MD 20892, USA. NR 44 TC 7 Z9 7 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD MAR PY 1996 VL 31 IS 1 BP 25 EP & PG 16 WC Nursing SC Nursing GA UA311 UT WOS:A1996UA31100004 PM 8604385 ER PT J AU Barrick, B Vogel, S AF Barrick, B Vogel, S TI Application of laboratory diagnostics in HIV nursing SO NURSING CLINICS OF NORTH AMERICA LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; WESTERN-BLOT; PLASMA VIREMIA; INFECTION; DISEASE; TYPE-1; COHORT; AIDS; IMMUNOPATHOGENESIS; INDIVIDUALS AB The HIV epidemic has challenged nursing to rethink the tools it uses and to consider how traditional medical tools may be used in the assessment of nursing problems. This article presents information for the direct care nurse on laboratory tests and how they may be used to meet the traditional needs of physiologic assessment and evaluation and to develop specific nursing interventions. This article discusses tests used for HIV infection, HN disease progression presence of microbiologic agents of opportunistic infections commonly associated with advanced HIV disease, and common laboratory tests and their special relevance to HIV. Nursing implications and interventions are discussed throughout the text. C1 NIAID,HIV RES CLIN,NATL INST HLTH,BETHESDA,MD 20892. RP Barrick, B (reprint author), NATL INST HLTH,WARREN GRANT MAGNUSON CLIN CTR,HIV RES CLIN,BLDG 10,ROOM 8C300,BETHESDA,MD 20892, USA. NR 47 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD MAR PY 1996 VL 31 IS 1 BP 41 EP & PG 17 WC Nursing SC Nursing GA UA311 UT WOS:A1996UA31100005 PM 8604386 ER PT J AU Hutchins, SA Eckes, R AF Hutchins, SA Eckes, R TI Clinical research - Considerations for prospective participants SO NURSING CLINICS OF NORTH AMERICA LA English DT Article ID TRIALS AB Many HIV-positive patients are involved in clinical trials. While working with the HIV-positive patient, the nurse is confronted with the challenge of a rapidly changing environment of collective knowledge. The nurse may meet a patient at any stage of drug or biologic development; therefore, it is very important to understand the process of clinical research. This article describes the purpose and process of clinical research, the patient perspective, ethical considerations, and the role of the nurse in biomedical research. RP Hutchins, SA (reprint author), NIH,HIV RES CLIN,WARREN GRANT MAGNUSON CLIN CTR,BLDG 10,ROOM 8C414,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 17 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD MAR PY 1996 VL 31 IS 1 BP 125 EP & PG 12 WC Nursing SC Nursing GA UA311 UT WOS:A1996UA31100010 PM 8604375 ER PT J AU Grady, C BechtelBoenning, C AF Grady, C BechtelBoenning, C TI HIV infection - Preface SO NURSING CLINICS OF NORTH AMERICA LA English DT Editorial Material C1 NIAID,NIH,BETHESDA,MD 20892. RP Grady, C (reprint author), NINR,NIH,BLDG 31,ROOM 5B10,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD MAR PY 1996 VL 31 IS 1 BP R15 EP R16 PG 2 WC Nursing SC Nursing GA UA311 UT WOS:A1996UA31100001 ER PT J AU Sherer, DM Salafia, CM Minior, VK Sanders, M Ernst, L Vintzileos, AM AF Sherer, DM Salafia, CM Minior, VK Sanders, M Ernst, L Vintzileos, AM TI Placental basal plate myometrial fibers: Clinical correlations of abnormally deep trophoblast invasion SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID FETAL GROWTH-RETARDATION; PRETERM DELIVERY; PATHOLOGY; INFANTS; LESIONS; TERM; BED AB Objective: To assess the incidence of placental basal plate myometrial fibers in preterm and term gestations and correlate this finding with clinical observations and placental histopathology. Methods: Placentas from 457 singleton births before 32 weeks' gestation and 108 uncomplicated singleton births after 37 weeks' gestation were examined histopathologically. Pregnancies complicated by maternal chronic hypertension, diabetes mellitus, coagulopathy, placenta previa, stillbirth, multiple fetuses, and fetal congenital anomalies were excluded from both groups. In the preterm group, 158 patients had preterm labor with intact membranes, 192 had preterm premature rupture of membranes (PROM), 31 had placental abruption without hypertension, and 76 had preeclampsia. Histopathology detected the presence of placental basal plate myometrial fibers, placental vascular lesions, and villous damage related to vascular insufficiency. Results: Forty-four of 457 (9.6%) of preterm placentas had basal plate myometrial fibers, compared with one of 108 (0.9%) term controls (P <.001). Uteroplacental vessels with abnormal physiologic changes were more frequent and placental weights were lower in cases-with basal plate myometrial fibers (P <.003 and P <.03, respectively). No other uteroplacental vascular lesions were related to basal plate myometrial fibers. The frequency of placental basal plate myometrial fibers was nine of 76 (12%) in cases complicated by preeclampsia, 21 of 192 (11%) cases of PROM, nine of 158 (5.7%) cases of preterm labor, and four of 31 (13%) cases of placental abruption without hypertension; these frequencies were not significantly different, and there was no significant relationship to gravidity, parity, mode of delivery, or birth weight. Conclusion: Placental basal plate myometrial fibers occur in ten times as many preterm births as term births. This finding is associated with both abnormal uteroplacental physiologic changes and decreased placental weight, and may explain the increased incidence of abnormalities of the third stage of labor associated with preterm delivery. C1 GEORGETOWN UNIV,MED CTR,DEPT OBSTET & GYNECOL,PERINATOL RES FACIL,DIV MATERNAL FETAL MED,NICHD,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20007. UNIV CONNECTICUT,CTR HLTH,DIV ANAT PATHOL,FARMINGTON,CT. UNIV CONNECTICUT,CTR HLTH,DIV MATERNAL FETAL MED,FARMINGTON,CT. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,ST PETERS MED CTR,DIV MATERNAL FETAL MED,NEW BRUNSWICK,NJ 08903. NR 27 TC 15 Z9 15 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD MAR PY 1996 VL 87 IS 3 BP 444 EP 449 DI 10.1016/0029-7844(95)00426-2 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TX742 UT WOS:A1996TX74200024 PM 8598971 ER PT J AU deSmet, MD AF deSmet, MD TI Low dose cyclosporin a therapy in treating chronic, noninfectious uveitis - Discussion SO OPHTHALMOLOGY LA English DT Editorial Material RP deSmet, MD (reprint author), NEI,IMMUNOL LAB,CLIN IMMUNOL SECT,BLDG 10,BETHESDA,MD 20892, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD MAR PY 1996 VL 103 IS 3 BP 373 EP 374 PG 2 WC Ophthalmology SC Ophthalmology GA UA469 UT WOS:A1996UA46900019 ER PT J AU George, RK Walton, RC Whitcup, SM Nussenblatt, RB AF George, RK Walton, RC Whitcup, SM Nussenblatt, RB TI Primary retinal vasculitis - Systemic associations and diagnostic evaluation SO OPHTHALMOLOGY LA English DT Article ID WEGENERS GRANULOMATOSIS; LUPUS-ERYTHEMATOSUS; UVEITIS; DISEASE AB Background: inflammation of the retinal vasculature without an infectious etiology, systemic disease association, or concomitant ocular disease is termed primary retinal vasculitis, and can result in severe and permanent vision loss. Patients with primary retinal vasculitis usually are subjected to an extensive but unrewarding diagnostic evaluation. This study was undertaken to determine the value of such a diagnostic workup, and to determine whether systemic diseases develop in these patients during the course of their illness. Methods: The clinical records of 25 patients seen between 1984 and 1994 with the referring diagnosis of primary retinal vasculitis were reviewed retrospectively. Recorded data included patient age, sex, race, medical history, medications, visual acuity, extent of retinal disease, and the results of their diagnostic evaluations. Results: On presentation, none of the patients had an underlying systemic disease attributable as the cause of their retinal vasculitis. Review of systems was suggestive of an underlying systemic disease in 1 of 25 patients. Diagnostic evaluation in this patient showed a positive antinuclear antibody value and a double-stranded DNA, suggestive of systemic lupus erythematosus. Subsequently, systemic lupus erythematosus was diagnosed based on the development of other diagnostic criteria. The review of systems was not suggestive of an underlying systemic disease in 24 of 25 patients. False-positive diagnostic test results were obtained in 5 (20.8%) of these 24 patients. No underlying systemic disease associated with the patients' retinal vasculitis subsequently developed in any of these five patients (mean follow-up, 4 years). Conclusion: Few diagnostic tests should be ordered in patients with retinal vasculitis in the absence of a medical history suggestive of underlying systemic disease. C1 NEI,NIH,IMMUNOL LAB,BETHESDA,MD 20892. NR 19 TC 30 Z9 32 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD MAR PY 1996 VL 103 IS 3 BP 384 EP 389 PG 6 WC Ophthalmology SC Ophthalmology GA UA469 UT WOS:A1996UA46900021 PM 8600413 ER PT J AU Shklar, G Schwartz, JL AF Shklar, G Schwartz, JL TI Vitamin E inhibits experimental carcinogenesis and tumour angiogenesis SO ORAL ONCOLOGY-EUROPEAN JOURNAL OF CANCER PART B LA English DT Article DE vitamin E; carcinogenesis; angiogenesis; TGF alpha ID EXPERIMENTAL ORAL CARCINOGENESIS; BETA-CAROTENE; EXPERIMENTAL CANCER; ALPHA-TOCOPHEROL; REGRESSION; CANTHAXANTHIN; PREVENTION; CARCINOMA; HAMSTERS AB In an experiment in which vitamin E inhibited carcinogenesis, it was found that tumour angiogenesis and tumour growth-factor alpha (TGF alpha) expression were also inhibited. Forty male golden hamsters were divided into four equal groups. Group 1 animals had the left buccal pouches painted three times weekly with 7,12-dimethylbenz(a)anthracene (DMBA) for 14 weeks. Group 2 animals had the same procedure of DMBA applications but also received alpha tocopherol. Groups 3 and 4 were vitamin E and untreated controls. Angiogenesis was studied with factor 8-related antigen (F8-RA) which identifies endothelial cells. TGF alpha was studied with the appropriate antibody. Staining was effected by the standard avidin-biotin horseradish peroxidase system. Mean tumour volume was significantly lower in the DMBA-vitamin E group compared to the tumour control group. Angiogenesis was significantly inhibited in the DMBA-vitamin E group and TGF alpha expression was also inhibited. It is suggested that inhibition of tumour angiogenesis by vitamin E may be an additional mechanism for the anticancer action of vitamin E. (C) 1996 Elsevier Science Ltd C1 NIDR,DIV MOLEC EPIDEMIOL,ORAL DIS & PREVENT PROGRAM,BETHESDA,MD 20892. RP Shklar, G (reprint author), HARVARD UNIV,SCH DENT MED,DIV ORAL PATHOL,DEPT ORAL MED & DIAGNOST SCI,188 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 39 TC 14 Z9 14 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0964-1955 J9 ORAL ONCOL JI Oral Oncol.-Eur. J. Cancer Pt. B PD MAR PY 1996 VL 32B IS 2 BP 114 EP 119 PG 6 WC Oncology; Dentistry, Oral Surgery & Medicine SC Oncology; Dentistry, Oral Surgery & Medicine GA UH982 UT WOS:A1996UH98200008 ER PT J AU Coghill, RC AF Coghill, RC TI Gate control theory and beyond - Populations of neurons and pain SO PAIN FORUM LA English DT Article ID SPINOTHALAMIC TRACT NEURONS; WIDE-DYNAMIC-RANGE; OLD-WORLD MONKEY; SPINAL-CORD; SPATIAL SUMMATION; PERCEPTION; RAT; CONNECTIONS; INTENSITY; STIMULI C1 NIDR,NATL INST HLTH,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. NR 44 TC 1 Z9 1 U1 0 U2 3 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 1058-9139 J9 PAIN FORUM JI Pain Forum PD SPR PY 1996 VL 5 IS 1 BP 40 EP 44 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA UB560 UT WOS:A1996UB56000007 ER PT J AU Rogers, MJ AF Rogers, MJ TI Rare codon usage in Escherichia coli and the expression of potentially toxic genes SO PARASITOLOGY TODAY LA English DT Letter ID RNA RP Rogers, MJ (reprint author), NIAID,PARASIT DIS LAB,GROWTH & DEV SECT,NIH,BETHESDA,MD 20892, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0169-4758 J9 PARASITOL TODAY JI Parasitol. Today PD MAR PY 1996 VL 12 IS 3 BP 124 EP 124 PG 1 WC Parasitology SC Parasitology GA TX133 UT WOS:A1996TX13300014 ER PT J AU Budka, H Aguzzi, A Brown, P Brucher, JM Bugiani, O Collinge, J Diringer, H Gullotta, F Haltia, M Hauw, JJ Ironside, JW Kretzschmar, HA Lantos, PL Masullo, C Pocchiari, M Schlote, W Tateishi, J Will, RG AF Budka, H Aguzzi, A Brown, P Brucher, JM Bugiani, O Collinge, J Diringer, H Gullotta, F Haltia, M Hauw, JJ Ironside, JW Kretzschmar, HA Lantos, PL Masullo, C Pocchiari, M Schlote, W Tateishi, J Will, RG TI Tissue handling in suspected Creutzfeldt-Jakob disease (CJD) and other human spongiform encephalopathies (prion diseases) SO PATHOLOGE LA German DT Article DE transmissible spongiform encephalopathies; prion diseases; Creutzfeldt-Jakob disease; infectivity; decontamination ID TRANSMISSION; VIRUS AB Despite many sensational and intimidating reports in the mass media, transmissible spongiform encephalopathies (prion diseases) are not contagious in the usual sense. Successful transmission requires both specific material (an affected individual's tissue, from or adjacent to CNS) and specific modes (mainly penetrating contact with the recipient). Nevertheless, specific safety precautions are mandatory to avoid accidental transmission and to decontaminate any infectivity. The autopsy is essential for definite diagnosis of these disorders. Recommendations are given here for safe performance of the autopsy, for neuropathology service and appropriate decontamination; they are based on the current literature and on precautions taken in most laboratories experienced in handling tissue from transmissible spongiform encephalopathies. In essence, special care must be taken to avoid penetrating wounds, possible contamination should be kept to a minimum, and potentially infectious material must be adequately decontaminated by specific means. The full English text of this Consensus Report was published in Brain Pathology 5: 319-322 (1995). C1 UNIV ZURICH, INST NEUROPATHOL, ZURICH, SWITZERLAND. NINCDS, NIH, LAB CENT NERVOUS SYST STUDIES, BETHESDA, MD 20892 USA. CATHOLIC UNIV LEUVEN, NEUROPATHOL UNIT, BRUSSELS, BELGIUM. ST MARYS HOSP, SCH MED, PRION DIS GRP, LONDON, ENGLAND. BUNDESGESUNDHEITSAMT, ROBERT KOCH INST, W-1000 BERLIN, GERMANY. UNIV MUNSTER, INST NEUROPATHOL, MUNSTER, GERMANY. UNIV HELSINKI, INST PATHOL, HELSINKI, FINLAND. HOP LA PITIE SALPETRIERE, LAB NEUROPATHOL R ESCOUROLLE, F-75651 PARIS, FRANCE. NATL CREUTZFELDT JAKOB DIS SURVEILLANCE UNIT, NEUROPATHOL LAB, EDINBURGH, MIDLOTHIAN, SCOTLAND. UNIV LONDON, INST PSYCHIAT, DEPT NEUROPATHOL, LONDON SE5 8AF, ENGLAND. UNIV CATTOLICA SACRO CUORE, INST NEUROL, I-00168 ROME, ITALY. IST SUPER SANITA, I-00161 ROME, ITALY. UNIV FRANKFURT, INST NEUROL, FRANKFURT, GERMANY. KYUSHU UNIV, INST NEUROL, DEPT NEUROPATHOL, FUKUOKA 812, JAPAN. UNIV GOTTINGEN, INST NEUROPATHOL, GOTTINGEN, GERMANY. RP Budka, H (reprint author), UNIV VIENNA, INST NEUROL, NEUES AKH 04J, POSTFACH 48, A-1097 VIENNA, AUSTRIA. RI Aguzzi, Adriano/A-3351-2008; OI Budka, Herbert/0000-0002-1933-1577 NR 20 TC 8 Z9 8 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0172-8113 J9 PATHOLOGE JI Pathologe PD MAR PY 1996 VL 17 IS 2 BP 171 EP 175 PG 5 WC Pathology SC Pathology GA UD748 UT WOS:A1996UD74800015 PM 8650149 ER PT J AU Kimberlin, D Powell, D Gruber, W Diaz, P Arvin, A Kumar, M Jacobs, R VanDyke, R Burchett, S Soong, SJ Lakeman, A Whitley, R AF Kimberlin, D Powell, D Gruber, W Diaz, P Arvin, A Kumar, M Jacobs, R VanDyke, R Burchett, S Soong, SJ Lakeman, A Whitley, R TI Administration of oral acyclovir suppressive therapy after neonatal herpes simplex virus disease limited to the skin, eyes and mouth: Results of a phase I/II trial SO PEDIATRIC INFECTIOUS DISEASE JOURNAL LA English DT Article DE newborn; herpes simplex; acyclovir; prophylaxis ID HIGH-DOSE ACYCLOVIR; INFECTION; VIDARABINE; PNEUMONIA AB Background. Neonatal herpes simplex virus (HSV) infections limited to the skin, eyes and mouth (SEM) can result in neurologic impairment. A direct correlation exists between the development of neurologic deficits and the frequency of cutaneous HSV recurrences. Thus, the National Institutes of Allergy and Infectious Diseases Collaborative Antiviral Study Group conducted a Phase I/II trial of oral acyclovir therapy for the suppression of cutaneous recurrences after SEM disease in 26 neonates. Methods. Infants less than or equal to 1 month of age with virologically confirmed HSV-S SEM disease were eligible for enrollment. Suppressive oral acyclovir therapy (300 mg/m(2)/dose given either twice daily or three times per day) was administered for 6 months. Results. Twelve (46%) of the 26 infants developed neutropenia (<1000 cells/mm(3)) while receiving acyclovir. Thirteen (81%) of the 16 infants who received drug 3 times per day experienced no recurrences of skin lesions while receiving therapy. In comparison, a previous Collaborative Antiviral Study Group study found that only 54% of infants have no cutaneous recurrences in the 6 months after resolution of neonatal HSV disease if oral acyclovir suppressive therapy is not initiated. In one infant, HSV DNA was detected in the cerebrospinal fluid during a cutaneous recurrence, and an acyclovir-resistant HSV mutant was isolated from another patient during the course of the study. Conclusions. Administration of oral acyclovir can prevent cutaneous recurrences of HSV after neonatal SEM disease. The effect of such therapy on neurologic outcome must be assessed in a larger, Phase III study. As such, additional investigation is necessary before routine use of suppressive therapy in this population can be recommended. C1 WASHINGTON UNIV, MED CTR, ST LOUIS, MO USA. SUNY SYRACUSE, SYRACUSE, NY USA. LOUISIANA STATE UNIV, NEW ORLEANS, LA 70112 USA. CHILDRENS HOSP PHILADELPHIA, PHILADELPHIA, PA 19104 USA. UNIV CINCINNATI, CINCINNATI, OH USA. HOSP INFANTIL MEXICO DR FEDERICO GOMEZ, MEXICO CITY, DF, MEXICO. COOK CHILDRENS MED CTR, FT WORTH, TX USA. BAPTIST MEM CTR E, MEMPHIS, TN USA. UNIV ALBERTA, EDMONTON, AB, CANADA. UNIV FLORIDA, GAINESVILLE, FL USA. DARTMOUTH HITCHCOCK MED CTR, LEBANON, NH USA. TUFTS UNIV NEW ENGLAND MED CTR, BOSTON, MA 02111 USA. DUKE UNIV, DURHAM, NC USA. COASTAL AREA HLTH EDUC CTR, WILMINGTON, NC USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. HCA WESLEY MED CTR, WICHITA, KS USA. UNIV SO CALIF, LOS ANGELES, CA USA. UNIV MISSOURI, KANSAS CITY, MO 64110 USA. EMORY UNIV, ATLANTA, GA 30322 USA. MARSHFIELD MED RES FDN, MARSHFIELD, WI 54449 USA. UNIV TEXAS SAN ANTONIO, MED BRANCH, GALVESTON, TX 77550 USA. UNIV IOWA, IOWA CITY, IA USA. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, RICHMOND, VA 23298 USA. BAYLOR COLL MED, HOUSTON, TX 77030 USA. UNIV WASHINGTON, SEATTLE, WA 98195 USA. UNIV CALIF SAN DIEGO, SAN DIEGO, CA 92103 USA. UNIV ALABAMA, DEPT PEDIAT, BIRMINGHAM, AL 35233 USA. NIH, BETHESDA, MD 20892 USA. UNIV ALABAMA, DEPT MICROBIOL, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT MED & BIOSTAT, BIRMINGHAM, AL USA. OHIO STATE UNIV, DEPT PEDIAT, COLUMBUS, OH 43210 USA. VANDERBILT UNIV, DEPT PEDIAT, NASHVILLE, TN USA. CHICAGO DEPT PUBL HLTH, COMMUNICABLE DIS DIV, CHICAGO, IL USA. STANFORD UNIV, DEPT PEDIAT, STANFORD, CA 94305 USA. CASE WESTERN RESERVE UNIV, DEPT PEDIAT, CLEVELAND, OH 44106 USA. UNIV ARKANSAS, DEPT PEDIAT, LITTLE ROCK, AR 72204 USA. TULANE UNIV, DEPT PEDIAT, NEW ORLEANS, LA 70118 USA. CHILDRENS HOSP, DEPT PEDIAT, BOSTON, MA 02115 USA. FU NIAID NIH HHS [N01-AI-15113, N01-AI-62554] NR 24 TC 77 Z9 80 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0891-3668 EI 1532-0987 J9 PEDIATR INFECT DIS J JI Pediatr. Infect. Dis. J. PD MAR PY 1996 VL 15 IS 3 BP 247 EP 254 DI 10.1097/00006454-199603000-00014 PG 8 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA UA252 UT WOS:A1996UA25200011 PM 8852914 ER PT J AU Hall, CB Chesney, PJ Gromisch, DS Halsey, NA Kohl, S Marcy, SM Marks, MI Nankervis, GA Overall, JC Pickering, LK Steele, RW Yogev, R Peter, G Berkelman, RL Orenstein, WA Hardegree, MC Jacobs, RF MacDonald, NE Rabinovich, NR Hall, MS Boucher, F Delage, G FordJones, E King, SE Speert, DP Tan, BJK Friesen, FR Marchessault, V Carlson, JAK Scheifele, DW Waters, JR AF Hall, CB Chesney, PJ Gromisch, DS Halsey, NA Kohl, S Marcy, SM Marks, MI Nankervis, GA Overall, JC Pickering, LK Steele, RW Yogev, R Peter, G Berkelman, RL Orenstein, WA Hardegree, MC Jacobs, RF MacDonald, NE Rabinovich, NR Hall, MS Boucher, F Delage, G FordJones, E King, SE Speert, DP Tan, BJK Friesen, FR Marchessault, V Carlson, JAK Scheifele, DW Waters, JR TI Meningococcal disease prevention and control strategies for practice-based physicians SO PEDIATRICS LA English DT Article ID CAPSULAR POLYSACCHARIDE VACCINE; SINGLE-DOSE CIPROFLOXACIN; A NEISSERIA-MENINGITIDIS; NASOPHARYNGEAL CARRIERS; EPIDEMIC; POPULATION; CHILDREN; INFANTS; OUTBREAK; CONTACTS AB Localized outbreaks of meningococcal disease in the United States and Canada continue to cause serious alarm within communities as a result of the fulminating pattern of the disease, high mortality rate, and high incidence among adolescents. The increasing number of outbreaks since 1991 has raised questions about the management and prevention of further cases during an outbreak. The purpose of this statement is to guide primary-care physicians in their role in infection control and prevention of both sporadic cases and outbreaks of invasive meningococcal disease. This statement provides information on the epidemiology of meningococcal disease, including definitions of sporadic, secondary, and coprimary cases, clusters of cases, and outbreaks. Data are presented on identification of cases, disease risk of contacts, and agents for chemoprophylaxis, and recommendations are given for: (I) risk assessment of contacts, (2) administration of chemoprophylaxis, (3) appropriate use of meningococcal. vaccine, (4) appropriate use of the microbiology laboratory, (5) the necessity for timely and appropriate reporting of invasive meningococcal disease to local public health authorities, and (6) information on counseling and public education that may be helpful during an outbreak to minimize public anxiety. An additional section, ''Information for Sharing,'' which uses a question-and-answer format and which may be helpful to parents and community and health care workers during an outbreak, is also provided. C1 CDCP,ATLANTA,GA. US FDA,ROCKVILLE,MD 20857. AMER THORAC SOC,NEW YORK,NY. NIH,BETHESDA,MD 20892. AMER ACAD PEDIAT,EVANSTON,IL. NR 69 TC 23 Z9 25 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAR PY 1996 VL 97 IS 3 BP 404 EP 412 PG 9 WC Pediatrics SC Pediatrics GA TY580 UT WOS:A1996TY58000023 ER PT J AU Klish, WJ Baker, SS Flores, CA Georgieff, MK Lake, AM Leibel, RL Udall, JN Cheney, M Daniels, PN Harris, SS Hubbard, VS Levin, E Prendergast, A Smith, AE Yetley, E Yip, R Zlotkin, S Lauer, RM Bell, EF AF Klish, WJ Baker, SS Flores, CA Georgieff, MK Lake, AM Leibel, RL Udall, JN Cheney, M Daniels, PN Harris, SS Hubbard, VS Levin, E Prendergast, A Smith, AE Yetley, E Yip, R Zlotkin, S Lauer, RM Bell, EF TI Aluminum toxicity in infants and children SO PEDIATRICS LA English DT Article ID CHRONIC-RENAL-FAILURE; PARENTERAL-NUTRITION; CALCIUM ACETATE; ENCEPHALOPATHY; DIALYSIS; INTOXICATION; ACCUMULATION; HYDROXIDE; UREMIA; BONE C1 BUR NUTR SCI,OTTAWA,ON,CANADA. USDA,WASHINGTON,DC 20250. NIDDKD,BETHESDA,MD 20892. NICHHD,BETHESDA,MD 20892. AMER DIETET ASSOC,CHICAGO,IL. US FDA,ROCKVILLE,MD 20857. CDCP,ATLANTA,GA 30341. NR 35 TC 35 Z9 36 U1 1 U2 3 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAR PY 1996 VL 97 IS 3 BP 413 EP 416 PG 4 WC Pediatrics SC Pediatrics GA TY580 UT WOS:A1996TY58000024 ER PT J AU Heyman, RB Adger, H Anglin, TM Fuller, PG Jacobs, EA Shah, RZ Tenenbein, M Armentano, M Boyd, GM Czechowicz, D Chilton, L Bordurtha, J FreelandHyde, BT Goodrich, J Grossman, D Jantz, J Mandell, F Baker, FW Bell, J Wilson, HL AF Heyman, RB Adger, H Anglin, TM Fuller, PG Jacobs, EA Shah, RZ Tenenbein, M Armentano, M Boyd, GM Czechowicz, D Chilton, L Bordurtha, J FreelandHyde, BT Goodrich, J Grossman, D Jantz, J Mandell, F Baker, FW Bell, J Wilson, HL TI Inhalant abuse SO PEDIATRICS LA English DT Article ID VOLATILE SUBSTANCE ABUSE; OPTIC NEUROPATHY; DRUG-USE; TOLUENE; ADDICTION; ACIDOSIS; YOUTH C1 NIAAA,ROCKVILLE,MD 20852. NIDA,LEXINGTON,KY 40583. NR 37 TC 27 Z9 27 U1 2 U2 3 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAR PY 1996 VL 97 IS 3 BP 420 EP 423 PG 4 WC Pediatrics SC Pediatrics GA TY580 UT WOS:A1996TY58000026 ER PT J AU Mienville, JM Barker, JL AF Mienville, JM Barker, JL TI Immature properties of large-conductance calcium-activated potassium channels in rat neuroepithelium SO PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY LA English DT Article DE large-conductance Ca-activated K channels; single-channel recording; development; telencephalon; neuroepithelium; proteolytic modifications; trypsin; charybdotoxin ID CA-2+-ACTIVATED K+ CHANNELS; HIPPOCAMPAL-NEURONS; SPINAL NEURONS; MUSCLE-CELLS; MEMBRANE; KINETICS; BILAYERS; BRAIN AB The pharmacological and biophysical properties of large-conductance Ca-activated K (BK) channels from embryonic rat telencephalic neuroepithelium were investigated with in situ patch-clamp techniques. A fraction of these channels exhibited properties characteristic of BK channels recorded in well differentiated cells, including normal gating mode (BKN channels). The vast majority of BK channels expressed distinctive properties, the most conspicuous being their buzz gating mode (BKB channels). BKB channels were insensitive to a concentration of charybdotoxin that completely and reversibly blocked BKN channels. In contrast with the strict dependence of BKN channel activation on cytoplasmic Ca, BKB channels displayed substantially high open probability (P-o) after inside-out patch excision in a Ca-free medium. Intracellular trypsin down-regulated the P-o of BKB channels, which then exhibited a greater sensitivity to cytoplasmic Ca, mainly in the positive direction (increased P-o with increased Ca). This suggested a modulatory role for Ca as opposed to its gating role in BKN channels. Ca ions also reduced current amplitude of both types of channels. BKB channels were less voltage sensitive than BKN channels, but this was not correlated with their lower Ca sensitivity. We speculate that BKB channels may represent immature forms in the developmental expression of BK channels. RP Mienville, JM (reprint author), NINCDS,NIH,NEUROPHYSIOL LAB,BLDG 36,ROOM 2CO2,36 CONVENT DR,MSC 4066,BETHESDA,MD 20892, USA. NR 36 TC 12 Z9 12 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0031-6768 J9 PFLUG ARCH EUR J PHY JI Pflugers Arch. PD MAR PY 1996 VL 431 IS 5 BP 763 EP 770 DI 10.1007/BF02253841 PG 8 WC Physiology SC Physiology GA UB048 UT WOS:A1996UB04800013 PM 8596728 ER PT J AU Elmer, GI Gorelick, DA Goldberg, SR Rothman, RB AF Elmer, GI Gorelick, DA Goldberg, SR Rothman, RB TI Acute sensitivity vs context-specific sensitization to cocaine as a function of genotype SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE sensitization; cocaine; behavior genetics; locomotor activity ID VENTRAL TEGMENTAL AREA; BEHAVIORAL SENSITIZATION; NUCLEUS-ACCUMBENS; DEPENDENT SENSITIZATION; AMPHETAMINE; MICE; MORPHINE; EXPRESSION; STRAINS; MOUSE AB Individual variability in the acute and chronic effects of psychomotor stimulants is due, in part, to genetic factors. The purpose of this series of studies was to utilize a behavioral model of sensitization, namely increased locomotor activity, to assess individual variability in sensitization to the chronic effects of cocaine and its relationship to the acute stimulant effects of cocaine. Because the degree of sensitization is proportional to the training dose, genetic differences in acute sensitivity to cocaine were assessed and incorporated into the sensitization paradigm. Acute sensitivity and context-dependent sensitization were determined in six inbred mouse strains. Large quantitative and qualitative differences were found in the acute potency and efficacy of cocaine to stimulate locomotor activity. The ED(50) was higher in the strains in which cocaine was most efficacious. Context-specific sensitization was determined via chronic administration of equiactive doses of cocaine (ED(50)) specifically paired with the test apparatus or with the home colony. Sensitization was time, environment, and genotype dependent. The differences in the number of trials required to show sensitization were unrelated to the acute locomotor stimulant effects of cocaine. These findings suggest that acute cocaine-induced locomotor activity and context-specific sensitization reflect different pharmacological properties of cocaine. C1 NIDA, NIH, DIV INTRAMURAL RES, CLIN PSYCHOPHARMACOL SECT, BALTIMORE, MD 21224 USA. NIDA, NIH, DIV INTRAMURAL RES, PHARMACOTHERAPY SECT, BALTIMORE, MD 21224 USA. RP Elmer, GI (reprint author), NIDA, NIH,DIV INTRAMURAL RES, BEHAV PHARMACOL & GENET SECT,4940 EASTERN AVE, POB 5180, BALTIMORE, MD 21224 USA. NR 47 TC 23 Z9 23 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD MAR PY 1996 VL 53 IS 3 BP 623 EP 628 DI 10.1016/0091-3057(95)02062-4 PG 6 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA TX845 UT WOS:A1996TX84500021 PM 8866964 ER PT J AU Wong, G Sarviharju, M Toropainen, M Matecka, D Korpi, ER AF Wong, G Sarviharju, M Toropainen, M Matecka, D Korpi, ER TI Pharmacologic actions of subtype-selective and novel GABAergic ligands in rat lines with differential sensitivity to ethanol SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE alcohol sensitivity; benzodiazepine receptors; GABA(A) receptor subtypes; zolpidem; bretazenil ZG-63; loreclezole; selected rat lines ID INSENSITIVE BENZODIAZEPINE RECEPTORS; GABA-A RECEPTORS; INDUCED MOTOR IMPAIRMENT; LOW ALCOHOL SENSITIVITY; RO 15-4513; PARTIAL AGONIST; BINDING-SITES; DIAZEPAM; LORECLEZOLE; ZOLPIDEM AB Alcohol-nontolerant (ANT) rats, produced by selective breeding for high sensitivity to motor-impairing effects of ethanol, have a point mutation in the cerebellar gamma-aminobutyric acid type A (GABA(A)) receptor alpha 6 subunit, which has been proposed to underlie enhanced sensitivity to benzodiazepine agonists as well. We compared ANT and alcohol-tolerant (AT) rats using behavioral and neurochemical methods to assess the significance of alpha 6- and non alpha 6-containing GABA(A) receptor subtypes. Motor performance in a tilting plane test was largely unaffected by a type I benzodiazepine receptor-preferring agonist, zolpidem [1-10 mg/kg, intraperitoneally (IP)], partial benzodiazepine agonists bretazenil and ZG-63 (both at 40 mg/kg, IF), and a novel broad-spectrum anticonvulsant loreclezole (40 mg/kg, IF) in both ANT and AT rats. In contrast, diazepam (10 mg/kg, IF) impaired performance of the ANT but not AT animals. These data, supported by results from blain regional autoradiography of [H-3]Ro15-4513 and membrane binding of [H-3]ZG-63 and [S-35]TBPS as influenced by these ligands, strongly suggest that only ligands with full agonist actions on mutant (ANT) but not wild-type (AT) alpha 6-containing GABA(A) receptors are able to produce motor impairment in the ANT rats. C1 ALKO GRP LTD,BIOMED RES CTR,SF-00101 HELSINKI,FINLAND. NIDDKD,NIH,MED CHEM LAB,BETHESDA,MD 20892. NR 40 TC 21 Z9 21 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD MAR PY 1996 VL 53 IS 3 BP 723 EP 730 DI 10.1016/0091-3057(95)02076-4 PG 8 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA TX845 UT WOS:A1996TX84500034 PM 8866977 ER PT J AU Sabra, K Wilson, H Gallelli, JF AF Sabra, K Wilson, H Gallelli, JF TI Isolators in pharmacy practice - Guidelines used in the United Kingdom and Ireland SO PHARMACOPEIAL FORUM LA English DT Article C1 NIH,WARREN G MAGNUSON CLIN CTR,BETHESDA,MD 20892. RP Sabra, K (reprint author), ST JAMES HOSP,DUBLIN 8,IRELAND. NR 3 TC 2 Z9 2 U1 0 U2 0 PU US PHARMACOPEIAL CONVENTION PI ROCKVILLE PA 12601 TWINBROOK PKWY, ROCKVILLE, MD 20852 SN 0363-4655 J9 PHARMACOPEIAL FORUM JI Pharmacop. Forum PD MAR-APR PY 1996 VL 22 IS 2 BP 2216 EP 2219 PG 4 WC Medicine, Legal; Pharmacology & Pharmacy SC Legal Medicine; Pharmacology & Pharmacy GA UA254 UT WOS:A1996UA25400006 ER PT J AU Paruszewski, R RostafinskaSuchar, G Strupinska, M Jaworski, P Stables, JP AF Paruszewski, R RostafinskaSuchar, G Strupinska, M Jaworski, P Stables, JP TI Synthesis and anticonvulsant activity of some amino acid derivatives .1. Alanine derivatives SO PHARMAZIE LA English DT Article ID ANTIEPILEPTIC DRUG DEVELOPMENT; NMDA RECEPTOR; EPILEPSY; ANTAGONISTS; POTENT; SERIES AB Fifteen amides of N-substituted D-Ala, DL-Ala and beta Ala have been designed and synthesized as potential anticonvulsants. All obtained amides as well as one intermediate (8) were evaluated in the maximal electroshock seizure (MES) test, the subcutaneous Metrazol seizure threshold (sc Met) test and the rotorod neurotoxicity (Tox) test in mice. According to the classification of the Anticonvulsant Screening Project (ASP) of the Antiepileptic Drug Development Program (ADDP) eight compounds received class I, three class II and five class III designations. Two of the most active compounds (20, 24) were tested quantitatively. They exhibited, after i.p. administration in mice, a large protective index (PI) 3.2 for 20 and 4.3 for 24 and after oral administration in rat PI > 18 for 20 and > 14 for 24. C1 MED UNIV,DEPT PHARMACEUT CHEM,WARSAW,POLAND. NINCDS,DIV CONVULS DEV & NEUROMUSCULAR DISORDERS,NIH,BETHESDA,MD. NR 13 TC 15 Z9 16 U1 0 U2 3 PU GOVI-VERLAG GMBH PI ESCHBORN PA PHARMAZEUTISCHER VERLAG GINNHEIMER STRASSE 26, D-65760 ESCHBORN, GERMANY SN 0031-7144 J9 PHARMAZIE JI Pharmazie PD MAR PY 1996 VL 51 IS 3 BP 145 EP 148 PG 4 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA UB856 UT WOS:A1996UB85600002 PM 8900864 ER PT J AU Rashid, MA Gustafson, KR Cardellina, JH Boyd, MR AF Rashid, MA Gustafson, KR Cardellina, JH Boyd, MR TI A benzoic acid glycoside from Geniostoma antherotrichum SO PHYTOCHEMISTRY LA English DT Article DE Geniostoma antherotrichum; loganiaceae; benzoic acid glycoside; HIV-inhibitory tannins ID NATURAL-PRODUCTS AB Fractionation of an HIV-inhibitory organic extract of Geniostoma antherotrichum afforded a glycoside derivative, which has been characterized as 2-hydroxy-3-O-beta-D-glucopyranosyl-benzoic acid (1) on the basis of spectral analyses. The HIV-inhibitory activity of the extract was traced to polymeric tannins, while 1 was found to be inactive in the National Cancer Institute's primary anti-HIV screen. C1 UNIV DHAKA,DEPT PHARM,DHAKA 1000,BANGLADESH. RP Rashid, MA (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,LAB DRUG DISOCVERY RES & DEV,BLDG 1052,RM 121,FREDERICK,MD 21702, USA. NR 7 TC 9 Z9 10 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9422 J9 PHYTOCHEMISTRY JI Phytochemistry PD MAR PY 1996 VL 41 IS 4 BP 1205 EP 1207 DI 10.1016/0031-9422(95)00768-7 PG 3 WC Biochemistry & Molecular Biology; Plant Sciences SC Biochemistry & Molecular Biology; Plant Sciences GA TX847 UT WOS:A1996TX84700036 PM 8728720 ER PT J AU Izumi, S Slayden, OD Rubin, JS Brenner, RM AF Izumi, S Slayden, OD Rubin, JS Brenner, RM TI Keratinocyte growth factor and its receptor in the rhesus macaque placenta during the course of gestation SO PLACENTA LA English DT Article ID MESENCHYMAL-EPITHELIAL INTERACTIONS; TROPHOBLASTIC INVASION; INSITU HYBRIDIZATION; ANTIBODY KI-67; LOCALIZATION; EXPRESSION; ANTIGEN; CELLS; DIFFERENTIATION; PURIFICATION AB Keratinocyte growth factor (KGF) is synthesized and secreted exclusively by mesenchymal cells, and acts through its receptor (KGFR) to stimulate epithelial proliferation. In vivo, KGF and KGFR comprise a mesenchymal-epithelial cell paracrine system that can mediate epithelial cell mitosis. In preliminary work, we noted that KGF was expressed in the rhesus monkey placenta, and we now report on the expression of placental KGF and KGFR mRNAs during the course of gestation in this species. In-situ hybridization revealed that during early gestation, KGF mRNA was strongly expressed in placental mesenchymal cells. These cells, which were also immunoreactive for vimentin, were mainly located on the periphery of the mesenchymal cores of both anchoring and floating villi. KGFR mRNA was expressed in the adjacent trophoblastic epithelium, which was immunoreactive for cytokeratin. In-situ hybridization revealed that KGF mRNA expression was very high in the youngest placentae (34-days gestation) and decreased gradually to minimal levels by late gestation (157 days). Northern blot analysis indicated also that the KGF MRNA signal was strongest in early gestation samples and weakest by late gestation. Analysis for KGFR mRNA by a reverse transcriptase-polymerase chain reaction technique showed that KGFR mRNA expression could be detected at all stages. However, in-situ hybridization indicated that KGFR mRNA expression was highest in early gestation placentae and least in the oldest placentae. Autoradiographs of frozen sections of placenta that had been incubated with [I-125]KGF to detect receptor binding showed that grain density over the trophoblast was highest in the youngest and least in the oldest placentae. PCNA and Ki-67 expression followed this same temporal trend. We conclude that the KGF/KGFR system may be important in proliferation of the placental trophoblast during early- to mid-pregnancy in rhesus monkeys. (C) 1996 W. B. Saunders Company Ltd C1 OREGON REG PRIMATE RES CTR,DIV REPROD SCI,BEAVERTON,OR 97006. NAGASAKI UNIV,SCH MED,DEPT ANAT 3,NAGASAKI 852,JAPAN. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. FU NICHD NIH HHS [HD07675, HD19182, HD18185] NR 43 TC 16 Z9 16 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0143-4004 J9 PLACENTA JI Placenta PD MAR-APR PY 1996 VL 17 IS 2-3 BP 123 EP 135 DI 10.1016/S0143-4004(96)80005-1 PG 13 WC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology SC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology GA UF160 UT WOS:A1996UF16000005 PM 8730882 ER PT J AU Goldman, D AF Goldman, D TI Interdisciplinary perceptions of genetics and behavior SO POLITICS AND THE LIFE SCIENCES LA English DT Article; Proceedings Paper CT University-of-Maryland Conference on Research on Genetics and Criminal Behavior - Scientific Issues, Social and Political Implications CY SEP 22-24, 1995 CL ASPEN INST, WYE CTR, QUEENSTOWN, MD SP Univ Maryland, School Public Affairs, Inst Philos & Public Policy HO ASPEN INST, WYE CTR RP Goldman, D (reprint author), NIAAA,NEUROGENET LAB,12501 WASHINGTON AVE,ROOM 2,ROCKVILLE,MD 20852, USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BEECH TREE PUBLISHING PI GUILDFORD PA 10 WATFORD CLOSE, GUILDFORD, SURREY, ENGLAND GU1 2EP SN 0730-9384 J9 POLIT LIFE SCI JI Polit. Life Sci. PD MAR PY 1996 VL 15 IS 1 BP 97 EP 98 PG 2 WC Biology; History & Philosophy Of Science; Social Issues SC Life Sciences & Biomedicine - Other Topics; History & Philosophy of Science; Social Issues GA UM151 UT WOS:A1996UM15100024 PM 11655030 ER PT J AU Glasgow, RE Sorensen, G Giffen, C Shipley, RH Corbett, K Lynn, W AF Glasgow, RE Sorensen, G Giffen, C Shipley, RH Corbett, K Lynn, W TI Promoting worksite smoking control policies and actions: The Community Intervention Trial for Smoking Cessation (COMMIT) Experience SO PREVENTIVE MEDICINE LA English DT Article AB Background. As an important aspect of the COMMIT trial, worksite smoking-control consultations and supports were provided to employers in 11 diverse, moderate-sized communities. After a 4-year intervention period (1989-1992), impacts on worksite policies, support resources for smokers, and employee perceptions were assessed in these communities and in 11 matched Comparison communities. Methods. Data from two surveys are reported here. In each of the 22 COMMIT communities, a sample of worksites within each of four size strata were surveyed to determine worksite policies, activities, and resources regarding smoking. Data from employees were obtained from independent community-wide surveys of community residents. Results. Overall, 44% of the worksites surveyed reported having smokefree policies, with no differences between Intervention and Comparison communities. Thirty-seven percent of Intervention community worksites reported offering smoking cessation resources or assistance for employees during the period of the study, compared to 31% of Comparison community worksites (P = 0.04). Employees in Intervention communities, relative to those in Comparison communities, reported greater awareness of stop-smoking resources, but equivalent increases in worksite smoking bans. Conclusion. Although the level of worksite smoking-cessation activities was higher in Intervention than in Comparison communities, there remains a substantial need to increase the level of such activities and to integrate such activities with restrictive smoking policies. (C) 1996 Academic Press, Inc. C1 HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02138. INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. DUKE UNIV,MED CTR,DURHAM,NC 27708. VET AFFAIRS MED CTR,DURHAM,NC 27708. UNIV COLORADO,DEPT ANTHROPOL,DENVER,CO 80217. NCI,NIH,BETHESDA,MD 20892. RP Glasgow, RE (reprint author), OREGON RES INST,1715 FRANKLIN BLVD,EUGENE,OR 97403, USA. FU NCI NIH HHS [CN55513-38] NR 25 TC 18 Z9 18 U1 1 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0091-7435 J9 PREV MED JI Prev. Med. PD MAR-APR PY 1996 VL 25 IS 2 BP 186 EP 194 DI 10.1006/pmed.1996.0045 PG 9 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA UK038 UT WOS:A1996UK03800013 PM 8860284 ER PT J AU Caplan, LS Helzlsouer, KJ Shapiro, S Wesley, MN Edwards, BK AF Caplan, LS Helzlsouer, KJ Shapiro, S Wesley, MN Edwards, BK TI Reasons for delay in breast cancer diagnosis SO PREVENTIVE MEDICINE LA English DT Article ID SURVIVAL; STAGE; WOMEN AB Background. A study of system delay, the time between the initial medical consultation and the establishment of a diagnosis, in breast cancer patients revealed that almost 40% of women reported delays of at least 4 weeks. The objective of this study was to explore the reasons for these prolonged intervals between initial medical consultation and establishment of a diagnosis. Methods. A total of 367 female breast cancer patients from the National Cancer Institute's Black/White Cancer Survival Study were studied, Medical systems involved in the diagnosis and treatment of these women included hospital outpatient and emergency room, private clinic, public clinic, private doctor, and health maintenance organization. Results. In about 25% of the cases, the delay was attributed by the woman to the patient herself, and the most common reason she gave was that she felt that the problem was not important. In about 45% of the cases, the provider and the health care system were said to be responsible for the delay through difficulties in scheduling or physician inaction, while in another 17% both the patient and the system were responsible. Conclusions. This study looked at the issue of how the behaviors of women and their providers contribute to the timing of breast cancer diagnosis. It is one of the only studies to examine the woman's role in delay. It is clear from this study that additional work is needed to look at this question. However, the results of this study suggest that efforts must be made to reduce the time needed to get an appointment with a physician or a diagnostic test, as well as to educate physicians and the women themselves regarding the importance of breast symptoms and the value of prompt evaluation, diagnosis, and treatment. (C) 1996 Academic Press, Inc. C1 SUNY STONY BROOK,DEPT PREVENT MED,DIV EPIDEMIOL,STONY BROOK,NY 11794. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT HLTH POLICY & MANAGEMENT,DIV HLTH SERV RES,BALTIMORE,MD 21218. INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. NCI,OFF ASSOCIATE DIRECTOR,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. NR 21 TC 66 Z9 69 U1 3 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0091-7435 J9 PREV MED JI Prev. Med. PD MAR-APR PY 1996 VL 25 IS 2 BP 218 EP 224 DI 10.1006/pmed.1996.0049 PG 7 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA UK038 UT WOS:A1996UK03800017 PM 8860288 ER PT J AU FREDERICKSON, DS AF FREDERICKSON, DS TI SHANNON,JAMES,AUGUSTINE (AUGUST-9,1904 MAY-20,1994) SO PROCEEDINGS OF THE AMERICAN PHILOSOPHICAL SOCIETY LA English DT Item About an Individual RP FREDERICKSON, DS (reprint author), NATL LIB MED,BETHESDA,MD 20209, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER PHILOSOPHICAL SOC PI PHILADELPHIA PA 104 SOUTH FIFTH ST, PHILADELPHIA, PA 19106-3387 SN 0003-049X J9 P AM PHILOS SOC JI Proc. Amer. Philos. Soc. PD MAR PY 1996 VL 140 IS 1 BP 106 EP 113 PG 8 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA UC718 UT WOS:A1996UC71800010 ER PT J AU Chanock, RM AF Chanock, RM TI Reminiscences of Albert Sabin and his successful strategy for the development of the live oral poliovirus vaccine SO PROCEEDINGS OF THE ASSOCIATION OF AMERICAN PHYSICIANS LA English DT Article ID SEQUENCE; MUTATION; VIRUS RP Chanock, RM (reprint author), NIAID, NIH,INFECT DIS LAB,BLDG 7,ROOM 100,7 CTR DR, MSC 0720, BETHESDA, MD USA. NR 32 TC 3 Z9 4 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 1081-650X J9 P ASSOC AM PHYSICIAN JI Proc. Assoc. Am. Phys. PD MAR PY 1996 VL 108 IS 2 BP 117 EP 126 PG 10 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA UC169 UT WOS:A1996UC16900001 PM 8705731 ER PT J AU Romero, R Munoz, H Gomez, R Parra, M Polanco, M Valverde, V Hasbun, J Garrido, J Ghezzi, F Mazor, M Tolosa, JE Mitchell, MD AF Romero, R Munoz, H Gomez, R Parra, M Polanco, M Valverde, V Hasbun, J Garrido, J Ghezzi, F Mazor, M Tolosa, JE Mitchell, MD TI Increase in prostaglandin bioavailability precedes the onset of human parturition SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID AMNIOTIC-FLUID; LABOR; PREGNANCY AB The traditional paradigm that prostaglandins (PGs) are of central importance in the initiation of labor has been challenged. A group of investigators has recently reported that the amniotic fluid concentrations of PGE(2) and PGF(2 alpha) increase only late in the course of labor implying that 'the accumulation of prostaglandins in amniotic fluid is an after-effect of labor and not indicative of a role of these compounds in the initiation of human parturition'. The present study was conducted to determine whether amniotic fluid prostaglandin concentrations increase prior to the onset of human labor, the central question in this controversy. Three amniocenteses were performed in 17 women with intrahepatic cholestasis of pregnancy - the first two prior to the onset of labor and the third during early spontaneous labor. PGE(2) and PGF(2 alpha) were measured with sensitive and specific radioimmunoassays. Amniotic fluid concentrations of PGE(2) and PGF(2 alpha) increased prior to the onset of spontaneous labor. An additional increase in the concentrations of PGE(2) and PGF(2 alpha) was found in samples obtained in early labor. We conclude that an increase in prostaglandin bioavailability precedes the onset of spontaneous human parturition. C1 UNIV CHILE,SANTIAGO,CHILE. UNIV UTAH,SALT LAKE CITY,UT. RP Romero, R (reprint author), NICHHD,PERINATOL RES BRANCH,INTRAMURAL DIV,BETHESDA,MD 20892, USA. RI Mitchell, Murray/A-8639-2010; OI Mitchell, Murray/0000-0002-6167-7176; Ghezzi, Fabio/0000-0003-3949-5410 NR 24 TC 81 Z9 82 U1 0 U2 4 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD MAR PY 1996 VL 54 IS 3 BP 187 EP 191 DI 10.1016/S0952-3278(96)90015-0 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA UG246 UT WOS:A1996UG24600005 PM 8860106 ER PT J AU Yamazaki, T Hinck, AP Wang, YX Nicholson, LK Torchia, DA Wingfield, P Stahl, SJ Kaufman, JD Chang, CH Domaille, PJ Lam, PYS AF Yamazaki, T Hinck, AP Wang, YX Nicholson, LK Torchia, DA Wingfield, P Stahl, SJ Kaufman, JD Chang, CH Domaille, PJ Lam, PYS TI Three-dimensional solution structure of the HIV-1 protease complexed with DMP323, a novel cyclic urea-type inhibitor, determined by nuclear magnetic resonance spectroscopy SO PROTEIN SCIENCE LA English DT Article DE comparison to crystal structure; cyclic urea inhibitor; HIV-1 protease; protease inhibitor; protein flexibility; protein structure; NMR ID HUMAN IMMUNODEFICIENCY VIRUS; DISTANCE GEOMETRY; LARGER PROTEINS; SPECTRA; H-1-NMR; N-15; NMR AB The three-dimensional solution structure of the HIV-1 protease homodimer, MW 22.2 kDa, complexed to a potent, cyclic urea-based inhibitor, DMP323, is reported. This is the first solution structure of an HIV protease/inhibitor complex that has been elucidated. Multidimensional heteronuclear NMR spectra were used to assemble more than 4,200 distance and angle constraints. Using the constraints, together with a hybrid distance geometry/simulated annealing protocol, an ensemble of 28 NMR structures was calculated having no distance or angle violations greater than 0.3 Angstrom or 5 degrees, respectively. Neglecting residues in disordered loops, the RMS deviation (RMSD) for backbone atoms in the family of structures was 0.60 Angstrom relative to the average structure. The individual NMR structures had excellent covalent geometry and stereochemistry, as did the restrained minimized average structure. The latter structure is similar to the 1.8-Angstrom X-ray structure of the protease/DMP323 complex (Chang CH et al., 1995, Protein Science, submitted); the pairwise backbone RMSD calculated for the two structures is 1.22 Angstrom. As expected, the mismatch between the structures is greatest in the loops that are disordered and/or flexible. The flexibility of residues 37-42 and 50-51 may be important in facilitating substrate binding and product release, because these residues make up the respective hinges and tips of the protease flaps. Flexibility of residues 4-8 may play a role in protease regulation by facilitating autolysis. C1 NIH,PROT EXPRESS LAB,BETHESDA,MD 20892. NIDR,STRUCT MOLEC BIOL UNIT,BETHESDA,MD 20892. DUPONT MERCK PHARMACEUT CO,DEPT CHEM & PHYS SCI,WILMINGTON,DE 19880. NR 37 TC 63 Z9 64 U1 1 U2 4 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0961-8368 J9 PROTEIN SCI JI Protein Sci. PD MAR PY 1996 VL 5 IS 3 BP 495 EP 506 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TY946 UT WOS:A1996TY94600011 PM 8868486 ER PT J AU Brando, LJ Yolken, R Herman, MM Kleinman, JE Ross, CA Torrey, EF AF Brando, LJ Yolken, R Herman, MM Kleinman, JE Ross, CA Torrey, EF TI Analysis of the DRPLA triplet repeat in brain tissue and leukocytes from schizophrenics SO PSYCHIATRIC GENETICS LA English DT Article DE DRPLA; schizophrenia; triplet repeats ID EXPRESSION; GENES AB An expansion of the CAG triplet in the human gene called atrophin-1 or CTG-B37 causes the neuropsychiatric disease known as dentatorubral-pallidoluysian atrophy (DRPLA). We have examined the genomic DNA from brains and peripheral blood leukocytes (PBLs) of schizophrenic and non-schizophrenic individuals and PBLs from a cohort of monozygotic twins discordant or concordant for schizophrenia, for expansions of the CTG-B37 region. AU samples, including non-schizophrenic/normal controls, had 7-22 CAG repeats in this region. Thus we found no evidence for an expansion of the DRPLA triplet repeat associated with schizophrenia when compared to controls. Our data suggest that an expansion in the CTG-B37 gene is not linked to or responsible for the disease schizophrenia. C1 JOHNS HOPKINS UNIV,DEPT PEDIAT,STANLEY LAB STUDY SCHIZOPHRENIA & BIPOLAR DIS,BALTIMORE,MD 21218. NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,WASHINGTON,DC 20032. JOHNS HOPKINS UNIV,DEPT PSYCHIAT,MOLEC NEUROBIOL LAB,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,DEPT NEUROSCI,BALTIMORE,MD 21205. RI Ross, Christopher/H-8395-2013 NR 16 TC 14 Z9 14 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8829 J9 PSYCHIATR GENET JI Psychiatr. Genet. PD SPR PY 1996 VL 6 IS 1 BP 1 EP 5 DI 10.1097/00041444-199621000-00001 PG 5 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA UC044 UT WOS:A1996UC04400001 PM 8925251 ER PT J AU Guedj, F Cao, Q Cravchik, A Ram, A Badner, J Gershon, ES Gejman, PV AF Guedj, F Cao, Q Cravchik, A Ram, A Badner, J Gershon, ES Gejman, PV TI Analysis of DRPLA trinucleotide repeats in schizophrenia SO PSYCHIATRIC GENETICS LA English DT Article DE anticipation; dentarubral; pallidoluysian atrophy; DRPLA; expansion; schizophrenia; sequences ID SCHIZOAFFECTIVE DISORDER C1 NIMH,UNIT MOL CLIN INVEST,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. NR 7 TC 1 Z9 1 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8829 J9 PSYCHIATR GENET JI Psychiatr. Genet. PD SPR PY 1996 VL 6 IS 1 BP 33 EP 34 DI 10.1097/00041444-199621000-00007 PG 2 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA UC044 UT WOS:A1996UC04400007 PM 8925256 ER PT J AU Klerman, GL Leon, AC Wickramaratne, P Warshaw, MG Mueller, TI Weissman, MM Akiskal, H AF Klerman, GL Leon, AC Wickramaratne, P Warshaw, MG Mueller, TI Weissman, MM Akiskal, H TI The role of drug and alcohol abuse in recent increases in depression in the US SO PSYCHOLOGICAL MEDICINE LA English DT Article ID MAJOR DEPRESSION; SECULAR TRENDS; PSYCHIATRIC-DISORDERS; UNITED-STATES; COLLABORATIVE PROGRAM; HOSPITALIZED-PATIENTS; DIAGNOSTIC INTERVIEW; MENTAL-DISORDERS; AGE; PREVALENCE AB Previous studies have reported an increase in depression among recent birth cohorts. Concurrent with the increase in rates of depression, there have been increases in rates of drug and alcohol abuse and dependence. This study sought to determine if the recent increase in rates of depression could be attributed to co-mol-bid alcohol and drug abuse. The data derived from two studies: (1) a sample of relatives of probands with affective disorder; and (2) a community survey of the US population. The piecewise exponential statistical model was applied to evaluate the association of gender, age, period and birth cohort with rates of major depressive disorder (MDD) separately for those with, and without, diagnoses of alcohol or drug abuse. Elevated rates of MDD occurred among those with co-morbid drug and alcohol abuse in both the family and community samples. However, there were also temporal increases in rates of MDD in those with no such co-morbidity. Specifically there were effects of age and gender for both studies; in addition, there was a period effect in the family study and a birth cohort effect in the community sample. The recent increases in depression in the US cannot be accounted for solely by concurrent increases in co-morbid drug and alcohol abuse. Temporal (period and cohort) effects on rates of depression occur in addition to the contribution of co-morbid drug and alcohol abuse or dependence. C1 CORNELL UNIV MED COLL,DEPT PSYCHIAT,NEW YORK,NY 10021. BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI. COLUMBIA UNIV,COLL PHYS & SURG,DEPT PSYCHIAT,NEW YORK,NY 10027. NEW YORK STATE PSYCHIAT INST & HOSP,DEPT GEN & GENET EPIDEMIOL,NEW YORK,NY. NIMH,OFF DIRECTOR,ROCKVILLE,MD 20857. OI Weissman, Myrna/0000-0003-3490-3075 FU NIMH NIH HHS [R0-1-MH-43044, UO-1-MH-43077] NR 41 TC 15 Z9 15 U1 2 U2 6 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD MAR PY 1996 VL 26 IS 2 BP 343 EP 351 PG 9 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA UA855 UT WOS:A1996UA85500013 PM 8685290 ER PT J AU Faraone, SV Blehar, M Pepple, J Moldin, SO Norton, J Nurnberger, JI Malaspina, D Kaufmann, CA Reich, T Cloninger, CR DePaulo, JR Berg, K Gershon, ES Kirch, DG Tsuang, MT AF Faraone, SV Blehar, M Pepple, J Moldin, SO Norton, J Nurnberger, JI Malaspina, D Kaufmann, CA Reich, T Cloninger, CR DePaulo, JR Berg, K Gershon, ES Kirch, DG Tsuang, MT TI Diagnostic accuracy and confusability analyses: An application to the diagnostic interview for genetic studies SO PSYCHOLOGICAL MEDICINE LA English DT Article ID ATTENTION-DEFICIT DISORDER; EYE TRACKING DYSFUNCTIONS; LATENT STRUCTURE-ANALYSIS; REPEATED SCREENING-TESTS; PSYCHIATRIC-DIAGNOSIS; LINKAGE ANALYSIS; SCHIZOPHRENIA; RELIABILITY; ERROR; SENSITIVITY AB The dominant, contemporary paradigm for developing and refining diagnoses relies heavily on assessing reliability with kappa coefficients and virtually ignores a core component of psychometric practice: the theory of latent structures. This article describes a psychometric approach to psychiatric nosology that emphasizes the diagnostic accuracy and confusability of diagnostic categories. We apply these methods to the Diagnostic Interview for Genetic Studies (DIGS), a structured psychiatric interview designed by the NIMH Genetics Initiative for genetic studies of schizophrenia and bipolar disorder. Our results show that sensitivity and specificity were excellent for both DSM-III-R and RDC diagnoses of major depression, bipolar disorder, and schizophrenia. In contrast, diagnostic accuracy was substantially lower for subtypes of schizoaffective disorder - especially for the DSM-III-R definitions. Both the bipolar and depressed subtypes of DSM-III-R schizoaffective disorder had excellent specificity but poor sensitivity. The RDC definitions also had excellent specificity but were more sensitive than the DSM-III-R schizoaffective diagnoses. The source of low sensitivity for schizoaffective subtypes differed for the two diagnostic systems. For RDC criteria, the schizoaffective subtypes were frequently confused with one another; they were less frequently confused with other diagnoses. In contrast, the DSM-III-R subtypes were often confused with schizophrenia, but not with each other. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS MENTAL HLTH CTR,DEPT PSYCHIAT,INST PSYCHIAT EPIDEMIOL & GENET,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. JOHNS HOPKINS UNIV,DEPT PSYCHIAT,BALTIMORE,MD. NIMH,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892. NIMH,EXTRAMURAL RES PROGRAM,BETHESDA,MD 20892. WASHINGTON UNIV,DEPT PSYCHIAT,ST LOUIS,MO. INDIANA UNIV,DEPT PSYCHIAT,BLOOMINGTON,IN 47405. COLUMBIA UNIV,DEPT PSYCHIAT,NEW YORK,NY. MED COLL GEORGIA,AUGUSTA,GA 30912. RP Faraone, SV (reprint author), VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,940 BELMONT ST,BROCKTON,MA 02401, USA. RI Cloninger, Claude/F-5357-2012; OI Cloninger, Claude/0000-0003-3096-4807; Nurnberger, John/0000-0002-7674-1767; Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [UO1 MH46274, UO1 MH46276, UO1 MH46318] NR 50 TC 70 Z9 71 U1 0 U2 4 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD MAR PY 1996 VL 26 IS 2 BP 401 EP 410 PG 10 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA UA855 UT WOS:A1996UA85500019 PM 8685296 ER PT J AU Bradley, MM Cuthbert, BN Lang, PJ AF Bradley, MM Cuthbert, BN Lang, PJ TI Lateralized startle probes in the study of emotion SO PSYCHOPHYSIOLOGY LA English DT Article DE startle; blink reflex; emotion; laterality; hemispheric specialization; affect ID HEMISPHERE AB Two experiments are reported in which affective modulation of the startle reflex elicited by monaurally presented acoustic probes was further examined. An earlier study in our laboratory obtained significant modulation by affect for probes presented to the left ear, but no significant effect for probes presented to the right ear. Experiment 1 replicated the procedures used in that experiment and obtained the same pattern of effects. Experiment 2 changed the presentation of monaural probes from a blocked to a mixed presentation and again obtained a similar pattern. Modulatory differences in reflex magnitude between pleasant and unpleasant stimuli were consistently large and reliable for reflexes elicited by left ear probes but weak and unreliable for reflexes elicited by right ear probes. RP Bradley, MM (reprint author), UNIV FLORIDA,NIMH,CTR STUDY EMOT & ATTENT,BOX 100165 HSC,GAINESVILLE,FL 32610, USA. FU NIMH NIH HHS [MH52384, MH37757, MH43973] NR 21 TC 42 Z9 43 U1 2 U2 11 PU SOC PSYCHOPHYSIOL RES PI WASHINGTON PA 1010 VERMONT AVE NW SUITE 1100, WASHINGTON, DC 20005 SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PD MAR PY 1996 VL 33 IS 2 BP 156 EP 161 DI 10.1111/j.1469-8986.1996.tb02119.x PG 6 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA TY381 UT WOS:A1996TY38100006 PM 8851243 ER PT J AU Weise, RE Blehar, MC Maser, JD Akiskal, HS AF Weise, RE Blehar, MC Maser, JD Akiskal, HS TI Competence models in adult psychopathology: A report on a National Institute of Mental Health Workshop SO PSYCHOTHERAPY LA English DT Article ID LIFE EVENTS; DEPRESSION; PERSONALITY; CHILDREN; RECOVERY; ILLNESS; STRESS; WOMEN AB Philosophers of science have repeatedly demonstrated that more than one theoretical construct can be applied to any set of observations (Hempel, 1965; Millon, 1991). With the advent of DSM-III (1980), the predominant clinical psychological/psychiatric nosology shifted from psychoanalytic, with emphases on pathological internal processes, to a new medical model focusing on definable sets of disorders. The practical consequences of these orientations have been to assess patients in terms of a variety of deficiencies that are deemed in need of therapeutic correction. Although the ''Third Force'' or Humanistic Movement led by Maslow and Rogers (DeCarvalho, 1991) provided the initiative for more strength-oriented or competence models, the predominant orientation in clinical psychology and psychiatry remains focused on the psychopathology of disease. In order to consider the usefulness of employing a ''strengths approach'' to augment the traditional risk factor model in adult mood and related disorders, the National Institute of Mental Health convened a workshop focused on psychological strengths. The workshop, titled ''Personal Resilience in Adversity and Psychopathology,'' was organized by the N.I.M.H. Mood, Anxiety, and Personality Disorders Branch. Workshop participants included Drs. Lyn Abramson, Hagop Akiskal, Lorna Benjamin, Norman Garmezy, Rodney Lowman, Frederick Rhodewalt, Martin Seligman, Steven Wolin, and Sybil Wolin. RP Weise, RE (reprint author), NIMH,5600 FISHERS LANE,ROOM 10C-16,ROCKVILLE,MD 20857, USA. NR 44 TC 3 Z9 3 U1 1 U2 3 PU AMER PSYCHOLOGICAL ASSOC, DIV PSYCHOTHERAPY PI PHOENIX PA 3900 E CAMELBACK RD #200, PHOENIX, AZ 85018 SN 0033-3204 J9 PSYCHOTHER JI Psychotherapy PD SPR PY 1996 VL 33 IS 1 BP 61 EP 67 DI 10.1037/0033-3204.33.1.61 PG 7 WC Psychology, Clinical SC Psychology GA VB910 UT WOS:A1996VB91000007 ER PT J AU Alciati, MH Glanz, K AF Alciati, MH Glanz, K TI Using data to plan public health programs: Experience from state cancer prevention and control programs SO PUBLIC HEALTH REPORTS LA English DT Article ID BREAST-CANCER AB IN 1989 THE National Cancer Institute funded the second round of Data-Based intervention Research (DBIR) cooperative agreements with state health agencies to implement a four-phase cancer prevention and control planning model that would establish ongoing cancer prevention and control programs. Activities included identifying and analyzing relevant data to develop a state cancer control plan. The authors reviewed the data analysis and planning activities of five DBIR projects to understand: how states use different types of available data to make public health planning decisions, in what ways available data were sufficient or insufficient for this planning, and the perceived costs and benefits of a data-based planning approach. Many of the sources of and ways in which health statistics and behavioral data were used were consistent across states. Sources and use of data on the availability and utilization of health services and on cancer control policies were less consistent Data were most useful in making decisions to address specific cancers, to target populations or regions, to identify general barriers, and to influence policy makers and the public. Data were less influential in identifying specific barriers within target populations and determining what proven intervention components should be implemented and how. The process of pulling this information together and involving working groups and coalitions was considered very beneficial in establishing the credibility of the state health agency in addressing the state's cancer problem. This process relied on a national infrastructure that provided financial resources, sources of data, and research results. C1 NCI,PUBL HLTH AGY SECT,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. UNIV HAWAII,CANC RES CTR HAWAII,HONOLULU,HI 96822. RP Alciati, MH (reprint author), PUBL HLTH SERV,NATL ACT PLAN BREAST CANC,OFF WOMENS HLTH,DEPT HLTH & HUMAN SERV,WASHINGTON,DC 20201, USA. OI Alciati, Marianne/0000-0001-6294-1090 NR 18 TC 10 Z9 10 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD MAR-APR PY 1996 VL 111 IS 2 BP 165 EP 172 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UD059 UT WOS:A1996UD05900041 PM 8606917 ER PT J AU JamisDow, CA Choyke, PL Jennings, SB Linehan, WM Thakore, KN Walther, MM AF JamisDow, CA Choyke, PL Jennings, SB Linehan, WM Thakore, KN Walther, MM TI Small (<=3-cm) renal masses: Detection with CT versus US and pathologic correlation SO RADIOLOGY LA English DT Article DE computed tomography (CT), comparative studies; kidney neoplasms; ultrasound (US), comparative studies; von Hippel-Lindau disease ID IMAGING FEATURES; CELL CARCINOMAS; TOMOGRAPHY AB PURPOSE: To determine the sensitivities of computed tomography (CT) and ultrasound (US) for detection and characterization of surgically verified small renal lesions. MATERIALS AND METHODS: Twenty-one patients with von Hippel-Lindau disease or hereditary papillary renal cancer underwent CT and US before partial nephrectomy or enucleation; 205 renal masses were removed (92% were <3 cm). Detection rates and accuracy of CT and US in the characterization of renal morphology were correlated with lesion size. RESULTS: CT and US detection rates for lesions of 0-5 mm were respectively 47% and 0%; 5-10 mm, 60% and 21%; 10-15 mm, 75% and 28%; 15-20 mm, 100% and 58%; 20-25 mm, 100% and 79%; and 25-30 mm, 100% and 100%. Among the lesions 10-35 mm, 80% and 82% were correctly characterized with CT and US, respectively. CONCLUSION: A substantial proportion of lesions under 1 cm were not detected with either modality. Neither CT nor US was superior in the characterization of lesions 3 cm or less. CT and particularly US screening studies in patients with von Hippel-Lindau disease should be interpreted cautiously because missed or mischaracterized small renal lesions are a frequent problem in these patients. C1 NIH,HENRY M JACKSON FDN,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,MED BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NCI,SURG BRANCH,UROL ONCOL DIV,BETHESDA,MD 20892. NR 12 TC 144 Z9 154 U1 1 U2 5 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD MAR PY 1996 VL 198 IS 3 BP 785 EP 788 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TW212 UT WOS:A1996TW21200031 PM 8628872 ER PT J AU Brown, KE Young, NS AF Brown, KE Young, NS TI Parvoviruses and bone marrow failure SO STEM CELLS LA English DT Review DE parvovirus B19 infection; bone marrow diseases; red cell aplasia; hematopoiesis; diagnosis; treatment ID RED-CELL APLASIA; IDIOPATHIC THROMBOCYTOPENIC PURPURA; HEMATOPOIETIC PROGENITOR CELLS; HUMAN-SERUM PARVOVIRUS; B19 PARVOVIRUS; TRANSIENT ERYTHROBLASTOPENIA; HEREDITARY SPHEROCYTOSIS; MALIGNANT HISTIOCYTOSIS; HEMOPHAGOCYTIC SYNDROME; PRODUCTIVE INFECTION AB Parvovirus B19, the only known human pathogenic parvovirus, is highly tropic to human bone marrow and replicates only in erythroid progenitor cells. The basis of this erythroid tropism is the tissue distribution of the B19 cellular receptor, globoside (blood group P antigen), In individuals with underlying hemolytic disorders, infection with parvovirus B19 is the primary cause of transient aplastic crisis, In immunocompromised patients, persistent B19 infection may develop that manifests as pure red cell aplasia and chronic anemia. B19 infection in utero can result in fetal death, hydrops fetalis or congenital anemia. Diagnosis is based on examination of the bone marrow and B19 virological studies, Treatment of persistent infection with immunoglobulin leads to a rapid, marked resolution of the anemia. RP Brown, KE (reprint author), NHLBI,NIH,HEMATOL BRANCH,BLDG 10,ROOM 7C218,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 95 TC 40 Z9 40 U1 0 U2 1 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 1066-5099 J9 STEM CELLS JI Stem Cells PD MAR PY 1996 VL 14 IS 2 BP 151 EP 163 PG 13 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA UC727 UT WOS:A1996UC72700001 PM 8991535 ER PT J AU Evans, CH AF Evans, CH TI Cytokines and viral anti-immune genes SO STEM CELLS LA English DT Review DE anti-immune gene; complement; cytokine; homolog; interleukin; MHC gene presentation; receptor decoy; virus pirating of host defense genes ID MYXOMA VIRUS; RECEPTOR; LEUKOREGULIN; PROTEINS; DEFENSES; FAMILY AB Cytokines, the pleomorphic and pleiotropic director proteins of an increasingly defined diversity of differentiation and growth, are potent modulators of immune function and homeostasis, The antiviral and immunostimulatory actions of cytokines, like the interferons, have also been recognized for many years, In more recent developments, virus genomes were discovered in 1990 to contain anti-immune genes that control the synthesis of host cell proteins that disarm immune defenses. Many of the virus anti-immune genes are directed against cytokines, Recent discoveries of cytokine homologs and cytokine receptor homologs, and other viral gene products that disarm host immune defenses, provide a molecular basis for improved understanding of virus diseases and new targets for development of innovative therapeutic approaches against viral, cancer and perhaps a number of other diseases. RP Evans, CH (reprint author), NCI,NIH,BIOL LAB,BLDG 37,ROOM 2A17,BETHESDA,MD 20892, USA. NR 24 TC 4 Z9 4 U1 1 U2 1 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 1066-5099 J9 STEM CELLS JI Stem Cells PD MAR PY 1996 VL 14 IS 2 BP 177 EP 184 PG 8 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA UC727 UT WOS:A1996UC72700003 PM 8991537 ER PT J AU Alexander, NJ Kim, HK Blye, RR Blackmore, PF AF Alexander, NJ Kim, HK Blye, RR Blackmore, PF TI Steroid specificity of the human sperm membrane progesterone receptor SO STEROIDS LA English DT Article DE progesterone; steroidal heterocycles; hormonal assays; Ca2+ influx; human sperm membrane receptor; acrosome reaction; calcium ionophore, A23187; 3D molecular modeling; conformational analysis; superposition ID ACROSOME REACTION; FOLLICULAR-FLUID; HUMAN SPERMATOZOA; BINDING; LOCALIZATION; AGGREGATION; PROTEIN; ABILITY; INFLUX AB The aim of this study was to evaluate the effect of several abeopregnane, steroidal heterocycles (A/B-transandrostano [2,3-d]isoxazole, and 17-spiroandrostano[2,3-c]furazan), and 6 alpha, 11 beta, 16 alpha-trisubstituted 19-nor-pregnadienedione on the influx of extracellular Ca2+ in human sperm. These steroidal compounds had minimal genomic progestational, androgenic, oi estrogenic activity with the exception of 16 alpha-ethyl-6 alpha-methyl-11 beta-(4-N,N-dimethylaminophenyl)-19-norpregna-4,9-diene-3,20-dione which was four times more progestational than progesterone. Some of the steroidal compounds, e.g., 16 alpha-ethyl-6 alpha-methyl-11 beta-(4-N,N-dimethylaminophenyl)-19-nor-pregna-4,9-diene-3,20-dione and 2',3',4',5'-tetrahydrospiro[furan-2'beta,17-androstano] [2,3-c]furazan produced an influx of Ca2+ into human spermatozoa. These studies indicate that high (10 mu M) concentrations of certain steroidal compounds are selective for the sperm membrane progesterone receptor; since most of them have minimal genomic activity. The steroidal compounds that elicited an influx of Ca2+ caused an initial high influx but were not as potent as progesterone, since no effects were observed below 1 mu M, whereas progesterone at 1 mu M produced a maximum effect. Progesterone as well as the steroidal compounds caused a modest increase in the number of acrosome-reacted spermatozoa. Molecular modeling revealed that 5 alpha-dihydro-2,3-fused and 4,4-dimethyl-5-ene-2,3-fused steroidal heterocycles possessing different conformations compared to that of progesterone are responsible for elevation of Ca2+. In conclusion, a unique, non-genomic progesterone receptor is present on human spermatozoa and several steroidal compounds that do not have progestational effects may activate this sperm membrane receptor, resulting in Ca2+ influx. C1 EASTERN VIRGINIA MED SCH,DEPT PHARMACOL,NORFOLK,VA 23501. RP Alexander, NJ (reprint author), NICHHD,NIH,POPULAT RES CTR,CONTRACEPT DEV BRANCH,BETHESDA,MD 20892, USA. FU NICHD NIH HHS [HD-129492] NR 44 TC 23 Z9 23 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0039-128X J9 STEROIDS JI Steroids PD MAR PY 1996 VL 61 IS 3 BP 116 EP 125 DI 10.1016/0039-128X(95)00202-2 PG 10 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA TY956 UT WOS:A1996TY95600003 PM 8852828 ER PT J AU Nishida, K Markey, SP AF Nishida, K Markey, SP TI Platelet-activating factor in brain regions after transient ischemia in gerbils SO STROKE LA English DT Article DE platelet-activating factor; spectrum analysis, mass; gerbils ID TUMOR NECROSIS FACTOR; ALVEOLAR MACROPHAGES; RAT-BRAIN; POLYMORPHONUCLEAR LEUKOCYTES; FOREBRAIN ISCHEMIA; HUMAN-NEUTROPHILS; ARACHIDONIC-ACID; FACTOR PAF; INJURY; BIOSYNTHESIS AB Background and Purpose Platelet-activating factor (PAF) has been reported to be an active mediator in ischemic brain damage on the basis of indirect pharmacological data from PAF antagonists. The direct measurement of PAF in neuronal tissues has not been reported previously in analogous animal models. We have examined regional brain PAF concentration changes during the reperfusion period after ischemia in gerbils to obtain direct evidence for the involvement of PAF with ischemic brain damage and reported gas chromatography/mass spectrometry (GC/MS) methods of PAF quantitative analysis in brain tissues. Methods After transient (10 minutes) ischemia followed by controlled periods (0 to 96 hours) of reperfusion and recovery, regional PAF concentrations were determined in gerbil brain tissue. Quantitative analysis of PAF in brain regions is per formed using an electron-capture negative chemical ionization GC/MS method, modified for brain tissue. Results The level of PaF was increased significantly and maximally in hippocampus (211%), cortex (168%), and thalamus (169%) after 1 hour of reperfusion. In contrast, there were no significant changes of PAF in any brain region from 6 hours to 96 hours after reperfusion. Conclusions PAF is increased in gerbil brain in response to ischemia at early stages of reperfusion. PAF increases could contribute to the onset and progress of ischemic neuropathology. C1 NIMH, CLIN SCI LAB, ANALYT BIOCHEM SECT, BETHESDA, MD 20892 USA. NR 35 TC 33 Z9 38 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0039-2499 EI 1524-4628 J9 STROKE JI Stroke PD MAR PY 1996 VL 27 IS 3 BP 514 EP 518 PG 5 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA TZ958 UT WOS:A1996TZ95800030 PM 8610322 ER PT J AU Hurley, CK Steiner, N Hoyer, RJ Menchaca, E Mitton, W Simonis, T Hartzman, RJ Johnson, AH Ng, J AF Hurley, CK Steiner, N Hoyer, RJ Menchaca, E Mitton, W Simonis, T Hartzman, RJ Johnson, AH Ng, J TI Novel HLA-B alleles, B*8201, B*3515 and B*5106, add to the complexity of serologic identification of HLA types SO TISSUE ANTIGENS LA English DT Article DE HLA-B; B*8201; B*3515; B*5106 ID MHC CLASS-I; HISTOCOMPATIBILITY ANTIGEN; POSITIVE SELECTION; PEPTIDE-BINDING; MOLECULES; SPECIFICITY; RECOGNITION; RESOLUTION; REPERTOIRE; EPITOPES AB Three class I alleles, B*8201, B*3515 and B*5106, have been described using DNA and cDNA sequencing. The B*8201 allele is most structurally related to B*5602, differing from it by 14 nucleotide substitutions resulting in 5 amino acid differences. The other two alleles, B*3515 and B*5106, differ from their most closely related HLA-B alleles by 2-3 nucleotide substitutions resulting in 1-2 amino acid substitutions, respectively. The majority of nucleotide substitutions marking these new alleles are observed in other HLA-B alleles suggesting that gene conversion and/or reciprocal recombination have created this diversity. All of the amino acid substitutions are predicted to alter the antigen binding site of the HLA-B molecule. The newly defined HLA-B allelic products were originally defined by their unusual serologic reactivity patterns. The B*8201 allelic product is serologically typed as a B ''blank'' or as a variant of B22 or B45. These patterns and the serologic reactivity of the other newly described allelic products are consistent with the protein sequence homology among specific HLA-B molecules. While serology remains a powerful tool for detecting HLA diversity, alleles generated by events resulting in the sharing of HLA sequence polymorphisms among alleles at a locus will continue to create complexity in the interpretation of typing results. C1 GEORGETOWN UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,WASHINGTON,DC. WILFORD HALL USAF MED CTR,LACKLAND AFB,TX 78236. USN,MED RES INST,BETHESDA,MD. NIH,HLA LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20007. NR 29 TC 21 Z9 22 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD MAR PY 1996 VL 47 IS 3 BP 179 EP 187 DI 10.1111/j.1399-0039.1996.tb02538.x PG 9 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA UG189 UT WOS:A1996UG18900002 PM 8740766 ER PT J AU Williams, RC Hanson, RL Pettitt, DJ Sievers, ML Nelson, RG Knowler, WC AF Williams, RC Hanson, RL Pettitt, DJ Sievers, ML Nelson, RG Knowler, WC TI HLA*A2 confers mortality risk for cardiovascular disease in Pimans SO TISSUE ANTIGENS LA English DT Article DE cardiovascular disease; HLA*A2; mortality rate ratio; Pima Indians ID RIVER-INDIAN-COMMUNITY; DIABETES-MELLITUS; HISTOCOMPATIBILITY COMPLEX; ALPHA-2 HELIX; HLA; ARIZONA; PREVALENCE; LONGEVITY; FREQUENCY; ADMIXTURE AB A sample of 1465 full heritage Piman Indians from Arizona were typed for the serological antigens of the HLA class I loci and then incorporated into a survival study that ended December 31, 1991. The total follow-up time was 11,749 person-years with an average of 8.0 years per person. During the study 298 persons died, 54 from cardiovascular disease (CVD). Allele HLA*A2 conferred a 4.94 fold rate for death from CVD (95% C.I. 1.91 - 12.77). When controlled for the potential confounding variables, cholesterol, mean blood pressure, smoking, body mass index, rheumatoid factor titer, and nephropathy, the mortality rate ratio (MRR) was 5.42 (95% C.I. 1.98 - 14.82). There was no statistically significant association of mortality with other HLA-A or HLA-B alleles, or for causes of death not related to cardiovascular disease. C1 BLOOD SYST INC,HISTOCOMPATIBIL LAB,SCOTTSDALE,AZ. NIDDKD,DIABET & ARTHRIT EPIDEMIOL SECT,PHOENIX,AZ. NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,PHOENIX,AZ. RP Williams, RC (reprint author), ARIZONA STATE UNIV,DEPT ANTHROPOL,BOX 872402,TEMPE,AZ 85287, USA. RI Nelson, Robert/B-1470-2012; Hanson, Robert/O-3238-2015 OI Hanson, Robert/0000-0002-4252-7068 NR 34 TC 3 Z9 3 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD MAR PY 1996 VL 47 IS 3 BP 188 EP 193 DI 10.1111/j.1399-0039.1996.tb02539.x PG 6 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA UG189 UT WOS:A1996UG18900003 PM 8740767 ER PT J AU Blazka, ME Elwell, MR Holladay, SD Wilson, RE Luster, MI AF Blazka, ME Elwell, MR Holladay, SD Wilson, RE Luster, MI TI Histopathology of acetaminophen-induced liver changes: Role of interleukin 1 alpha and tumor necrosis factor alpha SO TOXICOLOGIC PATHOLOGY LA English DT Article DE female B6C3F1 mice; antibody; proinflammatory; hepatotoxic; centrilobular congestion ID INDUCED HEPATIC NECROSIS; ACTIVATED MACROPHAGES; ALCOHOLIC HEPATITIS; RECEPTOR ANTAGONIST; POTENTIAL ROLE; BINDING; INVIVO; HEPATOTOXICITY; INFLAMMATION; HEPATOCYTES AB Administration of 500 mg/kg acetaminophen (APAP) to female B6C3F1 mice resulted in well-documented pathophysiological changes in the liver manifested as increased serum concentration of liver enzymes (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and serum sorbitol dehydrogenase), centrilobular congestion, and hepatocellular degeneration and necrosis. The role of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha) and interleukin 1 alpha (IL-1 alpha), on the hepatotoxicity of APAP was examined at 4, 8, 12, and 24 hr following APAP administration. Neutralization of TNF-alpha or IL-1 alpha with specific antibodies partially prevented the hepatotoxic effects of APAP at the 4- and 8-hr time points. In addition, prior administration of anti-TNF-alpha antibodies shortened the recovery time following APAP treatment. While IL-I receptor antagonist (IL-1ra) had only a modest protective effect against APAP-induced liver damage, as determined by serum enzyme release, IL-1ra had no effect on the degree of hepatic congestion or necrosis at any of the time points examined. On the other hand, administration of antibodies against IL-lra exacerbated APAP-induced liver toxicity. These results suggest that TNF-alpha and IL-1 alpha play an important role in the degree of damage and recovery that the Liver undergoes following APAP intoxication. C1 NIEHS,ENVIRONM IMMUNOL & NEUROBIOL SECT,RES TRIANGLE PK,NC 27709. NR 36 TC 95 Z9 99 U1 1 U2 1 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PD MAR-APR PY 1996 VL 24 IS 2 BP 181 EP 189 PG 9 WC Pathology; Toxicology SC Pathology; Toxicology GA UE430 UT WOS:A1996UE43000006 PM 8992608 ER PT J AU Elwell, MR Dunnick, JK Hailey, JR Haseman, JK AF Elwell, MR Dunnick, JK Hailey, JR Haseman, JK TI Chemicals associated with decreases in the incidence of mononuclear cell leukemia in the Fischer rat SO TOXICOLOGIC PATHOLOGY LA English DT Article DE chemotherapy; toxicity; carcinogenicity; spleen ID GRANULAR LYMPHOCYTE LEUKEMIA; SALMONELLA MUTAGENICITY TESTS; F344 RATS; ANILINE HYDROCHLORIDE; STATISTICAL ISSUES; TRANSPLANT MODEL; BODY-WEIGHT; CARCINOGENICITY; SARCOMAS; TERM AB A significant treatment-related decrease in the incidence of mononuclear cell leukemia (MCL) was identified in Fischer-344/N rats for 20 chemicals tested in the National Toxicology Program's 2-yr carcinogenicity bioassay. Fourteen of the 20 chemicals caused decreases of MCL in both male and female rats; 6 of the 20 caused a significant decrease only in males and a marginal or no decrease in female rats. Seventeen of the chemicals associated with a decrease in MCL had a free aromatic amine or nitro functional groups that could be metabolized to free amines. With 1 exception, all 14 chemicals causing a decrease in MCL in both sexes produced spleen toxicity in the 13-wk studies. Reduced body weight and decreased survival, related either to toxicity or to an increase in other types of lethal neoplasms, did not contribute to the decreases in MCL observed in chemical exposure groups. Thirteen of the 20 chemicals were positive in Salmonella tests, and 15 were associated with increases in neoplasms at other sites in rats and/or mice, suggesting that different metabolites could be responsible for these varied biological effects. C1 NIEHS,EXPT TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. NR 41 TC 19 Z9 19 U1 0 U2 0 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PD MAR-APR PY 1996 VL 24 IS 2 BP 238 EP 245 PG 8 WC Pathology; Toxicology SC Pathology; Toxicology GA UE430 UT WOS:A1996UE43000012 PM 8992614 ER PT J AU Germolec, DR Henry, EC Maronpot, R Foley, JF Adams, NH Gasiewicz, TA Luster, MI AF Germolec, DR Henry, EC Maronpot, R Foley, JF Adams, NH Gasiewicz, TA Luster, MI TI Induction of CYP1A1 and ALDH-3 in lymphoid tissues from Fisher 344 rats exposed to 2,3,7,8-tetrachlorodibenzodioxin (TCDD) SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID CYTOSOLIC ALDEHYDE DEHYDROGENASE; CYTOCHROME-P450IA1 MESSENGER-RNA; ARYL-HYDROCARBON HYDROXYLASE; POLYMERASE CHAIN-REACTION; AH RECEPTOR; ANTIBODY-RESPONSES; CELL-LINE; EXPRESSION; LYMPHOCYTES; INVITRO AB The immune system is a primary target for toxic insult by a number of drugs and environmental chemicals, many of which require activation to toxic metabolites by drug-metabolizing enzymes. We compared the induction of drug-metabolizing enzymes, including cytochrome P450 1A1 (CYP1A1) and aldehyde dehydrogenase (ALDH), in lymphoid tissues of F344 rats following treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). ALDH was induced in both the spleen and the thymus after TCDD treatment, with maximal expression at 9 and 15 days, respectively. Thymic microsomal preparations from TCDD-treated animals expressed elevated levels of inducible CYP1A1 as compared to microsomes from the spleens of treated animals or tissues from control rats. TCDD treatment also resulted in increased ethoxyresorufin-O-deethylase (EROD) activity in the thymus. There were no detectable mRNA transcripts for CYP1A1 in peripheral blood or splenic lymphocytes from treated animals; however, CYP1A1 transcripts were induced in isolated thymocytes, whole spleen, and whole thymus. In vitro exposure to TCDD did not result in induction of immunoreactive CYP1A1 in thymocytes unless simultaneously activated with the mitogen, phytohemagluttinin (PHA). Immunohistochemical localization of CYP1A1 in immune tissues indicated that cells other than the lymphoid populations are responsible for the increased CYP1A1 expression. The pattern of CYP1A1 induction was related to the expression of the Ah receptor (AhR) in immune tissues. Western blot analyses demonstrated less AhR present in peripheral blood lymphoid cells and spleen, as compared to whole tissues. These studies indicate that while drug-metabolizing enzymes are present in immune tissues, the induction of enzymes is selective in different lymphoid cells. (C) 1996 Academic Press, Inc. C1 NIEHS,LAB EXPT PATHOL,RES TRIANGLE PK,NC 27709. UNIV ROCHESTER,DEPT ENVIRONM MED,ROCHESTER,NY 14642. N CAROLINA STATE UNIV,DEPT TOXICOL,RALEIGH,NC 27695. RP Germolec, DR (reprint author), NIEHS,ENVIRONM IMMUNOL & NEUROBIOL SECT,RES TRIANGLE PK,NC 27709, USA. NR 51 TC 27 Z9 28 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD MAR PY 1996 VL 137 IS 1 BP 57 EP 66 DI 10.1006/taap.1996.0057 PG 10 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA TY926 UT WOS:A1996TY92600007 PM 8607142 ER PT J AU Korelitz, JJ Busch, MP Kleinman, SH Williams, AE Zuck, TF Gilcher, RO Ownby, HE Chien, HC Nemo, GJ AF Korelitz, JJ Busch, MP Kleinman, SH Williams, AE Zuck, TF Gilcher, RO Ownby, HE Chien, HC Nemo, GJ TI Relationship between antibody to hepatitis B core antigen and retroviral infections in blood from volunteer donors SO TRANSFUSION LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; POSTTRANSFUSION HEPATITIS; NON-A; C VIRUS; SURFACE-ANTIGEN; PREVALENCE; TRANSMISSION; POPULATION; DECREASE; TESTS AB Background: The value of the test for antibody to hepatitis B core antigen (anti-HBc) as a surrogate screening assay in the time before sensitive, virus-specific screening tests were available has been well established. There is significant debate, however, about the residual value of anti-HBc screening after the implementation of human immunodeficiency virus (HIV)-, human T-lymphotropic virus (HTLV)-, and hepatitis C virus (HCV)-specific assays and, in particular, about its utility as a lifestyle marker to identify persons at risk for retrovirus infections. Study Design and Methods: Screening tests for antibodies to HIV, HTLV, and HBc, as well as confirmatory or supplemental test results for anti-HIV and anti-HTLV, were obtained from approximately 2.8 million donations collected from 1991 through 1993 by five blood centers within the United States. The sensitivity, positive predictive value, and relative prevalence of anti-HBe for each retrovirus were calculated and compared among demographic subgroups. Results: The overall relationship between anti-HBc and anti-HIV was similar to that between anti-HBc and anti-HTLV. When calculated from the measured endpoint of the prevalence of anti-HIV-positive and anti-HTLV-positive donations, the sensitivities were 31.1 and 26.2 percent, the positive predictive values were 0.18 and 0.21 percent, and the relative prevalences were 30.1 and 23.8, respectively. Among 27 anti-HIV-seroconverting donors and 9 anti-HTLV-seroconverting donors, the sensitivities were 7.4 percent (95% CI: 0.9-24.3%) and 0 percent (95% CI: 0.0-28.3%), respectively. It was estimated that for each HIV-infected window-period donation detected by anti-HBc, from 19,000 to 81,000 HIV-noninfected donations are discarded. Similarly, more than 33,000 HTLV-noninfected donations are likely to be discarded for each HTLV-infected donation detected by anti-HBc. Conclusion: Although anti-HBc-reactive donations are more likely to be seropositive for a retrovirus than are anti-HBc-nonreactive donations, the low positive predictive value limits the test's effectiveness. If the anti-HBc test is retained in the blood donor setting, efforts should be focused on reducing the number of false-positive results. C1 IRWIN MEM BLOOD CTR,RES & SCI SERV,SAN FRANCISCO,CA. AMER RED CROSS,JEROME H HOLLAND LAB,ROCKVILLE,MD. UNIV CINCINNATI,MED CTR,HOXWORTH BLOOD CTR,CINCINNATI,OH 45267. OKLAHOMA BLOOD INST,OKLAHOMA CITY,OK. AMER RED CROSS,BLOOD SERV,SE MICHIGAN REG,DETROIT,MI. NHLBI,TRANSFUS MED SCI RES GRP,BETHESDA,MD 20892. RP Korelitz, JJ (reprint author), WESTAT CORP,1650 RES BLVD,ROCKVILLE,MD 20850, USA. FU NHLBI NIH HHS [N01-HB-47114, N01-HB-97078, N01-HB-97079] NR 41 TC 14 Z9 16 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD MAR PY 1996 VL 36 IS 3 BP 232 EP 237 DI 10.1046/j.1537-2995.1996.36396182141.x PG 6 WC Hematology SC Hematology GA UE234 UT WOS:A1996UE23400009 PM 8604508 ER PT J AU Hengen, PN AF Hengen, PN TI Is RNase-free really RNase for free? SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Article AB Methods and reagents is a unique monthly column that highlights current discussions in the newsgroup bionet.molbio.methds-reagnts, available on the Internet. This month's column discusses some contamination problems seen with the use of commercial RNase-free enzyme preparations, as well as a few other tips. For details on how to partake in the newsgroup, see the accompanying box. RP Hengen, PN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702, USA. NR 6 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0968-0004 J9 TRENDS BIOCHEM SCI JI Trends Biochem.Sci. PD MAR PY 1996 VL 21 IS 3 BP 112 EP 113 DI 10.1016/S0968-0004(96)30010-8 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UA955 UT WOS:A1996UA95500008 PM 8882585 ER PT J AU Lau, CL AF Lau, CL TI Cellular signals and responses in development SO TRENDS IN CELL BIOLOGY LA English DT Editorial Material RP Lau, CL (reprint author), NHLBI,NIH BLDG 10,ROOM 8N202,10 CTR DR,MSC 1762,BETHESDA,MD 20892, USA. NR 18 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0962-8924 J9 TRENDS CELL BIOL JI Trends Cell Biol. PD MAR PY 1996 VL 6 IS 3 BP 114 EP 116 DI 10.1016/0962-8924(96)81002-6 PG 3 WC Cell Biology SC Cell Biology GA TX599 UT WOS:A1996TX59900007 ER PT J AU Krsmanovic, LZ Stojilkovic, SS Catt, KJ AF Krsmanovic, LZ Stojilkovic, SS Catt, KJ TI Pulsatile gonadotropin-releasing hormone release and its regulation SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID IMMORTALIZED HYPOTHALAMIC NEURONS; GNRH NEURONS; EXPRESSION AB Several proposals have been put forward to explain the pulsatile pattern of gonadotropin-releasing hormone (GnRH) secretion form the hypothalamus, and the receptor-mediated modulation of such pulsatility. The mechanisms underlying these phenomena are not well defined bur the findings of intrinsic rhythmic activity of GnRH neurons, and the presence of autocrine GnRH action therein, have identified important elements in the episodic mode of neuropeptide release. RP Krsmanovic, LZ (reprint author), NICHHD,ENDOCRINOL & REPROD RES BRANCH,NIH,BETHESDA,MD 20892, USA. NR 16 TC 26 Z9 26 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD MAR PY 1996 VL 7 IS 2 BP 56 EP 59 DI 10.1016/1043-2760(96)00007-0 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UC208 UT WOS:A1996UC20800004 PM 18406726 ER PT J AU McLeod, HL FernandezSalguero, P Gonzalez, FJ AF McLeod, HL FernandezSalguero, P Gonzalez, FJ TI Pyrimidines and CNS regulation - Reply SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Letter ID 5-FLUOROURACIL C1 NCI,MOLEC CARCINOGENESIS LAB,NIH,BETHESDA,MD 20892. RP McLeod, HL (reprint author), UNIV ABERDEEN,DEPT MED & THERAPEUT,POLWARTH BLDG,ABERDEEN AB9 2ZD,SCOTLAND. NR 8 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0165-6147 J9 TRENDS PHARMACOL SCI JI Trends Pharmacol. Sci. PD MAR PY 1996 VL 17 IS 3 BP 107 EP 107 DI 10.1016/0165-6147(96)81584-7 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UG757 UT WOS:A1996UG75700007 ER PT J AU Jacobson, KA vonLubitz, DKJE Daly, JW Fredholm, BB AF Jacobson, KA vonLubitz, DKJE Daly, JW Fredholm, BB TI Adenosine receptor ligands: Differences with acute versus chronic treatment SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Review ID TERM CAFFEINE TREATMENT; LOCOMOTOR-ACTIVITY; MICE; WITHDRAWAL; TOLERANCE; BRAIN; A(1); SUSCEPTIBILITY; UPREGULATION; ANTAGONISTS AB Adenosine receptors have been the target of intense research with respect to potential use of selective ligands in a variety of therapeutic areas. Caffeine and theophylline are adenosine receptor antagonists, and over the past three decades a wide range of selective agonists and antagonists for adenosine receptor subtypes have been developed. A complication to the therapeutic use of adenosine receptor ligands is the observation that the effects of acute administration of a particular ligand can be diametrically opposite to the chronic effects of the same ligand. This 'effect inversion' is discussed here by Ken Jacobson and colleagues, and has been observed for effects on cognitive processes, seizures and ischaemic damage. C1 KAROLINSKA INST, DEPT PHYSIOL & PHARMACOL, SECT MOL NEUROPHARMACOL, S-17177 STOCKHOLM, SWEDEN. NIDDKD, BIOORGAN CHEM LAB, NIH, BETHESDA, MD 20892 USA. RP Jacobson, KA (reprint author), NIDDKD, MOL RECOGNIT SECT, NIH, BETHESDA, MD 20892 USA. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999] NR 50 TC 197 Z9 199 U1 0 U2 2 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0165-6147 J9 TRENDS PHARMACOL SCI JI Trends Pharmacol. Sci. PD MAR PY 1996 VL 17 IS 3 BP 108 EP 113 DI 10.1016/0165-6147(96)10002-X PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UG757 UT WOS:A1996UG75700008 PM 8936347 ER PT J AU Milstien, JB Gellin, BG Kane, M diFabio, JL Homma, A AF Milstien, JB Gellin, BG Kane, M diFabio, JL Homma, A TI Global DTP manufacturing capacity and capability. Status report: January 1995 SO VACCINE LA English DT Article DE DTP vaccine; quality control; vaccine production AB A recently completed survey of 63 manufacturers of diphtheria-tetanus-pertussis (DTP) vaccine and its components in 42 countries shows that there is potentially a large excess installed capacity for DTP production. However, many manufacturers ave not producing to capacity, and demand and supply for this vaccine are not matched in individual countries, About half of all countries producing DTP vaccine and its components do not have fully functional national control systems, and some countries are performing none of the critical functions for an effective control of quality. Thus, potential for export of excess capacity is limited. The data collected indicate much homogeneity in the preparation of diphtheria and tetanus toxoids. Nearly all manufacturers use the same seeds and similar purification methods, but there is variability in whether purification is done before or after conversion of toxin to toroid, About 10% of all manufacturers do not meet WHO-defined standards of purity for these toroids. There is much move heterogeneity in the pertussis seed strains and the methods of purification used. The formulation of DTP vaccine differs considerably among producers. Potency testing is not being done by the WHO-recommended method by about 50% of manufacturers on lots of diphtheria and tetanus toxoids for release. Testing of irreversibility of conversion of toxin to toroid, a WHO-specified safety test, is also not being clone on each lot of diphtheria toroid by 15% of manufacturers surveyed nor on each lot of tetanus toroid vaccine by 30% of manufacturers surveyed. Access to technology to develop new DTP-based combination vaccines will be delayed if these manufacturers cannot ensure consistent high quality vaccine for their target populations. The results and conclusions suggest areas for future activities to strengthen the supply and quality of DTP and DTP-based combination vaccines. Copyright (C) 1996 Elsevier Science Ltd. C1 NIAID,NIH,BETHESDA,MD. PAN AMER HLTH ORG,WASHINGTON,DC. RP Milstien, JB (reprint author), WHO,GLOBAL PROGRAMME VACCINES & IMMUNIZAT,CH-1211 GENEVA,SWITZERLAND. NR 3 TC 12 Z9 12 U1 0 U2 2 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0264-410X J9 VACCINE JI Vaccine PD MAR PY 1996 VL 14 IS 4 BP 313 EP 320 DI 10.1016/0264-410X(95)00181-Y PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA UG716 UT WOS:A1996UG71600012 PM 8744559 ER PT J AU Mizukami, H Young, NS Brown, KE AF Mizukami, H Young, NS Brown, KE TI Adeno-associated virus type 2 binds to a 150-kilodalton cell membrane glycoprotein SO VIROLOGY LA English DT Article ID ADENOASSOCIATED VIRUS; STRUCTURAL PROTEINS; INTEGRATION; LINE; PARVOVIRUS; SEQUENCE; GENOME; SITE AB Early events, including the identification of the cellular receptor, have not yet been described for adeno-associated virus (AAV) infection. In this study, the binding characteristics of AAV-2 to human cells were examined in two different assays. In a liquid-phase assay, in which binding of biotinylated virus to cells in suspension was measured, AAV-2 showed specific binding to four different permissive cell lines: HeLa S3, 293, D6, and KB cells. In contrast, AAV-2 binding to erythrocytes or to the nonpermissive cell line UT-7/Epo was negligible. AAV-2 binding showed saturation kinetics. Both binding and infectivity of AAV-2 were abolished by trypsin treatment of cells, with significant recovery of bindings after 8 hr of culture, suggesting that virus attachment occurs through a protein that can be regenerated on the cell surface. in a second, virus overlay assay, we assessed binding of [S-35]methionine-labeled AAV-2 to membrane proteins that had been transferred to nitrocellulose after electrophoretic separation. In this assay, virus attachment was shown to a 150-kDa protein. This protein was present in membranes from the AAV-2 permissive cell lines but not detected in membranes from erythrocytes or UT-7/Epo cells. Enzymatic deglycosylation studies suggested that N-linked glycans are required for AAV-2 binding. A 150-kDa glycoprotein might serve as the cellular receptor for AAV-2. (C) 1996 Academic Press, Inc. RP Mizukami, H (reprint author), NIH,HEMATOL BRANCH,BLDG 10,ROOM 7C103,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Mizukami, Hiroaki/D-7674-2013 OI Mizukami, Hiroaki/0000-0001-8954-874X NR 38 TC 62 Z9 66 U1 0 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD MAR 1 PY 1996 VL 217 IS 1 BP 124 EP 130 DI 10.1006/viro.1996.0099 PG 7 WC Virology SC Virology GA TY211 UT WOS:A1996TY21100013 PM 8599196 ER PT J AU Crook, T Ludwig, RL Marston, NJ Willkomm, D Vousden, KH AF Crook, T Ludwig, RL Marston, NJ Willkomm, D Vousden, KH TI Sensitivity of p53 lysine mutants to ubiquitin-directed degradation targeted by human papillomavirus E6 SO VIROLOGY LA English DT Article ID WILD-TYPE P53; CELLULAR-RESPONSE; DNA DAMAGE; PROTEIN; TRANSACTIVATION; ONCOPROTEIN; BINDING; ANTIGEN; ASSOCIATION; EXPRESSION AB The activity of the p53 tumor suppressor protein is regulated, at least in part, through the stability of the protein. p53 degradation in normal cells is controlled by ubiquitin-dependent proteolysis, and activation of p53 following DNA damage is associated with an increase in the stability of the protein. The human papillomavirus-encoded E6 protein abrogates p53 function by targeting it for rapid degradation, also through the ubiquitin pathway. Although the p53 protein is ubiquitinated following interaction with E6, we show here that none of the lysine residues within p53 are specifically required for E6-targeted degradation. Mutation of lysine residues within the C-terminus of p53 resulted in resistance to E6-mediated degradation in vitro, although the ability of the two proteins to form a complex was not affected. The same mutant was efficiently targeted for degradation in cells, however, illustrating a lack of correlation between the in vitro and the in vivo assays. (C) 1996 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. INST CANC RES,HADDOW LABS,SUTTON SM2 5NG,SURREY,ENGLAND. UNIV LUBECK,D-23538 LUBECK,GERMANY. FU CIT NIH HHS [CHRX-CT92-0005] NR 49 TC 41 Z9 41 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD MAR 1 PY 1996 VL 217 IS 1 BP 285 EP 292 DI 10.1006/viro.1996.0115 PG 8 WC Virology SC Virology GA TY211 UT WOS:A1996TY21100029 PM 8599213 ER PT J AU Semmes, OJ Majone, F Cantemir, C Turchetto, L Hjelle, B Jeang, KT AF Semmes, OJ Majone, F Cantemir, C Turchetto, L Hjelle, B Jeang, KT TI HTLV-1 and HTLV-II tax: Differences in induction of micronuclei in cells and transcriptional activation of viral LTRs SO VIROLOGY LA English DT Article ID PRIMARY HUMAN-LYMPHOCYTES; LEUKEMIA-VIRUS TYPE-1; ENDEMIC POPULATION; CYTOMEGALO-VIRUS; CELLULAR FACTORS; GENE; PROTEIN; TRANSFORMATION; RETROVIRUS; EXPRESSION AB Human T-cell leukemia virus (HTLV) types I and II are highly related viruses that differ in disease manifestations. HTLV-I has been linked unmistakably to adult T-cell leukemia-lymphoma. On the other hand, there is little evidence that prior infection with HTLV-II increases risk for lymphoproliferative disorders. Both viruses encode homologous transcriptional-activating proteins (respectively designated as Tax1 and Tax2) which have been suggested to be important mediators of viral pathogenesis. Previously, we reported that Tax1 is a potent inducer of micronuclei formation in cells. Here, we present evidence that Tax2 lacks micronuclei inductive ability. We contrast this phenotypic difference between Tax1 and Tax2 at the cellular level with their similarities at the molecular level in transcriptional activation. (C) 1996 Academic Press, Inc. C1 NIAID,NIH,MOLEC MICROBIOL LAB,MOL VIROL SECT,BETHESDA,MD 20892. UNIV PADUA,DIPARTIMENTO BIOL,PADUA,ITALY. UNIV NEW MEXICO,DEPT PATHOL,SCH MED,ALBUQUERQUE,NM 87131. RI Jeang, Kuan-Teh/A-2424-2008 NR 52 TC 74 Z9 74 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD MAR 1 PY 1996 VL 217 IS 1 BP 373 EP 379 DI 10.1006/viro.1996.0126 PG 7 WC Virology SC Virology GA TY211 UT WOS:A1996TY21100040 PM 8599225 ER PT J AU Chow, JC AF Chow, JC TI Health and international security SO WASHINGTON QUARTERLY LA English DT Article RP Chow, JC (reprint author), NIH,FOGARTY INT CTR,BLDG 10,BETHESDA,MD 20892, USA. NR 13 TC 3 Z9 3 U1 0 U2 0 PU MIT PRESS PI CAMBRIDGE PA 55 HAYWARD ST JOURNALS DEPT, CAMBRIDGE, MA 02142 SN 0163-660X J9 WASH QUART JI Wash. Q. PD SPR PY 1996 VL 19 IS 2 BP 63 EP 77 PG 15 WC International Relations; Law SC International Relations; Government & Law GA TY900 UT WOS:A1996TY90000004 ER PT J AU Fraticelli, A Serrano, CV Bochner, BS Capogrossi, MC Zweier, JL AF Fraticelli, A Serrano, CV Bochner, BS Capogrossi, MC Zweier, JL TI Hydrogen peroxide and superoxide modulate leukocyte adhesion molecule expression and leukocyte endothelial adhesion SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE free radical; oxidant; inflammation; selectin expression; integrin expression ID MYOCARDIAL REPERFUSION INJURY; FREE-RADICAL GENERATION; POLYMORPHONUCLEAR LEUKOCYTES; NEUTROPHIL ADHESION; XANTHINE-OXIDASE; CELL-ADHESION; ACTIVATION; ATHEROSCLEROSIS; REOXYGENATION; INFLAMMATION AB While endothelial oxidant generation and subsequent leukocyte chemotaxis and activation are important mechanisms of tissue damage in ischemic organs, it is not known if oxidant generation may be involved in triggering the subsequent leukocyte-mediated injury which occurs. Questions remain whether particular oxidants and oxygen-free radicals are capable of modulating the expression of leukocyte adhesion molecules and effecting leukocyte endothelial adhesion. Studies were performed to determine the effect of different biologically occurring oxidant molecules and oxygen free radicals including: . O-2(-); . OH, and H2O2 on the expression of integrin and selectin adhesion molecules on the surface of human PMNs and to determine the effect of these alterations on PMN adhesion to the endothelium. Adhesion molecule expression on the surface of human PMNs was measured by immunofluorescence flow cytometry. Electron paramagnetic resonance spectroscopy was applied to characterize the presence of exogenous free radical generation as well as that from activated PMNs. It was observed that these oxidants can cause up-regulation of CD11b and CD18 expression with shedding of L-selectin. The kinetics and dose-response of these effects were analyzed and their functional significance determined by measuring PMN adhesion to cultured human aortic endothelial monolayers. These studies demonstrate that oxygen free radicals and non-radical oxidants can directly trigger PMN activation and adhesion to vascular endothelium. C1 JOHNS HOPKINS BAYVIEW MED CTR,MOLEC & CELLULAR BIOPHYS LABS,BALTIMORE,MD 21224. JOHNS HOPKINS BAYVIEW MED CTR,JOHNS HOPKINS MED INST,EPR CTR,DEPT MED,DIV CARDIOL,BALTIMORE,MD 21224. JOHNS HOPKINS BAYVIEW MED CTR,JOHNS HOPKINS MED INST,DEPT MED,DIV CLIN IMMUNOL,BALTIMORE,MD 21224. NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. RI Serrano Junior, Carlos Vicente/I-2729-2013 FU NHLBI NIH HHS [HL-38324, HL-52315] NR 38 TC 109 Z9 115 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4889 J9 BBA-MOL CELL RES JI Biochim. Biophys. Acta-Mol. Cell Res. PD FEB 29 PY 1996 VL 1310 IS 3 BP 251 EP 259 DI 10.1016/0167-4889(95)00169-7 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UA095 UT WOS:A1996UA09500001 PM 8599602 ER PT J AU Bunnell, BA Morgan, RA AF Bunnell, BA Morgan, RA TI Gene therapy for AIDS SO MOLECULES AND CELLS LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; CYTOTOXIC LYMPHOCYTES-T; HUMAN ADENOSINE-DEAMINASE; LONG-TERM EXPRESSION; WILD-TYPE VIRUS; ANTISENSE RNA; RETROVIRAL VECTORS; HIV-INFECTION; INTRACELLULAR IMMUNIZATION; SEROPOSITIVE INDIVIDUALS C1 NIH, NATL CTR HUMAN GENOME RES, CLIN GENE THERAPY BRANCH, BETHESDA, MD 20892 USA. NR 110 TC 0 Z9 0 U1 0 U2 1 PU KOREAN SOC MOLECULAR & CELLULAR BIOLOGY PI SEOUL PA 635-4, YUCKSAM-DONG, GANGNAM-GU, SEOUL 135-703, SOUTH KOREA SN 1016-8478 J9 MOL CELLS JI Mol. Cells PD FEB 29 PY 1996 VL 6 IS 1 BP 1 EP 12 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TY477 UT WOS:A1996TY47700001 ER PT J AU Partiot, A Grafman, J Sadato, N Flitman, S Wild, K AF Partiot, A Grafman, J Sadato, N Flitman, S Wild, K TI Brain activation during script event processing SO NEUROREPORT LA English DT Article DE scripts; temporal order; PET; planning; frontal lobes ID MEMORY; REPRESENTATION; LOCALIZATION; KNOWLEDGE AB REGIONAL cerebral blood flow was measured with positron emission tomography in seven normal volunteers while they performed various script event verification tasks. The left frontal lobe, left anterior cingulate and the anterior part of the left superior temporal gyrus were more activated in the script event membership and action categorization conditions, whereas the right frontal lobe, left superior temporal gyrus and the middle temporal gyrus bilaterally were more activated in the script event temporal order verification condition. These results indicate that the temporal ordering of script events and determining whether an event belongs to a particular script or action category are processed by distinctive distributed neuronal networks. C1 NINCDS,COGNIT NEUROSCI SECT,MED NEUROL BRANCH,NIH,BETHESDA,MD 20892. NINCDS,HUMAN MOTOR CONTROL SECT,MED NEUROL BRANCH,NIH,BETHESDA,MD 20892. FUKUI MED SCH,DEPT RADIOL,FUKUI 91011,JAPAN. OI Grafman, Jordan H./0000-0001-8645-4457 NR 42 TC 52 Z9 52 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD FEB 29 PY 1996 VL 7 IS 3 BP 761 EP 766 DI 10.1097/00001756-199602290-00020 PG 6 WC Neurosciences SC Neurosciences & Neurology GA UK478 UT WOS:A1996UK47800020 PM 8733740 ER PT J AU Matsunaga, T Mukhin, AG London, ED AF Matsunaga, T Mukhin, AG London, ED TI Regionally distinct stoichiometry for N-methyl-D-aspartate receptor domains in brain SO NEUROREPORT LA English DT Article DE dizocilpine; CGP39653; dichlorokynurenic acid; frontal cortex; hippocampus; striatum; cerebellum; spinal cord; rat; radioligand binding ID GLYCINE BINDING-SITES; NMDA-RECEPTOR; RAT-BRAIN; H-3 CGP-39653; RADIOLIGAND; MODULATION; GLUTAMATE; KINETICS; COMPLEX; ACID AB A stoichiometric analysis of N-methyl-D-aspartate (NMDA) receptor binding was conducted using [H-3]dizocilpine, [H-3]dichlorokynurenic acid and [H-3]CGP39653, and membranes from various brain regions of rats. The ratio of the density of [H-3]CGP39653 binding to [H-3]dizocilpine binding was >1 in frontal cortex and hippocampus, approximate to 1 in striatum and spinal cord and <1 in cerebellum. When [H-3]dichlorokynurenic acid binding was compared with [H-3]dizocilpine binding, the ratios were >1 in frontal cortex, hippocampus and striatum, 3-4 in cerebellum, and approximate to 2 in spinal cord. These observations suggest that a single channel complex may have more than one binding site for NMDA and/or glycine and that the stoichiometry between the binding domains of the NMDA receptor varies regionally. C1 NIDA,NEUROIMAGING & DRUG ACT SECT,INTRAMURAL RES PROGRAM,NATL INST HLTH,BALTIMORE,MD 21224. GEORGETOWN UNIV,DEPT NEUROL & PHARMACOL,WASHINGTON,DC 20007. JOHNS HOPKINS MED INST,DEPT RADIOL,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201. NR 24 TC 3 Z9 3 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD FEB 29 PY 1996 VL 7 IS 3 BP 833 EP 837 DI 10.1097/00001756-199602290-00036 PG 5 WC Neurosciences SC Neurosciences & Neurology GA UK478 UT WOS:A1996UK47800036 PM 8733756 ER PT J AU Iams, JD Goldenberg, RL Meis, PJ Mercer, BM Moawad, A Das, A Thom, E McNellis, D Copper, RL Johnson, F Roberts, JM Hauth, JC Northern, A Neely, C MuellerHeubach, E Swain, M Frye, A Lindheimer, M Jones, P Brown, MEL Siddiqi, TA Elder, N Coombs, T VanHorn, J Bain, R Leuchtenburg, L Fischer, M Harger, JH Cotroneo, M Stallings, C Yaffe, S Catz, C Klebanoff, M Landon, MB Schneider, J Mueller, C Carey, JC Meier, A Liles, E Newman, RB Collins, BA Metcalf, T Odell, V Sibai, B Ramsey, R Fricke, JL Treadwell, M Norman, GS AF Iams, JD Goldenberg, RL Meis, PJ Mercer, BM Moawad, A Das, A Thom, E McNellis, D Copper, RL Johnson, F Roberts, JM Hauth, JC Northern, A Neely, C MuellerHeubach, E Swain, M Frye, A Lindheimer, M Jones, P Brown, MEL Siddiqi, TA Elder, N Coombs, T VanHorn, J Bain, R Leuchtenburg, L Fischer, M Harger, JH Cotroneo, M Stallings, C Yaffe, S Catz, C Klebanoff, M Landon, MB Schneider, J Mueller, C Carey, JC Meier, A Liles, E Newman, RB Collins, BA Metcalf, T Odell, V Sibai, B Ramsey, R Fricke, JL Treadwell, M Norman, GS TI The length of the cervix and the risk of spontaneous premature delivery SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID PRETERM DELIVERY; CONTROLLED TRIAL; ULTRASONOGRAPHY; PREDICTION; PREGNANCY; CERCLAGE; WOMEN AB Background. The role of the cervix in the pathogenesis of premature delivery is controversial. In a prospective, multicenter study of pregnant women, we used vaginal ultrasonography to measure the length of the cervix; we also documented the incidence of spontaneous delivery before 35 weeks' gestation. Methods. At 10 university-affiliated prenatal clinics, we performed vaginal ultrasonography at approximately 24 and 28 weeks of gestation in women with singleton pregnancies. We then assessed the relation between the length of the cervix and the risk of spontaneous preterm delivery. Results. We examined 2915 women at approximately 24 weeks of gestation and 2531 of these women again at approximately 28 weeks. Spontaneous preterm delivery (at less than 35 weeks) occurred in 126 of the women (4.3 percent) examined at 24 weeks. The length of the cervix was normally distributed at 24 and 28 weeks (mean [+/-SD], 35.2+/-8.3 mm and 33.7+/-8.5 mm, respectively). The relative risk of preterm delivery increased as the length of the cervix decreased. When women with shorter cervixes at 24 weeks were compared with women with values above the 75th percentile, the relative risks of preterm delivery among the women with shorter cervixes were as follows: 1.98 for cervical lengths at or below the 75th percentile (40 mm), 2.35 for lengths at or below the 50th percentile (35 mm), 3.79 for lengths at or below the 25th percentile (30 mm), 6.19 for lengths at or below the 10th percentile (26 mm), 9.49 for lengths at or below the 5th percentile (22 mm), and 13.99 for lengths at or below the Ist percentile (13 mm) (P<0.001 for values at or below the 50th percentile; P=0.008 for values at or below the 75th percentile). For the lengths measured at 28 weeks, the corresponding relative risks were 2.80, 3.52, 5.39, 9.57, 13.88, and 24.94 (P<0.001 for values at or below the 50th percentile; P=0.003 for values at the 75th percentile). Conclusions. The risk of spontaneous preterm delivery is increased in women who are found to have a short cervix by vaginal ultrasonography during pregnancy. C1 UNIV ALABAMA,DEPT OBSTET & GYNECOL,BIRMINGHAM,AL 35294. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT OBSTET & GYNECOL,WINSTON SALEM,NC 27103. UNIV TENNESSEE,DEPT OBSTET & GYNECOL,MEMPHIS,TN 38103. UNIV CHICAGO,DEPT OBSTET & GYNECOL,CHICAGO,IL 60637. GEORGE WASHINGTON UNIV,CTR BIOSTAT,DEPT OBSTET & GYNECOL,WASHINGTON,DC. NICHHD,DEPT OBSTET & GYNECOL,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT OBSTET & GYNECOL,PITTSBURGH,PA. UNIV CINCINNATI,CINCINNATI,OH. MED UNIV S CAROLINA,CHARLESTON,SC 29425. UNIV OKLAHOMA,OKLAHOMA CITY,OK. WAYNE STATE UNIV,DETROIT,MI. MAGEE WOMENS HOSP,PITTSBURGH,PA 15213. RP Iams, JD (reprint author), OHIO STATE UNIV,DEPT OBSTET & GYNECOL,1654 UPHAM DR,COLUMBUS,OH 43210, USA. FU NICHD NIH HHS [U10-HD-21410, U10-HD-27915, U10-HD-27917] NR 14 TC 839 Z9 870 U1 1 U2 28 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 29 PY 1996 VL 334 IS 9 BP 567 EP 572 DI 10.1056/NEJM199602293340904 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA TW696 UT WOS:A1996TW69600004 PM 8569824 ER PT J AU Landesman, SH Burns, D AF Landesman, SH Burns, D TI Quantifying HIV SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID INFECTION C1 NICHHD,NIH,CTR RES MOTHERS & CHILDREN,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,ROCKVILLE,MD. RP Landesman, SH (reprint author), SUNY HLTH SCI CTR,DEPT MED,DIV INFECT DIS,450 CLARKSON AVE,BOX 122,BROOKLYN,NY 11203, USA. NR 14 TC 11 Z9 11 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 28 PY 1996 VL 275 IS 8 BP 640 EP 641 DI 10.1001/jama.275.8.640 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA TW627 UT WOS:A1996TW62700026 PM 8594247 ER PT J AU Zahn, TP Leonard, HL Swedo, SE Rapoport, JL AF Zahn, TP Leonard, HL Swedo, SE Rapoport, JL TI Autonomic activity in children and adolescents with obsessive-compulsive disorder SO PSYCHIATRY RESEARCH LA English DT Article DE electrodermal activity; heart rate; tic disorder ID GLUCOSE-METABOLISM; RESPONSES; CLOMIPRAMINE; INTERVIEW AB Electrodermal activity and heart rate were recorded from 55 children and adolescents with obsessive-compulsive disorder (OCD) and 58 normal subjects in a protocol that included rest and mild stress periods, and nonsignal and signal stimuli, to determine if autonomic activity might be involved in the pathogenesis of OCD or might be related to important clinical differences. Few differences were observed between OCD and normal subjects despite adequate power to detect small differences due to the large number of subjects. Thus, autonomic activity appears not to be an important etiological factor in childhood OCD. However, electrodermal activity showed consistent positive correlations with ratings of the severity of OCD symptoms (but not with anxiety or depression ratings), suggesting that severely afflicted cases are autonomically sensitive to OCD-related stimuli or, conversely, that low electrodermal activity may be protective of symptom severity. Patients with a coexisting tic disorder (not Tourette's syndrome) had larger electrodermal responses to a novel stimulus and higher heart rate variability than those without ties but did not differ from normal subjects. These few differences seem insufficient to support the hypothesis of a separate etiology of OCD cases with a coexisting tic disorder. C1 NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. RP Zahn, TP (reprint author), NIMH,PSYCHOL & PSYCHOPATHOL LAB,BLDG 10,ROOM 4C110,10 CTR DR,MSC 1366,BETHESDA,MD 20892, USA. NR 37 TC 11 Z9 11 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD FEB 28 PY 1996 VL 60 IS 1 BP 67 EP 76 DI 10.1016/0165-1781(95)02846-3 PG 10 WC Psychiatry SC Psychiatry GA TZ321 UT WOS:A1996TZ32100008 PM 8852868 ER PT J AU Lange, N AF Lange, N TI Statistical approaches to human brain mapping by functional magnetic resonance imaging SO STATISTICS IN MEDICINE LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; SIGNAL; NOISE; NMR; IMAGES; NEUROANATOMY; LOCALIZATION; VARIANCE; SYSTEMS; MODELS AB Proper use of functional neuro-imaging through effective experimental design and modern statistical analysis provides new insights in current brain research. This tutorial has two aims: to describe aspects of this technology to applied statisticians and to provide some statistical ideas to neuroscientists unfamiliar with quantitative analytic methods that accommodate randomness. Introductory background material and ample references to current literature on the physics of magnetic resonance imaging, Fourier methods for image reconstruction and measures of image quality are included. Two of the statistical approaches mentioned here are extensions of established methods for longitudinal data analysis to the frequency domain. A recent case study provides real-world instances of approaches, problems and open questions encountered in current functional neuro-imaging research and an introduction to the analysis of spatial time series in this context. RP Lange, N (reprint author), NIH,FED BLDG,ROOM 7C04,BETHESDA,MD 20892, USA. NR 94 TC 55 Z9 56 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD FEB 28 PY 1996 VL 15 IS 4 BP 389 EP 428 DI 10.1002/(SICI)1097-0258(19960229)15:4<389::AID-SIM285>3.0.CO;2-J PG 42 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA TY774 UT WOS:A1996TY77400004 PM 8668868 ER PT J AU Fay, MP Gennings, C AF Fay, MP Gennings, C TI Non-parametric two-sample tests for repeated ordinal responses SO STATISTICS IN MEDICINE LA English DT Article ID RIDIT ANALYSIS; MODELS AB Consider data on two groups of clusters, where each cluster consists of many units that respond on an ordinal scale. We develop a Mann-Whitney type test to determine whether a typical response from the first group is larger (or smaller) than a typical response from the second group. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. RP Fay, MP (reprint author), NCI,BIOMETRY BRANCH,DIV CANC PREVENT & CONTROL,EXECUT PLAZA N,SUITE 344,6130 EXECUT BLVD MSC 735,BETHESDA,MD 20892, USA. RI Fay, Michael/A-2974-2008; OI Fay, Michael P./0000-0002-8643-9625 NR 22 TC 6 Z9 6 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD FEB 28 PY 1996 VL 15 IS 4 BP 429 EP 442 DI 10.1002/(SICI)1097-0258(19960229)15:4<429::AID-SIM139>3.0.CO;2-I PG 14 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA TY774 UT WOS:A1996TY77400005 PM 8668869 ER PT J AU Lynn, RB Cao, GY Considine, RV Hyde, TM Caro, JF AF Lynn, RB Cao, GY Considine, RV Hyde, TM Caro, JF TI Autoradiographic localization of leptin binding in the choroid plexus of ob/ob and db/db mice SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID INVITRO AUTORADIOGRAPHY; RAT-BRAIN AB The obese gene product, leptin, is synthesized in adipose tissue and is a circulating factor regulating body weight. To identify the location of leptin receptors in the brain we have performed an autoradiographic study of the binding of [I-125]leptin to frozen sections of mouse brain. Dense specific binding of [I-125]leptin was found only in the choroid plexus which is located in the dorsal part of the third ventricle and lateral ventricles. Specific binding of [I-125]leptin was found in the oblob and db/db mice. These findings further our understanding of the sites and mechanism of action of leptin on brain centers regulating body weight. (C) 1996 Academic Press, Inc. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT MED,DIV GASTROENTEROL & HEPATOL,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT MED,DIV ENDOCRINOL & METAB,PHILADELPHIA,PA 19107. NIMH,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. FU NIDDK NIH HHS [DK45592, DK02094] NR 12 TC 101 Z9 102 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD FEB 27 PY 1996 VL 219 IS 3 BP 884 EP 889 DI 10.1006/bbrc.1996.0328 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TZ799 UT WOS:A1996TZ79900035 PM 8645274 ER PT J AU Kohno, Y Sei, Y Koshiba, M Kim, HO Jacobson, KA AF Kohno, Y Sei, Y Koshiba, M Kim, HO Jacobson, KA TI Induction of apoptosis in HL-60 human promyelocytic leukemia cells by adenosine A(3) receptor agonists SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID MOLECULAR-CLONING; CAMPTOTHECIN; EXPRESSION AB The effects of adenosine (ADO) analogs on cells of the human promyelocytic HL-60 line were examined. ADO A(3) receptor agonists, N-6-(3-iodobenzyl)adenosine-5'-N-methylcarboxamide (IB-MECA, 30-60 mu M) and 2-chloro-N-6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (CI-IB-MECA, 10-30 mu M) induced apoptotic cell death. In contrast, neither an A(1)/A(2) antagonist (XAC) nor other selective ADO receptor agonists (CPA, NECA and CGS21680) induced apoptosis at concentrations of less than or equal to 30 mu M. Both IB-MECA and CI-IB-MECA significantly induced Ca2+ release from intracellular Ca2+ pools followed by Ca2+ influx, suggesting the presence of phospholipase C-coupled ADO A(3) receptors on HL-60 cells. This was further supported by the presence of mRNA of ADO A3 receptor in the cells. These results suggest that activation of ADO A(3) receptors is responsible for the ADO-induced apoptosis in HL-60 cells and could be of potential therapeutic value in the treatment of leukemia. (C) 1996 Academic Press, Inc. C1 NIDDK,NIH,MOLEC RECOGNIT SECT,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NIDDK,NIH,NEUROSCI LAB,BETHESDA,MD 20892. NIAID,NIH,IMMUNOL LAB,BETHESDA,MD 20892. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999] NR 29 TC 143 Z9 149 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD FEB 27 PY 1996 VL 219 IS 3 BP 904 EP 910 DI 10.1006/bbrc.1996.0331 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TZ799 UT WOS:A1996TZ79900038 PM 8645277 ER PT J AU Naghashfar, Z DiPaolo, JA Woodworth, CD Passaniti, A AF Naghashfar, Z DiPaolo, JA Woodworth, CD Passaniti, A TI Immortalization of human adult prostatic adenocarcinoma cells by human papilloma virus HPV16 and -18 DNA SO CANCER LETTERS LA English DT Article DE human prostatic cell; immortalization; human papilloma virus DNA ID POLYMERASE CHAIN-REACTION; PRIMARY HUMAN KERATINOCYTES; CERVICAL-CARCINOMA; GENE-EXPRESSION; TYPE-18 E6; E7 GENES; CANCER; TRANSFORMATION; SUFFICIENT; LINE AB Primary prostate epithelial and prostate adenocarcinoma cells cultured in serum-free medium grew for up to 10 passages before senescence. Cells from prostate adenocarcinoma of a 55-year-old patient without lymph node involvement were transfected with plasmids containing recombinant human papilloma virus HPV16 or HPV18 DNA and the selectable neomycin-resistance gene. After G-418 selection, cells underwent crisis, and surviving cells infected with retroviruses encoding the HPV18 E6/E7 genes (HPV-PAC1), transfected with a head-to-tail dimer of the complete HPV16 genome (HPV-PAC2), or transfected with HPV18 E6/E7 early genes (HPV-PAC3) were established. HPV-PAC1 and HPV-PAC2 cultures appeared morphologically similar to primary cultures even after 40 passages. However, HPV-PAC2 cultures had a clonal morphology. All lines were positive for cytokeratin 18, had acquired vimentin expression, and contained either HPV16 or HPV18 sequences integrated into host DNA. None was tumorigenic in nude mice or formed colonies in soft agar. These cells did not secrete prostate specific antigen nor respond to androgen although tamoxifen inhibited the growth of the cells. Immunohistochemistry showed no evidence of p53 overexpression. Further characterization of these cell lines and examination of their response to chemotherapeutic agents may provide relevant information for the study of hormone-independent PC. C1 NIA,GERONTOL RES CTR,NIH,BIOL CHEM LAB,BALTIMORE,MD 21224. NCI,BIOL LAB,NIH,BETHESDA,MD 20892. NR 42 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD FEB 27 PY 1996 VL 100 IS 1-2 BP 47 EP 54 DI 10.1016/0304-3835(95)04071-4 PG 8 WC Oncology SC Oncology GA TW796 UT WOS:A1996TW79600010 PM 8620453 ER PT J AU Niles, JL Bottinger, EP Saurina, GR Kelly, KJ Pan, GL Collins, AB McCluskey, RT AF Niles, JL Bottinger, EP Saurina, GR Kelly, KJ Pan, GL Collins, AB McCluskey, RT TI The syndrome of lung hemorrhage and nephritis is usually an ANCA-associated condition SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS; ANTINEUTROPHIL-CYTOPLASMIC ANTIBODIES; BASEMENT-MEMBRANE ANTIBODIES; SYSTEMIC VASCULITIS; WEGENERS GRANULOMATOSIS; GOODPASTURES-SYNDROME; PULMONARY HEMORRHAGE; NEUTROPHIL CYTOPLASM; AUTO-ANTIGEN; AUTOANTIBODIES AB Background: In the absence of evidence of arteritis or Wegener's granulomatosis, the syndrome of lung hemorrhage and nephritis has been commonly associated with anti-glomerular basement membrane (GBM) antibodies. However, it has been increasingly recognized that many cases are associated with antineutrophil cytoplasmic antibodies (ANCAs). Objective: To review available clinical and pathologic findings to determine the diseases accounting for lung hemorrhage and nephritis. Methods: We studied the records of 750 patients from whom serum samples were sent to our laboratory for anti-GEM antibody assays between 1981 and 1993 and found 88 patients with evidence of lung hemorrhage and nephritis. Serum samples were retested, using current methods, for anti-GEM antibodies (against noncollagenous 1 domain of the alpha 3 chain of type IV collagen) and for antibodies to proteinase 3 and myeloperoxidase-the two types of ANCA of diagnostic value. Results: Of 88 patients with evidence of lung hemorrhage and nephritis, 48 had ANCAs, six had anti-GBM antibodies, and seven had both. In 48 patients with ANCAs, the pathologic findings that accounted for the pulmonary renal syndrome were pauci-immune necrotizing and crescentic glomerulonephritis and pulmonary capillaritis. Only eight had convincing evidence (during life) of Wegener's granulomatosis and only one other had documented arteritis. In 27 patients without ANCAs or anti-GBM antibodies, a variety of unrelated renal and pulmonary diseases were found. Conclusions: The largest group of patients who present with the syndrome of lung hemorrhage and nephritis have ANCAs and not anti-GBM antibodies. Appropriate tests for antibodies to proteinase 3, antibodies to myeloperoxidase, and anti-GBM antibodies provide reliable guides for making a diagnosis in patients with this pulmonary renal syndrome. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NCI,BETHESDA,MD 20892. RP Niles, JL (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,COX 5,BOSTON,MA 02114, USA. NR 41 TC 124 Z9 130 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD FEB 26 PY 1996 VL 156 IS 4 BP 440 EP 445 DI 10.1001/archinte.156.4.440 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA TW328 UT WOS:A1996TW32800011 PM 8607730 ER PT J AU Giedd, JN Rumsey, JM Castellanos, FX Rajapakse, JC Kaysen, D Vaituzis, AC Vauss, YC Hamburger, SD Rapoport, JL AF Giedd, JN Rumsey, JM Castellanos, FX Rajapakse, JC Kaysen, D Vaituzis, AC Vauss, YC Hamburger, SD Rapoport, JL TI A quantitative MRI study of the corpus callosum in children and adolescents SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE adolescent; child; corpus callosum; development; MRI; myelination; sex ID ATTENTION-DEFICIT DISORDER; SEXUAL DIMORPHISM; CHRONIC-SCHIZOPHRENIA; BRAIN; COMMISSUROTOMY; HYPERACTIVITY; CONNECTIONS; CONTROVERSY; MORPHOLOGY; PARENT AB Total midsagittal area and seven subdivisions of the corpus callosum were measured on magnetic resonance images of 114 healthy boys and girls, aged 4 to 18. Striking variability of size was noted for all measures. Total midsagittal corpus callosum area increased in a robust and linear fashion from ages 4 to 18 (slope = 13.1 mm(2)/year, P = 0.0001 and slope = 11.1 mm(2)/year, P = 0.0001 for females and males, respectively). Posterior and mid regions demonstrated greater age-related changes than anterior regions with the rostrum and genu (anterior regions) having reached adult sizes in the youngest of our subjects. There were no significant effects of sex for any measures. These findings support anatomical studies indicating ongoing myelination of higher association areas throughout adolescence, but raise intriguing questions about anterior-posterior gradients of interhemispheric myelination. RP Giedd, JN (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,10 CTR DR,MSC-1600,BETHESDA,MD 20892, USA. RI Giedd, Jay/A-3080-2008; Rajapakse, Jagath/B-8485-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015 OI Rajapakse, Jagath/0000-0001-7944-1658; Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978 NR 69 TC 83 Z9 83 U1 2 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD FEB 26 PY 1996 VL 91 IS 2 BP 274 EP 280 DI 10.1016/0165-3806(95)00193-X PG 7 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA TX931 UT WOS:A1996TX93100015 ER PT J AU Paliogianni, F Hama, N Mavrothalassitis, GJ Thyphronitis, G Boumpas, DT AF Paliogianni, F Hama, N Mavrothalassitis, GJ Thyphronitis, G Boumpas, DT TI Signal requirements for interleukin 4 promoter activation in human T cells SO CELLULAR IMMUNOLOGY LA English DT Article ID CHROMOSOMAL GENE; PHORBOL ESTER; LYMPHOCYTES-T; CALCINEURIN; TRANSCRIPTION; IL-4; CAMP; PROSTAGLANDIN-E2; CYCLOSPORINE; T-HELPER-1 AB We have studied the signal requirements for human IL-4 promoter activation in Jurkat T cells by the use of DNA transfection assays with vectors carrying the IL-4 promoter linked to a reporter gene, Stimulation with calcium (Ca2+) ionophores (ionomycin), but not with phorbol esters (phorbol myristate acetate, PMA) or cyclic AMP elevating agents (prostaglandin Ea(2) PGE(2)), induced the transcriptional activity of the IL-4 promoter by similar to 3-fold. Costimulation with ionomycin and PGE(2) resulted in the same level of IL-4 promoter activity as the stimulation with ionomycin alone. In contrast, costimulation with ionomycin and PMA decreased the activity of the IL-4 promoter by similar to 40% compared to stimulation with ionomycin alone. Induction of IL-4 promoter by ionomycin was partially inhibited (similar to 50% inhibition) in the presence of as high as 2 mu g/ml cyclosporin A (CsA), an inhibitor of the Ca+/calmodulin-dependent phosphatase calcineurin. Under the same conditions, only 0.1 mu g/ml of CsA inhibited by >95% the transactivation of the IL-2 promoter in response to ionomycin and PMA. Transfection of a deletion mutant of the calcineurin catalytic subunit (Delta CaM-AI) known to have Ca2+-independent, constitutive phosphatase activity increased IL-4 promoter activity by similar to 14-fold. Stimulation with ionomycin of cells transfected with low doses of Delta CaM-AI, further induced IL-4 promoter activity by similar to 2-fold, These results identify the Ca2+-signaling system as a key component of the signal transduction pathway leading to IL-4 promoter activation in Jurkat T cells and suggest a major role of calcineurin in its regulation. (C) 1996 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,MOLEC ONCOL LAB,FREDERICK,MD 21702. INST PASTEUR,F-59019 LILLE,FRANCE. RP Paliogianni, F (reprint author), NIDDKD,NIH,KIDNEY DIS SECT,BLDG 10,ROOM 3N112,BETHESDA,MD 20892, USA. NR 34 TC 20 Z9 20 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD FEB 25 PY 1996 VL 168 IS 1 BP 33 EP 38 DI 10.1006/cimm.1996.0046 PG 6 WC Cell Biology; Immunology SC Cell Biology; Immunology GA TY854 UT WOS:A1996TY85400004 PM 8599837 ER PT J AU Schwabe, M Cox, GW Bosco, MC Prohaska, R Kung, HF AF Schwabe, M Cox, GW Bosco, MC Prohaska, R Kung, HF TI Multiple cytokines inhibit interleukin-6-dependent murine hybridoma/plasmacytoma proliferation SO CELLULAR IMMUNOLOGY LA English DT Article ID B-CELL HYBRIDOMAS; HUMAN-MONOCYTES; GROWTH-FACTOR; BSF-2 IL-6; TGF-BETA; EXPRESSION; RECEPTOR; ARREST; GAMMA AB A panel of cytokines was tested for inhibitors of interleukin-6 (IL-6)-dependent cell proliferation. Murine type I and II interferons (mIFNs) strongly inhibited proliferation of IL-6-dependent B9 and 7TD1 cells in a dose-dependent manner. Human tumor necrosis factor-alpha (hTNF-alpha) and human transforming growth factor-beta (hTGF-beta) potently inhibited B9 and to a lesser extent 7TD1 cells, while hIL-11, human oncostatin M (hOSM), and human leukemia inhibitory factor (hLIF) had no inhibitory effects on IL-6-dependent growth, Conversely, IL-11 and OSM but not LIF stimulated B9 and 7TD1 cell growth, However, compared with IL-6, up to 1000-fold higher IL-11 and OSM concentrations were required to induce maximal cell proliferation. Increasing concentrations of IL-6 (up to 100 ng/ml) could not overcome the antiproliferative effects of mIFNs, hTNF-alpha, and hTGF-beta. Supernatants from mIFN-gamma and lipopolysaccharide (LPS)-treated mouse macrophages (ANA-1 cell line) were tested in B9 cell assays to identify cytokines among stimulatory and inhibitory biological activities that can inhibit IL-6-dependent proliferation, Undiluted or relatively concentrated supernatants from ANA-1 macrophages treated with mIFN-gamma and/or LPS did not contain detectable IL-6 bioactivity. However, diluted samples contained considerable amounts of detectable IL-6 bioactivity (nanogram levels), Testing the same samples for IL-6 immunoreactivity using enzyme-linked immunoabsorbent assay revealed comparable levels of mIL-6, We conclude that IFNs, TNF-alpha, and TGF-beta and possibly other factors are potent, dominant inhibitors of IL-6-dependent plasmacytoma/hybridoma growth in vitro. (C) 1996 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. UNIV VIENNA,INST BIOCHEM,A-1030 VIENNA,AUSTRIA. RP Schwabe, M (reprint author), UNIV VIENNA,INST BIOCHEM,ROOM 3506,DR BOHR GASSE 9,A-1030 VIENNA,AUSTRIA. RI Bosco, Maria Carla/J-7928-2016 OI Bosco, Maria Carla/0000-0003-1857-7193 NR 27 TC 11 Z9 11 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD FEB 25 PY 1996 VL 168 IS 1 BP 117 EP 121 DI 10.1006/cimm.1996.0056 PG 5 WC Cell Biology; Immunology SC Cell Biology; Immunology GA TY854 UT WOS:A1996TY85400014 PM 8599834 ER PT J AU Davenport, EA Nettesheim, P AF Davenport, EA Nettesheim, P TI Type I collagen gel modulates extracellular matrix synthesis and deposition by tracheal epithelial cells SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID LAMININ A-CHAIN; ENDOTHELIAL-CELLS; DIFFERENTIATION; EXPRESSION; SUBSTRATUM; INHIBITION; SECRETION; POLARITY; INVITRO; GENE AB Extracellular matrix (ECM) molecules, including those present in basement membranes, are known to play an important role in morphogenesis and differentiation. Primary rat tracheal epithelial (RTE) cells grown on permeable membranes in air-liquid interface (ALI) cultures differentiate into mucous and ciliated cells. We previously showed that RTE cell differentiation is accelerated and enhanced on type I collagen gel-coated membranes. The purpose of this study was to determine whether type I collagen gel matrix also regulates basement membrane formation by RTE cells and whether this correlates with differentiation. Therefore, we examined the synthesis and deposition of several ECM molecules by RTE cells maintained on uncoated and type I collagen gel coated permeable membranes in ALI cultures. Fibronectin, thrombospondin-l, and alpha-1 type IV collagen gene expression were down regulated in cultures maintained on type I collagen gel-coated membranes and in differentiated cultures. Fibronectin and laminin alpha, beta, and gamma protein levels also were decreased slightly in response to type I collagen gel and differentiation. Deposition of fibronectin and laminin were dependent on type I collagen gel substratum. While fibronectin and laminin deposition were evident underlying both undifferentiated and differentiated cultures on type I collagen gel, deposition of these proteins on uncoated membranes was not readily detectable in undifferentiated cultures and was limited to patches of fibronectin deposition beneath differentiated cultures. Evidence suggestive of a discontinuous basal lamina-like structure was most apparent underlying differentiated cultures on type I collagen gel. These data demonstrate that ECM RNA and protein expression by RTE cells in ALI cultures are down-regulated by type I collagen gel whereas differentiation and ECM deposition are accelerated and enhanced on type I collagen gel. (C) 1996 Academic Press, Inc. C1 NIEHS,PULM PATHOBIOL LAB,AIRWAY CELL BIOL GRP,RES TRIANGLE PK,NC 27709. NR 42 TC 17 Z9 17 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD FEB 25 PY 1996 VL 223 IS 1 BP 155 EP 162 DI 10.1006/excr.1996.0069 PG 8 WC Oncology; Cell Biology SC Oncology; Cell Biology GA TX234 UT WOS:A1996TX23400018 PM 8635488 ER PT J AU SingerLahat, D Ma, AL Felder, CC AF SingerLahat, D Ma, AL Felder, CC TI Independent induction of morphological transformation of CHO cells by receptor-activated cyclic AMP synthesis or by receptor-operated calcium influx SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE receptor; phospholipase C; adenylate cyclase; receptor-operated calcium channel; morphological transformation of cells; second messengers ID MUSCARINIC ACETYLCHOLINE-RECEPTOR; ARACHIDONIC-ACID RELEASE; CA2+ INFLUX; MITOGENESIS; GENES; EXPRESSION; SUBTYPES AB Morphological transformation of Chinese hamster ovary (CHO) cells can be induced by exogenous addition of cyclic AMP (cAMP) or through the stimulation of G protein-coupled receptors ectopically expressed in these cells. The morphological transformation has been shown to represent a phenotypic suppres sion of CHO cell tumorigenic potential. Studies were undertaken to determine which receptor-activated signal transduction pathway initiates the progression from a tumorigenic to a non-tumorigenic phenotype. Stimulation of CHO cells expressing the dopamine D1 receptor (CHOD1) with a D1 selective agonist, SKF38393, resulted in an increase in cAMP accumulation which correlated with morphologic transformation. SKF38393 had no effect on intracellular calcium levels, arguing against a requirement for phospholipase C or calcium mobilization in the D1-stimulated morphology change. Tn contrast, stimulation of muscarinic m5 (CHOm5) or vasopressin V1a (CHOV1a) receptors expressed in CHO cells with carbachol or arginine vasopressin (AVP), respectively, did result in an increase in intracellular calcium and a morphology change. The time course of carbachol-stimulated calcium influx correlated with the time course of morphological transformation, but not with carbachol-stimulated cAMP or inositol, 1,4,5-trisphosphate (IP3) accumulation. Furthermore, no increase in cAMP accumulation was observed in AVP-stimulated CHOV1a cells, suggesting a cAMP-independent stimulation of the transformation process. Carbachol-stimulated CHO cells expressing the m2 muscarinic receptor (CHOm2) failed to undergo a morphological transformation, yet released IP3. Therefore, phospholipase C-mediated signal transduction is not sufficient for the morphological transformation of CHO cells. It appears that receptor-stimulated morphologic transformation of CHO cells can be induced via two independent signaling pathways, mediated by adenylate cyclase or receptor-operated calcium channels. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. NR 22 TC 6 Z9 6 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD FEB 23 PY 1996 VL 51 IS 4 BP 495 EP 502 DI 10.1016/0006-2952(95)02226-0 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TV998 UT WOS:A1996TV99800015 PM 8619896 ER PT J AU Coso, OA Teramoto, H Simonds, WF Gutkind, JS AF Coso, OA Teramoto, H Simonds, WF Gutkind, JS TI Signaling from G protein-coupled receptors to c-Jun kinase involves beta gamma subunits of heterotrimeric G proteins acting on a Ras and Rac1-dependent pathway SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article AB Stimulation of a variety of cell surface receptors enhances the enzymatic activity of mitogen-activated protein kinases (MAPKs). MAPKs have been classified in three subfamilies: extracellular signal-regulated kinases (ERKs), Stress-activated protein kinases or c-Jun NH2-terminal kinases (SAPKs/JNKs), and p38 kinase. Whereas the pathway linking cell surface receptors to ERKs has been partially elucidated, the mechanism of activation of JNKs is still poorly understood. Recently, we have shown that stimulation of G protein-coupled receptors can effectively induce JNK in NIH 3T3 cells (Coso, O. A., Chiariello, M., Kalinec, G., Kyriakis, J. M., Woodgett, J., and Gutkind, J. S. (1995) J. Biol. Chem. 270, 5620-5624). In the present study, we have used the transient expression in COS-7 cells of m1 and m2 muscarinic receptors (mAChRs) as a model system to study the signaling pathway linking G protein-coupled receptors to JNK. We show that stimulation of either muscarinic receptor subtype leads to JNK activation; however, this effect was not mimicked by expression of activated forms of alpha(s), alpha(i2), alpha(q), or alpha(13) G protein alpha subunits. In contrast, overexpression of G beta gamma subunits potently induced JNK activity. Furthermore, we show that signaling from mi and m2 mAChRs to JNK involves beta gamma subunits of heterotrimeric G proteins, acting on a Ras and Rac1-dependent pathway. C1 NIDR,CELLULAR DEV & ONCOL LAB,MOL SIGNALING UNIT,BETHESDA,MD 20892. NIDDK,BETHESDA,MD 20892. RI Gutkind, J. Silvio/A-1053-2009 NR 21 TC 190 Z9 193 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 3963 EP 3966 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000002 PM 8626724 ER PT J AU Gong, DW Bi, S Pratley, RE Weintraub, BD AF Gong, DW Bi, S Pratley, RE Weintraub, BD TI Genomic structure and promoter analysis of the human obese gene SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSCRIPTION AB The human gene encoding the homolog of the mouse obese (ob) gene was isolated and partially characterized. The human ob gene consists of three exons and two introns and spans about 18 kilobase pairs (kb), encoding a 3.5-kb cDNA. A 3-kb 5'-flanking region of the gene was cloned and transient transfection assay with luciferase reporter confirmed the promoter activity in differentiated F442-A adipocytes. Potential regulatory elements are discussed in this report. C1 NIDDK,PHOENIX EPIDEMIOL & CLIN RES BRANCH,BETHESDA,MD 20892. RP Gong, DW (reprint author), NIDDK,MOL & CELLULAR ENDOCRINOL BRANCH,BLDG 10,RM 8D14,10 CTR DR,MSC 1758,BETHESDA,MD 20892, USA. NR 18 TC 169 Z9 173 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 3971 EP 3974 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000004 PM 8626726 ER PT J AU Potterf, SB Muller, J Bernardini, I Tietze, F Kobayashi, T Hearing, VJ Gahl, WA AF Potterf, SB Muller, J Bernardini, I Tietze, F Kobayashi, T Hearing, VJ Gahl, WA TI Characterization of a melanosomal transport system in murine melanocytes mediating entry of the melanogenic substrate tyrosine SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LEUKOCYTE GRANULAR FRACTIONS; LYSOSOMAL MEMBRANE-TRANSPORT; HUMAN FIBROBLAST LYSOSOMES; RAT-THYROID CELLS; CYSTINE TRANSPORT; AMINO-ACIDS; STIMULATION; NUTRITION; MELANOMA; DISEASE AB In this study, we identify a transport system for tyrosine, the initial precursor of melanin synthesis, in the melanosomes of murine melanocytes. Melanosomes preloaded with tyrosine demonstrated countertransport of 10 mu M [H-3]tyrosine, indicating carrier-mediated transport. Melanosomal tyrosine transport was saturable, with an apparent K-m for tyrosine transport of 54 mu M and a maximal velocity of 15 pmol of tyrosine/unit of hexosaminidase/min. Transport was temperature-dependent (E(alpha) = 7.5 kcal/mol) and showed stereospecificity for the L-isomer of tyrosine. Aromatic, neutral hydrophobic compounds (such as tryptophan and phenylalanine), as well as the small, bulky neutral amino acids (such as leucine, isoleucine, and methionine) competed for tyrosine transport. Tyrosine transport was inhibited by the classical system L analogue, 2-aminobicyclo[2.2.1]heptane-2-carboxylic acid and by monoiodotyrosine, but not by cystine, lysine, glutamic acid, or 2-(methylamino)isobutyric acid. Tyrosine transport showed no dependence on Na+ or K+, and did not require an acidic environment or the availability of free thiols. These results demonstrate the existence of a neutral amino acid carrier in murine melanocyte melanosomes which resembles the rat thyroid FRTL-5 lysosomal system h. This transport system is critical to the function of the melanosome since tyrosine is the essential substrate required for the synthesis of the pigment melanin. C1 NICHHD,SECT HUMAN BIOCHEM GENET,HERITABLE DISORDERS BRANCH,BETHESDA,MD 20892. NCI,CELL BIOL LAB,BETHESDA,MD 20892. US FDA,DIV VIRAL PROD,CTR BIOL EVALUAT & RES,ROCKVILLE,MD 20852. NIDDK,MOL & CELLULAR BIOL LAB,BETHESDA,MD 20892. NR 35 TC 38 Z9 38 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4002 EP 4008 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000010 PM 8626732 ER PT J AU Guyton, KZ Liu, YS Gorospe, M Xu, QB Holbrook, NJ AF Guyton, KZ Liu, YS Gorospe, M Xu, QB Holbrook, NJ TI Activation of mitogen-activated protein kinase by H2O2 - Role in cell survival following oxidant injury SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SIGNAL-TRANSDUCTION; GENE-PRODUCT; PHOSPHORYLATION; CARCINOGENESIS; EXPRESSION; PATHWAY; RAS AB The mitogen-activated protein kinase (MAPK) family is comprised of key regulatory proteins that control the cellular response to both proliferation and stress signals. In this study we investigated the factors controlling MAPK activation by H2O2 and explored the impact of altering the pathways to kinase activation on cell survival following H2O2 exposure. Potent activation (10-20-fold) of extracellular signal-regulated protein kinase (ERK2) occurred within 10 min of H2O2 treatment, whereupon rapid inactivation ensued, H2O2 activated ERK2 in several cell types and also moderately activated (3-5-fold) both c-Jun N-terminal kinase and p38/RK/CSBP, Additionally, H2O2 increased the mRNA expression of MAPK-dependent genes c-jun, c-fos, and MAPK phosphatase-1. Suramin pretreatment completely inhibited H2O2 stimulation of ERK2, highlighting a role for growth factor receptors in this activation, Further, ERK2 activation by H2O2 was blocked by pretreatment with either N-acetyl-cysteine, o-phenanthroline, or mannitol, indicating that metal-catalyzed free radical formation mediates the initiation of signal transduction by H2O2. H2O2-stimulated activation of ERK2 was abolished in PC12 cells by inducible or constitutive expression of the dominant negative Ras-N-17 allele. Interestingly, PC12/Ras-N-17 cells were more sensitive than wild-type PC12 cells to H2O2 toxicity. Moreover, NIH 3T3 cells expressing constitutively active MAPK kinase (MEK, the immediate upstream regulator of ERK) were more resistant to H2O2 toxicity, while those expressing kinase-defective MEK were more sensitive, than cells expressing wild-type MEK. Taken together, these studies provide insight into mechanisms of MAPK regulation by H2O2 and suggest that ERK plays a critical role in cell survival following oxidant injury. C1 NIA,GERONTOL RES CTR,GENE EXPRESS & AGING SECT,NIH,BALTIMORE,MD 21224. RI Liu, Yusen/E-3527-2011 NR 42 TC 1015 Z9 1039 U1 1 U2 24 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4138 EP 4142 DI 10.1074/jbc.271.7.3604 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000031 PM 8626753 ER PT J AU Witteveen, CFB Giovanelli, J Kaufman, S AF Witteveen, CFB Giovanelli, J Kaufman, S TI Reduction of quinonoid dihydrobiopterin to tetrahydrobiopterin by nitric oxide synthase SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; L-ARGININE; METHYLENETETRAHYDROFOLATE REDUCTASE; BIOCHEMICAL-CHARACTERIZATION; DIHYDROPTERIDINE REDUCTASE; MURINE MACROPHAGES; LIVER; PURIFICATION; COFACTOR; INHIBITION AB Rat cerebellar nitric oxide synthase (NOS) purified from transfected human kidney cells catalyzes an NADPH-dependent reduction of quinonoid dihydrobiopterin (qBH(2)) to tetrahydrobiopterin (BH4). Reduction of qBH(2) at 25 mu M proceeds at a rate that is comparable with that of the overall reaction (citrulline synthesis) and requires calcium ions and calmodulin for optimal activity; NADH has only 10% of the activity of NADPH. The reduction rate with the quinonoid form of 6-methyldihydropterin is approximately twice that with qBH(2). 7,8-Dihydrobiopterin had negligible activity. Neither 7,8-dihydrobiopterin nor BH4 affected the rate of qBH(2) reduction. Reduction is inhibited by the flavoprotein inhibitor diphenyleneiodonium, whereas inhibitors of electron transfer through heme (7-nitroindazole and N-nitroarginine) stimulated the rate to a small extent, Methotrexate, which inhibits a variety of enzymes catalyzing dihydrobiopterin reduction, did not inhibit. These studies provide the first demonstration of the reduction of qBH(2) to BH4 by NOS and indicate that the reduction is catalyzed by the flavoprotein ''diaphorase'' activity of NOS. This activity is located on the reductase (C-terminal) domain, whereas the high affinity BH4 site involved in NOS activation is located on the oxygenase (N-terminal) domain. The possible significance of this reduction of qBH(2) to the essential role of BH4 in NOS is discussed. C1 NIMH,NEUROCHEM LAB,BETHESDA,MD 20892. NR 52 TC 36 Z9 36 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4143 EP 4147 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000032 PM 8626754 ER PT J AU Cawley, NX Chen, HC Beinfeld, MC Loh, YP AF Cawley, NX Chen, HC Beinfeld, MC Loh, YP TI Specificity and kinetic studies on the cleavage of various prohormone mono- and paired-basic residue sites by yeast aspartic protease 3 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID OPIOMELANOCORTIN-CONVERTING ENZYME; KEX2-LIKE ENDOPROTEASE; CELL-LINE; PRECURSOR CLEAVAGE; MONOBASIC SITES; PURIFICATION; FURIN; PITUITARY; GENE; RAT AB The specificity and relative efficiency of cleavage of mono and paired-basic residue processing sites by YAP3p was determined in vitro for a number of prohormone substrates: human ACTH(1-39), bovine proinsulin, porcine cholecystokinin 33, cholecystokinin (CCK) 13-33, dynorphin A(1-11), dynorphin B(1-13), and amidorphin. YAP3p generated ACTH(1-15) from ACTH(1-39) It cleaved proinsulin at the paired-basic residue sites of the B-C junction as well as the C-A junction. Leu-enkephalin-Arg and Leu-enkephalin-Arg-Arg were generated from dynorphin A and dynorphin B, respectively. YAP3p generated Met-enkephalin-Lys-Lys from amidorphin showing that cleavage by this enzyme can occur at a lone pair of Lys residues. CCK33 was cleaved at Lys(23) and Arg(9), each containing an upstream Arg residue at the P6 and P5 position, respectively, K-m values were between 10(-4) and 10(-5) M for the various substrates, with the highest affinity exhibited for the tetrabasic site of ACTH(1-39) (1.8 x 10(-5) M) The tetrabasic residue site of ACTH(1-39) was cleaved with the highest relative efficiency (k(cat)/K-m = 3.1 x 10(6) M(-1) s(-1)), while that of the monobasic site of CCK13-33 and the paired-basic site of proinsulin B-C junction, were cleaved less efficiently at 4.2 x 10(4) M(-1) s(-1) and 1.6 x 10(4) M(-1) s(-1), respectively. C1 NICHHD, DEV NEUROBIOL LAB, NIH, BETHESDA, MD 20892 USA. NICHHD, ENDOCRINE & REPROD RES BRANCH, NIH, BETHESDA, MD 20892 USA. UNIFORMED SERV UNIV HLTH SCI, DEPT BIOCHEM, BETHESDA, MD 20814 USA. ST LOUIS UNIV, MED CTR, DEPT PHARMACOL & PHYSIOL SCI, ST LOUIS, MO 63104 USA. FU NINDS NIH HHS [NS18667, NS31602] NR 43 TC 33 Z9 33 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4168 EP 4176 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000036 PM 8626758 ER PT J AU Berlett, BS Levine, RL Stadtman, ER AF Berlett, BS Levine, RL Stadtman, ER TI Comparison of the effects of ozone on the modification of amino acid residues in glutamine synthetase and bovine serum albumin SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; METAL-CATALYZED OXIDATION; HYDROXYL RADICALS; PROTEINS; DEGRADATION; DAMAGE; WATER; DERIVATIZATION; INACTIVATION; OZONATION AB During exposure to ozone, the methionine and aromatic amino acid residues of Escherichia coli glutamine synthetase (GS) and bovine serum albumin (BSA) are oxidized rapidly in the order Met > Trp > Tyr approximate to His > Phe. The loss of His is matched by a nearly equivalent formation of aspartate or of a derivative that is converted to aspartic acid upon acid hydrolysis. Conversion of His to aspartate was confirmed by showing that the oxidation of E. coli protein in which all His residues were uniformly labeled with C-14 gave rise to C-14-labeled aspartic acid in 80% yield and also by the demonstration that His residues in the tripeptides Ala-His-Ala or Ala-Ala-His gave rise to nearly stoichiometric amounts of aspartic acid whereas oxidation of His-Ala-Ala yielded only 36% aspartate. The oxidation of BSA and GS led to formation, respectively, of 11 and 3.3 eq of carbonyl groups and 0.5 and 0.3 eq of quinoprotein per subunit. Although BSA and GS contain nearly identical amounts of each kind of aromatic amino acid residues, oxidation of these residues in BSA was about 1.5-2.0 times faster than in GS indicating that the susceptibility to oxidation is dependent on the primary, secondary, tertiary, and quaternary structure of the protein. C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. RI Levine, Rodney/D-9885-2011 NR 47 TC 86 Z9 92 U1 3 U2 7 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4177 EP 4182 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000037 PM 8626759 ER PT J AU Krebsbach, PH Nakata, K Bernier, SM Hatano, O Miyashita, T Rhodes, CS Yamada, Y AF Krebsbach, PH Nakata, K Bernier, SM Hatano, O Miyashita, T Rhodes, CS Yamada, Y TI Identification of a minimum enhancer sequence for the type II collagen gene reveals several core sequence motifs in common with the link protein gene SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHLORAMPHENICOL ACETYLTRANSFERASE; PROCOLLAGEN GENE; MAMMALIAN-CELLS; CULTURED-CELLS; 1ST INTRON; EXPRESSION; TRANSCRIPTION; PROMOTER; DOMAIN; CARTILAGE AB The type II collagen gene (Col2a1) is expressed primarily in chondrocytes. Transcription of Col2a1 is mediated by cell-specific regulatory elements located within the promoter and first intron. Here, we map a minimal enhancer and identify elements that determine cartilage-specific Col2a1 expression by analyzing the activity of a series of chimeric genes consisting of rat Col2a1 first intron deletion mutants ligated to the chloramphenicol acetyltransferase reporter gene. We show that a 100-base pair (bp) segment within the first intron is the minimum size necessary for high level, cell type-specific expression of Col2a1. Sequence analysis of this 100-bp Col2a1 enhancer revealed several sequence motifs similar to motifs present within the regulatory region of the link protein gene, another cartilage gene. These motifs include an AT-rich element, a C1 motif and a C3 motif. Deletion of any of these elements reduced Col2a1 enhancer activity in chick embryo chondrocytes. We also tested enhancer-mediated activity in CFK2 cells which differentiate to a chondrogenic phenotype and begin to express type II collagen mRNA after extended culture. In stably transfected CFK2 cells, constructs containing the 100-bp enhancer were activated during the transition from prechondrogenic to chondrogenic cell populations and deletions within the enhancer strongly down-regulated activity. Chondrocyte-specific DNA-protein complexes were identified using nuclear extracts prepared from chick embryo chondrocytes and P-32-labeled oligonucleotides from these regions of the first intron. These results suggest that interaction of chondrocyte specific nuclear factors with multiple core elements from a small region within the first intron are important for cell-type specific Col2a1 enhancer activity. C1 NIDR,DEV BIOL LAB,NIH,BETHESDA,MD 20892. NR 35 TC 62 Z9 62 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4298 EP 4303 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000055 PM 8626777 ER PT J AU Hoeg, JM Vaisman, BL Demosky, SJ Meyn, SM Talley, GD Hoyt, RF Feldman, S Berard, AM Sakai, N Wood, D Brousseau, ME Marcovina, S Brewer, HB SantamarinaFojo, S AF Hoeg, JM Vaisman, BL Demosky, SJ Meyn, SM Talley, GD Hoyt, RF Feldman, S Berard, AM Sakai, N Wood, D Brousseau, ME Marcovina, S Brewer, HB SantamarinaFojo, S TI Lecithin:cholesterol acyltransferase overexpression generates hyperalpha-lipoproteinemia and a nonatherogenic lipoprotein pattern in transgenic rabbits SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DIFFERENT ALLELIC MUTATIONS; LIPID TRANSFER PROTEINS; FISH EYE SYNDROME; PLASMA; GENE; LCAT; EXPRESSION AB Cholesterol esterification within plasma lipoprotein particles is catalyzed by lecithin:cholesterol acyltransferase (LCAT). The impact of the overexpression of this enzyme on plasma concentrations of the different plasma lipoproteins in an animal model expressing cholesteryl ester transfer protein was evaluated by generating rabbits expressing human LCAT. A 6.2-kilobase human genomic DNA construct was injected into the pronuclei of rabbit embryos. Of the 1002 embryos that were injected, 3 founder rabbits were characterized that expressed the human LCAT gene. As in mice and humans, the principal sites of mRNA expression in these rabbits is in the liver and brain, indicating that the regulatory elements required for tissue-specific expression among these species are similar. The alpha-LCAT activity correlated with the number of copies of LCAT that integrated into the rabbit DNA. Compared with controls, the high expressor LCAT-transgenic rabbits total and high density lipoprotein (HDL) cholesterol concentrations were increased 1.5-2.5-fold with a 3.1-fold increase in the plasma cholesterol esterification rate. Analysis of the plasma lipoproteins by fast protein liquid chromatography indicates that these changes reflected an increased concentration of apolipoprotein E-enriched, HDL(1)-sized particles, whereas atherogenic apolipoprotein B particles disappeared from the plasma. The concentrations of plasma HDL cholesterol were highly correlated with both human LCAT mass (r = 0.93; p = 0.001) and the log LCAT activity (r = 0.94; p < 0.001) in the transgenic rabbits. These results indicate that overexpression of LCAT in the presence of cholesteryl ester transfer protein leads to both hyperalphalipoproteinemia and reduced concentrations of atherogenic lipoproteins. C1 NHLBI,LAB ANIM MED & SURG,NIH,BETHESDA,MD 20892. UNIV WASHINGTON,SCH MED,DEPT MED,NW LIPID RES LABS,SEATTLE,WA 98195. RP Hoeg, JM (reprint author), NHLBI,MOLEC DIS BRANCH,NIH,BLDG 10,RM 7N115,10 CTR DR MSC 1666,BETHESDA,MD 20892, USA. NR 37 TC 87 Z9 88 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4396 EP 4402 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000068 PM 8626790 ER PT J AU Krebsbach, PH Lee, SK Matsuki, Y Kozak, CA Yamada, RM Yamada, Y AF Krebsbach, PH Lee, SK Matsuki, Y Kozak, CA Yamada, RM Yamada, Y TI Full-length sequence, localization, and chromosomal mapping of ameloblastin - A novel tooth-specific gene SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN; ENAMEL; BONE; PHOSPHOPROTEIN; PURIFICATION; SIALOPROTEIN AB We report the full-length sequencing, cell type-specific expression, and immunolocalization of a novel gene expressed in rat incisors, which we have designated ameloblastin. Northern blot analysis of RNA from multiple rat and mouse tissues demonstrated high levels of expression of two distinct transcripts of approximately 2.0 and 1.6 kilobase pairs that were expressed only in teeth. In situ hybridization using a digoxigenin-labeled RNA probe showed that the tissue distribution of ameloblastin was limited to the ameloblast in rat incisors. Immunohistochemical staining of rat incisors using a polyclonal antibody raised against a fusion protein revealed a unique localization pattern. Ameloblastin was found to be expressed during the differentiation of inner enamel epithelium into ameloblasts, with intense localization in the Tomes' processes of secretory ameloblasts. In contrast to amelogenin, only modest amounts of ameloblastin were detected in enamel matrix. The ameloblastin gene encodes an open reading frame of 422 amino acids corresponding to a putative protein of 45 kDa. The predicted protein is acidic (pI = 5.54) and the most abundant amino acids are Pro (15.2%), Gly (9.9%), and Leu (9.9%). We have also mapped the ameloblastin gene, Ambn, to a locus on mouse chromosome 5 near other genes associated with mineralized tissues. Thus, ameloblastin represents a unique ameloblast-specific gene product that may be important in enamel matrix formation and mineralization. C1 NIDR,DEV BIOL LAB,NIH,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,NIH,BETHESDA,MD 20892. OI Yamada, Kenneth/0000-0003-1512-6805 NR 35 TC 227 Z9 240 U1 0 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4431 EP 4435 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000072 PM 8626794 ER PT J AU Wang, YS Macke, JP Abella, BS Andreasson, K Worley, P Gilbert, DJ Copeland, NG Jenkins, NA Nathans, J AF Wang, YS Macke, JP Abella, BS Andreasson, K Worley, P Gilbert, DJ Copeland, NG Jenkins, NA Nathans, J TI A large family of putative transmembrane receptors homologous to the product of the Drosophila tissue polarity gene frizzled SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FACTOR MESSENGER-RNAS; MOLECULAR-CLONING; RAT-BRAIN; PROTEIN; MOUSE; ORGANIZATION; SEQUENCES; ALIGNMENT; WINGLESS; ENCODES AB In Drosophila melanogaster, the frizzled gene plays an essential role in the development of tissue polarity as assessed by the orientation of cuticular structures. Through a combination of random cDNA sequencing, degenerate polymerase chain reaction amplification, and low stringency hybridization we have identified six novel frizzled homologues from mammals, at least 11 from zebrafish, several from chicken and sea urchin, and one from Caenorhabditis elegans. The complete deduced amino acid sequences of the mammalian and nematode homologues share with the Drosophila frizzled protein a conserved amino-terminal cysteine-rich domain and seven putative transmembrane segments. Each of the mammalian homologues is expressed in a distinctive set of tissues in the adult, and at least three are expressed during embryogenesis. As hypothesized for the Drosophila frizzled protein, the frizzled homologues are likely to act as transmembrane receptors for as yet unidentified ligands. These observations predict the existence of a family of signal transduction pathways that are homologous to the pathway that determines tissue polarity in Drosophila. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT OPHTHALMOL,BALTIMORE,MD 21205. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. JOHNS HOPKINS UNIV,SCH MED,HOWARD HUGHES MED INST,BALTIMORE,MD 21205. RP Wang, YS (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205, USA. RI Abella, Benjamin/G-3579-2010 NR 43 TC 305 Z9 320 U1 0 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4468 EP 4476 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000078 PM 8626800 ER PT J AU Wondrak, EM Nashed, NT Haber, MT Jerina, DM Louis, JM AF Wondrak, EM Nashed, NT Haber, MT Jerina, DM Louis, JM TI A transient precursor of the HTV-1 protease - Isolation, characterization, and kinetics of maturation SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-1 PROTEASE; ESCHERICHIA-COLI; PROTEINASES; INHIBITION; PARTICLES; FUSION; SALT; GAG AB Recently, the mechanism of autoprocessing of the protease (PR) of the human immunodeficiency virus type 1 from the model polyprotein, MBP-Delta TF-PR-Delta Pol, which contains the protease linked to short native flanking sequences (Delta TF and Delta Pol) fused to the maltose binding protein (MBP) of Escherichia coli, was reported (Louis, J. M., Nashed, N. T., Parris, G. D., Kimmel, A. R., and Jerina, D. M. (1994) Proc, Natl Acad Sci. U.S.A. 91, 7970-7974). According to this mechanism, intramolecular cleavage of the N-terminal strands of the dimeric MBP-Delta TF-PR-Delta Pol protein leads to the formation of the PR-Delta Pol intermediate, which is subsequently converted to the mature protease by cleavage of the C-terminal strands. We now report the purification and characterization of the PR-Delta Pol intermediate and the kinetics of its processing to the mature protease. Unlike the MBP-Delta TF-PR-Delta Pol precursor, PR-Delta Pol has proteolytic activity similar to that of the mature enzyme at pH 5.0. The pH rate profile for k(cat)/K-m is similar to that of the mature protease above pH 4.0. Although the PR-Delta Pol is more sensitive than the mature protease toward denaturing reagents, both the enzymatic activity and the intrinsic fluorescence of PR-Delta Pol are linearly dependent on the protein concentration, indicating that the protein is largely in its dimeric form above 10 nM. In contrast to the first-order kinetics observed for the proteolytic reaction at the N terminus of the protease, the proteolytic reaction at the C terminus of the protease is second order in protein concentration. These results are discussed in terms of a mechanism in which the C-terminally located Delta Pol peptide chains are cleaved intermolecularly to release the mature protease. C1 NIDDK, MOL MECHANISMS DEV SECT, CELLULAR & DEV BIOL LAB, NIH, BETHESDA, MD 20892 USA. NIDDK, SECT OXIDAT MECHANISMS, BIOORGAN CHEM LAB, NIH, BETHESDA, MD 20892 USA. NR 23 TC 49 Z9 49 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4477 EP 4481 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000079 PM 8626801 ER PT J AU Lee, JH Jang, SI Yang, JM Markova, NG Steinert, PM AF Lee, JH Jang, SI Yang, JM Markova, NG Steinert, PM TI The proximal promoter of the human transglutaminase 3 gene - Stratified squamous epithelial-specific expression in cultured cells is mediated by binding of Sp1 and ets transcription factors to a proximal promoter element SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN EPIDERMAL TRANSGLUTAMINASE; HAIR FOLLICLE TRANSGLUTAMINASES; AMINO-ACID-SEQUENCE; KERATINOCYTE TRANSGLUTAMINASE; TRANSGENIC MICE; RETINOIC ACID; GUINEA-PIG; PROTRANSGLUTAMINASE-E; ENVELOPE PRECURSOR; HUMAN LORICRIN AB The transglutaminase 3 enzyme is expressed during the late stages of the terminal differentiation of the epidermis and in certain cell types of the hair follicle. The enzyme is thought to be critically involved in the crosslinking of structural proteins and in the formation of the cornified cell envelope, thereby contributing to rigid structures that play vital roles in shape determination and/or barrier functions. To explore the mechanisms regulating the expression of the transglutaminase 3 gene (TGM3), 3.0 kilobase pairs of sequences upstream from the transcription start site were assessed for their ability to control the expression of a chloramphenicol acetyltransferase reporter gene. Deletion analyses in transiently transfected epidermal keratinocytes defined sequences between -126 and -91 as the proximal promoter region of the gene, and which can confer epithelial-specific expression to the TGM3 gene in vitro. Mutation and DNA-protein binding analyses indicated that a complex interaction between adjacent Sp1- and ets-like recognition motifs with their cognate binding factors is required for the function of the TGM3 promoter. As these TGM3 sequences can confer promoter/enhancer activity to reporter genes at a level comparable to the powerful SV40 promoter, they may be useful for gene therapy in keratinocytes. C1 NIAMS,NIH,SKIN BIOL LAB,BETHESDA,MD 20892. NR 75 TC 88 Z9 88 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 23 PY 1996 VL 271 IS 8 BP 4561 EP 4568 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW960 UT WOS:A1996TW96000090 PM 8626812 ER PT J AU Hinton, DM MarchAmegadzie, R Gerber, JS Sharma, M AF Hinton, DM MarchAmegadzie, R Gerber, JS Sharma, M TI Characterization of pre-transcription complexes made at a bacteriophage T4 middle promoter: Involvement of the T4 MotA activator and the T4 AsiA protein, a sigma(70) binding protein, in the formation of the open complex SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE bacteriophage; transcription; activation; MotA; AsiA ID COLI RNA-POLYMERASE; ESCHERICHIA-COLI; ALPHA-SUBUNIT; ADP-RIBOSYLTRANSFERASE; REGION SEQUENCES; SIGMA-70 SUBUNIT; DNA; RECOGNITION; MUTANT; POLYPEPTIDES AB Bacteriophage T4 middle promoters have excellent matches to the -10 consensus sequence for the sigma(70) subunit of Escherichia coli RNA polymerase, but a binding site for the T4 transcriptional activator MotA replaces the sigma(70)-35 consensus. E. coli RNA polymerase transcribes from middle promoters with or without the activator. In contrast, transcription by T4-modified E. coli RNA polymerase, which is present during T4 infection, requires MotA. We show that transcription by unmodified polymerase from the T4 middle promoter P-uvsX is independent of the specific sequences within the -35 region, and the DNase I footprint obtained with unmodified polymerase and P-uvsX resembles those seen previously with E. coli ''extended -10'' promoters. In contrast, although T4-modified polymerase alone binds P-uvsX, promoter unwinding and detection of a DNase I footprint requires MotA. This footprint is significantly different from that obtained with unmodified polymerase, starting upstream of around position -20. Previous work has indicated that the T4 AsiA protein, which binds tightly to sigma(70), is the phage modification required for MotA activation. We show that in the presence of AsiA, MotA, and otherwise unmodified polymerase, DNase I protection of P-uvsX is now similar to that obtained with the fully modified polymerase and MotA up to around position -40. However, protection upstream of -40 is still similar to that seen with unmodified polymerase. Our results support the idea that MotA-dependent activation requires AsiA binding to sigma(70) to achieve specific protein-DNA contacts within the -20 to -40 region of a middle promoter. (C) 1996 Academic Press Limited RP Hinton, DM (reprint author), NIDDKD,NIH,MOL & CELLULAR BIOL LAB,BLDG 8,ROOM 2A-13,BETHESDA,MD 20892, USA. NR 39 TC 45 Z9 45 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD FEB 23 PY 1996 VL 256 IS 2 BP 235 EP 248 DI 10.1006/jmbi.1996.0082 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW565 UT WOS:A1996TW56500005 PM 8594193 ER PT J AU Yazynin, SA Deyev, SM Jucovic, M Hartley, RW AF Yazynin, SA Deyev, SM Jucovic, M Hartley, RW TI A plasmid vector with positive selection and directional cloning based on a conditionally lethal gene SO GENE LA English DT Article DE barnase; barstar; polylinker; ribonuclease ID BARNASE; EXPRESSION; STRAINS; BARSTAR AB A plasmid vector with a multiple cloning site (MCS) for positive selection of cloned inserts in Escherichia coli (Ec) has been devised, based on the expression plasmid (pMT416) for the bacterial ribonuclease barnase (Barn). The host is protected from the lethal effect of moderate expression of barn by expression of the gene bars, encoding its inhibitor, barstar (Bars), placed on the same plasmid. Full expression, however, is lethal. Induction is also lethal with the derived plasmid, pMT440, which has the pUC19 MCS inserted into barn. Under inducing conditions, transformation by the vector is lethal unless the product of the modified barn is inactivated by insertion of cloned DNA fragments into the MCS, Plasmid pMT440 is, therefore, a generally useful selective cloning vector not requiring any special strain of Ec. C1 NIDDK,CELLULAR & DEV BIOL LAB,NIH,BETHESDA,MD 20892. RUSSIAN ACAD SCI,VA ENGELHARDT MOLEC BIOL INST,MOSCOW 117984,RUSSIA. SLOVAK ACAD SCI,INST MOLEC BIOL,BRATISLAVA 84251,SLOVAKIA. RI Deyev, Sergey/F-8191-2014 OI Deyev, Sergey/0000-0002-3952-0631 NR 11 TC 17 Z9 18 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD FEB 22 PY 1996 VL 169 IS 1 BP 131 EP 132 DI 10.1016/0378-1119(95)00814-4 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA TX640 UT WOS:A1996TX64000023 PM 8635737 ER PT J AU Druey, KM Blumer, KJ Kang, VH Kehrl, JH AF Druey, KM Blumer, KJ Kang, VH Kehrl, JH TI Inhibition of C-protein-mediated MAP kinase activation by a new mammalian gene family SO NATURE LA English DT Article ID PHEROMONE RESPONSE PATHWAY; ALPHA-FACTOR PHEROMONES; SACCHAROMYCES-CEREVISIAE; G1 ARREST; A-FACTOR; DESENSITIZATION; PHOSPHORYLATION; RECEPTOR AB A GENERAL property of signal transduction pathways is that prolonged stimulation decreases responsiveness, a phenomenon termed desensitization. Yeast cells stimulated with mating pheromone activate a heterotrimeric G-protein-linked, MAP-kinase-dependent signalling pathway that induces G1-phase cell-cycle arrest and morphological differentiation (reviewed in refs 1, 2). Eventually the cells desensitize to pheromone and resume growth(3). Genetic studies have demonstrated the relative importance of a desensitization mechanism that uses the SST2 gene product, Sst2p(4-7). Here we identify a mammalian gene family termed RGS (for regulator of G-protein signalling) that encodes structural and functional homologues of Sst2p. Introduction of RGS family members into yeast blunts signal transduction through the pheromone-response pathway. Like SST2 (refs 8-10), they negatively regulate this pathway at a point upstream or at the level of the G protein. The RGS family members also markedly impair MAP kinase activation by mammalian G-protein-linked receptors, indicating the existence and importance of an SST2-like desensitization mechanism in mammalian cells. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,DEPT CELL BIOL & PHYSIOL,ST LOUIS,MO 63110. RI Blumer, Kendall/C-5268-2012 NR 28 TC 385 Z9 392 U1 0 U2 8 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 22 PY 1996 VL 379 IS 6567 BP 742 EP 746 DI 10.1038/379742a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TW567 UT WOS:A1996TW56700057 PM 8602223 ER PT J AU Latronico, AC Anasti, J Arnhold, IJP Rapaport, R Mendonca, BB Bloise, W Castro, M Tsigos, C Chrousos, GP AF Latronico, AC Anasti, J Arnhold, IJP Rapaport, R Mendonca, BB Bloise, W Castro, M Tsigos, C Chrousos, GP TI Testicular and ovarian resistance to luteinizing hormone caused by inactivating mutations of the luteinizing hormone-receptor gene SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID GONADOTROPIN C1 NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. CHILDRENS HOSP NEW JERSEY, DEPT PEDIAT ENDOCRINOL & METAB, NEWARK, NJ USA. UNIV & MED DENT NEW JERSEY, NEW JERSEY MED SCH, NEWARK, NJ USA. UNIV SAO PAULO, HOSP CLIN, DIV ENDOCRINOL, BR-05508 SAO PAULO, BRAZIL. RI Castro, Margaret/A-4918-2009; Mendonca, Berenice/C-2827-2012; ARNHOLD, IVO/D-2672-2012; OI Latronico Xavier, Ana Claudia/0000-0001-6782-693X NR 25 TC 217 Z9 225 U1 0 U2 3 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 22 PY 1996 VL 334 IS 8 BP 507 EP 512 DI 10.1056/NEJM199602223340805 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA TV686 UT WOS:A1996TV68600005 PM 8559204 ER PT J AU Karl, M Saviolakis, GA Gravanis, A Chrousos, GP Margioris, AN AF Karl, M Saviolakis, GA Gravanis, A Chrousos, GP Margioris, AN TI The PC12 rat pheochromocytoma cell line expresses the prodynorphin gene and secretes the 8 kDa dynorphin product SO REGULATORY PEPTIDES LA English DT Article DE PC12; pheochromocytoma; dynorphin; opioid ID PHENYLETHANOLAMINE N-METHYLTRANSFERASE; BOVINE ADRENAL-MEDULLA; INSITU HYBRIDIZATION; CHROMAFFIN CELLS; PROENKEPHALIN-A; OPIOID-PEPTIDES; MESSENGER-RNAS; OPIATE BINDING; PITUITARY; ENKEPHALINS AB Most adrenal chromaffin cells synthesize opioids derived from proenkephalin but not from prodynorphin. However, human pheochromocytomas and the PC12 rat pheochromocytoma cell line synthesize dynorphins. The aim of this study was to confirm the presence of the authentic prodynorphin transcript and its dynorphin product in PC12 cells. We have found that the sequence of a 458 bp cDNA fragment derived from RT-PCR amplification of total PC12 RNA was in complete accordance with the published sequence of the equivalent region of the prodynorphin gene. It encodes the potent endogenous kappa opioid agonists alpha-neo-endorphin, dynorphin A and dynorphin B. Furthermore, immunoaffinity-purified PC12 cell extracts were subjected to RP-HPLC. Most of its IR-dynorphin eluted on a peak exhibiting the retention time of similarly treated rat anterior pituitary. The expression of the prodynorphin gene in pheochromocytomas can be explained as either the result of (a) the process of dedifferentiation of chromaffin cells to pheochromocytoma which may thus cause the expression of a previously unexpressed prodynorphin or that (b) those pheochromocytomas expressing the prodynorphin gene derive from the few, centrally located chromaffin cells, which express this gene even under normal conditions. C1 NICHHD, NIH, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. WALTER REED ARMY INST RES, DEPT MED NEUROSCI, WASHINGTON, DC 20307 USA. UNIV CRETE, SCH MED, DEPT PHARMACOL, GR-71110 IRAKLION, GREECE. UNIV CRETE, SCH MED, DEPT CLIN CHEM, GR-71110 IRAKLION, GREECE. NR 37 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD FEB 22 PY 1996 VL 61 IS 2 BP 99 EP 104 DI 10.1016/0167-0115(95)00144-1 PG 6 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA TY798 UT WOS:A1996TY79800003 PM 8852811 ER PT J AU McKenna, IM Bare, RM Waalkes, MP AF McKenna, IM Bare, RM Waalkes, MP TI Metallothionein gene expression in testicular interstitial cells and liver of rats treated with cadmium SO TOXICOLOGY LA English DT Article DE cadmium; metallothionein; testicular interstitial cells; liver ID DIETARY ZINC-DEFICIENCY; ISOLATED LEYDIG-CELLS; BINDING PROTEINS; I GENE; TESTES; TOXICITY; MICE; RESISTANCE; CARCINOGENESIS; PURIFICATION AB The rodent testes are generally more susceptible to cadmium (Cd)-induced toxicity than the liver. Cd induces predominantly testicular interstitial cell (TIC) tumors. In order to clarify the molecular mechanism underlying tissue differences in Cd sensitivity, we compared Cd-induced metallothionein (MT) gene expression, MT protein accumulation, and Cd retention in freshly isolated TICs and liver. Adult male Fischer rats received a s.c. injection of 4.0 mu mol Cd/kg or vehicle and 24 h later tissues were sampled and TICs isolated. MT-I and MT-II mRNA levels were determined by slot-blot analysis followed by densitometry scanning, and MT was estimated by the Cd-heme method. Testicular lesions were not grossly or histologically observed in rats treated with 4 mu mol Cd/kg. Both MT mRNA and MT (as determined by Cd-binding capacity) were constitutively present in TICs as well as the liver. TICs isolated from Cd-treated rats accumulated more Cd (4-fold), and had higher levels of MT-I (1.9-fold) and MT-II (1.4-fold) mRNAs over control, but contained less MT (30% decrease) than TICs isolated from control animals. Cd exposure substantially increased hepatic Cd content (6000-fold), MT (58-fold), and MT-I mRNA (5.3-fold), but did not increase MT-II mRNA. Thus, our findings indicate that, although low-dose Cd exposure results in increases of MT mRNA in TICs it does not enhance MT synthesis within these cells. The inability to induce the metal-detoxicating MT-protein, in response to Cd, might account for higher susceptibility of testes to Cd toxicity and carcinogenesis relative to liver. RP McKenna, IM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,INORGAN CARCINOGENESIS SECT,FREDERICK,MD 21702, USA. NR 45 TC 25 Z9 31 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0300-483X J9 TOXICOLOGY JI Toxicology PD FEB 22 PY 1996 VL 107 IS 2 BP 121 EP 130 DI 10.1016/0300-483X(95)03252-B PG 10 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA TX423 UT WOS:A1996TX42300004 PM 8599171 ER PT J AU Rodriguez, RE Misra, M Diwan, BA Riggs, CW Kasprzak, KS AF Rodriguez, RE Misra, M Diwan, BA Riggs, CW Kasprzak, KS TI Relative susceptibilities of C57BL/6, (C57BL/6xC3H/He)F-1, and C3H/He mice to acute toxicity and carcinogenicity of nickel subsulfide SO TOXICOLOGY LA English DT Article DE nickel; toxicity; carcinogenesis; mice ID LIPID-PEROXIDATION; DIFFERENT STRAINS; RAT SERUM; DISSOLUTION; SYSTEMS; DAMAGE; CELLS; LIVER AB The aim of this study was to compare susceptibility of mice of different strains to the toxicity and carcinogenicity of nickel subsulfide (Ni3S2), a water insoluble compound suspected to damage cells through oxidative mechanisms. Groups of 30 male mice of each strain, C57BL/6 (C57BL), (C57BL/6 x C3H/He)F-1 (B6C3F1), and C3H/He (C3H), were injected with single doses of 0.5-10 mg of Ni3S2/site into the thigh muscle and observed for up to 78 weeks, The highest Ni3S2 dose was lethal within 1 week to C57BL(93%) > B6C3F1 (80%) > C3H(53%) mice. The most susceptible C57BL mice also had the most severe necrotic/inflammatory kidney damage, compared with that in the other mice. The final incidence of local sarcomas at the 5 mg Ni3S2 dose was: C3H (97%) > B6C3F1 (76%) > C57BL (40% of mice at risk, i.e. those surviving at least 25 weeks; P < 0.05 or better as compared to the incidence in C3H mice). The relatively highest acute toxicity of Ni3S2 in C57BL mice, observed in the present study, concurred with the weakest antioxidant response to systemic water-soluble nickel(II), resulting in reduction in glutathione (GSH) level and increased lipid peroxidation (LPO) in their kidneys and livers, two main targets of acute nickel toxicity, reported by us previously (Toxicol. Lett. 1991, 57, 269; ibid. 1991, 58, 121). Ni3S2 deposited in the muscle, therefore, constitutes a source of soluble nickel that can reach and damage distant organs. The strongest tumor response in C3H mice relative to other strains did, in turn, concur with the lowest base levels of GSH and highest LPO in their muscle, the target for Ni3S2 carcinogenesis. Thus, the acute toxicity and carcinogenicity of Ni3S2 and Ni3S2-derived soluble nickel(II) in mice seem to depend, at least in part, on antioxidant capacity of target organs, which varies among different strains. C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. SAIC FREDERICK,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DATA MANAGEMENT SERV INC,FREDERICK,MD 21702. NR 24 TC 26 Z9 26 U1 0 U2 3 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0300-483X J9 TOXICOLOGY JI Toxicology PD FEB 22 PY 1996 VL 107 IS 2 BP 131 EP 140 DI 10.1016/0300-483X(95)03251-A PG 10 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA TX423 UT WOS:A1996TX42300005 PM 8599172 ER PT J AU LuYao, GL Potosky, AL Albertsen, PC Wasson, JH Barry, MJ Wennberg, JE AF LuYao, GL Potosky, AL Albertsen, PC Wasson, JH Barry, MJ Wennberg, JE TI Follow-up prostate cancer treatments after radical prostatectomy: A population-based study SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID CARCINOMA; MEDICARE; PRESERVATION; MANAGEMENT; MORBIDITY; OUTCOMES AB Background: Radical prostatectomy is one of the most commonly used curative procedures for the treatment of localized prostate cancer. The probability that a patient will undergo additional cancer therapy after this procedure is largely unknown. Purpose: The objective was to determine the likelihood of additional cancer therapy after radical prostatectomy. Methods: Data for this study were derived from a linked dataset that combined information from the Surveillance, Epidemiology, and End Results Program and Medicare hospital and physician claims. Records were included in this study if patient histories met the following criteria: (a) residing in Connecticut, Washington (Seattle-Puget Sound), or Georgia (Metropolitan Atlanta); (b) having been diagnosed with prostate cancer during the period from January 1, 1985, through December 31, 1991; (c) undergoing radical prostatectomy by December 31, 1992; and (d) having no evidence of other types of cancer. Patients were considered to have had additional cancer therapy if they had had radiation therapy, orchiectomy, and/or androgen-deprivation therapy by injection after radical prostatectomy. The interval between the initial treatment and any follow-up treatment was calculated from the date of radical prostatectomy to the Ist day of the follow-up cancer therapy. All presented probabilities are based on Kaplan-Meier estimates. Results: The study population consisted of 3494 Medicare patients, 3173 of whom underwent radical prostatectomy within 3 months of prostate cancer diagnosis. Although radical prostatectomy is often reserved for localized cancer, less than 60% (1934) of patients whose records were included in this study had organ-confined disease, according to final surgical pathology. Overall, the 5-year cumulative incidence of having any additional cancer treatment after radical prostatectomy reached 34.9% (95% confidence interval [CI] = 31.5% -38.5%). For patients with pathologically organ-confined cancer, the 5-year cumulative incidence was 24.3% (95% CI = 20.0%-29.3%) overall and ranged from 15.6% (95% CI = 9.7%-24.5%) for well-differentiated cancer (Gleason scores 2-4) to 41.5% (95% CI = 27.9%-58.4%) for poorly differentiated cancer (Gleason scores 8-10). The corresponding figures for pathologically regional cancer were 22.7% (95% CI = 12.9%-40.5%) and 68.1% (95% CI = 58.7%-77.1%). Conclusion: Further treatment of prostate cancer was done in about one third of patients who had had a radical prostatectomy with curative intent and in about one quarter of patients who were found to have organ-confined disease. Implications: Given the common requirement for follow-up cancer treatments after radical prostatectomy and the uncertainties about the effectiveness of the various follow-up treatment strategies, further investigation of these treatments is warranted. C1 NCI,DIV CANC PREVENT & CONTROL,SURVEILLANCE PROGRAM,BETHESDA,MD 20892. UNIV CONNECTICUT,DIV UROL,DEPT SURG,FARMINGTON,CT. MASSACHUSETTS GEN HOSP,MED PRACTICES EVALUAT CTR,BOSTON,MA 02114. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,CTR EVALUAT CLIN SCI,HANOVER,NH 03756. FU AHRQ HHS [HS08397, HS06336] NR 40 TC 146 Z9 150 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD FEB 21 PY 1996 VL 88 IS 3-4 BP 166 EP 173 DI 10.1093/jnci/88.3-4.166 PG 8 WC Oncology SC Oncology GA TV723 UT WOS:A1996TV72300011 PM 8632490 ER PT J AU Dimitrov, DS Apostolova, M AF Dimitrov, DS Apostolova, M TI The limit of PCR amplification SO JOURNAL OF THEORETICAL BIOLOGY LA English DT Letter RP Dimitrov, DS (reprint author), NCI,MATH BIOL LAB,NIH,BETHESDA,MD 20892, USA. NR 2 TC 6 Z9 6 U1 0 U2 3 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-5193 J9 J THEOR BIOL JI J. Theor. Biol. PD FEB 21 PY 1996 VL 178 IS 4 BP 425 EP 426 DI 10.1006/jtbi.1996.0041 PG 2 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA UD481 UT WOS:A1996UD48100012 PM 8733480 ER PT J AU Davis, DA Dorsey, K Wingfield, PT Stahl, SJ Kaufman, J Fales, HM Levine, RL AF Davis, DA Dorsey, K Wingfield, PT Stahl, SJ Kaufman, J Fales, HM Levine, RL TI Regulation of HIV-1 protease activity through cysteine modification SO BIOCHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; SITE-DIRECTED MUTAGENESIS; DNA-BINDING DOMAIN; ESCHERICHIA-COLI; CONSERVED CYSTEINE; PROTEINASE DIMER; S-THIOLATION; INVITRO; CELLS; GLUTATHIONE AB The homodimeric protease of the human immunodeficiency virus 1 contains two cysteine residues per monomer which are highly conserved among viral isolates. However, these cysteine residues are not essential for catalytic activity which raises the question of why they are conserved. We have found previously that these cysteine residues are unusually susceptible to oxidation by metal ions, and this results in inhibition of protease activity. Recombinant protease mutants (C67A, C95A, and the double mutant C67A,C95A) were prepared to assess the possible role of these cysteines in redox regulation of the enzyme. Mixed disulfides were formed between the cysteine residues of the enzymes and low molecular weight thiols. Enzyme activity was lost when a mixed disulfide was formed between 5,5'-dithiobis(2-nitrobenzoic acid) and cysteine 95, while the same mixed disulfide at cysteine 67 reduced activity by 50%. This effect was reversible as normal activity could be restored when the enzyme was treated with dithiothreitol. The cysteines could also be modified with the common cellular thiol glutathione. Modification with glutathione was verified by mass spectrometry of the protein peaks obtained from HPLC separation. Glutathiolation of cysteine 95 abolished activity whereas modification at cysteine 67 increased the k(cat) by more than 2-fold with no effect on K-m. In addition, glutathiolation at cysteine 67 markedly stabilized the enzyme activity presumably by reducing autoproteolysis. These results demonstrate one possible mechanism for regulation of the HIV-1 protease through cysteine modification and identify additional targets for affecting protease activity other than the active site. C1 NHLBI, NIH, BIOCHEM LAB, BETHESDA, MD 20892 USA. OFF DIRECTOR, PROT EXPRESS LAB, BETHESDA, MD 20892 USA. NHLBI, BIOPHYS CHEM LAB, BETHESDA, MD 20892 USA. RI Levine, Rodney/D-9885-2011 NR 45 TC 75 Z9 76 U1 1 U2 7 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 20 PY 1996 VL 35 IS 7 BP 2482 EP 2488 DI 10.1021/bi951525k PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TW345 UT WOS:A1996TW34500048 PM 8652592 ER PT J AU Shiloach, J Kaufman, J Guillard, AS Fass, R AF Shiloach, J Kaufman, J Guillard, AS Fass, R TI Effect of glucose supply strategy on acetate accumulation, growth, and recombinant protein production by Escherichia coli BL21 (lambda DE3) and Escherichia coli JM109 SO BIOTECHNOLOGY AND BIOENGINEERING LA English DT Article DE Escherichia coli; acetate; protein, recombinant ID PSEUDOMONAS-AERUGINOSA; EXOTOXIN-A; EXPRESSION; CULTURES; BATCH; EXCRETION; STRAINS; SYSTEM; STAT AB Two Escherichia coli strains, widely used for the produc tion of various recombinant proteins, were compared for their pre-induction growth and acetate accumulation patterns. The strains studied were E. coli BL21 (lambda DE3), transformed with a plasmid encoding Pseudomonas exotoxin A, and an E. coli K12 derived strain, JM109, carrying a plasmid encoding maltose-binding protein fused with HIV protease. Cultures were grown in controlled bench-top fermenters to the optimal pre-induction density in both high glucose batch and low glucose fed batch strategies. The results showed the superiority of E. coli BL21 (lambda DES) as a host for a recombinant protein expression system. For example, JM109 responds differently to high glucose concentration and to low glucose concentration. Its acetate concentration was as high as 10 g/L in a batch mode and 5 g/L in a fed batch mode. In comparison, strain BL21 (lambda DE3) reached 2 g/L acetate when grown in batch mode and not more than 1 g/L acetate when grown in a fed batch mode. E. cell BL21 (lambda DE3), most likely, possesses an acetate self-control mechanism which makes it possible to grow to the desired pre-induction density in a high glucose medium using simple batch propagation techniques. Such a technique is cost effective, reproducible, and easy to scale up. (C) 1996 John Wiley & Sons, Inc. RP Shiloach, J (reprint author), NIH,BIOTECHNOL UNIT,BLDG 6,ROOM B1-33,BETHESDA,MD 20892, USA. NR 24 TC 95 Z9 103 U1 4 U2 16 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3592 J9 BIOTECHNOL BIOENG JI Biotechnol. Bioeng. PD FEB 20 PY 1996 VL 49 IS 4 BP 421 EP 428 DI 10.1002/(SICI)1097-0290(19960220)49:4<421::AID-BIT9>3.0.CO;2-R PG 8 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA TR945 UT WOS:A1996TR94500009 PM 18623597 ER PT J AU Ishwad, CS Ferrell, RE Rossie, KM Appel, BN Johnson, JT Myers, EN Law, JC Srivastava, S Gollin, SM AF Ishwad, CS Ferrell, RE Rossie, KM Appel, BN Johnson, JT Myers, EN Law, JC Srivastava, S Gollin, SM TI Loss of heterozygosity of the short arm of chromosomes 3 and 9 in oral cancer SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID CELL CARCINOMA; DELETION; REGIONS; HEAD; NECK AB Loss of heterozygosity (LOH) on chromosomes 3p and 9p has been documented in a variety of malignancies, which suggests the presence of tumor suppressor gene loci on these chromosomes. We have studied 77 oral carcinomas for LOH using 16 microsatellite markers distributed over 5 human chromosomes. Fifty-five (710/0) of these tumors showed LOH at one or more loci. A significant proportion of LOH at the informative tumors was observed at chromosomes 3p and 9p: 58% and 48%, respectively. A majority of the tumors showed lesser at multiple loci on chromosomes 3p or 9p or on both. Our results suggest that tumor suppressor genes located on the short arms of chromosomes 3 and 9 may be involved in the pathogenesis of oral carcinoma. These regions of deletion observed in oral cancers overlap those reported in other neoplasms. However, we did not find any evidence of these changes in tumor margins with early pathological changes. (C) 1996 Wiley-Liss, Inc. C1 UNIV PITTSBURGH,DEPT DIAGNOST DENT SCI,PITTSBURGH,PA 15261. UNIV PITTSBURGH,DEPT OTOLARYNGOL,PITTSBURGH,PA 15261. UNIV PITTSBURGH,INST CANC,PITTSBURGH,PA. NIH,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. RP Ishwad, CS (reprint author), UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT HUMAN GENET,130 DESOTO ST,PITTSBURGH,PA 15261, USA. NR 20 TC 41 Z9 41 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD FEB 20 PY 1996 VL 69 IS 1 BP 1 EP 4 PG 4 WC Oncology SC Oncology GA TX092 UT WOS:A1996TX09200001 PM 8600052 ER PT J AU Srivastava, S Rossi, SC AF Srivastava, S Rossi, SC TI Early detection research program at the NCI SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT Workshop on Genetic Screening for Colorectal Cancer CY APR 10-11, 1995 CL BETHESDA, MD ID NONPOLYPOSIS COLORECTAL-CANCER; C-MYC; BREAST CARCINOMAS; POOR PROGNOSIS; GENE; IDENTIFICATION; MUTATIONS; DIAGNOSIS; BENIGN; POLYPS AB The Early Detection Branch, Division of Cancer Prevention and Control, National Cancer Institute, has created a program called The Early Detection Research Network (EDRN). EDRN's mission is to support translational research leading to early detection of cancer. The objectives are to (i) establish a network of institutions with the facilities, resources, personnel and interest to undertake biomarker research in early cancer detection; (ii) advance the understanding of the molecular basis of tumorigenesis in relation to screening, early detection and risk assessment; (iii) identify potential biomarkers that can be used as outcome measures or as intermediate end-points for cancer screening studies and (iv) respond to late-breaking developments in the field of biomarkers in a timely fashion. This program has the singular purpose of studying biologic, molecular and genetic markers relevant to the early detection of prostate, colorectal, lung, head and neck, bladder and breast cancers. (C) 1996 Wiley-Liss, Inc. * RP Srivastava, S (reprint author), NCI,NIH,EARLY DETECT & COMMUNITY ONCOL PROGRAM,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,BETHESDA,MD 20892, USA. NR 25 TC 18 Z9 18 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD FEB 20 PY 1996 VL 69 IS 1 BP 35 EP 37 DI 10.1002/(SICI)1097-0215(19960220)69:1<35::AID-IJC8>3.0.CO;2-X PG 3 WC Oncology SC Oncology GA TX092 UT WOS:A1996TX09200008 PM 8600056 ER PT J AU Brown, ML Kessler, LG AF Brown, ML Kessler, LG TI Use of gene tests to detect hereditary predisposition to cancer: What do we know about cost effectiveness? SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT Workshop on Genetic Screening for Colorectal Cancer CY APR 10-11, 1995 CL BETHESDA, MD ID COLORECTAL-CANCER AB Mutations in 4 genes associated with DNA repair have been shown to be associated with hereditary non-polyposis colon cancer (HNPCC) in families which display unusually high risk for colorectal cancer. laboratory tests for mutations in these genes will soon be commercially available, raising the possibility that population-wide gene testing to identify individuals with an inherited susceptibility to colorectal cancer could be conducted. The purpose of our report is to explore the economic implications of conducting a program of population-wide screening for HNPCC compared with alternative programs which would be restricted to families already known to be at high risk for HNPCC. Rather than provide a definitive answer to these questions, our purpose is to indicate priority areas of research which need to be conducted before such a definitive analysis can be done. An exploratory analysis has been conducted to determine which factors are most important in determining the cost-effectiveness of a genetic testing program for HNPCC. The base case analysis focuses on current uncertainty about the population prevalence of the HNPCC genotype and phenotype, factors which are central to the cost-effectiveness of population-wide screening. Uncertainty in parameters related to the cost and effectiveness of screening and preventive interventions for HNPCC were explored using additional sensitivity analyses. Favorable levels of cost-effectiveness for population-wide screening are achieved only when the most favorable assumptions about HNPCC prevalence and the cost and effectiveness of screening and preventive interventions are made. (C) 1996 Wiley-Liss, Inc.* RP Brown, ML (reprint author), NCI,DIV CANC PREVENT & CONTROL,SURVEILLANCE PROGRAM,APPL RES BRANCH,BETHESDA,MD 20892, USA. NR 18 TC 19 Z9 19 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD FEB 20 PY 1996 VL 69 IS 1 BP 55 EP 57 DI 10.1002/(SICI)1097-0215(19960220)69:1<55::AID-IJC14>3.0.CO;2-J PG 3 WC Oncology SC Oncology GA TX092 UT WOS:A1996TX09200014 PM 8600063 ER PT J AU Szakmary, A Huang, SM Chang, DT Beachy, PA Sander, M AF Szakmary, A Huang, SM Chang, DT Beachy, PA Sander, M TI Overexpression of a Rrp1 transgene reduces the somatic mutation and recombination frequency induced by oxidative DNA damage in Drosophila melanogaster SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ESCHERICHIA-COLI; APURINIC ENDONUCLEASE; REPAIR ENZYMES; CELL-DIVISION; MUTANT; CLEAVAGE; PROTEIN; ASSAY AB Recombination repair protein 1 (Rrp1) includes a C-terminal region homologous to several DNA repair proteins, including Escherichia coli exonuclease III and human APE, that repair oxidative and alkylation damage to DNA, The nuclease activities of Rrp1 include apurinic/apyrimidinic endonuclease, 3'-phosphodiesterase, 3'-phosphatase, and 3'-exonuclease. As shown previously, the C-terminal nuclease region of Rrp1 is sufficient to repair oxidative- and alkylation-induced DNA damage in repair-deficient E. coli mutants. DNA strand-transfer and single-stranded DNA renaturation activities are associated with the unique N-terminal region of Rrp1, which suggests possible additional functions that include recombinational repair or homologous recombination. By using the Drosophila w/w(+) mosaic eye system, which detects loss of heterozygosity as changes in eye pigmentation, somatic mutation and recombination frequencies were determined in transgenic flies overexpressing wild-type Rrp1 protein from a heat-shock-inducible transgene. A large decrease in mosaic clone frequency is observed when Rrp1 overexpression precedes treatment with gamma-rays, bleomycin, or paraquat, In contrast, Rrp1 overexpression does not alter the spot frequency after treatment with the alkylating agents methyl methanesulfonate or methyl nitrosourea. A reduction in mosaic clone frequency depends on the expression of the Rrp1 transgene and on the nature of the induced DNA damage, These data suggest a lesion-specific involvement of Rrp1 in the repair of oxidative DNA damage. C1 NIEHS, MOLEC GENET LAB, RES TRIANGLE PK, NC 27709 USA. JOHNS HOPKINS UNIV, SCH MED, HOWARD HUGHES MED INST, DEPT MOLEC BIOL & GENET, BALTIMORE, MD 21205 USA. NR 46 TC 14 Z9 16 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 20 PY 1996 VL 93 IS 4 BP 1607 EP 1612 DI 10.1073/pnas.93.4.1607 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TW698 UT WOS:A1996TW69800048 PM 8643678 ER PT J AU Wijmenga, C Gregory, PE Hajra, A Schrock, E Ried, T Eils, R Liu, PP Collins, FS AF Wijmenga, C Gregory, PE Hajra, A Schrock, E Ried, T Eils, R Liu, PP Collins, FS TI Core binding factor beta-smooth muscle myosin heavy chain chimeric protein involved in acute myeloid leukemia forms unusual nuclear rod-like structures in transformed NIH 3T3 cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID VIRUS ENHANCERS; RECEPTOR-DELTA; GENE; RUNT; FUSION; AML1 AB Patients with the M4Eo subtype of acute myeloid leukemia almost invariably are found to have an inversion of chromosome 16 in their leukemic cells, which results in a gene fusion between the transcription factor called core binding factor beta (CBF beta) on 16q and a smooth muscle myosin heavy chain (SMMHC) gene on 16p, Subcellular localizations of the wild-type CBF beta and the CBF beta-SMMHC fusion protein were determined by immunofluorescence of NIH 3T3 cells that overexpress wild-type or fusion protein. Normal CBF beta showed an unexpected perinuclear pattern consistent with primary localization in the Golgi complex, The CBF beta-SMMHC fusion protein had a very different pattern. Nuclear staining included rod-like crystalline structures as long as 11 mu m. The heterodimeric partner of CBF beta, CBF alpha, formed part of this complex. Cytoplasmic staining included stress fibers that colocalized with actin, probably as a consequence of the myosin heavy chain component of the fusion protein, Deletion of different regions of the CBF beta portion of the fusion protein showed that binding to CBF alpha was not required for nuclear translocation, However, deletion of parts of the SMMHC domain of the fusion protein involved in myosin-mediated filament formation resulted in proteins that did not form rod-like structures. These observations confirm previous indirect evidence that the CBF beta-SMMHC fusion protein is capable of forming macromolecular nuclear aggregates and suggests possible models for the mechanism of leukemic transformation. C1 NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892. UNIV HEIDELBERG,INTERDISCIPLINARY CTR SCI COMP,HEIDELBERG,GERMANY. RP Wijmenga, C (reprint author), NATL CTR HUMAN GENOME RES,LAB GENE TRANSFER,BLDG 31,ROOM 4B09,31 CTR DR,BETHESDA,MD 20892, USA. RI Liu, Paul/A-7976-2012; Wijmenga, Cisca/D-2173-2009; Eils, Roland/B-6121-2009; OI Liu, Paul/0000-0002-6779-025X; Eils, Roland/0000-0002-0034-4036; Wijmenga, Cisca/0000-0002-5635-1614 NR 24 TC 27 Z9 27 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 20 PY 1996 VL 93 IS 4 BP 1630 EP 1635 DI 10.1073/pnas.93.4.1630 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TW698 UT WOS:A1996TW69800052 PM 8643682 ER PT J AU Venkateshan, CN Narayanan, R Espey, MG Moffett, JR Gajdusek, DC Gibbs, CJ Namboodiri, MAA AF Venkateshan, CN Narayanan, R Espey, MG Moffett, JR Gajdusek, DC Gibbs, CJ Namboodiri, MAA TI Immunocytochemical localization of the endogenous neuroexcitotoxin quinolinate in human peripheral blood monocytes macrophages and the effect of human T-cell lymphotropic virus type I infection SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE quinolinic acid; interferon gamma; kynurenine; tryptophan; neurotoxicity ID TROPICAL SPASTIC PARAPARESIS; HTLV-I; INDOLEAMINE 2,3-DIOXYGENASE; CEREBROSPINAL-FLUID; BACTERIAL LIPOPOLYSACCHARIDE; IMMUNODEFICIENCY-VIRUS; INVITRO INFECTION; L-TRYPTOPHAN; MOUSE LUNG; ACID AB Quinolinate (Quin), a metabolite in the kynurenine pathway of tryptophan degradation and a neurotoxin that appears to act through the N-methyl-D-aspartate receptor system, was localized in cultured human peripheral blood monocytes/macrophages (PBMOs) by using a recently developed immunocytochemical method, Quin immunoreactivity (Quin-IR) was increased in gamma interferon (IFN-gamma)-stimulated monocytes/macrophages (MOs), In addition, the precursors, tryptophan and kynurenine, significantly increased Quin-IR, Infection of MOs by human T-cell lymphotropic virus type I (HTLV-I) in vitro substantially increased both the number of Quin-IR cells and the intensity of Quin-IR, At the peak of the Quin-IR response, about 40% of the cells were Quin-IR positive, In contrast, only about 2-5% of the cells were positive for HTLV-I, as detected by both immunofluorescence for the HTLV-I antigens and PCR techniques for the HTLV-I Tax gene. These results suggest that HTLV-I-induced Quin production in MOs occurs by an indirect mechanism, perhaps via cytokines produced by the infection but not directly by the virus infection per se, The significance of these findings to the neuropathology of HTLV-I infection is discussed. C1 GEORGETOWN UNIV,DEPT BIOL,WASHINGTON,DC 20057. RP Venkateshan, CN (reprint author), NINCDS,NIH,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892, USA. NR 46 TC 14 Z9 14 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 20 PY 1996 VL 93 IS 4 BP 1636 EP 1641 DI 10.1073/pnas.93.4.1636 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TW698 UT WOS:A1996TW69800053 PM 8643683 ER PT J AU Arispe, N Pollard, HB Rojas, E AF Arispe, N Pollard, HB Rojas, E TI Zn2+ interaction with Alzheimer amyloid beta protein calcium channels SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE giant amyloid beta-protein channel; lipid bilayer; zinc-binding motif; zinc blockade ID BILAYER-MEMBRANES; DISEASE; BINDING; INSULIN; ZINC; NEUROTOXICITY; TRANSITION; PRECURSOR; ALUMINUM; NEURONS AB The Alzheimer disease 40-residue amyloid beta protein (A beta P[1-40]) forms cation-selective channels across acidic phospholipid bilayer membranes with spontaneous transitions over a wide range of conductances ranging from 40 to 4000 pS. Zn2+ has been reported to bind to A beta P[1-40] with high affinity, and it has been implicated in the formation of amyloid plaques, We now report the functional consequences of such Zn2+ binding for the A beta P[1-40] channel. Provided the A beta P[1-40] channel is expressed in the low conductance (<400 pS) mode, Zn2+ blocks the open channel in a dose-dependent manner, For A beta P[1-40] channels in the giant conductance mode (>400 pS), Zn2+ doses in the millimolar range were required to exert substantial blockade. The Zn2+ chelator o-phenanthroline reverses the blockade. We also found that Zn2+ modulates A beta P[1-40] channel gating and conductance only from one side of the channel, These data are consistent with predictions of our recent molecular modeling studies on A beta P[1-40] channels indicating asymmetric Zn2+-A beta P[1-40] interactions at the entrance to the pore. RP Arispe, N (reprint author), NIDDKD,NIH,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. NR 33 TC 179 Z9 182 U1 2 U2 10 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 20 PY 1996 VL 93 IS 4 BP 1710 EP 1715 DI 10.1073/pnas.93.4.1710 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TW698 UT WOS:A1996TW69800066 PM 8643694 ER PT J AU Brining, SK Smith, DV AF Brining, SK Smith, DV TI Distribution and synaptology of glossopharyngeal afferent nerve terminals in the nucleus of the solitary tract of the hamster SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Review DE horseradish peroxidase; taste; medulla oblongata; synaptic vesicles; electron microscopy ID SUPERIOR LARYNGEAL NERVE; TASTE BUD DISTRIBUTION; HORSERADISH-PEROXIDASE METHOD; PRIMARY SENSORY NEURONS; UPPER ALIMENTARY-TRACT; BRAIN-STEM NEURONS; CHORDA TYMPANI; CENTRAL PROJECTIONS; GUSTATORY SENSITIVITIES; TRANSGANGLIONIC DEGENERATION AB The distribution and synaptology of the afferent fibers of the glossopharyngeal nerve (IXN) in the hamster were studied by using horseradish peroxidase (HRP) histochemistry visualized with light and electron microscopy. Crystals of HRP were applied to the trunk of IXN in the vicinity of the petrosal ganglion. The densest IXN afferent label was distributed within the nucleus of the solitary tract (nst), just caudal to but overlapping with the area of termination of the facial nerve. Labeled IXN fibers extended rostrally to the principal trigeminal nucleus and caudally to the cervical spinal cord. There was significant labeling within the spinal trigeminal complex; the area postrema and the medullary reticular formation contained some labeled fibers. Ultrastructurally, the synaptic arrangements of anterogradely labeled IXN fibers were examined in the nst. Quantitative measures were taken of the area, maximum diameter, perimeter, and vesicles of labeled endings and the length of their synaptic junctions with dendritic processes. These endings were compared to comparable endings in control material and to published descriptions of VIIth nerve afferent terminals in the hamster nst. The synaptic relations of IXN afferent endings were predominantly with dendritic spines and shafts. The majority (86.6%) of IXN afferent endings were with dendritic processes that were not in apparent contact with other, unlabeled processes. Only 13.4% of IXN synaptic relationships were with dendritic processes that were also contacted by unlabeled vesicle-containing processes. This is in contrast to 31.2% of facial nerve afferent endings in the nst which make synaptic contact with such processes. There were more direct synaptic contacts between facial endings and unlabeled vesicle-containing processes (26.1%) than between IXN endings and unlabeled vesicle-containing processes (1.3%). Thus, unlike the glomerular-like endings of the gustatory fibers of the VIIth nerve, less complex relations appeared to characterize IXN synapses in the nst. These differences were related to the differential physiology of gustatory fibers in the VIIth nerve and IXN. (C) 1996 Wiley-Liss, Inc. C1 UNIV MARYLAND, SCH MED, DEPT ANAT, BALTIMORE, MD 21201 USA. RP Brining, SK (reprint author), NIA, NEUROSCI LAB,NIH,BLDG 10,10 CTR DR,MSC 1582, ROOM 6C-103, BETHESDA, MD 20892 USA. FU NIDCD NIH HHS [DC00066, DC00353] NR 116 TC 26 Z9 27 U1 1 U2 1 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0021-9967 EI 1096-9861 J9 J COMP NEUROL JI J. Comp. Neurol. PD FEB 19 PY 1996 VL 365 IS 4 BP 556 EP 574 PG 19 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA TV769 UT WOS:A1996TV76900004 PM 8742302 ER PT J AU Brew, BJ Wesselingh, SL Gonzales, M Heyes, MP Price, RW AF Brew, BJ Wesselingh, SL Gonzales, M Heyes, MP Price, RW TI How HIV leads to neurological disease SO MEDICAL JOURNAL OF AUSTRALIA LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; NERVOUS-SYSTEM; INFECTION; DEMENTIA; ABNORMALITIES; BRAIN C1 FLINDERS MED CTR, DEPT MICROBIOL & INFECT DIS, ADELAIDE, SA, AUSTRALIA. ROYAL MELBOURNE HOSP, DEPT ANAT PATHOL, NEUROPATHOL LAB, MELBOURNE, VIC, AUSTRALIA. NIMH, CLIN SCI LAB, BETHESDA, MD 20892 USA. UNIV CALIF SAN FRANCISCO, DEPT NEUROL, SERV NEUROL, SAN FRANCISCO, CA 94143 USA. RP Brew, BJ (reprint author), NATL CTR HIV EPIDEMIOL & CLIN RES, SYDNEY, NSW, AUSTRALIA. RI Brew, Bruce/J-6513-2012 NR 19 TC 11 Z9 13 U1 0 U2 1 PU AUSTRALASIAN MED PUBL CO LTD PI PYRMONT PA LEVEL 2, 26-32 PYRMONT BRIDGE RD, PYRMONT, NSW 2009, AUSTRALIA SN 0025-729X J9 MED J AUSTRALIA JI Med. J. Aust. PD FEB 19 PY 1996 VL 164 IS 4 BP 233 EP 234 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA TY143 UT WOS:A1996TY14300015 PM 8604196 ER PT J AU vonBorstel, RC Drake, JW Loeb, LA AF vonBorstel, RC Drake, JW Loeb, LA TI Mechanisms of antimutagenesis and anticarcinogenesis - Foreword SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Editorial Material RP vonBorstel, RC (reprint author), NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD FEB 19 PY 1996 VL 350 IS 1 BP 1 EP 3 DI 10.1016/0027-5107(96)90041-X PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TY150 UT WOS:A1996TY15000001 ER PT J AU Drake, JW AF Drake, JW TI The antievolutionary component of antimutagenesis and anticarcinogenesis: Where do mutation rates come from and where are they going? SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article; Proceedings Paper CT 4th International Conference on Mechanisms of Antimutagenesis and Anticarcinogenesis CY SEP 04-09, 1994 CL BANFF, CANADA SP IGEN Inc, Rockville, Tyler Res Instruments Corp, Edmonton, US Natl Canc Inst, US EPA, Kellogg Co, Alberta Heritage Fdn Med Res, Univ Alberta, Dairy Farmers Canada, Dairy Nutr Council Alberta, Nat Sci & Engn Res Council Canada, Raylo Chem, Edmonton, Genet Soc Can RP Drake, JW (reprint author), NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD FEB 19 PY 1996 VL 350 IS 1 BP 5 EP 8 DI 10.1016/0027-5107(95)00084-4 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TY150 UT WOS:A1996TY15000002 PM 8657196 ER PT J AU Schaaper, RM AF Schaaper, RM TI Suppressors of Escherichia coli mutT: Antimutators for DNA replication errors SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article; Proceedings Paper CT 4th International Conference on Mechanisms of Antimutagenesis and Anticarcinogenesis CY SEP 04-09, 1994 CL BANFF, CANADA SP IGEN Inc, Rockville, Tyler Res Instruments Corp, Edmonton, US Natl Canc Inst, US EPA, Kellogg Co, Alberta Heritage Fdn Med Res, Univ Alberta, Dairy Farmers Canada, Dairy Nutr Council Alberta, Nat Sci & Engn Res Council Canada, Raylo Chem, Edmonton, Genet Soc Can DE E-coli antimutator strain; mutator, mutT; gene; dnaE; DNA polymerase; fidelity of DNA replication; 8-oxo-dGTP ID POLYMERASE; SPECIFICITY; MUTATIONS; FIDELITY; STRAINS; SPECTRA AB Previous studies in our laboratory used a papillation assay to identify a set of mutations in the E. coli dnaE gene that confer increased accuracy of DNA replication (antimutators). These antimutators were isolated as suppressors of the high mutability of a mismatch-repair-defective mutL strain, in which the majority of mutations represent uncorrected replication errors (mainly A . T --> G . C and G . C --> A . T transitions). In the present study, we have sought suppressors of the high mutability of a mutT mutator strain. mutT strains produce a high frequency of A . T --> C . G transversions due to their lack of the mutT-encoded 8-oxo-dGTPase, leading to a high frequency of A (8-oxoG) mispairing errors. Following localized mutagenesis of the dnaE-dnaQ region of the chromosome, two strong suppressors of mutT mutability were obtained, both residing in the dnaE gene (dnaE940 and dnaE941). When subsequently tested in a mutL strain, these two alleles also proved antimutators in this background, dnaE941 being significantly stronger than the previously isolated antimutators. The results suggest that the DNA polymerase may use similar mechanisms to discriminate against A .(8-oxoG) transversion mispairs and A . C or T . G transition mispairs. The findings may also have significance for the interpretation of the antimutator effect conferred by these dnaE alleles in a wild-type (mut(+)) background. RP Schaaper, RM (reprint author), NIEHS,MOLEC GENET LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 17 TC 16 Z9 16 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD FEB 19 PY 1996 VL 350 IS 1 BP 17 EP 23 DI 10.1016/0027-5107(95)00086-0 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TY150 UT WOS:A1996TY15000004 PM 8657178 ER PT J AU Wachsman, JT AF Wachsman, JT TI The beneficial effects of dietary restriction: Reduced oxidative damage and enhanced apoptosis SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article; Proceedings Paper CT 4th International Conference on Mechanisms of Antimutagenesis and Anticarcinogenesis CY SEP 04-09, 1994 CL BANFF, CANADA SP IGEN Inc, Rockville, Tyler Res Instruments Corp, Edmonton, US Natl Canc Inst, US EPA, Kellogg Co, Alberta Heritage Fdn Med Res, Univ Alberta, Dairy Farmers Canada, Dairy Nutr Council Alberta, Nat Sci & Engn Res Council Canada, Raylo Chem, Edmonton, Genet Soc Can DE oxidative damage; carcinogenesis; aging; caloric restriction; apoptosis; glucocorticoids; poly(ADP-ribose) polymerase (PARP) ID HYDROGEN-PEROXIDE RELEASE; PROGRAMMED CELL-DEATH; FOOD RESTRICTION; POLY(ADP-RIBOSE) POLYMERASE; PHYSIOLOGICAL CONSEQUENCES; MITOCHONDRIAL-DNA; GENE CED-3; GENERATION; METABOLISM; INHIBITION AB There is compelling evidence for the central role of oxidative damage in the aging process and for the participation of reactive oxygen species in tumor initiation and promotion. Caloric restriction (CR) or energy restriction retards age-associated increases in mitochondrial free-radical production and reduces the accumulation of oxidatively damaged cell components. CR has also been shown to slow down age-related declines in various repair capabilities, including some types of DNA repair. It is proposed that inhibitors of mitochondrial electron transport and/or uncouplers of oxidative phosphorylation (rotenone, amytal, amiodarone, valinomycin, etc.), when used at extremely low doses, could mimic the effects of CR in model systems. The objective is to lower mitochondrial free-radical production by decreasing the fraction of electron carriers in the reduced state. In addition to a variety of other effects, CR has been shown to increase the rate of apoptosis, particularly in preneoplastic cells, and in general, to promote elevated levels of free glucocorticoids (GCs). GCs are known to induce tissue-specific apoptosis and to upregulate gap-junction-mediated intercellular communication (GJIC). Tumor promoters like phorbol eaters have the opposite effect, in that they inhibit both the process of apoptosis and GJIC. The enzyme poly (ADP-ribose) polymerase (PARP) is thought to play a central role in apoptosis, in a manner that has been highly conserved in evolution. There is good evidence that the apoptosis-associated Ca/Mg-dependent DNA endonuclease is maintained in a latent form by being poly (ADP-ribosylated). Apoptosis would require the removal of this polymer from the endonuclease, and, most likely, its removal from topoisomerase II and histone H1 as well. The role of poly (ADP-ribose) in apoptosis, carcinogenesis, and aging could be studied by the use of modulators of PARP activity (3-aminobenzamide, 3-nitrosobenzamide, 1% ethanol, etc.), inhibitors of poly (ADP-ribose) glycohydrolase activity (ethacridine, 43 degrees C, etc.), and inhibitors of the PARP-specific protease (interleuken-1 beta converting enzyme (ICE)-like protease). Also, it would be of interest to determine if CR can decrease the half-life of poly (ADP-ribose), upregulate GJIC, and modulate the activities of PARP, the glycohydrolase, and the PARP-specific protease, factors potentially important in these processes. RP Wachsman, JT (reprint author), NIEHS,ENVIRONM TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709, USA. NR 74 TC 69 Z9 72 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD FEB 19 PY 1996 VL 350 IS 1 BP 25 EP 34 DI 10.1016/0027-5107(95)00087-9 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TY150 UT WOS:A1996TY15000005 PM 8657188 ER PT J AU Negishi, M Iwasaki, M Juvonen, RO Sueyoshi, T Darden, TA Pedersen, LG AF Negishi, M Iwasaki, M Juvonen, RO Sueyoshi, T Darden, TA Pedersen, LG TI Structural flexibility and functional versatility of cytochrome P450 and rapid evolution SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article; Proceedings Paper CT 4th International Conference on Mechanisms of Antimutagenesis and Anticarcinogenesis CY SEP 04-09, 1994 CL BANFF, CANADA SP IGEN Inc, Rockville, Tyler Res Instruments Corp, Edmonton, US Natl Canc Inst, US EPA, Kellogg Co, Alberta Heritage Fdn Med Res, Univ Alberta, Dairy Farmers Canada, Dairy Nutr Council Alberta, Nat Sci & Engn Res Council Canada, Raylo Chem, Edmonton, Genet Soc Can DE cytochrome P450; rapid evolution; functional versatility; site-directed mutagenesis ID AMINO-ACID; SUBSTRATE SPECIFICITIES; HYDROXYLASE-ACTIVITIES; CRYSTAL-STRUCTURE; MUTATION; 15-ALPHA-HYDROXYLASE; SUPERFAMILY; DETERMINANT; RESIDUE-209; METABOLISM AB P450 represents a large group of heme-thiolate enzymes that exhibit remarkably diverse activities for the metabolism of numerous endogenous and exogenous chemicals. Recent site-directed mutagenesis studies indicate that a single mutation at any of the key residues can be enough to alter the substrate and/or product specificities in the P450 activities. Molecular modeling predicts that these key residues are located within the substrate heme pocket. Structural elements involved in diversifying P450 activity appear to correspond to the B' helix, the F helix and the F/G interhelical loop in the bacterial P450s. Structures represented by these regions are extremely variable despite the fact that the core of the P450 substrate pocket is well conserved. A mutation within these regions may result in a significant geometrical alteration of the pocket and lead to diversify the P450 activity. Phylogenetical analysis shows a relatively high rate of nonsynonymous substitution within these substrate binding regions. The functional versatility of P450 can thus be largely accounted for in terms of pocket change brought about by rapid mutations. C1 NIEHS,LAB QUANTITAT & COMPUTAT BIOL,RES TRIANGLE PK,NC 27709. RP Negishi, M (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,PHARMACOGENET SECT,RES TRIANGLE PK,NC 27709, USA. RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 37 TC 25 Z9 25 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD FEB 19 PY 1996 VL 350 IS 1 BP 43 EP 50 DI 10.1016/0027-5107(95)00089-5 PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TY150 UT WOS:A1996TY15000007 PM 8657195 ER PT J AU Haseman, JK Johnson, FM AF Haseman, JK Johnson, FM TI Analysis of national toxicology program rodent bioassay data for anticarcinogenic effects SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article; Proceedings Paper CT 4th International Conference on Mechanisms of Antimutagenesis and Anticarcinogenesis CY SEP 04-09, 1994 CL BANFF, CANADA SP IGEN Inc, Rockville, Tyler Res Instruments Corp, Edmonton, US Natl Canc Inst, US EPA, Kellogg Co, Alberta Heritage Fdn Med Res, Univ Alberta, Dairy Farmers Canada, Dairy Nutr Council Alberta, Nat Sci & Engn Res Council Canada, Raylo Chem, Edmonton, Genet Soc Can ID ANIMAL CARCINOGENICITY; TUMOR-INCIDENCE; MELATONIN; RATS; MICE AB We reanalyzed data from 218 two-year rodent carcinogenicity studies carried out by the National Toxicology Program (NTP). These data were originally collected for the purpose of identifying potential human carcinogens. However, the objective of our analysis was to investigate the frequency of possible anticarcinogenic effects in these data, since recurring cases of chemical-associated tumor reductions have been noted in the course of these studies over time. Our analysis reveals that most (> 90%) NTP-tested chemicals show at least one statistically significant (p < 0.05) decrease in site-specific tumor incidence. Because of the large number of statistical comparisons made in a long-term bioassay, random variability can account for many of these tumor decreases. However, we found that certain tumors (predominantly those with a high spontaneous incidence) show chemically related decreases far more frequently than chance expectation. Many of these decreases, particularly those for pituitary and mammary gland tumors, adrenal pheochromocytoma and uterine polyps in rats and liver and lung tumors in mice, are associated with the reduced body weights frequently observed in the dosed groups. The chemically related decreased incidences of leukemia in rats appear to be related to spleen damage, i.e., chemically related splenic toxicity is evident for most chemicals showing decreased incidences of leukemia. While random variability, associations with body weight and splenic toxicity can account for most of the decreased tumor incidences observed in NTP studies, there are other tumor decreases that could not be totally explained by these factors. Further investigations of possible mechanisms of action are underway. These data are relevant to the concept of chemoprevention as well as to the task of using long-term laboratory animal studies to predict enhanced human environmental-cancer risk for regulatory purposes. RP Haseman, JK (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 26 TC 40 Z9 40 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD FEB 19 PY 1996 VL 350 IS 1 BP 131 EP 141 DI 10.1016/0027-5107(95)00098-4 PG 11 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TY150 UT WOS:A1996TY15000016 PM 8657174 ER PT J AU Thomas, DC Umar, A Kunkel, TA AF Thomas, DC Umar, A Kunkel, TA TI Microsatellite instability and mismatch repair defects in cancer cells SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article; Proceedings Paper CT 4th International Conference on Mechanisms of Antimutagenesis and Anticarcinogenesis CY SEP 04-09, 1994 CL BANFF, CANADA SP IGEN Inc, Rockville, Tyler Res Instruments Corp, Edmonton, US Natl Canc Inst, US EPA, Kellogg Co, Alberta Heritage Fdn Med Res, Univ Alberta, Dairy Farmers Canada, Dairy Nutr Council Alberta, Nat Sci & Engn Res Council Canada, Raylo Chem, Edmonton, Genet Soc Can DE mutator phenotype; carcinogenesis; microsatellite instability; DNA replication fidelity; DNA repair ID NONPOLYPOSIS COLON-CANCER; ESCHERICHIA-COLI; COLORECTAL-CANCER; DNA-REPLICATION; MUTATIONS; TOLERANT; HOMOLOG; ERRORS C1 NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709. NR 29 TC 30 Z9 37 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD FEB 19 PY 1996 VL 350 IS 1 BP 201 EP 205 DI 10.1016/0027-5107(95)00112-3 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TY150 UT WOS:A1996TY15000023 PM 8657182 ER PT J AU Gill, M Vallada, H Collier, D Sham, P Holmans, P Murray, R McGuffin, P Nanko, S Owen, M Antonarakis, S Housman, D Kazazian, H Nestadt, G Pulver, AE Straub, RE MacLean, CJ Walsh, D Kendler, KS DeLisi, L Polymeropoulos, M Coon, H Byerley, W Lofthouse, R Gershon, E Golden, L Crow, T Freedman, R Laurent, C BodeauPean, S dAmato, T Jay, M Campion, D Mallet, J Wildenauer, DB Lerer, B Albus, M Ackenheil, M Ebstein, RP Hallmayer, J Maier, W Gurling, H Curtis, D Kalsi, G Brynjolfsson, J Sigmundson, T Petursson, H Blackwood, D Muir, W StClair, D He, L Maguire, S Moises, HW Hwu, HG Yang, L Wiese, C Tao, L Liu, XH Kristbjarnason, H Levinson, DF Mowry, BJ DonisKeller, H Hayward, NK Crowe, RR Silverman, JM Nancarrow, DJ Read, CM AF Gill, M Vallada, H Collier, D Sham, P Holmans, P Murray, R McGuffin, P Nanko, S Owen, M Antonarakis, S Housman, D Kazazian, H Nestadt, G Pulver, AE Straub, RE MacLean, CJ Walsh, D Kendler, KS DeLisi, L Polymeropoulos, M Coon, H Byerley, W Lofthouse, R Gershon, E Golden, L Crow, T Freedman, R Laurent, C BodeauPean, S dAmato, T Jay, M Campion, D Mallet, J Wildenauer, DB Lerer, B Albus, M Ackenheil, M Ebstein, RP Hallmayer, J Maier, W Gurling, H Curtis, D Kalsi, G Brynjolfsson, J Sigmundson, T Petursson, H Blackwood, D Muir, W StClair, D He, L Maguire, S Moises, HW Hwu, HG Yang, L Wiese, C Tao, L Liu, XH Kristbjarnason, H Levinson, DF Mowry, BJ DonisKeller, H Hayward, NK Crowe, RR Silverman, JM Nancarrow, DJ Read, CM TI A combined analysis of D22S278 marker alleles in affected sib-pairs: Support for a susceptibility locus for schizophrenia at chromosome 22q12 SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE linkage analysis; sib pair analysis; functional psychosis; candidate locus ID LINKAGE ANALYSIS; GENETIC-LINKAGE; STRATEGIES; FAMILIES AB Several groups have reported weak evidence for linkage between schizophrenia and genetic markers located on chromosome 22q using the lod score method of analysis. However these findings involved different genetic markers and methods of analysis, and so were not directly comparable. To resolve this issue we have performed a combined analysis of genotypic data from the marker D22S278 in multiply affected schizophrenic families derived from 11 independent research groups worldwide. This marker was chosen because it showed maximum evidence for linkage in three independent datasets (Vallada et al., Am J Med Genet 60:139-146, 1995; Polymeropoulos et al., Neuropsychiatr Genet 54:93-99, 1994; Lasseter et al., Am J Med Genet, 60:172-173, 1995. Using the affected sib-pair method as implemented by the program ESPA, the combined dataset showed 252 alleles shared compared with 188 alleles not shared (chi-square 9.31, 1df, P = 0.001) where parental genotype data was completely known. When sib-pairs for whom parental data was assigned according to probability were included the number of alleles shared was 514.1 compared with 437.8 not shared (chi-square 6.12, 1df, P = 0.006). Similar results were obtained when a likelihood ratio method for sib-pair analysis was used. These results indicate that may be a susceptibility locus for schizophrenia at 22q12. (C) 1996 Wiley-Liss, Inc. C1 INST PSYCHIAT, DEPT PSYCHOL MED, LONDON SE5 8AF, ENGLAND. UNIV WALES COLL CARDIFF, COLL MED, DEPT PSYCHOL MED, CARDIFF, S GLAM, WALES. TEIKYO UNIV, DEPT PSYCHIAT, TOKYO, JAPAN. UNIV GENEVA, GENEVA, SWITZERLAND. MIT, BOSTON, MA USA. UNIV PENN, PHILADELPHIA, PA 19104 USA. JOHNS HOPKINS UNIV, BALTIMORE, MD USA. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, DEPT HUMAN GENET & PSYCHIAT, RICHMOND, VA 23298 USA. ST LOMANS HOSP, DUBLIN, IRELAND. SUNY STONY BROOK, DEPT PSYCHIAT, STONY BROOK, NY 11794 USA. UNIV UTAH, SALT LAKE CITY, UT USA. CLIN RES CTR, HARROW HA1 3UJ, MIDDX, ENGLAND. NIMH, CLIN NEUROGENET BRANCH, BETHESDA, MD 20892 USA. UNIV UTAH, SCH MED, DEPT PSYCHIAT, SALT LAKE CITY, UT 84112 USA. UNIV COLORADO, HLTH SCI CTR, DENVER, CO USA. CNRS, LAB GENET MOL NEUROTRANSMISS & PROC NEUROGENERATI, PARIS, FRANCE. UNIV MUNICH, HOSP PSYCHIAT, W-8000 MUNICH, GERMANY. UNIV MAINZ, HOSP PSYCHIAT, MAINZ, GERMANY. HADASSAH HERZOG PSYCHOGENET PROGRAM, JERUSALEM, ISRAEL. UCL, SCH MED, LONDON W1N 8AA, ENGLAND. BORGARSPITALINN, DEPT PSYCHIAT, REYKJAVIK, ICELAND. ROYAL EDINBURGH & ASSOCIATED HOSP, DEPT PSYCHIAT, WESTERN GEN HOSP, MRC HUMAN GENET UNIT, EDINBURGH, MIDLOTHIAN, SCOTLAND. KIEL UNIV HOSP, DEPT PSYCHIAT, GENET MOLEC LAB, KIEL, GERMANY. NATL TAIWAN UNIV HOSP, DEPT PSYCHIAT, TAIPEI, TAIWAN. W CHINA UNIV, DEPT PSYCHIAT, CHENGDU, PEOPLES R CHINA. NATL UNIV HOSP REYKJAVIK, DEPT PSYCHIAT, REYKJAVIK, ICELAND. MED COLL PENN, DEPT PSYCHIAT, PHILADELPHIA, PA 19129 USA. HAHNEMANN UNIV, PHILADELPHIA, PA 19102 USA. UNIV QUEENSLAND, BRISBANE, QLD, AUSTRALIA. WASHINGTON UNIV, SCH MED, DEPT SURG, ST LOUIS, MO 63110 USA. QUEENSLAND INST MED RES, BRISBANE, QLD 4006, AUSTRALIA. UNIV IOWA HOSP & CLIN, DEPT PSYCHIAT, DES MOINES, IA USA. MT SINAI SCH MED, DEPT PSYCHIAT, NEW YORK, NY USA. STATE MENTAL HOSP, HAAR, GERMANY. RI turton, miranda/F-4682-2011; Gurling, Hugh/A-5029-2010; McGuffin, Peter/A-1565-2012; Antonarakis, Stylianos/N-8866-2014; Holmans, Peter/F-4518-2015; Vallada, Homero/D-1333-2014; OI murray, robin/0000-0003-0829-0519; McGuffin, Peter/0000-0002-9888-2907; Antonarakis, Stylianos/0000-0001-8907-5823; Holmans, Peter/0000-0003-0870-9412; Vallada, Homero/0000-0001-5123-8295; Gill, Michael/0000-0003-0206-5337 FU Medical Research Council [G9309834] NR 26 TC 168 Z9 171 U1 2 U2 8 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD FEB 16 PY 1996 VL 67 IS 1 BP 40 EP 45 DI 10.1002/(SICI)1096-8628(19960216)67:1<40::AID-AJMG6>3.0.CO;2-W PG 6 WC Genetics & Heredity SC Genetics & Heredity GA TY403 UT WOS:A1996TY40300007 PM 8678112 ER PT J AU Wu, S Moomaw, CR Tomer, KB Falck, JR Zeldin, DC AF Wu, S Moomaw, CR Tomer, KB Falck, JR Zeldin, DC TI Molecular cloning and expression of CYP2J2, a human cytochrome P450 arachidonic acid epoxygenase highly expressed in heart SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LIVER MICROSOMAL CYTOCHROME-P-450; ENDOGENOUS EPOXYEICOSATRIENOIC ACIDS; RAT-KIDNEY; ENANTIOFACIAL SELECTIVITY; STENOTOMUS-CHRYSOPS; COS CELLS; METABOLISM; OXYGENASE; IDENTIFICATION; LOCALIZATION AB A cDNA encoding a human cytochrome P450 arachidonic acid epoxygenase was isolated from a human liver cDNA library. Sequence analysis revealed that this 1,876-base pair cDNA contained an open reading frame and encoded a new 502-amino acid protein designated CYP2J2. Blot hybridization analysis of RNA prepared from human tissues revealed that CYP2J2 was highly expressed in the heart. Recombinant CYP2J2 protein was prepared using the baculovirus expression system and purified to near electrophoretic homogeneity. The enzyme metabolized arachidonic acid predominantly via olefin epoxidation to all four regioisomeric cis-epoxyeicosatrienoic acids (catalytic turnover 65 pmol of product formed/nmol of cytochrome P450/min at 30 degrees C). Epoxidation of arachidonic acid by CYP2J2 at the 14,15-olefin was highly enantioselective for (14R,15S)-epoxyeicosatrienoic acid (76% optical purity). Immunoblotting of microsomal fractions prepared from human tissues using a polyclonal antibody raised against the recombinant hemoprotein confirmed primary expression of CYP2J2 protein in human heart. The in vivo significance of CYP2J2 was suggested by documenting the presence of epoxyeicosatrienoic acids in the human heart using gas chromatography/mass spectroscopy. importantly, the chirality of CYP2J2 products matched that of the epoxyeicosatrienoic acid enantiomers present, in vivo, in human heart. We propose that CYP2J2 is one of the enzymes responsible for epoxidation of endogenous arachidonic acid pools in human heart and that epoxyeicosatrienoic acids may, therefore, play important functional roles in cardiac physiology. C1 NIEHS, PULM PATHOBIOL LAB, NIH, RES TRIANGLE PK, NC 27709 USA. UNIV TEXAS, SW MED CTR, DEPT MOLEC GENET, DALLAS, TX 75235 USA. NIEHS, MOLEC BIOPHYS LAB, NIH, RES TRIANGLE PK, NC 27709 USA. RI Tomer, Kenneth/E-8018-2013; OI Falck, John/0000-0002-9219-7845 FU NIGMS NIH HHS [GM31278, GM37922] NR 76 TC 314 Z9 325 U1 2 U2 7 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 16 PY 1996 VL 271 IS 7 BP 3460 EP 3468 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TV724 UT WOS:A1996TV72400022 PM 8631948 ER PT J AU Liu, YS Guyton, KZ Gorospe, M Xu, QB Kokkonen, GC Mock, YD Roth, GS Holbrook, NJ AF Liu, YS Guyton, KZ Gorospe, M Xu, QB Kokkonen, GC Mock, YD Roth, GS Holbrook, NJ TI Age-related decline in mitogen-activated protein kinase activity in epidermal growth factor-stimulated rat hepatocytes SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IMMEDIATE-EARLY GENE; DNA-SYNTHESIS; PHOSPHATASE; COMPLEX; JUN; FOS AB A number of studies have demonstrated that the proliferative capacity of cells declines with aging. In particular, epidermal growth factor (EGF)-stimulated DNA synthesis is reduced in hepatocytes from aged rats relative to young rats. Growth factor stimulation activates a genetic program in large part regulated by a family of mitogen-activated protein kinases (MAPK) that phosphorylate and thereby activate transcription factors involved in controlling the expression of proliferation-associated genes. In the present study, we compared the activation of the extracellular signal-regulated kinase 2 (ERK2) and c-Jun N-terminal kinase 1 (JNK1) MAPK in EGF-stimulated hepatocytes derived from young (6-month) and aged (24-month) rats. JNK activity was not appreciably altered by EGF treatment of cells from either age group, In contrast, ERK2 was highly activated by EGF treatment, but the magnitude of activation was significantly lower in hepatocytes of aged animals compared to those of young animals (7-fold versus 20-fold, respectively). The reduced ERK2 activity in response to EGF was associated with decreased c-fos and c-jun mRNA expression and lower levels of AP-1 transcription factor DNA binding activity in the aged hepatocytes. Finally, the basal expression of MAPK phosphatase 1, a MAPK-regulated gene involved in regulating MAPK activity, was higher in aged hepatocytes. Taken together, these findings suggest that an alteration in the balance between MAP kinase-phosphatase activities could con tribute to the age-related decline in proliferative capacity. C1 NIA,GERONTOL RES CTR,GENE EXPRESS & AGING SECT,BALTIMORE,MD 21224. NIA,MOLEC PHYSIOL & GENET SECT,CELLULAR & MOLEC BIOL LAB,BALTIMORE,MD 21224. RI Liu, Yusen/E-3527-2011 NR 36 TC 80 Z9 82 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 16 PY 1996 VL 271 IS 7 BP 3604 EP 3607 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TV724 UT WOS:A1996TV72400042 PM 8631968 ER PT J AU Austin, SJ Fujimoto, W Marvin, KW Vollberg, TM Lorand, L Jetten, AM AF Austin, SJ Fujimoto, W Marvin, KW Vollberg, TM Lorand, L Jetten, AM TI Clotting and regulation of cornifin beta, a new member of the cornifin/spr family - Suppression by retinoic acid receptor-selective retinoids SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRACHEAL EPITHELIAL-CELLS; CROSS-LINKED ENVELOPE; HUMAN EPIDERMAL-CELLS; SQUAMOUS DIFFERENTIATION; KERATINOCYTE; EXPRESSION; GENE; TRANSGLUTAMINASE; INVOLUCRIN; PROTEINS AB In this study, we describe the isolation and characterization of a cDNA clone C12 that encodes a new member of the cornifin/small proline-rich protein (spr) family, which we have named cornifin beta, C12 encodes a 1.1-kilobase pair mRNA and a 24,3-kDa cytosolic protein with a high proline content (19%). Its total amino acid sequence exhibits a 37-66% identity while the first 30 amino acids at the amino terminus are 87% identical to that of members of the cornifin family, At its carboxyl terminus, cornifin beta contains 21 tandem repeats of an octapeptide, Cornifin beta expression is restricted to several squamous epithelia, It is highly expressed in esophagus, tongue, and oral mucosa but, in contrast to cornifin alpha, is not detectable in the epidermis. Both retinoic acid and a retinoid selective for the nuclear retinoic acid receptors were very potent suppressors of cornifin beta expression while an analog selective for the nuclear retinoid X receptors was much less effective, suggesting that a specific retinoid signaling pathway is involved in this suppression, Cornifin beta can function through some of its Gln residues as an amine acceptor in transglutaminase-catalyzed cross-linking reactions, These results indicate that cornifin beta functions as a cross-linked envelope precursor. C1 NIEHS,PULM PATHOBIOL LAB,CELL BIOL SECT,NIH,RES TRIANGLE PK,NC 27709. NR 32 TC 26 Z9 27 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 16 PY 1996 VL 271 IS 7 BP 3737 EP 3742 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TV724 UT WOS:A1996TV72400062 PM 8631988 ER PT J AU Shinomiya, K Inokuchi, N Gnabre, JN Muto, M Kabasawa, Y Fales, HM Ito, Y AF Shinomiya, K Inokuchi, N Gnabre, JN Muto, M Kabasawa, Y Fales, HM Ito, Y TI Countercurrent chromatographic analysis of ovalbumin obtained from various sources using the cross-axis coil planet centrifuge SO JOURNAL OF CHROMATOGRAPHY A LA English DT Article DE counter-current chromatography; cross-axis coil planet centrifuge; ovalbumin; proteins ID ROTARY SEALS; EFFICIENCY; APPARATUS; PHASE AB The present studies have been conducted to investigate the cause of an unusually broad peak of ovalbumin obtained by countercurrent chromatography (CCC) reported earlier [K. Shinomija et al., J. Chromatogr., 644 (1993) 215]. A series of CCC experiments using our prototyte of the cross-axis coil planet centrifuge revealed that commercial ovalbumin products were classified into two groups: group A formed two peaks of ovalbumin at pH 7.0 and 5.8, while group B showed a relatively sharp single peak in a broad range of pH. Electrophoresis indicated that the group A ovalbumin consisted of both natural and denatured products: the natural ovalbumin is a monomer (M(r) 45 000) whereas the denatured products form dimers (M(r) 90 000). The abnormally broad peak obtained from the group A ovalbumin at pH 9 is apparently caused by the heterogeneity of the sample protein. C1 JOHNS HOPKINS UNIV, DEPT BIOL, BALTIMORE, MD 21218 USA. NIHON UNIV, COLL SCI & TECHNOL, SCI & TECHNOL RES INST, MACHINE SHOP, FUNABASHI, CHIBA 274, JAPAN. NHLBI, BIOPHYS CHEM LAB, NIH, BETHESDA, MD 20892 USA. RP NIHON UNIV, COLL PHARM, 7-7-1 NARASHINODAI, FUNABASHI, CHIBA 274, JAPAN. NR 4 TC 21 Z9 21 U1 1 U2 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 EI 1873-3778 J9 J CHROMATOGR A JI J. Chromatogr. A PD FEB 16 PY 1996 VL 724 IS 1-2 BP 179 EP 184 DI 10.1016/0021-9673(95)00911-6 PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA TX704 UT WOS:A1996TX70400018 PM 8819795 ER PT J AU Ma, Y Sokoloski, E Ito, Y AF Ma, Y Sokoloski, E Ito, Y TI pH-zone refining counter-current chromatography of polar catecholamines using di-(2-ethylhexyl)phosphoric acid as a ligand SO JOURNAL OF CHROMATOGRAPHY A LA English DT Article DE pH-zone refining counter-current chromatography; counter-current chromatography; catecholamines; di-(2-ethylhexyl)phosphoric acid ID SEPARATION AB The use of di-(2-ethylhexyl)phosphoric acid (DEHPA) as a ligand in the stationary phase effectively increased the partition coefficient of polar catecholamines. pH-Zone refining counter-current chromatography of six components, i.e. five catecholamines and one amino acid (DOPA), was successfully performed using a two-phase solvent system composed of methyl tert.-butyl ether and water by adding DEHPA (20%) and ammonium acetate (200 mM) to the organic phase and KCl (50 mM) to the aqueous mobile phase. DOPA was eluted first as a normal peak followed by the five catecholamines which formed a succession of highly concentrated rectangular peaks associated with sharp impurity peaks at their borders (UV tracing at 280 nn). Both pH and standard partition coefficient of collected fractions indicated minimum overlap between the main peaks. Each component was identified by NMR analysis. C1 NHLBI,BIOPHYS CHEM LAB,NATL INST HLTH,BETHESDA,MD 20892. NR 19 TC 9 Z9 10 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 J9 J CHROMATOGR A JI J. Chromatogr. A PD FEB 16 PY 1996 VL 724 IS 1-2 BP 348 EP 353 DI 10.1016/0021-9673(95)00999-X PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA TX704 UT WOS:A1996TX70400038 PM 8819796 ER PT J AU Anderssen, N Jacobs, DR Sidney, S Bild, DE Sternfeld, B Slattery, ML Hannan, P AF Anderssen, N Jacobs, DR Sidney, S Bild, DE Sternfeld, B Slattery, ML Hannan, P TI Change and secular trends in physical activity patterns in young adults: A seven-year longitudinal follow-up in the coronary artery risk development in young adults study (CARDIA) SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE exercise; longitudinal studies; racial stocks ID MINNESOTA-HEART-SURVEY; BODY-MASS INDEX; CARDIOVASCULAR-DISEASE; SOCIOECONOMIC-FACTORS; SKINFOLD THICKNESS; HEALTH; TIME; EXERCISE; FITNESS; DETERMINANTS AB Levels and changes in self-reported physical activity over a 7-year period were examined to determine tracking and to estimate the proportion of total cohort change attributable to secular trends. A population-based sample of 2,328 men and 2,787 women aged 18-30 years at baseline (52% black and 48% white) from Birmingham, Alabama, Chicago, Illinois, Minneapolis, Minnesota, and Oakland, California, were examined four times between 1985-1986 and 1992-1993. The intraclass correlation for up to four measures was 0.57 for the entire sample, varying between 0.57 for white men and 0.42 for black women, indicating a moderate tendency for tracking. The energy expenditure in physical activity at each examination was greatest in black men and, compared with black men, about 5% less in white men, 30% less in white women, and 50% less in black women, The total cohort decrease in mean physical activity was approximately 30% in each race-sex group, The secular trend accounted for 38% of the total cohort change in black men, 43% in black women, 52% in white men, and 81% in white women, Physical activity declined sharply during the early years of adulthood, partly because of secular trend. Young adults are therefore an important target group for physical activity promotion programs to reverse individual and populationwide declines prior to middle age. Am J Epidemiol 1996;143:351-62. C1 UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55454. UNIV BERGEN,CTR HLTH PROMOT,BERGEN,NORWAY. KAISER PERMANENTE MED CARE PROGRAM,DIV RES,OAKLAND,CA 94611. NHLBI,DIV CLIN APPLICAT,BETHESDA,MD 20892. UNIV UTAH,SCH MED,SALT LAKE CITY,UT. RI Loureiro, Nuno/I-6400-2012 OI Loureiro, Nuno/0000-0002-1166-3219 FU NHLBI NIH HHS [N01-HC-48048, N01-HC-48047, N01-HC-48049] NR 51 TC 108 Z9 110 U1 0 U2 4 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 15 PY 1996 VL 143 IS 4 BP 351 EP 362 PG 12 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TU989 UT WOS:A1996TU98900006 PM 8633619 ER PT J AU Carroll, RJ Freedman, LS Hartman, AM AF Carroll, RJ Freedman, LS Hartman, AM TI Use of semiquantitative food frequency questionnaires to estimate the distribution of usual intake SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE calibration; cohort studies; diet surveys; epidemiologic methods; nutrition; questionnaires; statistics; study design ID LIMITATIONS; REPRODUCIBILITY; VALIDITY; DIET AB The authors consider whether semiquantitative food frequency questionnaires can be used to survey a population to estimate the distribution of usual intake. They take as an assumption that, if they were possible to obtain, the mean of many food records or recalls would be an accurate representation of an individual's usual diet. They then assume that nutrient intake as measured by a questionnaire follows a linear regression model when regressed against the usual intake of that nutrient, If the coefficients in this regression relation were known, then the distribution of usual intake could be constructed from the responses to the questionnaire. Since one generally does not know the values of the coefficients, they need to be estimated from a calibration study in which respondents complete the questionnaire together with multiple food records or recalls. This can be done either through an internal subset of the data or through an independent external study. With an internal substudy, the authors find that food frequency questionnaires typically provide little information about the distribution of usual intake in addition to that obtained from the multiple records or recalls in the substudy. When the substudy is external, if it is small then having very large numbers of subjects completing food frequency questionnaires in the survey is no more efficient than having a few subjects completing food records or recalls. However, if the external substudy is large and accurately characterizes the relation between the questionnaire response and usual intake, food frequency questionnaires can provide a cost-efficient way of estimating the distribution of usual intake. These results do not apply to the different problem of correcting relative risks for the effects of measurement error. Am J Epidemiol 1995;143:392-404. C1 NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,BETHESDA,MD 20892. TEXAS A&M UNIV,DEPT STAT,COLLEGE STN,TX 77843. NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,BETHESDA,MD 20892. FU NCI NIH HHS [CA-57030] NR 17 TC 19 Z9 20 U1 0 U2 3 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 15 PY 1996 VL 143 IS 4 BP 392 EP 404 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TU989 UT WOS:A1996TU98900010 PM 8633623 ER PT J AU Minor, JR Piscitelli, SC AF Minor, JR Piscitelli, SC TI Thalidomide in diseases associated with human immunodeficiency virus infection SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY LA English DT Letter ID NECROSIS-FACTOR-ALPHA; ULCERS RP Minor, JR (reprint author), NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT PHARM,CLIN PHARMACOKINET RES LAB,10 CTR DR,MSC-1196,BETHESDA,MD 20892, USA. NR 16 TC 5 Z9 5 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 1079-2082 J9 AM J HEALTH-SYST PH JI Am. J. Health-Syst. Pharm. PD FEB 15 PY 1996 VL 53 IS 4 BP 429 EP 431 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TW767 UT WOS:A1996TW76700017 PM 8673666 ER PT J AU Hsu, FF Lakshmi, V Rothman, N Bhatnager, VK Hayes, RB Kashyap, R Parikh, DJ Kashyap, SK Turk, J Zenser, T Davis, B AF Hsu, FF Lakshmi, V Rothman, N Bhatnager, VK Hayes, RB Kashyap, R Parikh, DJ Kashyap, SK Turk, J Zenser, T Davis, B TI Determination of benzidine, N-acetylbenzidine, and N,N'-diacetylbenzidine in human urine by capillary gas chromatography negative ion chemical ionization mass spectrometry SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID LIQUID-CHROMATOGRAPHY; METABOLITES; BINDING; INVITRO; HAMSTER; INVIVO; DNA AB We report an isotope dilution mass spectrometry method using capillary gas chromatography/negative ion chemical ionization to quantitate urine concentrations of benzidine (BZ) and of its acetylated metabolites N-acetylbenzidine (ABZ) and N,N'-diacetylbenzidine (DABZ). Urine samples were purified by solid-phase extraction columns, reduced with LiAlH4/THF, and derivatized with pentafluoropropionic anhydride. The derivatives were measured by selected ion monitoring relative to deuterium-labeled internal standards. A detection limit as low as 0.5, 0.8, and 1.5 ppt for BZ, ABZ, and DABZ, respectively, can easily be achieved. Urinary concentrations of ABZ substantially exceed those of either BZ or of DABZ in workers exposed to BZ or BZ-based dyes. This method has been successfully used to measure BZ, ABZ, and DABZ in 1.0-ml urine samples collected from workers involved in manufacturing BZ and BZ-based dyes. The method should be applicable to the measurement of other aromatic amines and their acetylated metabolites. (C) 1996 Academic Press, Inc. C1 ST LOUIS UNIV,SCH MED,VA MED CTR,ST LOUIS,MO 63125. ST LOUIS UNIV,SCH MED,DEPT BIOCHEM,ST LOUIS,MO 63125. ST LOUIS UNIV,SCH MED,DIV GERIATR MED,ST LOUIS,MO 63125. NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. INDIAN NATL INST OCCUPAT HLTH,AHMEDABAD 380016,GUJARAT,INDIA. RP Hsu, FF (reprint author), WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110, USA. FU NCRR NIH HHS [RR-00954]; NIADDK NIH HHS [AM-20579] NR 18 TC 29 Z9 29 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD FEB 15 PY 1996 VL 234 IS 2 BP 183 EP 189 DI 10.1006/abio.1996.0070 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA TW972 UT WOS:A1996TW97200009 PM 8714596 ER PT J AU Zimmerman, SB Murphy, LD AF Zimmerman, SB Murphy, LD TI Electrophoresis of polyethylene glycols and related materials as sodium dodecyl sulfate complexes SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID POLY(ETHYLENE OXIDE); PROTEINS; SOLUBILIZATION; PRECIPITATION; SURFACTANT; MECHANISM; BEHAVIOR; POLYMER; WATER AB Polyethylene glycol (PEG) and polyethylene glycol derivatives are analyzed by a modification of the sodium dodecyl sulfate-polyacrylamide stacking gel electrophoresis procedure of Kurfurst. Gels using a discontinuous buffer system but which do not have a separate stacking gel are used without loss of resolution and with less tendency to form artifactual multiple or distorted bands. Examination of several commercial preparations of PEGs and PEG derivatives on such gels indicates heterogeneity other than the expected unimodal size distributions. SDS-gel electrophoresis of proteins or other materials in samples containing PEGs may yield gels with zones of contamination from the PEGs. Methods of reducing such contamination are suggested. (C) 1996 Academic Press, Inc. RP Zimmerman, SB (reprint author), NIDDK,MOLEC BIOL LAB,NATL INST HLTH,BETHESDA,MD 20892, USA. NR 22 TC 13 Z9 15 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD FEB 15 PY 1996 VL 234 IS 2 BP 190 EP 193 DI 10.1006/abio.1996.0071 PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA TW972 UT WOS:A1996TW97200010 PM 8714597 ER PT J AU Masur, H Shelhamer, J AF Masur, H Shelhamer, J TI Empiric outpatient management of HIV-related pneumonia: Economical or unwise? SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material RP Masur, H (reprint author), NIH,BLDG 10,ROOM 4D43,10 CTR DR,MSC 1662,BETHESDA,MD 20892, USA. NR 0 TC 21 Z9 22 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD FEB 15 PY 1996 VL 124 IS 4 BP 451 EP 453 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA TV220 UT WOS:A1996TV22000011 PM 8554256 ER PT J AU Seki, K Sheu, FS Huang, KP AF Seki, K Sheu, FS Huang, KP TI Binding of myristoylated alanine-rich protein kinase C substrate to phosphoinositides attenuates the phosphorylation by protein kinase C SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE protein kinase C; MARCKS; neurogranin; neuromodulin; phospholipids ID PROMINENT CELLULAR SUBSTRATE; RAT-BRAIN; PHOSPHATIDYLINOSITOL 4,5-BISPHOSPHATE; MEMBRANE PHOSPHOLIPIDS; CALMODULIN-BINDING; PLASMA-MEMBRANE; 87-KDA PROTEIN; BOVINE BRAIN; MARCKS; PURIFICATION AB The myristoylated alanine-rich protein kinase C substrate (MARCKS) is a peripheral membrane protein that undergoes phosphorylation-dependent translocation between membrane and cytosol, MARCKS binds to acidic phospholipids with high affinity (K-d less than 0.5 mu M) but binds poorly to neutral phospholipids. Although interaction of MARCKS with acidic phospholipids lacks specificity when determined by binding assay, these phospholipids exert distinctive effects on the phosphorylation of this protein by protein kinase C (PKC), Preincubation of MARCKS with phosphatidylserine (PS) or phosphatidylglycerol enhanced the phosphorylation; whereas with phosphatidic acid, phosphatidylinositol (PI), phosphatidylinositol-4-phosphate, or phosphatidylinositol-4,5-bisphosphate inhibited the phosphorylation of this substrate by PKC, Phosphoinositide inhibition of MARCKS phosphorylation was apparently directed at the substrate rather than at the kinase as the phosphorylation of two other phospholipid-binding PKC substrates, neuromodulin and neurogranin, exhibited different responses from those of MARCKS. Furthermore, the inhibition of phosphoinositides on MARCKS phosphorylation was seen with PKC isozymes alpha, beta, gamma, and delta and with the catalytic fragment of PKC, protein kinase M. A 25-amino-acid synthetic peptide corresponding to the phosphorylation site domain (PSD) of MARCKS, but not to the myristoylated N-terminal peptide, competed equally effectively with MARCKS in binding to either PS- or PI-containing vesicles, suggesting that both phospholipids bind to the PSD of MARCKS, Binding of PI to MARCKS inhibited PKC phosphorylation of all three phosphorylation sites, These results suggest that phosphoinositides and PS bind at different residues within the MARCKS PSD, so that the resulting phospholipid/MARCKS complexes are differentially phosphorylated by PKC. (C) 1996 Academic Press, Inc. C1 NICHHD, NIH, ENDOCRINOL & REPROD RES BRANCH, METAB REGULAT SECT, BETHESDA, MD 20892 USA. RI SHEU, Fwu-Shan/G-6435-2011 OI SHEU, Fwu-Shan/0000-0002-2784-2529 NR 48 TC 14 Z9 14 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0003-9861 EI 1096-0384 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD FEB 15 PY 1996 VL 326 IS 2 BP 193 EP 201 DI 10.1006/abbi.1996.0065 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TW966 UT WOS:A1996TW96600003 PM 8611023 ER PT J AU Jaffe, ES AF Jaffe, ES TI Classification of natural killer (NK) cell and NK-like T-cell malignancies SO BLOOD LA English DT Editorial Material ID EPSTEIN-BARR-VIRUS; RENAL-TRANSPLANT PATIENT; NON-HODGKINS-LYMPHOMA; CLINICOPATHOLOGICAL ENTITY; LEUKEMIA LYMPHOMA; GAMMA-DELTA; LOCALIZATION; LYMPHOCYTES; INVOLVEMENT; RECIPIENT RP Jaffe, ES (reprint author), NCI,HEMATOPATHOL SECT,PATHOL LAB,BLDG 10,ROOM 2N 202,10 CTR DR MSC-1500,BETHESDA,MD 20892, USA. NR 43 TC 205 Z9 209 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1996 VL 87 IS 4 BP 1207 EP 1210 PG 4 WC Hematology SC Hematology GA TV523 UT WOS:A1996TV52300001 PM 8608206 ER PT J AU Taub, DD Longo, DL Murphy, WJ AF Taub, DD Longo, DL Murphy, WJ TI Human interferon-inducible protein-10 induces mononuclear cell infiltration in mice and promotes the migration of human T lymphocytes into the peripheral tissues of human peripheral blood lymphocytes-SCID mice SO BLOOD LA English DT Article ID CYTOKINE FAMILY; IP-10; GAMMA; EXPRESSION; MIP-1-BETA; CHEMOATTRACTANT; MIP-1-ALPHA; MONOCYTES; CHEMOKINE; ADHESION AB The human cytokine, interferon-inducible protein-10 (IP-10), is a small glycoprotein secreted by activated monocytes, T cells, keratinocytes, astrocytes, and endothelial cells and is structurally related to the alpha subfamily of chemotactic cytokines called chemokines (Taub and Oppenheim, Cytokine 5:175, 1993). However, in contrast to other alpha chemokines that induce neutrophil migration, IP-10 has been shown to chemoattract monocytes and T lymphocytes in vitro, suggesting a role in T-cell-mediated immune responses. We therefore examined the effects of human IP-10 after in vivo administration. IP-10 induces significant mononuclear cell infiltration after subcutaneous injections in normal mice. In an effort to study the in vivo effects of IP-10 on human leukocyte migration, we then examined the ability of recombinant human IP-10 (rhIP-10) to induce human T-cell infiltration using a human/severe combined immune deficiency (SCID) mouse model. SCID mice received an intraperitoneal injection of human peripheral blood lymphocytes (10(8) cells), followed by a subcutaneous injection of rhIP-10 (1 mu g/injection) in the hind flank for 4 hours or sequential injections for 3 days. The skin and underlying tissue from the rhIP-10 injection site were then biopsied and examined for the extent of mononuclear cell infiltration. rhIP-10 again induced significant mononuclear cell accumulation 72 hours after injection. Immunohistologic evaluation determined that a significant number of human CD3(+) T cells were recruited in response to rhIP-10 injections. These results show that rhIP-10 is capable of inducing human T-cell migration in vivo and may play an important role in monocyte and lymphocyte recruitment into inflammatory sites. C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,CLIN SERV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,OFF ASSOCIATE DIRECTOR,FREDERICK,MD 21702. NR 37 TC 103 Z9 106 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1996 VL 87 IS 4 BP 1423 EP 1431 PG 9 WC Hematology SC Hematology GA TV523 UT WOS:A1996TV52300027 PM 8608232 ER PT J AU Yaswen, L Kulkarni, AB Fredrickson, T Mittleman, B Schiffmann, R Payne, S Longenecker, G Mozes, E Karlsson, S AF Yaswen, L Kulkarni, AB Fredrickson, T Mittleman, B Schiffmann, R Payne, S Longenecker, G Mozes, E Karlsson, S TI Autoimmune manifestations in the transforming growth factor-beta 1 knockout mouse SO BLOOD LA English DT Article ID BETA TGF-BETA; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; SYSTEMIC LUPUS-ERYTHEMATOSUS; DNA ANTIBODY IDIOTYPES; MYELIN BASIC-PROTEIN; INFLAMMATORY DISEASE; MICE; CELLS; EXPRESSION; MUTATION AB Targeted disruption of the transforming growth factor-beta 1 (TGF-beta 1) gene in mice results in the development of a massive multifocal inflammatory disease in many tissues. Because no detectable pathogen was identified, we examined whether autoimmune mechanisms played a role in initiating or maintaining the inflammatory disease. The serum of TGF-beta 1 knockout mice contained elevated titers of antibodies to nuclear antigens (ssDNA, dsDNA, Sm, and RNP), as well as reactivity against the 16/6 idiotype (16/6 Id). In addition, Ig deposits were detected in renal glomeruli of TGF-beta 1 knockout mice. Transplantation of TGF-beta 1 knockout hematopoietic cells into normal irradiated recipients resulted in a similar profile of autoantibody production as well as in the induction of inflammatory lesions. Our results describe autoimmune activity that ensues when the TGF-beta 1 cytokine is absent. This is a US government work. There are no restrictions on ifs use. C1 NINCDS,DEV & METAB NEUROL BRANCH,UNIT MOUSE GNET & HUMAN DIS MODELS,MOLEC & MED GENET SECT,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,REGISTRY EXPTL CANC,BETHESDA,MD. NR 34 TC 128 Z9 132 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1996 VL 87 IS 4 BP 1439 EP 1445 PG 7 WC Hematology SC Hematology GA TV523 UT WOS:A1996TV52300029 PM 8608234 ER PT J AU Donahue, RE Kirby, MR Metzger, ME Agricola, BA Sellers, SE Cullis, HM AF Donahue, RE Kirby, MR Metzger, ME Agricola, BA Sellers, SE Cullis, HM TI Peripheral blood CD34(+) cells differ from bone marrow CD34(+) cells in Thy-1 expression and cell cycle status in nonhuman primates mobilized or not mobilized with granulocyte colony-stimulating factor and/or stem cell factor SO BLOOD LA English DT Article ID MEDIATED GENE-TRANSFER; PROGENITOR CELLS; HEMATOPOIETIC-CELLS; G-CSF; TRANSPLANTATION; INTERLEUKIN-3; PRECURSORS; CULTURE AB Granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) have been shown to stimulate the circulation of hematopoietic progenitor cells in both mice and nonhuman primates, We evaluated the immunophenotype and cell cycle status of CD34(+) cells isolated from the bone marrow (BM) and leukapheresis product of cytokine-mobilized nonhuman primates. CD34(+) cells were isolated from rhesus macaques that had received no cytokine therapy, 100 mu g/kg/d G-CSF, 200 mu g/kg/d SCF, or a combination of both 100 mu g/kg/d G-CSF and 200 mu g/kg/d SCF as a subcutaneous injection for 5 days. BM was aspirated before (day 0) and on the last day (day 5) of cytokine administration. On days 4 and 5, peripheral blood (PB) mononuclear cells were collected using a novel method of leukapheresis. Threefold more PB mononuclear cells were collected from animals receiving G-CSF alone or G-CSF and SCF than from animals that had received either SCF alone or no cytokine therapy. CD34(+) cells were positively selected using an immunoadsorptive system from the BM, PB, and/or leukapheresis product. Threefold and 10-fold more CD34(+) cells were isolated from the leukapheresis product of animals receiving G-CSF or G-CSF and SCF, respectively, than from animals receiving no cytokine therapy or SCF alone, The isolated CD34(+) cells were immunophenotyped using CD34-allophycocyanin, CD38-fluorescein isothiocyanate, and Thy-l-phycoerythrin. These cells were later stained with 4',6-diamidino-2-phenylindole for simultaneous DNA analysis and immunophenotyping. BM-derived CD34(+) cells did not differ significantly in cell cycle status and Thy-1 or CD38 phenotype before or after G-CSF and/or SCF administration. Similarly, CD34(+) cells isolated from the leukapheresis product did not differ significantly in immunophenotype or cell cycle status before or after G-CSF and/or SCF administration. However, there were consistent differences in both immunophenotype and cell cycle status between BM- and PB-derived CD34(+) cells, CD34(+) cells isolated from the PB consistently had a smaller percentage of cells in the S+G2/M phase of the cell cycle and had a higher percentage of cells expressing Thy-1 than did CD34(+) cells isolated from the BM. A greater proportion of PB-derived CD34(+) cells were in the S+G2/M phase of the cell cycle after culture in media supplemented with interleukin-6 and SCF. However, culturing decreased the proportion of CD34(+) cells expressing Thy-1. (C) 1996 by The American Society of Hematology. C1 BAXTER HLTHCARE CORP,FENWAL DIV,DEERFIELD,IL. RP Donahue, RE (reprint author), NHLBI,NIH,HEMATOL BRANCH,5 RES CT,ROCKVILLE,MD 20850, USA. NR 39 TC 99 Z9 101 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1996 VL 87 IS 4 BP 1644 EP 1653 PG 10 WC Hematology SC Hematology GA TV523 UT WOS:A1996TV52300054 PM 8608259 ER PT J AU Waterhouse, D Carman, WJ Schottenfeld, D Gridley, G McLean, S AF Waterhouse, D Carman, WJ Schottenfeld, D Gridley, G McLean, S TI Cancer incidence in the rural community of Tecumseh, Michigan - A pattern of increased lymphopoietic neoplasms SO CANCER LA English DT Article DE cohort study; nested case-control study; insecticides; herbicides; non-Hodgkin's lymphomas; Hodgkin's disease; chronic lymphocytic leukemia ID NON-HODGKINS-LYMPHOMA; RISK-FACTORS; TIME TRENDS; COHORT AB BACKGROUND. The Tecumseh Community Health Study (TCHS), initiated in 1959 at the University of Michigan School of Public Health, has provided a resource for long term prospective studies of the incidence of cancer in the setting of a midwestern rural farming community. METHODS. A survey of total and site specific cancer incidence among 7016 male and female adult residents from 1959-1987 was conducted, and the observed number compared with the expected number, based on the age-sex-race-calendar period-and site-specific cancer incidence rates reported by the Connecticut tumor registry. Based on the results of this survey, a hypothesis was advanced concerning the potential risks of exposures to insecticides and herbicides. This was pursued by analyzing for each county in Michigan the comparative annual number of acres and percentage of acreage treated with agricultural chemicals in 1978 and for the period 1982-1987. Finally, because of the availability of information on lifestyle risk factors that had been collected in the 1960s on all participants, a nested case-control study was implemented. RESULTS. The standardized incidence ratio (SIR), based on the observed number divided by the expected number of invasive cancer cases (all sites combined [excluding nonmelanoma skin cancer]), was not significant in females (SIR, 0.95; 95% confidence interval [CI], 0.86-1.05) nor males (SIR, 0.91; 95% CI, 0.81-1.01). A significant increase was demonstrated for males and females combined in the incidence of lymphopoietic neoplasms, namely non-Hodgkin's lymphoma, Hodgkin's disease, and chronic lymphocytic leukemia; the combined SIR was 1.40 (95% CI, 1.03-1.86; P = 0.03). In the Department of Commerce surveys of counties in Michigan, the Tecumseh area (Lenawee County) was ranked highest with respect to the average annual number of acres (240,000 or more) and the percent of acreage (40%) sprayed with herbicides and insecticides. A comparison of temporal trends for cancer incidence since 1973 was reviewed for the Wayne-Oakland-Macomb tricounty area, in which the survey estimated that less than 80,000 acres per year, or less than 8% of acreage, were treated with pesticides. The comparison of the Tecumseh cohort, for all sites combined, was not significantly different from expectation in females (SIR, 1.01; 95% CI, 0.89-1.14), and was decreased by more than 10% in males (SIR, 0.88; 95% CI, 0.77-1.00). However, the SIR for non-Hodgkin's lymphoma in females was significantly elevated (SIR, 1.92; 95% CI, 1.07-3.11, P = 0.02); the trend for increased risks of lymphomas and leukemias was also evident in males. In the nested case-control study, based on risk factor information documented prior to diagnosis, the relative risk of a family history of lymphoma, leukemia, or multiple myeloma was significantly increased among patients with lymphoproliferative neoplasms (odds ratio, 3.81; 95% CI, 1.49-9.79; P = 0.005). CONCLUSIONS. This prospective epidemiologic study conducted in a rural farming community in Michigan has found significant increases in the incidence of lymphoproliferative cancers. A plausible hypothesis, consistent with the preliminary findings, is that the reported cancer pattern is an expression of risk resulting from sustained environmental exposures to agricultural chemicals, perhaps in conjunction with familial or genetic factors. (C) 1996 American Cancer Society. C1 UNIV MICHIGAN,SCH PUBL HLTH,DEPT EPIDEMIOL,ANN ARBOR,MI 48109. ONCOL CONSULTANTS INC,CINCINNATI,OH. NATL CANC INST,EPIDEMIOL & BIOSTAT PROGRAM,ROCKVILLE,MD. NR 31 TC 41 Z9 44 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD FEB 15 PY 1996 VL 77 IS 4 BP 763 EP 770 DI 10.1002/cncr.1996.2820770402 PG 8 WC Oncology SC Oncology GA TU581 UT WOS:A1996TU58100024 PM 8616770 ER PT J AU Takatsuka, J Takahashi, N De Luca, LM AF Takatsuka, J Takahashi, N De Luca, LM TI Retinoic acid metabolism and inhibition of cell proliferation: An unexpected liaison SO CANCER RESEARCH LA English DT Article ID ACUTE PROMYELOCYTIC LEUKEMIA; CHICK LIMB BUD; DIFFERENTIATION THERAPY; SPATIAL-DISTRIBUTION; INVIVO METABOLISM; CYTOCHROME-P-450; IDENTIFICATION; INDUCTION; INVITRO; BINDING AB The rationale for the use of all-trans-retinoic acid (RA) as an anticancer agent is based on its ability to inhibit growth and promote differentiation of some neoplastic cells. However, RA is not effective in all conditions of cell culture, and in some cases, it may stimulate cell growth. We used a serum-free culture system to study the effect of RA on cell proliferation. Following 2 days of RA exposure, 9 of a total of 15 cell lines showed an inhibition of cell growth (RA-sensitive), while 6 of 15 cell lines showed resistance to RA (RA-resistant cells). Metabolic studies and high-performance liquid chromatography analysis of the cell-associated and medium extracts from cells incubated with [H-3]RA revealed that all nine RA-sensitive cells showed a very high activity to metabolize RA to polar metabolites found in the medium. In sharp contrast, RA-resistant cells retained about 60% of the original RA at 76 h. However, conditioned medium from the sensitive cells was without activity on the growth of sensitive and resistant cells. We conclude that a relationship exists between RA inhibition of cell growth and intracellular RA metabolism. These data may help design useful strategies in cancer therapy by retinoids and dispel the notion that RA itself is responsible for the inhibition of cell growth. C1 NCI, CELLULAR CARCINOGENESIS & TUMOR PROMOT, BETHESDA, MD 20892 USA. HOSHI UNIV, DEPT HYG CHEM, SHINAGAWA KU, TOKYO 142, JAPAN. NR 28 TC 86 Z9 88 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1996 VL 56 IS 4 BP 675 EP 678 PG 4 WC Oncology SC Oncology GA TV219 UT WOS:A1996TV21900004 PM 8630993 ER PT J AU Jacoby, RF Marshall, DJ Newton, MA Novakovic, K Tutsch, K Cole, CE Lubet, RA Kelloff, GJ Verma, A Moser, AR Dove, WF AF Jacoby, RF Marshall, DJ Newton, MA Novakovic, K Tutsch, K Cole, CE Lubet, RA Kelloff, GJ Verma, A Moser, AR Dove, WF TI Chemoprevention of spontaneous intestinal adenomas in the Apc (Min) mouse model by the nonsteroidal anti-inflammatory drug piroxicam SO CANCER RESEARCH LA English DT Article ID COLORECTAL-CANCER; NEOPLASIA; MUTATION; MUCOSA AB C57BL/6J-Min/+ mice (n = 56), heterozygous for a nonsense mutation in the Apc gene, sere randomized at weaning to seven groups, including groups treated with piroxicam at 0, 50, 100, and 200 ppm in the AIN93G diet. After only 6 weeks of treatment, intestinal adenomas and aberrant crypt foci were counted, and serum levels of piroxicam and thromboxane B-2 were quantitated. Tumor multiplicity was decreased in a dose-dependent manner from 17.3 +/- 2.7 in the control to 2.1 +/- 1.1 (12%) in the high-dose piroxicam group (P < 0.001). Thromboxane B-2 levels in plasma also decreased monotonically in parallel to the decrease in tumor multiplicity, consistent with the prostaglandin inhibitory effect of piroxicam. The Min mouse model demonstrates that the nonsteroidal anti-inflammatory drug piroxicam has strong biological and therapeutic effects, potentially useful for prevention of the early adenoma stage of tumor development. C1 UNIV WISCONSIN,DEPT MED,DIV GASTROENTEROL,MADISON,WI 53792. UNIV WISCONSIN,DEPT HUMAN ONCOL,MADISON,WI 53792. CTR COMPREHENS CANC,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT BIOSTAT,MADISON,WI 53792. NCI,CHEMOPREVENT LAB,DCPC,BETHESDA,MD 20892. UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706. FU NCI NIH HHS [CA14520, CA59352, CA50585] NR 20 TC 293 Z9 294 U1 0 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1996 VL 56 IS 4 BP 710 EP 714 PG 5 WC Oncology SC Oncology GA TV219 UT WOS:A1996TV21900011 PM 8631000 ER PT J AU Bae, I Smith, ML Sheikh, MS Zhan, QM Scudiero, DA Friend, SH OConnor, PM Fornace, AJ AF Bae, I Smith, ML Sheikh, MS Zhan, QM Scudiero, DA Friend, SH OConnor, PM Fornace, AJ TI An abnormality in the p53 pathway following gamma-irradiation in many wild-type p53 human melanoma lines SO CANCER RESEARCH LA English DT Article ID TUMOR-SUPPRESSOR GENE; GROWTH-ARREST; GADD45 GENE; DNA-DAMAGE; PROTEIN; ACTIVATION; RADIATION; CELLS; APOPTOSIS AB DNA-damaging agents such as ionizing radiation (IR) activate the tumor suppressor p53, and, in turn, p53 transactivates a number of downstream effector genes such as GADD45, CIP1/WAF1, and MDM2. The induction of these downstream genes following IR appears to be strictly dependent upon the presence of wild-type functional p53 known to evoke G(1) arrest. In this study, we characterized 56 cell lines from 9 different tumor types viith predetermined p53 genotype by measuring the induction of GADD45, CIP1/WAF1, and MDM2 relative mRNA levels after IR. A higher fraction of melanoma lines had wild-type (wt) p53 (5/8, or 63%) compared to the nonmelanoma lines (11/48, or 23%). Most wt p53 (nonmelanoma) cell lines (11/12, or 92%) showed clear induction of both GADD45 and CIP1/WAF1. On the other hand, many wt p53 melanoma lines (4/5, or 80%) showed normal induction of CIP1/WAF1, but little or no induction of GADD45. Despite this defect in GADD45 induction, we found that all wt p53 melanoma lines exhibited strong G(1) arrest and increased levels of p53 protein after IR. The results demonstrated that radiation-induced G(1) arrest could occur by the p53-CIP1/WAF1 pathway without appreciable induction of GADD45 in melanoma lines. Time course experiments demonstrated prolonged induced expression of CIP1/WAF1 mRNA transcripts in melanoma lines in which GADD45 induction was lacking, suggesting some sort of compensatory mechanism involving CIP1/WAF1, in cell lines with defective GADD45 induction. We could reproduce this compensatory effect in RKO colon carcinoma cells in which GADD45 expression was blocked by constitutive antisense vectors. These findings reveal that defective induction of GADD45 following IR is common in human melanoma cell lines. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,NIH,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,FREDERICK,MD 21702. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 42 TC 68 Z9 77 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1996 VL 56 IS 4 BP 840 EP 847 PG 8 WC Oncology SC Oncology GA TV219 UT WOS:A1996TV21900033 PM 8631022 ER PT J AU Frankel, AE FitzGerald, D Siegall, C Press, OW AF Frankel, AE FitzGerald, D Siegall, C Press, OW TI Advances in immunotoxin biology and therapy: A summary of the Fourth International Symposium on Immunotoxins SO CANCER RESEARCH LA English DT Editorial Material ID B-CELL NEOPLASMS; PHASE-I TRIAL; ANTI-B4-BLOCKED RICIN; LYMPHOMA; INFUSION C1 UNIV WASHINGTON,MED CTR,DEPT BIOL STRUCT,SEATTLE,WA 98195. UNIV WASHINGTON,MED CTR,DEPT MED,SEATTLE,WA 98195. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. NCI,BIOTHERAPY SECT,NIH,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121. FU NCI NIH HHS [R01CA55596, R13CAER66559] NR 13 TC 48 Z9 49 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1996 VL 56 IS 4 BP 926 EP 932 PG 7 WC Oncology SC Oncology GA TV219 UT WOS:A1996TV21900048 PM 8631036 ER PT J AU Rowan, S Ludwig, RL Haupt, Y Bates, S Lu, X Oren, M Vousden, KH AF Rowan, S Ludwig, RL Haupt, Y Bates, S Lu, X Oren, M Vousden, KH TI Specific loss of apoptotic but not cell-cycle arrest function in a human tumor derived p53 mutant SO EMBO JOURNAL LA English DT Article DE apoptosis; G(1) arrest; p53; transcriptional activation; tumor suppression ID WILD-TYPE P53; DNA-DAMAGING AGENTS; MONOCLONAL-ANTIBODIES; GENE AMPLIFICATION; BINDING-SITE; PROTEIN; TRANSCRIPTION; SUPPRESSION; IDENTIFICATION; TRANSFORMATION AB The p53 tumor-suppressor gene product is frequently inactivated in malignancies by point mutation. Although most tumor-derived p53 mutants show loss of sequence specific transcriptional activation, some mutants have been identified which retain this activity. One such mutant, p53175P, is defective for the suppression of transformation in rodent cells, despite retaining the ability to suppress the growth of p53-null human cells. We now demonstrate that p53175P can induce a cell-cycle arrest in appropriate cell types but shows loss of apoptotic function. Our results therefore support a direct role of p53 transcriptional activation in mediating a cell-cycle arrest and demonstrate that such activity is not sufficient for the full apoptotic response. These data suggest that either p53 can induce apoptosis through a transcriptionally independent mechanism, a function lost by p53175P, or that this mutant has specifically lost the ability to activate genes which contribute to cell death, despite activation of genes responsible for the G(1) arrest. This dissociation of the cell-cycle arrest and apoptotic activities of p53 indicates that inactivation of p53 apoptotic function without concomitant loss of growth inhibition can suffice to relieve p53-dependent tumor-suppression in vivo and thereby contribute to tumor development. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. WEIZMANN INST SCI,IL-76100 REHOVOT,ISRAEL. ST MARYS HOSP,SCH MED,LUDWIG INST CANC RES,LONDON W2 1PG,ENGLAND. NR 84 TC 281 Z9 285 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD FEB 15 PY 1996 VL 15 IS 4 BP 827 EP 838 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TX610 UT WOS:A1996TX61000014 PM 8631304 ER PT J AU Minucci, S Botquin, V Yeom, YI Dey, A Sylvester, I Zand, DJ Ohbo, K Ozato, K Scholer, HR AF Minucci, S Botquin, V Yeom, YI Dey, A Sylvester, I Zand, DJ Ohbo, K Ozato, K Scholer, HR TI Retinoic acid-mediated down-regulation of Oct3/4 coincides with the loss of promoter occupancy in vivo SO EMBO JOURNAL LA English DT Article DE embryonal carcinoma cells; embryonic stem cells; gene regulation; in vivo footprinting; POU ID BINDING TRANSCRIPTION FACTOR; THYROID-HORMONE; GENE-EXPRESSION; POU-DOMAIN; RXR-BETA; RECEPTORS; CELLS; DIFFERENTIATION; COMPLEX; ALPHA AB Oct3/4, a hallmark of the earliest stages of embryogenesis, is expressed in undifferentiated embryonal carcinoma (EC) and embryonic stem (ES) cells. Oct3/4 gene expression is dependent on the promoter region, the proximal enhancer and the newly identified distal enhancer. We have analysed in vivo occupancy of these elements. In undifferentiated EC and ES cells, strong footprints were detected at specific sites of all three regulatory elements. These were promptly lost upon RA treatment in ES cells and in P19 EC cells, in parallel with sharply reduced Oct3/4 mRNA levels, Thus, the occupancy of regulatory elements is coupled with Oct3/4 expression, and RA treatment causes coordinated factor displacement, leading to extinction of gene activity. In F9 EC cells, footprint was first abolished at the proximal enhancer. However, this loss of binding site occupancy did not result in a decrease in Oct3/4 mRNA levels. The partial factor displacement seen in F9 EC cells, combined with the observation that EC and ES cells utilize the proximal and distal enhancers in a differential manner, indicate the complex pattern of Oct3/4 gene regulation, which could reflect a cell type- and lineage-specific expression of the gene in vivo. C1 NICHHD,LAB MOLEC GROWTH REGULAT,BETHESDA,MD 20892. EUROPEAN MOLEC BIOL LAB,GENE EXPRESS PROGRAMME,D-69012 HEIDELBERG,GERMANY. RI Minucci, Saverio/J-9669-2012; OI Scholer, Hans/0000-0003-2643-5136 NR 34 TC 72 Z9 79 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD FEB 15 PY 1996 VL 15 IS 4 BP 888 EP 899 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TX610 UT WOS:A1996TX61000019 PM 8631309 ER PT J AU Izenwasser, S Newman, AH Cox, BM Katz, JL AF Izenwasser, S Newman, AH Cox, BM Katz, JL TI The cocaine-like behavioral effects of meperidine are mediated by activity at the dopamine transporter SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE dopamine transporter; cocaine; meperidine ID RAT CAUDATE-PUTAMEN; NUCLEUS-ACCUMBENS; LIGAND-BINDING; H-3 DOPAMINE; STRIATUM; RECEPTOR; NALTREXONE; INHIBITION; NALOXONE; MORPHINE AB Meperidine has atypical opioid receptor agonist effects and shares some structural features with the phenyltropane (WIN) analogs of cocaine. In combination with 0.1 mg/kg naltrexone, meperidine produced cocaine-like discriminative stimulus effects in monkeys, whereas morphine was inactive. Both cocaine and meperidine inhibited [H-3]dopamine uptake in chopped rat caudate putamen with comparable potencies; meperidine differed from cocaine in that its effects could be characterized as having predominantly a single high-affinity component. Morphine was not active in inhibiting [H-3]dopamine uptake, indicating that the effect of meperidine was not via a classic mu-opioid receptor agonist action. Further, meperidine but not morphine displaced [H-3]WIN 35,428 (2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane) binding. These data suggest that the actions of meperidine that are atypical of opioids are due to activity at the dopamine transporter. In addition, meperidine appears to interact predominantly with the high-affinity component of the dopamine transporter, and this high-affinity component may be the site of importance for the production of cocaine's behavioral effects. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PHARMACOL,BETHESDA,MD 20814. RP Izenwasser, S (reprint author), NIDA,NIH,DIV INTRAMURAL RES,PSYCOBIOL SECT,POB 5180,BALTIMORE,MD 21224, USA. RI Izenwasser, Sari/G-9193-2012; OI Katz, Jonathan/0000-0002-1068-1159 NR 44 TC 18 Z9 18 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD FEB 15 PY 1996 VL 297 IS 1-2 BP 9 EP 17 DI 10.1016/0014-2999(95)00696-6 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TX428 UT WOS:A1996TX42800002 PM 8851160 ER PT J AU Izenwasser, S Heller, B Cox, BM AF Izenwasser, S Heller, B Cox, BM TI Continuous cocaine administration enhances mu- but not delta-opioid receptor-mediated inhibition of adenylyl cyclase activity in nucleus accumbens SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE cocaine; opioid; caudate; nucleus accumbens ID DOPAMINE UPTAKE; BRAIN; RAT; BINDING AB Cocaine alters opioid receptor densities in rat brain. To investigate the functional consequences of such opioid receptor changes, adenylyl cyclase activity was measured in rat nucleus accumbens and caudate putamen following continuous cocaine administration (50 mg/kg/day, 7 days). In the nucleus accumbens chronic cocaine led to an increase in both the number of mu-opioid receptors and the maximal inhibition of adenylyl cyclase activity by DAMGO ([D-Ala(2),N-methyl-Phe(4),Glyol]enkephalin). There was no effect on inhibition of adenylyl cyclase activity by DPDPE ([D-Pen(2),D-Pen(5)]enkephalin). There were no changes in the caudate putamen. Thus, continuous cocaine administration for 7 days results in a selective increase in mu-opioid receptor-mediated effector function in the nucleus accumbens. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PHARMACOL,BETHESDA,MD 20814. RP Izenwasser, S (reprint author), NIDA,INTRAMURAL RES PROGRAM,PSYCHOBIOL SECT,POB 5180,BALTIMORE,MD 21224, USA. RI Izenwasser, Sari/G-9193-2012 NR 15 TC 37 Z9 38 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD FEB 15 PY 1996 VL 297 IS 1-2 BP 187 EP 191 DI 10.1016/0014-2999(95)00828-4 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TX428 UT WOS:A1996TX42800024 PM 8851182 ER PT J AU Du, Y Remmers, EF Goldmuntz, EA Zha, HB Mathern, P Ding, YP Kotake, S Szpirer, J Szpirer, C Wilder, RL AF Du, Y Remmers, EF Goldmuntz, EA Zha, HB Mathern, P Ding, YP Kotake, S Szpirer, J Szpirer, C Wilder, RL TI Linkage maps of rat chromosomes 15, 16, 17, 19, and X SO GENOMICS LA English DT Article ID POLYMORPHIC MARKERS; GENES; ASSIGNMENT; HYBRIDIZATION AB Linkage maps of rat chromosomes 15, 16, 17, 19, and X were constructed by multipoint genetic linkage analysis of 22 polymorphic markers in 40 F-2 progeny of Fischer (F344/N) and Lewis (LEW/N) inbred rat strains. These markers are associated with eight genes (angiotensin receptor A, M3 muscarinic acetylcholine receptor, heme oxygenase, endothelin receptor A, haptoglobin, tyrosine aminotransferase, phosphoribosylpyrophosphate synthetase subunit II, and 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase) and 14 anonymous loci. Linkage analysis placed the markers into five linkage groups covering 11.7, 7.9, 11.6, 42.5, and 5.1 cM. These linkage groups were assigned to rat chromosomes 15, 16, 17, 19, and X, respectively, either by mouse x rat somatic cell hybrid analysis or based on previously identified locations of several loci. In polymorphism analysis, these markers exhibited two to nine different alleles in 16 inbred rat strains. (C) 1996 Academic Press, Inc. C1 NIAMSD,NIH,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD 20892. FREE UNIV BRUSSELS,DEPT BIOL MOLEC,B-1640 RHODE ST GENESE,BELGIUM. NR 15 TC 7 Z9 7 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD FEB 15 PY 1996 VL 32 IS 1 BP 113 EP 116 DI 10.1006/geno.1996.0083 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA TW558 UT WOS:A1996TW55800014 PM 8786096 ER PT J AU BennettBaker, PE Kiousis, S Chandrasekharappa, SC King, SE Abel, KJ Collins, FS Weber, BL Chamberlain, JS AF BennettBaker, PE Kiousis, S Chandrasekharappa, SC King, SE Abel, KJ Collins, FS Weber, BL Chamberlain, JS TI Isolation of tetranucleotide repeat polymorphisms flanking the BRCA1 gene SO GENOMICS LA English DT Article ID FAMILIAL BREAST; OVARIAN-CANCER; REGION; CHROMOSOME-17Q12-Q21; MAP AB Large pools of cosmids from the BRCA1 region of human chromosome 17 were screened for tetranucleotide repeat polymorphisms by hybridizing shotgun subcloned pools with a mixture of 25 oligonucleotides. Identified subclones were PCR amplified and directly sequenced to design PCR primers for short tandem repeat polymorphism (STRP) analysis of family DNAs. With the identification of the BRCA1 gene and the observation that most mutations in this > 100-kb gene are unique, haplotyping and linkage analysis may play a significant role in diagnosis and carrier detection of BRCA1-associated breast and ovarian cancers. We report the characterization of 15 new STRPs flanking the BRCA1 locus. (C) 1996 Academic Press, Inc. C1 UNIV MICHIGAN,SCH MED,CTR HUMAN GENOME,DEPT HUMAN GENET,ANN ARBOR,MI 48109. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. UNIV PENN,DEPT INTERNAL MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT GENET,PHILADELPHIA,PA 19104. FU NHGRI NIH HHS [HG00209] NR 18 TC 1 Z9 1 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD FEB 15 PY 1996 VL 32 IS 1 BP 163 EP 167 DI 10.1006/geno.1996.0097 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA TW558 UT WOS:A1996TW55800028 PM 8786111 ER PT J AU Chung, DC Anglade, E Sullivan, DM Nussenblatt, RB Csaky, KG AF Chung, DC Anglade, E Sullivan, DM Nussenblatt, RB Csaky, KG TI Comparison of lipofection, calcium phosphate coprecipitation and adenovirus facilitated lipofection mediated ex vivo gene transfer into cultured human retinal pigmented epithelial cells. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 34 EP 34 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700034 ER PT J AU Marmorstein, AD Yeaman, C Bonilha, VL Anglade, E Csaky, K RodriguezBoulan, E AF Marmorstein, AD Yeaman, C Bonilha, VL Anglade, E Csaky, K RodriguezBoulan, E TI An exogenous plasma membrane protein is polarized on the apical surface of the retinal pigment epithelium (RPE) in vivo and in vitro. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 CORNELL UNIV,COLL MED,DEPT CELL BIOL & ANAT,NEW YORK,NY 10021. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 35 EP 35 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700035 ER PT J AU Borras, T Tamm, E Zigler, JS AF Borras, T Tamm, E Zigler, JS TI Efficiency and toxicity of gene delivery to the anterior segment of rabbits SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,LAB MECHANISMS OCULAR DIS,BETHESDA,MD 20892. NEI,NIH,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 39 EP 39 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700039 ER PT J AU Iuvone, PM AlonsoGomez, AL Bernard, M Klein, DC AF Iuvone, PM AlonsoGomez, AL Bernard, M Klein, DC TI Circadian and light-evoked regulation of serotonin N-acetyltransferase activity and mRNA levels in chicken retina SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 EMORY UNIV,ATLANTA,GA 30322. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 68 EP 68 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700068 ER PT J AU Wang, Y Zhang, J Yu, Z Detrick, B Hooks, JJ AF Wang, Y Zhang, J Yu, Z Detrick, B Hooks, JJ TI Apoptosis as a mechanism for tissue damage in murine coronavirus induced retinopathy. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NHLBI,NIH,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 175 EP 175 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700175 ER PT J AU Suzuki, S Li, Q Fukushima, A Ramada, A Nussenblatt, RB Caspi, RC Chan, CC AF Suzuki, S Li, Q Fukushima, A Ramada, A Nussenblatt, RB Caspi, RC Chan, CC TI Methimazole inhibits experimental autoimmune uveoretinitis (EAU) in the rat. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. KEIO UNIV,SCH MED,DEPT OPHTHALMOL,TOKYO,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 178 EP 178 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700178 ER PT J AU Hooks, JJ Wang, Y Detrick, B AF Hooks, JJ Wang, Y Detrick, B TI Coronavirus infection of the retina is associated with increased levels of cytokines (IL-1, IL-6 and IFN-gamma) within the vitreous. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 189 EP 189 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700189 ER PT J AU Iwata, F Caruso, RC McCain, LM Gahl, WA KaiserKupfer, MI AF Iwata, F Caruso, RC McCain, LM Gahl, WA KaiserKupfer, MI TI Visual function assessment in adults with nephropathic cystinosis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NICHHD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 488 EP 488 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700487 ER PT J AU Vinores, SA Chen, YS Klein, DA Vinores, MA Chan, CC Green, WR Campochiaro, PA AF Vinores, SA Chen, YS Klein, DA Vinores, MA Chan, CC Green, WR Campochiaro, PA TI Upregulation of vascular endothelial growth factor (VEGF) and its receptors in non-ischemic retinal disease SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205. NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 632 EP 632 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700631 ER PT J AU Sperbeck, S Jaworski, C Richardson, J Wistow, G AF Sperbeck, S Jaworski, C Richardson, J Wistow, G TI Alternative splicing of PAX-6 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,SECT MOLEC STRUCT & FUNCT,LMDB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 706 EP 706 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700704 ER PT J AU Nishima, N Tomarev, S AF Nishima, N Tomarev, S TI Identification of two genes homologous to the Drosophila eyes absent gene in an embryonic chicken lens SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMDB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 712 EP 712 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700710 ER PT J AU Cvekl, A Kashanchi, F Epstein, J Rauchman, M Maas, R Piatigorsky, J AF Cvekl, A Kashanchi, F Epstein, J Rauchman, M Maas, R Piatigorsky, J TI Pax6, a ''master gene'' for eye development: Target genes and mechanism of action SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NCI,MOLEC & DEV BIOL LAB,NEI,LAB MOLEC VIROL,NIH,BETHESDA,MD 20892. BRIGHAM & WOMENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 715 EP 715 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700713 ER PT J AU Tamm, ER Russell, P Johnson, DH Piatigorsky, J AF Tamm, ER Russell, P Johnson, DH Piatigorsky, J TI Trabecular meshwork accumulates alpha B-crystallin in response to heat shock, oxidative stress and culture conditions SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MAYO CLIN,DEPT OPHTHALMOL,ROCHESTER,MN. NEI,LMDB,NIH,BETHESDA,MD 20892. NEI,LMOD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 720 EP 720 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700718 ER PT J AU Tumminia, SJ Epstein, DL Tamm, E Russell, P AF Tumminia, SJ Epstein, DL Tamm, E Russell, P TI The effects of mechanical stretch on signal transduction in human and rhesus monkey trabecular meshwork (TM) cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMOD,NIH,BETHESDA,MD. NEI,LMDB,NIH,BETHESDA,MD. DUKE UNIV,MED CTR,DURHAM,NC. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 725 EP 725 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700723 ER PT J AU ParkerWilson, DM Qian, Y Tripathi, BJ Chepelinsky, AB AF ParkerWilson, DM Qian, Y Tripathi, BJ Chepelinsky, AB TI Molecular characterization of the aquaporin expressed in trabecular meshwork cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. UNIV SO CALIF,DEPT PATHOL,LOS ANGELES,CA 90089. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 726 EP 726 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700724 ER PT J AU CohenMichaeli, A Jacot, JL Rosner, M Solomon, AS AF CohenMichaeli, A Jacot, JL Rosner, M Solomon, AS TI Corneal findings in rabbits with inherited glaucoma SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SURASKI MED CTR,TEL AVIV,ISRAEL. NEI,NIH,BETHESDA,MD 20892. TEL AVIV UNIV,GOLDSCHLEGER EYE RES INST,TEL AVIV,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 893 EP 893 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700891 ER PT J AU Kador, PF Secchi, EF Lizak, MJ Rodriguez, L Blessing, K Sato, S AF Kador, PF Secchi, EF Lizak, MJ Rodriguez, L Blessing, K Sato, S TI Effect of sorbitol dehydrogenase inhibition on sugar cataract formation in galactose-fed and diabetic rats SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,LAB OCULAR THERAPEUT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 894 EP 894 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700892 ER PT J AU Tomarev, S Callaerts, P Kos, L Zinovieva, R Halder, G Gehring, W Piatigorsky, J AF Tomarev, S Callaerts, P Kos, L Zinovieva, R Halder, G Gehring, W Piatigorsky, J TI Pax-6 and eye development in invertebrates SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,LMDB,BETHESDA,MD 20892. UNIV BASEL,DEPT CELL BIOL,BASEL,SWITZERLAND. NCHGR,LMGD,BETHESDA,MD. RI Halder, Georg/F-2966-2015 OI Halder, Georg/0000-0001-7580-3236 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 927 EP 927 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700925 ER PT J AU Zadunaisky, JA Croft, DF Spring, KS AF Zadunaisky, JA Croft, DF Spring, KS TI Human trabecular meshwork cells receptors SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NYU,MED CTR,NEW YORK,NY. NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 948 EP 948 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700946 ER PT J AU Miller, DS Croft, DF Zadunaisky, JA AF Miller, DS Croft, DF Zadunaisky, JA TI Organic anion transport by human trabecular meshwork cells in culture. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIEHS,NIH,LAB CELLULAR & MOL PHARMACOL,RES TRIANGLE PK,NC 27709. NYU,MED CTR,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 951 EP 951 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700949 ER PT J AU Zigler, JS Qin, C Tumminia, SJ Russell, P AF Zigler, JS Qin, C Tumminia, SJ Russell, P TI Prevention of cataractous changes in cultured rat lenses by the hydroxylamine of Tempol (Tempol-H) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,NEI,LAB MECHANISMS OCULAR DIS,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 970 EP 970 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39700968 ER PT J AU Redmond, TM Kammer, J Yu, S Liu, SY AF Redmond, TM Kammer, J Yu, S Liu, SY TI Proximal and distal regions of homology in the mouse and human RPE65 gene 5' flanking sequences. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1530 EP 1530 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701528 ER PT J AU Schoen, TJ Mazuruk, K Chandrasekharappa, SC Guru, SC Chader, GJ Rodriguez, IR AF Schoen, TJ Mazuruk, K Chandrasekharappa, SC Guru, SC Chader, GJ Rodriguez, IR TI Genomic organization and chromosomal sublocalization of the human gene for the seventh largest subunit of RNA polymerase II to 11q13. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NATL CTR HUMAN GENOME RES,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1531 EP 1531 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701529 ER PT J AU TombranTink, J Kozak, C Chader, G AF TombranTink, J Kozak, C Chader, G TI Molecular characterization, chromosomal localization and gene expression of the mouse PEDF. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1535 EP 1535 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701533 ER PT J AU Okamoto, S Kinoshita, S Sato, S Kador, PF AF Okamoto, S Kinoshita, S Sato, S Kador, PF TI Development of an in vitro model of galactose-induced keratoepitheliopathy using a corneal epithelial cell line SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 KYOTO PREFECTURAL YOSANOUMI HOSP,DEPT OPHTHALMOL,KYOTO,JAPAN. KYOTO PREFECTURAL UNIV MED,KYOTO 602,JAPAN. JAPAN & NATL EYE INST,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1613 EP 1613 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701611 ER PT J AU Guo, J Sax, CM Piatigorsky, J Yu, FX AF Guo, J Sax, CM Piatigorsky, J Yu, FX TI Differential, expression of the transketolase gene in the adult, developing, and healing mouse cornea and other ocular tissues. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,SCHEPENS EYE RES INST,BOSTON,MA. NEI,NIH,MOLEC & DEV BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1634 EP 1634 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701632 ER PT J AU Salamon, C Piatigorsky, J Sax, CM AF Salamon, C Piatigorsky, J Sax, CM TI Cloning and characterization of the mouse transketolase gene: A gene preferentially expressed in the cornea SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,MOLEC & DEV BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1635 EP 1635 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701633 ER PT J AU Smith, JA Hudak, D Geiser, S Nussenblatt, RB Whitcup, SM AF Smith, JA Hudak, D Geiser, S Nussenblatt, RB Whitcup, SM TI Prognostic factors for visual acuity in sarcoid uveitis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1681 EP 1681 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701679 ER PT J AU Nagineni, CN Pardhasaradhi, K Martins, MC Detrick, B Hooks, JJ AF Nagineni, CN Pardhasaradhi, K Martins, MC Detrick, B Hooks, JJ TI Mechanisms of interferon induced inhibition of Toxoplasma gondii replication in human RPE cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. WALTER REED ARMY INST RES,WASHINGTON,DC. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1729 EP 1729 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701727 ER PT J AU Ursell, PG Spalton, DJ KerrMuir, M Burgess, FC Whitcup, SM Nussenblatt, RB AF Ursell, PG Spalton, DJ KerrMuir, M Burgess, FC Whitcup, SM Nussenblatt, RB TI The incidence of CME after routine phaco surgery SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 ST THOMAS HOSP,DEPT OPHTHALMOL,LONDON,ENGLAND. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1866 EP 1866 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701864 ER PT J AU Christen, W Ajani, U Glynn, R Manson, J Chew, E Buring, J Hennekens, C AF Christen, W Ajani, U Glynn, R Manson, J Chew, E Buring, J Hennekens, C TI Vitamin supplements and risk of age-related macular degeneration (AMD) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1918 EP 1918 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701916 ER PT J AU Garland, DL TaborDuglas, Y Datiles, MB AF Garland, DL TaborDuglas, Y Datiles, MB TI Crystallins in the nucleus of normal and cataractous human lenses SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1950 EP 1950 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701948 ER PT J AU Podgor, MJ AF Podgor, MJ TI Does your model address your question? SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,DIV BIOMETRY & EPIDEMIOL,STAT METHODS & ANAL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 1997 EP 1997 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39701995 ER PT J AU Wawrousek, EF Brady, JP AF Wawrousek, EF Brady, JP TI Preliminary characterization of alpha A-crystallin gene knockout mice SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2028 EP 2028 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702026 ER PT J AU Ferris, FL AF Ferris, FL TI Alternative treatment strategies for age-related macular degeneration SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,DIV BIOMETRY & EPIDEMIOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2051 EP 2051 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702049 ER PT J AU Sax, CM Salamon, C Kays, WT Yu, F Cuthbertson, RA Piatigorsky, J AF Sax, CM Salamon, C Kays, WT Yu, F Cuthbertson, RA Piatigorsky, J TI The transketolase (TKT) gene is abundantly and differentially expressed in the developing mouse cornea SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BOSTON,MA. SCHEPENS EYE RES INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2062 EP 2062 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702060 ER PT J AU Ramadan, A Nussenblatt, RB deSmet, MD AF Ramadan, A Nussenblatt, RB deSmet, MD TI Elevation of anti-heat shock protein 70 antibodies in patients with uveitis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,CLIN IMMUNOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2081 EP 2081 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702079 ER PT J AU Rizzo, LV Yamamoto, JH Gazzinelli, RT Silveira, C Kalil, J Belfort, R AF Rizzo, LV Yamamoto, JH Gazzinelli, RT Silveira, C Kalil, J Belfort, R TI Analysis of immunological parameters of patients with toxoplasmosis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. USP,DEPT OPHTHALMOL,SAO PAULO,BRAZIL. UNIV FED MINAS GERAIS,DEPT BIOCHEM IMMUNOL,BELO HORIZONT,MG,BRAZIL. UFSP,DEPT OPHTHALMOL,SAO PAULO,BRAZIL. RI Rizzo, Luiz Vicente/B-4458-2009; Belfort Jr, Rubens/E-2252-2012; Yamamoto, Joyce/B-6192-2015 OI Belfort Jr, Rubens/0000-0002-8422-3898; NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2083 EP 2083 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702081 ER PT J AU Liu, SY Redmond, TM AF Liu, SY Redmond, TM TI Role of RNA sequences in translational regulation of RPE65 gene SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2115 EP 2115 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702113 ER PT J AU Caruso, RC KaiserKupfer, MI AF Caruso, RC KaiserKupfer, MI TI Flicker electroretinography in gyrate atrophy SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2291 EP 2291 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702289 ER PT J AU ReuterAyres, LM Caruso, RC KaiserKupfer, MI AF ReuterAyres, LM Caruso, RC KaiserKupfer, MI TI The rate of dark adaptation measured with electroretinography SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALMOL GENET & CLIN SERV BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2302 EP 2302 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702300 ER PT J AU Vistica, BP Sun, SH Milam, AH Whitcup, SM Nussenblatt, RB Gery, I AF Vistica, BP Sun, SH Milam, AH Whitcup, SM Nussenblatt, RB Gery, I TI Cellular and humoral responses to recoverin in humans differ from responses against S-antigen or IRBP SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,SEATTLE,WA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2452 EP 2452 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702449 ER PT J AU Prendergast, RA Caspi, RR Iliff, CE AF Prendergast, RA Caspi, RR Iliff, CE TI EAU: Comparative studies on effector functions of normal and fluorescent-labeled T cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD. NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2456 EP 2456 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702453 ER PT J AU Hu, H Rizzo, LV Silver, PB Caspi, RR AF Hu, H Rizzo, LV Silver, PB Caspi, RR TI Uveitogenicity is associated with a Th1-like lymphokine profile: Cytokine-dependent modulation of primary and committed T cells in EAU. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2458 EP 2458 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702455 ER PT J AU Sun, B Sun, SH Caspi, RR AF Sun, B Sun, SH Caspi, RR TI Genetic susceptibility to EAU involves more than a predisposition to generate a TH1 or a TH2-type response SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2459 EP 2459 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702462 ER PT J AU Li, Q Sung, B Luyo, D Caspi, RR Chan, CC AF Li, Q Sung, B Luyo, D Caspi, RR Chan, CC TI Cytokine profile of experimental melanin-protein induced uveitis (EMIU): Expression and kinetics SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2460 EP 2460 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702457 ER PT J AU Koevary, SB Caspi, RR AF Koevary, SB Caspi, RR TI Prevention of experimental autoimmune uveoretinitis (EAU) by intrathymic S-antigen (S-Ag) injection SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NE COLL OPTOMETRY,DEPT BIOL SCI,BOSTON,MA. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2461 EP 2461 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702458 ER PT J AU Agarwal, RK Caspi, RR AF Agarwal, RK Caspi, RR TI Abrogation of resistance to experimental autoimmune uveoretinitis (EAU) by pertussis toxin in a genetically resistant rat strain is accompanied by enhanced production of IFN-gamma SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2462 EP 2462 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702459 ER PT J AU Nguyen, TA Crawford, MA Li, Q Li, Y Chan, CC AF Nguyen, TA Crawford, MA Li, Q Li, Y Chan, CC TI Ultrastructural comparison of experimental melanin induced uveitis (EMIU) and experimental autoimmune retinitis (EAU) in the Lewis rat SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET CLIN SERV BRANCH,NIH,BETHESDA,MD 20892. NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2463 EP 2463 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702460 ER PT J AU Li, Y Zhai, Y Li, Q Nussenblatt, RB Chan, CC AF Li, Y Zhai, Y Li, Q Nussenblatt, RB Chan, CC TI GP100, an melanocyte-lineage antigen, enhances experimental melanin-protein induced uveitis (EMIU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NCI,SURG BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2464 EP 2464 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702461 ER PT J AU Tarrant, T Rizzo, LV Silver, PB Caspi, RR AF Tarrant, T Rizzo, LV Silver, PB Caspi, RR TI TGF-beta suppresses antigen stimulation of a uveitogenic T cell line through an effect on antigen-presenting cells. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HHMI,NIH,RES SCHOLARS PROGRAM,BETHESDA,MD. NEI,IMMUNOL LAB,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2465 EP 2465 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702468 ER PT J AU deSmet, MD Kriete, M Chan, CC Raber, J Wiggert, B Rengarajan, K AF deSmet, MD Kriete, M Chan, CC Raber, J Wiggert, B Rengarajan, K TI HSP70 is expressed in Lewis rat eyes during experimental autoimmune uveitis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,CLIN IMMUNOL SECT,BETHESDA,MD 20892. NEI,IMMUNOPATHOL SECT,BETHESDA,MD 20892. NEI,VET RES & RESOURCES SECT,IMMUNOL LAB,BETHESDA,MD 20892. NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2466 EP 2466 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702463 ER PT J AU Bowers, WE Choudhury, A Padhye, NS Caspi, RR AF Bowers, WE Choudhury, A Padhye, NS Caspi, RR TI Role of choroidal dendritic cells in the induction of experimental autoimmune uveoretinitis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV S CAROLINA,SCH MED,DEPT MICROBIOL & IMMUNOL,COLUMBIA,SC 29208. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2470 EP 2470 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702467 ER PT J AU Fukushima, A Vistica, BP Caspi, RR Wawrousek, EF Kozhich, AT Whitecup, SM Gery, I AF Fukushima, A Vistica, BP Caspi, RR Wawrousek, EF Kozhich, AT Whitecup, SM Gery, I TI Lymphocyte stimulation and expression of cell adhesion molecules are critical for adoptive transfer of cellular immunity and disease SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2471 EP 2471 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702473 ER PT J AU Chaudhry, S Kozhich, AT Chan, CC Sredni, B Nussenblatt, RB Whitecup, SM AF Chaudhry, S Kozhich, AT Chan, CC Sredni, B Nussenblatt, RB Whitecup, SM TI The immunomodulator AS101 inhibits endotoxin-induced uveits in the rat. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. BAR ILAN UNIV,RAMAT GAN,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2477 EP 2477 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702474 ER PT J AU Jacot, JL Hosotani, H Glover, JP Lois, N Robison, WG AF Jacot, JL Hosotani, H Glover, JP Lois, N Robison, WG TI Diabetic-like loss of corneal sensitivity in the 50% galactose fed rat is ameliorated with topical administration of an aldose reductase inhibitor SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. OSAKA PREFECTURE HOSP,DEPT OPHTHALMOL,OSAKA,JAPAN. WILLS EYE HOSP & RES INST,CORNEA SERV,PHILADELPHIA,PA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2511 EP 2511 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702510 ER PT J AU Janjani, A DuglasTabor, Y Garland, DL AF Janjani, A DuglasTabor, Y Garland, DL TI Modification of human lens crystallins with fiber cell age SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2751 EP 2751 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702753 ER PT J AU Sergeev, YV Hope, JN Hejtmancik, FJ AF Sergeev, YV Hope, JN Hejtmancik, FJ TI Microdomain structure of terminal, extensions in beta A3- and beta B2-crystallins SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2752 EP 2752 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702748 ER PT J AU Glover, JP Jacot, JL Rao, CM Qin, C Zigler, JS Robison, WG AF Glover, JP Jacot, JL Rao, CM Qin, C Zigler, JS Robison, WG TI Glycation of lens proteins in relation to aldose reductase activity and galactose-induced cataracts SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,NEI,SECT PATHOPHYSIOL,BETHESDA,MD 20892. NIH,NEI,LENS & CATARACT BIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2770 EP 2770 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702766 ER PT J AU Nelson, R Schaffner, AE Li, YX Walton, MK AF Nelson, R Schaffner, AE Li, YX Walton, MK TI Glutamate and cGMP sensitivities of rat retinal neurons assayed by fluorescent potentiometric probe SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NINCDS,NIH,NEUROPHYSIOL LAB,BETHESDA,MD. US FDA,CBER,OTRR,DCTDA,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2910 EP 2910 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702906 ER PT J AU Loi, J Alexander, P StetlerStevenson, W Sheffield, JB AF Loi, J Alexander, P StetlerStevenson, W Sheffield, JB TI Immunohistochemical studies on the distribution of metalloproteinases in tissue sections of developing chick retinas. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TEMPLE UNIV,DEPT BIOL,PHILADELPHIA,PA 19122. NCI,OREGON HLTH SCI CTR,DEPT OPHTHALMOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2944 EP 2944 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702946 ER PT J AU Mazuruk, K Schoen, T Chader, GJ Rodriguez, IR AF Mazuruk, K Schoen, T Chader, GJ Rodriguez, IR TI Isolation and characterization of new candidate genes for macular degeneration. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2956 EP 2956 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702952 ER PT J AU Bernstein, SL Borst, DE Wong, PW AF Bernstein, SL Borst, DE Wong, PW TI Further characterization of expressed sequence tags (ESTs) from a human foveal cDNA library. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. USUHS,DEPT ANAT & CELL BIOL,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2958 EP 2958 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702954 ER PT J AU Lee, J Jiao, X Hejtmancik, JF KaiserKupfer, M Chader, GJ AF Lee, J Jiao, X Hejtmancik, JF KaiserKupfer, M Chader, GJ TI Isolation and characterization of a 32 kDa docosahexaenoic acid-binding protein missing from lymphocytes in humans with Bietti's crystalline dystrophy (BCD). SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2964 EP 2964 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702960 ER PT J AU Csaky, KG Sullivan, DM Lee, YJ Chung, DC Nussenblatt, RB Anglade, E AF Csaky, KG Sullivan, DM Lee, YJ Chung, DC Nussenblatt, RB Anglade, E TI The use of green fluorescent protein to monitor gene transfer in human retinal pigment epithelial cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 2967 EP 2967 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39702966 ER PT J AU Hejtmancik, JF Nestorowicz, A Li, Y VanTuinen, P Smith, RJH KaiserKupfer, M Permutt, MA Ayyagari, R AF Hejtmancik, JF Nestorowicz, A Li, Y VanTuinen, P Smith, RJH KaiserKupfer, M Permutt, MA Ayyagari, R TI A YAC contig encompassing the usher syndrome type 1C locus on chromosome SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 WASHINGTON UNIV,SCH MED,DIV METAB,ST LOUIS,MO 63130. NEI,BETHESDA,MD 20892. UNIV IOWA,DEPT OTOLARYNGOL,IOWA CITY,IA 52242. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3028 EP 3028 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703024 ER PT J AU Fong, DS Ferris, FL AF Fong, DS Ferris, FL TI Is myopia related to amplitude of accommodation? SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,SCH MED,JULES STEIN EYE INST,KING DREW MED CTR,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3139 EP 3139 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703135 ER PT J AU Datiles, MB Mahurkar, A Caruso, RC Vivino, M Magno, B AF Datiles, MB Mahurkar, A Caruso, RC Vivino, M Magno, B TI Effect of nuclear cataracts on visual function: Cone threshold measurements using computer assisted perimetry. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NIH,DIV COMP RES & TECHNOL,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3483 EP 3483 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703478 ER PT J AU Anglade, E Chung, D Sullivan, D Nussenblatt, RB Graham, F Csaky, K AF Anglade, E Chung, D Sullivan, D Nussenblatt, RB Graham, F Csaky, K TI A comparison of human and murine cytomegalovirus promoters on gene expression in adult rat ocular tissues SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,IMMUNOL LAB,BETHESDA,MD. MCMASTER UNIV,DEPT BIOL,HAMILTON,ON,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3543 EP 3543 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703537 ER PT J AU Magone, T Nussenblatt, RB Whitcup, SM AF Magone, T Nussenblatt, RB Whitcup, SM TI The utility of laser flare photometry (LFP) in screening for cytomegalovirus retinitis in patients with AIDS. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3546 EP 3546 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703540 ER PT J AU Chader, G Becerra, SP Taniwaki, T Sugita, Y Araki, T Schwartz, J AF Chader, G Becerra, SP Taniwaki, T Sugita, Y Araki, T Schwartz, J TI Neurotrophic effects of pigment epithelium-derived factor (PEDF): Neuron-survival and ''gliastatic'' activities. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NINCDS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3641 EP 3641 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703635 ER PT J AU Alberdi, E Becerra, SP AF Alberdi, E Becerra, SP TI PEDF-binding to glycosaminoglycans and proteoglycans SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3642 EP 3642 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703636 ER PT J AU Kutty, RK Kutty, G Duncan, T Rodriguez, IR Shim, K Stark, WS Wiggert, B AF Kutty, RK Kutty, G Duncan, T Rodriguez, IR Shim, K Stark, WS Wiggert, B TI Molecular cloning of a novel gene encoding a Drosophila retinoid- and fatty acid-binding glycoprotein expressed in cone (Semper) cells of the compound eye SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. ST LOUIS UNIV,ST LOUIS,MO 63103. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3694 EP 3694 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703688 ER PT J AU Kikuchi, T SunayashikiKusuzaki, K Abe, T Wawrousek, E Hamasaki, D Shinohara, T AF Kikuchi, T SunayashikiKusuzaki, K Abe, T Wawrousek, E Hamasaki, D Shinohara, T TI Expression of arrestin, phosducin, and opsin in highly restricted small numbers of cells in brain. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR OPHTHALM RES,BOSTON,MA 02115. NEI,NIH,LMDB,BETHESDA,MD. UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,MIAMI,FL 33136. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 3735 EP 3735 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703729 ER PT J AU Hackett, J Jacot, JL Kalaria, A Robison, WG AF Hackett, J Jacot, JL Kalaria, A Robison, WG TI Apoptosis in diabetic-like corneal epitheliopathy in the 50% galactose-fed rat model SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. UNIV MICHIGAN,DEPT MICROBIOL,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4002 EP 4002 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39703996 ER PT J AU Mitton, KP Tumminia, SJ Russell, P AF Mitton, KP Tumminia, SJ Russell, P TI Cleavage of MIP26 (aquaporin-0) accompanies cataractogenesis in transgenic mice expressing HIV-1 protease linked to the alpha A-crystallin promoter. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,LAB MECHANISMS OCULAR DIS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4074 EP 4074 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704068 ER PT J AU Zlokovic, BV Mackic, JB Zigler, JS Kaplowitz, N Kannan, R AF Zlokovic, BV Mackic, JB Zigler, JS Kaplowitz, N Kannan, R TI Lens transport of ascorbic acid in guinea pigs, normal, galactose-fed and with congenital cataract SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV SO CALIF,SCH MED,DEPT NEUROSURG,LOS ANGELES,CA 90033. UNIV SO CALIF,SCH MED,DEPT MED,LOS ANGELES,CA 90033. UNIV SO CALIF,SCH MED,DOHENY EYE INST,LOS ANGELES,CA 90033. NEI,NIH,LMOD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4079 EP 4079 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704073 ER PT J AU Bettelheim, FA Churchill, AC Robison, WG Zigler, JS AF Bettelheim, FA Churchill, AC Robison, WG Zigler, JS TI Dimethyl sulfoxide cataract SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 ADELPHI UNIV,GARDEN CITY,NY 11530. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4096 EP 4096 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704090 ER PT J AU Dillon, J Reszka, K Chignell, C AF Dillon, J Reszka, K Chignell, C TI The photochemistry of yellow lens protein as studied by ESR. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 COLUMBIA UNIV,DEPT OPHTHALMOL,NEW YORK,NY 10027. NIEHS,MOLEC BIOPHYS LAB,DEPT MATH & SCI,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4108 EP 4108 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704102 ER PT J AU Robison, WG Jacot, JL Glover, JP Feld, LG AF Robison, WG Jacot, JL Glover, JP Feld, LG TI Roles of aldose reductase and glycation in cataracts SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI, NIH, BETHESDA, MD 20892 USA. STATE UNIV NEW YORK BUFFALO, CHILDRENS HOSP, SCH MED & BIOMED SCI, BUFFALO, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 EI 1552-5783 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4112 EP 4112 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704106 ER PT J AU Secchi, EF Lizak, MJ Sato, S Kador, PF AF Secchi, EF Lizak, MJ Sato, S Kador, PF TI New perspectives in the use of 3-fluoro-3-deoxygalactose to investigate sugar cataract formation SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,LAB OCULAR THERAPEUT,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4127 EP 4127 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704121 ER PT J AU Qin, C Zigler, JS Borras, T AF Qin, C Zigler, JS Borras, T TI Transient cataract formation in cultured lenses following removing from medium containing high levels of glycerol SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,LAB MECHANISMS OCULAR DIS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4130 EP 4130 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704124 ER PT J AU Pleyer, U Kozhich, AT Lobanoff, MC Grammer, J Chan, CC Whitcup, SM AF Pleyer, U Kozhich, AT Lobanoff, MC Grammer, J Chan, CC Whitcup, SM TI The role of circulating macrophages in the pathogenesis of experimental autoimmune uveitis (EAU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HUMBOLDT UNIV BERLIN,BEREICH MED CHARITE,EYE CLIN,O-1040 BERLIN,GERMANY. NEI,NIH,BETHESDA,MD. UNIV TUBINGEN,DEPT SURG,D-72076 TUBINGEN,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4149 EP 4149 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704143 ER PT J AU Jones, LS Rizzo, LV Agarwal, R Silver, PB Caspi, RR AF Jones, LS Rizzo, LV Agarwal, R Silver, PB Caspi, RR TI Interferon gamma (IFN-gamma)-deficient mice are susceptible to induction of experimental autoimmune uveitis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,HHMI,RES SCHOLARS PROGRAM,BETHESDA,MD 20892. NEI,IMMUNOL LAB,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4150 EP 4150 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704144 ER PT J AU GuexCrosier, Y Raber, J Hakimi, J Kriete, M Chan, CC Roberge, FG AF GuexCrosier, Y Raber, J Hakimi, J Kriete, M Chan, CC Roberge, FG TI Humanized anti-IL-2 and anti-IL-15 receptor antibodies in the treatment of uveoretinitis in a monkey model. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. F HOFFMANN LA ROCHE & CO LTD,NUTLEY,NJ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4151 EP 4151 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704145 ER PT J AU BanerjeeBasu, S Tomarev, SI Duncan, MK Piatigorsky, J AF BanerjeeBasu, S Tomarev, SI Duncan, MK Piatigorsky, J TI Role of homeobox gene Prox1 during chicken lens development SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4170 EP 4170 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704164 ER PT J AU Li, X Cvekl, A Piatigorsky, J AF Li, X Cvekl, A Piatigorsky, J TI Expression of the chicken and duck delta 2-crystallin gene. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4171 EP 4171 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704165 ER PT J AU Rampalli, AM Gao, CY Chauthaiwale, VM Zelenka, PS AF Rampalli, AM Gao, CY Chauthaiwale, VM Zelenka, PS TI Formation of a novel pRb-containing complex during differentiation of lens fiber cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4172 EP 4172 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704166 ER PT J AU Frederikse, P Piatigorsky, J AF Frederikse, P Piatigorsky, J TI Heat shock transcription factor 2 (HSF2) and lens crystallin promoter dyad motifs: A mechanism for recruitment of stress-related proteins to the ocular lens SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4173 EP 4173 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704167 ER PT J AU Wistow, G Richardson, J Lee, D Friling, R Sperbeck, S Graham, C AF Wistow, G Richardson, J Lee, D Friling, R Sperbeck, S Graham, C TI zeta-crystallin: Pax-6 dependence and expression in lens epithelial cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,SECT MOLEC STRUCT & FUNCT,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4175 EP 4175 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704169 ER PT J AU Rengarajan, K Kutty, RK Wiggert, B AF Rengarajan, K Kutty, RK Wiggert, B TI Expression in yeast of a human IRBP peptide: Isolation and partial characterization SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4193 EP 4193 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704187 ER PT J AU Kansupada, KB Kitchen, BJ Mueller, BU Walton, RC Nussenblatt, RB Whitcup, SM AF Kansupada, KB Kitchen, BJ Mueller, BU Walton, RC Nussenblatt, RB Whitcup, SM TI Ocular manifestations in pediatric patients with aids SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4215 EP 4215 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704209 ER PT J AU Egwuagu, CE Mahdi, R Smith, JA Chan, CC Chepelinsky, AB AF Egwuagu, CE Mahdi, R Smith, JA Chan, CC Chepelinsky, AB TI Gamma interferon-expressing transgenic rats: A useful model of anterior and posterior uveitis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4229 EP 4229 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704223 ER PT J AU Chepelinsky, AB Robinson, ML Ash, J ParkerWilson, DM OhtakaMaruyama, C Overbeek, PA AF Chepelinsky, AB Robinson, ML Ash, J ParkerWilson, DM OhtakaMaruyama, C Overbeek, PA TI Secreted FGF-3 induces cell cycle withdrawal and differentiation of lens epithelia in transgenic mice SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. BAYLOR COLL MED,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4247 EP 4247 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704241 ER PT J AU Arora, JK Zelenka, PS AF Arora, JK Zelenka, PS TI A role for 22(S)-HETE in signal transduction initiated by EGF-receptor activation. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4250 EP 4250 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704244 ER PT J AU Chew, E Ferris, F Kador, P Wyman, M Remaley, N Podgor, M AF Chew, E Ferris, F Kador, P Wyman, M Remaley, N Podgor, M TI Effect of aldose reductase inhibitor on fluorescein angiographic lesions in galactose-fed dogs. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4287 EP 4287 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704281 ER PT J AU Rodriguez, IR Coon, SL Mazuruk, K Bernard, M Roseboom, P Klein, DC AF Rodriguez, IR Coon, SL Mazuruk, K Bernard, M Roseboom, P Klein, DC TI Structural organization, localization and expression of the human serotonin N-acetyltransferase gene SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NICHHD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4341 EP 4341 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704335 ER PT J AU Lackner, PA Neuenschwander, H Greentree, W Takahashi, Y Wyman, M Kador, PF AF Lackner, PA Neuenschwander, H Greentree, W Takahashi, Y Wyman, M Kador, PF TI Reversal studies can preserve retinal capillary pericytes in galactose-fed dogs SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,LAB OCULAR THERAPEUT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4442 EP 4442 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704436 ER PT J AU Haynes, JI Duncan, MK Piatigorsky, J AF Haynes, JI Duncan, MK Piatigorsky, J TI Murine alpha B-crystallin promoter activity during embryogenesis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,LMDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4489 EP 4489 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704482 ER PT J AU Rao, PV Zigler, JS Garland, D AF Rao, PV Zigler, JS Garland, D TI Identification and characterization of members of the Ras super family GTPases in the eye lens SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4493 EP 4493 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704486 ER PT J AU Singh, I Zelenka, PS Wagner, BJ AF Singh, I Zelenka, PS Wagner, BJ TI Expression of a 20S proteasome subunit and cyclin B during embryonic chicken lens development SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT BIOCHEM & MOLEC BIOL,NEWARK,NJ 07103. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT OPHTHALMOL,NEWARK,NJ 07103. NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4495 EP 4495 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704488 ER PT J AU Lo, WK Wen, XJ Shaw, AP Reese, TS AF Lo, WK Wen, XJ Shaw, AP Reese, TS TI Involvement of kinesin and microtubules in organelle transport during lens fiber cell differentiation SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MOREHOUSE SCH MED,DEPT ANAT,ATLANTA,GA 30310. NINCDS,NIH,NEUROBIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4497 EP 4497 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704490 ER PT J AU He, HY Gao, CY Zelenka, PS AF He, HY Gao, CY Zelenka, PS TI Cyclin B is associated with histone H1 kinase activity in differentiating rat lens fiber cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4506 EP 4506 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704499 ER PT J AU Russell, P Tumminia, SJ AF Russell, P Tumminia, SJ TI HIV-1 protease expression in the lenses of transgenic animals SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4510 EP 4510 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704503 ER PT J AU Duncan, MK Tomarev, SI Cvekl, A Piatigorsky, J AF Duncan, MK Tomarev, SI Cvekl, A Piatigorsky, J TI Developmental regulation of the chicken beta B1-crystallin promoter SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMBD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4523 EP 4523 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704516 ER PT J AU GopalSrivastava, R Cvekl, A Piatigorsky, J AF GopalSrivastava, R Cvekl, A Piatigorsky, J TI Regulation of the murine alpha B-crystallin gene in lens. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4527 EP 4527 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704520 ER PT J AU Kantorow, F Cvekl, A Piatigorsky, J AF Kantorow, F Cvekl, A Piatigorsky, J TI Regulation of PAX-6 gene expression in the lens SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20891. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4528 EP 4528 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704521 ER PT J AU Chan, CC Davis, VL Schoen, T Li, Q Korach, KS Chader, GJ AF Chan, CC Davis, VL Schoen, T Li, Q Korach, KS Chader, GJ TI The role of estrogen on cataract formation: A study of transgenic mice with mutation of estrogen receptor SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIEHS,LRDT,RES TRIANGLE PK,NC 27709. NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4534 EP 4534 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704527 ER PT J AU Carper, DA McGowan, MH Iwata, T AF Carper, DA McGowan, MH Iwata, T TI Promoter expression of the polyol pathway enzymes SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4543 EP 4543 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704536 ER PT J AU Esumi, N Sinha, D Paralkar, V Noonan, F Rox, GD Lang, R Wistow, G AF Esumi, N Sinha, D Paralkar, V Noonan, F Rox, GD Lang, R Wistow, G TI MIF: A lymphokine in lens SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMDB,NIH,SECT MOLEC STRUCT & FUNCT,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,WASHINGTON,DC. NYU,MED CTR,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4545 EP 4545 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704538 ER PT J AU Davidson, JK Tink, J Loyer, M Traboulsi, E Maumenee, I Koenekoop, RK AF Davidson, JK Tink, J Loyer, M Traboulsi, E Maumenee, I Koenekoop, RK TI Pigment epithelium derived factor as a candidate gene for Leber's congenital amaurosis SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MCGILL UNIV,MONTREAL CHILDRENS HOSP,RES INST,MONTREAL,PQ H3A 2T5,CANADA. NEI,NIH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,CTR HEREDITARY EYE DIS,BALTIMORE,MD 21218. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4548 EP 4548 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704541 ER PT J AU Heinzmann, C Kojis, TL Flodman, P Tiller, GE Heckenlively, JR Rodriguez, IR Chader, GJ Spence, MA Bateman, JB AF Heinzmann, C Kojis, TL Flodman, P Tiller, GE Heckenlively, JR Rodriguez, IR Chader, GJ Spence, MA Bateman, JB TI Fine mapping of an autosomal dominant Retinitis pigmentosa (ADRP) locus on chromosome 17p13.3 and analysis of a candidate gene SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,JULES STEIN EYE INST,DEPT OPHTHALMOL,LOS ANGELES,CA 90024. VANDERBILT UNIV,MED CTR,NASHVILLE,TN. NEI,NIH,BETHESDA,MD 20892. UCHSC,DEPT OPHTHALMOL,DENVER,CO. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4549 EP 4549 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704542 ER PT J AU Sullivan, DM Chung, DC Taichman, LB Nussenblatt, RB Anglade, E Csaky, KG AF Sullivan, DM Chung, DC Taichman, LB Nussenblatt, RB Anglade, E Csaky, KG TI Overexpression of ornithine-delta-aminotransferase in keratinocytes cultured from gyrate atrophy patients. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. SUNY STONY BROOK,DEPT ORAL BIOL,STONY BROOK,NY 11794. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4801 EP 4801 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704794 ER PT J AU Putilina, T Frank, E Iwata, T Chader, G Krause, M AF Putilina, T Frank, E Iwata, T Chader, G Krause, M TI Development and characterization of antibodies to CED-4 protein. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4812 EP 4812 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704805 ER PT J AU BeleckyAdams, T Tomarev, S Sundin, O McInnes, RR Ploder, L Adler, R AF BeleckyAdams, T Tomarev, S Sundin, O McInnes, RR Ploder, L Adler, R TI Correlation of Prox 1, Pax-6, and Chx 10 gene expression and phenotypic fate of chicken retinal precursor cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,WILMER EYE INST,DEPT OPHTHALMOL,BALTIMORE,MD 21205. NEI,NIH,LMBD,BETHESDA,MD 20892. HOSP SICK CHILDREN,DEPT GENET,TORONTO,ON M5G 1X8,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4818 EP 4818 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704811 ER PT J AU Nemesure, B Leske, MC Connell, AMS Hejtmancik, F Schachat, A AF Nemesure, B Leske, MC Connell, AMS Hejtmancik, F Schachat, A TI Barbados Family Study of Open-angle Glaucoma. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SUNY STONY BROOK,DEPT PREVENT MED,STONY BROOK,NY 11794. NEI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 4995 EP 4995 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39704988 ER PT J AU Kozhich, AT MillerRivero, NE Caspi, RR Nussenblatt, RB Gery, I AF Kozhich, AT MillerRivero, NE Caspi, RR Nussenblatt, RB Gery, I TI High MHC class II affinity of peptides is required for induction of oral tolerance. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 5126 EP 5126 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39705119 ER PT J AU Wong, P Ulyanova, T Lakins, J Darrow, R Tenniswood, M vanVeen, T Organisciak, D Chader, G AF Wong, P Ulyanova, T Lakins, J Darrow, R Tenniswood, M vanVeen, T Organisciak, D Chader, G TI Light-induced, oxidative-stress mediated retinal degeneration in rats: Immunolocalization of clusterin. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. GOTHENBURG UNIV,DEPT ZOOL,S-40031 GOTHENBURG,SWEDEN. W ALTON JONES CELL SCI CTR,LAKE PLACID,NY 12946. WRIGHT STATE UNIV,DEPT BIOCHEM & MOLEC BIOL,DAYTON,OH 45435. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 5155 EP 5155 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39705148 ER PT J AU KwitekBlack, AE Krizman, D Carmi, R Doggett, N Stone, EM Sheffield, VC AF KwitekBlack, AE Krizman, D Carmi, R Doggett, N Stone, EM Sheffield, VC TI Fine-mapping of Bardet-Biedl syndrome focus on chromosome 16 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV IOWA,DEPT PEDIAT,IOWA CITY,IA 52242. UNIV IOWA,DEPT OPHTHALMOL,IOWA CITY,IA 52242. BEN GURION UNIV NEGEV,IL-84105 BEER SHEVA,ISRAEL. LOS ALAMOS NATL LAB,LOS ALAMOS,NM 87545. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 5160 EP 5160 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39705153 ER PT J AU Rota, R Cirielli, C Blasi, MA Martinotti, S Toniato, E Capogrossi, M Procopio, A Balestrazzi, E AF Rota, R Cirielli, C Blasi, MA Martinotti, S Toniato, E Capogrossi, M Procopio, A Balestrazzi, E TI Adenovirus-mediated wild-type p53 gene transfer induces apoptosis and inhibits proliferation of human uveal melanoma cells. SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV LAQUILA,CHAIR OPHTHALMOL,LAQUILA,ITALY. IDI,LAB VASC PATHOL,ROME,ITALY. UNIV LAQUILA,DMS,LAQUILA,ITALY. NIA,NIH,LCS,GENE THERAPY UNIT,BALTIMORE,MD 21224. UNIV CHIETI,GENE THERAPY CTR,CHIETI,ITALY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 5187 EP 5187 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39705180 ER PT J AU Charukamnoetkanok, P Fukushima, A Whitcup, SM Gery, I Egwuagu, CE AF Charukamnoetkanok, P Fukushima, A Whitcup, SM Gery, I Egwuagu, CE TI Ocular-specific antigens are expressed in the thymus SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NIH,HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB 15 PY 1996 VL 37 IS 3 BP 5205 EP 5205 PG 1 WC Ophthalmology SC Ophthalmology GA TX397 UT WOS:A1996TX39705198 ER PT J AU Lenders, JWM Eisenhofer, G Abeling, NGGM Berger, W Murphy, DL Konings, CH Wagemakers, LMB Kopin, IJ Karoum, F vanGennip, AH Brunner, HG AF Lenders, JWM Eisenhofer, G Abeling, NGGM Berger, W Murphy, DL Konings, CH Wagemakers, LMB Kopin, IJ Karoum, F vanGennip, AH Brunner, HG TI Specific genetic deficiencies of the A and B isoenzymes of monoamine oxidase are characterized by distinct neurochemical and clinical phenotypes SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE catecholamines; Norrie disease; metabolism; metanephrines; dihydroxyphenylglycol ID NORRIE DISEASE PATIENTS; LIQUID-CHROMATOGRAPHY; PRESSOR SENSITIVITY; HUMAN PLATELET; X-CHROMOSOME; PLASMA; DELETION; AMINE; 3,4-DIHYDROXYPHENYLALANINE; METABOLISM AB Monoamine oxidase (MAO) exists as two isoenzymes and plays a central role in the metabolism of monoamine neurotransmitters. In this study we compared the neurochemical phenotypes of previously described subjects with genetically determined selective lack of MAO-A or a lack of both MAO-A and MAO-B with those of two subjects with a previously described X chromosome microdeletion in whom we now demonstrate selective MAO-B deficiency. Mapping of the distal deletion breakpoint demonstrates its location in intron 5 of the MAO-B gene, with the deletion extending proximally into the Norrie disease gene. In contrast to the borderline mental retardation and abnormal behavioral phenotype in subjects with selective MAO-A deficiency and the severe mental retardation in patients with combined MAO-A/MAO-B deficiency and Norrie disease. the MAO-B-deficient subjects exhibit neither abnormal behavior nor mental retardation. Distinct neurochemical profiles characterize the three groups of MAO-deficient patients. In MAO-A-deficient subjects, there is a marked decrease in deaminated catecholamine metabolites and a concomitant marked elevation of O-methylated amine metabolites. These neurochemical changes are only slightly exaggerated in patients with combined lack of MAO-A and MAO-B. In contrast. the only biochemical abnormalities detected in subjects with the MAO-B gene deletion are a complete absence of platelet MAO-B activity and an increased urinary excretion of phenylethylamine. The differences in neurochemical profiles indicate that, under normal conditions, MAO-A is considerably more important than MAO-B in the metabolism of biogenic amines, a factor likely to contribute to the different clinical phenotypes. C1 UNIV NIJMEGEN ST RADBOUD HOSP, DEPT HUMAN GENET, 6525 GA NIJMEGEN, NETHERLANDS. UNIV AMSTERDAM, ACAD MED CTR, DEPT PEDIAT, 1105 AZ AMSTERDAM, NETHERLANDS. UNIV AMSTERDAM, ACAD MED CTR, DEPT CLIN CHEM, 1105 AZ AMSTERDAM, NETHERLANDS. NIMH, NIH, CLIN SCI LAB, BETHESDA, MD 20892 USA. NINCDS, CLIN NEUROSCI BRANCH, BETHESDA, MD 20892 USA. NIMH, ST ELIZABETHS HOSP, CTR NEUROSCI, WASHINGTON, DC 20032 USA. FREE UNIV AMSTERDAM HOSP, DEPT CLIN CHEM, 1081 HV AMSTERDAM, NETHERLANDS. UNIV AMSTERDAM, DEPT OPHTHALMOGENET, OPHTHALM RES INST, 1105 AZ AMSTERDAM, NETHERLANDS. RP Lenders, JWM (reprint author), UNIV NIJMEGEN ST RADBOUD HOSP, DIV GEN INTERNAL MED, DEPT MED, GEERT GROOTEPLEIN ZUID 8, 6525 GA NIJMEGEN, NETHERLANDS. RI Brunner, Han/C-9928-2013; Lenders, J.W.M./L-4487-2015 NR 49 TC 91 Z9 91 U1 0 U2 4 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 EI 1558-8238 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB 15 PY 1996 VL 97 IS 4 BP 1010 EP 1019 DI 10.1172/JCI118492 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA UD037 UT WOS:A1996UD03700018 PM 8613523 ER PT J AU Quill, H AF Quill, H TI Anergy as a mechanism of peripheral T cell tolerance SO JOURNAL OF IMMUNOLOGY LA English DT Editorial Material ID PROTEIN-TYROSINE PHOSPHORYLATION; CLONAL ANERGY; ANTIGEN PRESENTATION; INDUCTION; COSTIMULATION; STIMULATION; INVITRO; ABSENCE; STATE; IL-4 RP Quill, H (reprint author), NIAID,NIH,DIV ALLERGY IMMUNOL & TRANSPLANTAT,SOLAR BLDG,ROOM 4A13,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 35 TC 55 Z9 63 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1996 VL 156 IS 4 BP 1325 EP 1327 PG 3 WC Immunology SC Immunology GA TU692 UT WOS:A1996TU69200001 PM 8568229 ER PT J AU Hayashi, S Chan, CC Gazzinelli, R Roberge, FG AF Hayashi, S Chan, CC Gazzinelli, R Roberge, FG TI Contribution of nitric oxide to the host parasite equilibrium in toxoplasmosis SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MURINE PERITONEAL-MACROPHAGES; ANTI-MICROBIAL ACTIVITY; NECROSIS-FACTOR-ALPHA; CD8+ LYMPHOCYTES-T; L-ARGININE; IFN-GAMMA; PROLIFERATIVE RESPONSES; SUPPRESSOR MACROPHAGES; CYTO-TOXICITY; GONDII AB We studied the effect of nitric oxide (NO) production on the evolution of toxoplasmosis in C57BL/6 mice, infection was induced by i.p. injection of Toxoplasma gondii strain ME49. NO synthesis was inhibited by treatment with aminoguanidine, a structural analogue of L-arginine. The severity of infection was evaluated by histopathologic examination of the brain, In the infected mice treated for 2 wk with aminoguanidine, we observed an increase in the number of toxoplasma tachyzoites and intracellular cysts accompanied by an exacerbated inflammation of the brain tissue compared with that in controls, When spleen cells from infected mice were stimulated in culture with toxoplasma Ag, there was a marked cytotoxic effect on cells collected during the acute stage of infection and an inhibition of proliferation of the remaining viable lymphocytes, These effects were correlated with high levels of NO and PGE(2) production, The suppression of NO synthesis prevented cell death and restored the lymphocyte proliferative response as well as lymphokine production, The neutralization of IFN-gamma or TNF-alpha had no effect on NO production in the cultures of infected mouse spleen cells, Cultures in which purified macrophages and lymphocytes from infected and naive mice were mixed indicated that the production of NO was dependent on lymphocyte activation, In the later stages of infection, when the production of NO was abating, preventing PGE(2) secretion with indomethacin also increased the lymphocyte proliferative response, We conclude that the opposing effects of NO in toxoplasmosis, which protects against Toxoplasma gondii and at the same time limits the immune response, probably contribute to the establishment of the characteristic chronic state of host parasite equilibrium. C1 NEI,NIH,IMMUNOL LAB,BETHESDA,MD 20892. NIAID,NIH,PARASIT DIS LAB,BETHESDA,MD 20892. UNIV FED MINAS GERAIS,DEPT BIOCHEM & IMMUNOL,BR-30161970 BELO HORIZONT,MG,BRAZIL. NR 48 TC 85 Z9 91 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1996 VL 156 IS 4 BP 1476 EP 1481 PG 6 WC Immunology SC Immunology GA TU692 UT WOS:A1996TU69200022 PM 8568250 ER PT J AU Kullberg, MC Berzofsky, JA Jankovic, DL Barbieri, S Williams, ME Perlmann, P Sher, A TroyeBlomberg, M AF Kullberg, MC Berzofsky, JA Jankovic, DL Barbieri, S Williams, ME Perlmann, P Sher, A TroyeBlomberg, M TI T cell-derived IL-3 induces the production of IL-4 by non-B, non-T cells to amplify the Th2-cytokine response to a non-parasite antigen in Schistosoma mansoni-infected mice SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SPLENIC NON-B; BONE-MARROW; HELMINTH INFECTION; DOWN-REGULATION; IGE SYNTHESIS; MAST-CELLS; INTERLEUKIN-4; BASOPHILS; MOUSE; LINES AB We describe a novel amplification mechanism underlying the increased early IL-4 production observed in Schistosoma mansoni-infected mice in response to a non-parasite Ag, sperm whale myoglobin (SwMb). Earlier studies have shown that splenic Fc epsilon R(+) non-B, non-T (NBNT) cells from schistosome-infected mice secrete IL-4 after stimulation with parasite Ag. We now demonstrate that purified NBNT cells from SwMb-immunized S. mansoni-infected mice do not respond directly to SwMb, but produce IL-4 in response to IL-3. Accordingly, we show that the early SwMb-specific IL-4 response of spleen cells (SC) from immunized infected mice is dependent on IL-3 and on CD4(+) T cells. Thus, most of the early SwMb-induced IL-4 from SC of infected mice appears to be produced by NBNT cells triggered by IL-3 synthesized by SwMb-specific CD4(+) T cells. IL-3-induced IL-4 production was also observed in purified NBNT cells from immunized uninfected mice, but the frequency and/or IL-4-producing capacity of splenic IL-3-responsive cells was found to be 8 to 16 times higher in immunized infected animals, IL-4 production by purified CD4(+) cells from immunized infected mice was also seen after SwMb stimulation, but this response showed slower kinetics than those of total SC, was IL-3-independent, and on average threefold greater than that by CD4(+) cells from immunized uninfected controls. Thus, increased SwMb-induced IL-4 production in immunized S. mansoni-infected mice results from direct synthesis by CD4(+) T cells, as well as their stimulation via IL-3 of an expanded population of NBNT cells. The latter pathway may serve as an amplification loop for Th2-cytokine responses. C1 NIAID,NIH,PARASIT DIS LAB,IMMUNOBIOL SECT,BETHESDA,MD 20892. NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,NIH,BETHESDA,MD 20892. NIAID,NIH,BIOL RES BRANCH,BETHESDA,MD 20892. RP Kullberg, MC (reprint author), UNIV STOCKHOLM,DEPT IMMUNOL,S-10691 STOCKHOLM,SWEDEN. RI Troye-Blomberg, Marita/B-9210-2016 OI Troye-Blomberg, Marita/0000-0002-2804-0325 NR 35 TC 21 Z9 21 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1996 VL 156 IS 4 BP 1482 EP 1489 PG 8 WC Immunology SC Immunology GA TU692 UT WOS:A1996TU69200023 PM 8568251 ER PT J AU Lafrenie, RM Wahl, LM Epstein, JS Hewlett, IK Yamada, KM Dhawan, S AF Lafrenie, RM Wahl, LM Epstein, JS Hewlett, IK Yamada, KM Dhawan, S TI HIV-1-Tat modulates the function of monocytes and alters their interactions with microvessel endothelial cells - A mechanism of HIV pathogenesis SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HUMAN VASCULAR ENDOTHELIUM; TAT PROTEIN; IV COLLAGENASE; AIDS PATIENTS; T-CELLS; INFECTION; MACROPHAGES; EXPRESSION; TYPE-1 AB Monocytes are major targets of HIV infection in patients with AIDS. In vitro infection of monocytes with HIV is associated with increased expression of beta(2) integrins, which increases both monocyte aggregation and monocyte/endothelial adhesion as well as monocyte metalloproteinase (MMP-9) expression. Treatment of primary monocytes with soluble HIV-Tat protein mimicked many of the properties of HIV infection of monocytes. Tat treatment up-regulated the expression of the beta(2) integrins, which was associated with the formation of large aggregates of monocytes and increased adhesion to endothelial monolayers. Treatment of monocytes with Tat increased their adhesion to both untreated and TNF-alpha-treated endothelial monolayers, and adhesion was inhibited by inclusion of anti-beta(2) and anti-ICAM-1 Abs. The increased adhesion of activated monocytes was accompanied by substantial disruption of the endothelial monolayers, with retraction or detachment of individual endothelial cells. Tat treatment of monocytes up-regulated the synthesis and release of the protease MMP-9, providing a potential mechanism to explain endothelial cell/basement membrane detachment. Thus, extracellular Tat is capable of activating monocytes even in the absence of HIV infection, Our studies demonstrate that many of the effects of HIV infection on monocyte homotypic and heterotypic adhesion, protease secretion, and disruption of the endothelium can be mimicked by treatment with HIV-Tat protein alone. These results suggest a mechanism where monocytes could be inappropriately activated by HIV-Tat, secreted by HIV-infected cells, causing them to extravasate into underlying tissues and ultimately contribute to tissue damage as seen during the progression of AIDS. C1 US FDA,CTR BIOL EVALUAT & RES,DIV TRANSFUS TRANSMITTED DIS,MOLEC VIROL LAB,ROCKVILLE,MD 20852. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NIDR,IMMUNOL LAB,BETHESDA,MD 20892. OI Yamada, Kenneth/0000-0003-1512-6805 NR 50 TC 111 Z9 115 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1996 VL 156 IS 4 BP 1638 EP 1645 PG 8 WC Immunology SC Immunology GA TU692 UT WOS:A1996TU69200042 PM 8568270 ER PT J AU Rizzo, LV Silver, P Wiggert, B Hakim, F Gazzinelli, RT Chan, CC Caspi, RR AF Rizzo, LV Silver, P Wiggert, B Hakim, F Gazzinelli, RT Chan, CC Caspi, RR TI Establishment and characterization of a murine CD4(+) T cell line and clone that induce experimental autoimmune uveoretinitis in B10.A mice SO JOURNAL OF IMMUNOLOGY LA English DT Article ID RETINOID-BINDING PROTEIN; BETA GENE USAGE; MULTIPLE-SCLEROSIS; REACTIVE ARTHRITIS; RECEPTOR; TH1; ANTIGEN; ALPHA; EAU; UVEITIS AB B10.A mice develop experimental autoimmune uveoretinitis after active immunization with the interphotoreceptor retinoid-binding protein (IRBP), CD4(+) T cells play an important role in the development of the disease, In this study we have isolated and characterized a CD4(+) T cell line and a T cell clone that induce experimental autoimmune uveoretinitis when transferred into naive B10.A mice, The cell line was isolated from draining lymph nodes of IRBP-immunized animals by repeated cycles of IRBP stimulation, The line was shown to be pathogenic after 4 rounds of in vitro stimulation with IRBP at 5 x 10(6) cells/mouse, A T cell clone derived from this line by limiting dilution was shown to be pathogenic when the same number of cells was injected; incidence and severity of disease, however, were much lower, After 16 rounds of IRBP-specific stimulation the cell line was pathogenic at 10(5) cells/mouse. Analysis of the VP repertoire revealed that at this point the line was mostly composed of V beta 8.2- and V beta 6-positive cells (>80% of the population), The uveitogenic clone expressed V beta 8.2. Both the T cell line and the clone elaborated an unrestricted lymphokine profile in vitro, However, when these cells were adoptively transferred into naive recipients, mRNA isolated from the uveitic retina showed only Th1 type cytokines, These data help to characterize the nature of pathogenic cells involved in ocular autoimmunity. C1 NCI,NIH,BETHESDA,MD 20892. NIAID,NIH,BETHESDA,MD 20892. UNIV FED MINAS GERAIS,DEPT BIOCHEM & IMMUNOL,BELO HORIZONT,MG,BRAZIL. RP Rizzo, LV (reprint author), NEI,NIH,IMMUNOL LAB,BLDG 10,ROOM 10N202,BETHESDA,MD 20892, USA. RI Rizzo, Luiz Vicente/B-4458-2009 NR 51 TC 79 Z9 79 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1996 VL 156 IS 4 BP 1654 EP 1660 PG 7 WC Immunology SC Immunology GA TU692 UT WOS:A1996TU69200044 PM 8568272 ER PT J AU Watkins, BA Davis, AE Fiorentini, S diMarzoVeronese, F Reitz, MS AF Watkins, BA Davis, AE Fiorentini, S diMarzoVeronese, F Reitz, MS TI Evidence for distinct contributions of heavy and light chains to restriction of antibody recognition of the HIV-1 principal neutralization determinant SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; MONOCLONAL-ANTIBODY; PHAGE SURFACES; V3 LOOP; LIBRARIES; ENVELOPE; ANTIGEN; GENE; GLYCOPROTEIN; SEQUENCE AB We have used phage Ab display technology to analyze two mAbs to HIV-1 envelope proteins gp120 and gp41, From the data obtained we are able to demonstrate that the recognition of the principal neutralization determinant of different strains of HIV-1 by neutralizing mAb M77 is restricted by its heavy and light chains in different ways, Native M77 is able to recognize and neutralize HIV-1 strain IIIB through binding to the gp120 V3 loop, M77 is unable to recognize strains of HIV-1 that differ on either the left or right side of the V3 loop tip. A chain-switched Fab fragment containing the M77 Fd fragment and a different light chain was able to recognize HIV-1 strains that differ from IIIB on the left side but not the right side of the V3 loop tip. C1 NCI,NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 39 TC 12 Z9 12 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1996 VL 156 IS 4 BP 1676 EP 1683 PG 8 WC Immunology SC Immunology GA TU692 UT WOS:A1996TU69200047 PM 8568275 ER PT J AU Zhang, QL Lin, PX Shi, D Xian, H Webster, HD AF Zhang, QL Lin, PX Shi, D Xian, H Webster, HD TI Vasoactive intestinal peptide: Mediator of laminin synthesis in cultured Schwann cells SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE neuropeptide; VIP; peripheral nerve; glia; VIP receptor; nerve regeneration ID DORSAL-ROOT GANGLION; PERIPHERAL-NERVE; AXONAL-TRANSPORT; GENE-EXPRESSION; RAT; VIP; NEURONS; POLYPEPTIDE; INJURY; GROWTH AB To learn more about neuropeptide-induced glial responses which accompany axon regeneration, we studied effects of VIP on laminin production by cultured Schwann cells, Schwann cells were isolated from sciatic nerves of neonatal mice, purified, and incubated for 5 days in either control medium (DMEM + 15% FCS) or control medium containing 10(-7)-10(-11) M VIP, At 10(-7) and 10(-8) M VIP, laminin levels measured by enzyme-linked immunosorbent assay were significantly higher (55% and 35%) than those in control cultures, Lower VIP concentrations (10(-9)-10(-11) M) produced smaller increases which were not significant, Low-affinity VIP receptors which mediated this effect were demonstrated on Schwann cells by radioligand binding studies, The increased Schwann cell synthesis of laminin induced by VIP was blocked when either a VIP antagonist or a VIP receptor antagonist was added to the VIP-containing incubation medium, In contrast to astrocytes, when Schwann cells were loaded with fura-2, VIP did not increase cytosolic Ca2+, This indicates that Schwann cells and astrocytes may have different intracellular transduction pathways; their receptor subtypes also may differ, We suggest that the VIP-induced increase in laminin synthesis which we have observed in cultured Schwann cells may also occur in vivo and might be an important component of axon-Schwann cell interactions during nerve regeneration. (C) 1996 Wiley-Liss, Inc. C1 NINCDS,NIH,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. NINCDS,NIH,NEUROCHEM LAB,BETHESDA,MD 20892. NINCDS,NIH,NEUROPHYSIOL LAB,BETHESDA,MD 20892. NIDDKD,NIH,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 53 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD FEB 15 PY 1996 VL 43 IS 4 BP 496 EP 502 DI 10.1002/(SICI)1097-4547(19960215)43:4<496::AID-JNR11>3.0.CO;2-0 PG 7 WC Neurosciences SC Neurosciences & Neurology GA TY121 UT WOS:A1996TY12100011 PM 8699536 ER PT J AU Li, LP Darden, T Hiskey, R Pedersen, L AF Li, LP Darden, T Hiskey, R Pedersen, L TI Homology modeling and molecular dynamics simulations of the Gla domains of human coagulation factor IX and its G[12]A mutant SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID GAMMA-CARBOXYGLUTAMIC ACID; BOVINE PROTHROMBIN FRAGMENT-1; K-DEPENDENT PROTEINS; MEMBRANE-BINDING; HEMOPHILIA-B; RESIDUES; IONS; SITE; MUTATION; VARIANT AB We have tested molecular dynamics as a predictive tool for stability of protein structure. We first used the X-ray crystallographic coordinates of bovine prothrombin fragment 1 to model the structure of the cia domain of human factor IX, an essential coagulation protein. In addition, a mutant protein that differs in only a single amino acid (G[12]A) but is associated with one form of Hemophilia B was also modeled. Simulations performed in an identical fashion for both proteins, with considerable care to accommodate long-range forces in these highly ionic systems, indicated that substantial distortions occur in the mutant structure relative to the wild type factor IX. Surprisingly, the Gla domain (residues 1-34) of the wild type and mutant remain similar. Instead, it is the interaction of the added Ala at position 12 in the mutant that repels the post-Gla region (residues >33, the C-terminal helix) region. C1 NIEHS,RES TRIANGLE PK,NC 27709. RP Li, LP (reprint author), UNIV N CAROLINA,DEPT CHEM,CB 3290,CHAPEL HILL,NC 27599, USA. RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 52 TC 8 Z9 8 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3654 J9 J PHYS CHEM-US JI J. Phys. Chem. PD FEB 15 PY 1996 VL 100 IS 7 BP 2475 EP 2479 DI 10.1021/jp952190j PG 5 WC Chemistry, Physical SC Chemistry GA TV694 UT WOS:A1996TV69400003 ER PT J AU Zhou, HX Szabo, A AF Zhou, HX Szabo, A TI Theory and simulation of stochastically-gated diffusion-influenced reactions SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID BROWNIAN DYNAMICS; BIMOLECULAR REACTIONS; KINETICS; REACTIVITY AB The kinetics of the irreversible diffusion-influenced reaction between a protein (P) and a ligand (L) is studied when [L] much greater than [P] and the reactivity is stochastically gated due to conformational fluctuations of one of the species. If gating is due to the ligand, we show that the Smoluchowski rate equation, d[P(t)]/dt = -k(t)[L][P(t)], can be generalized by simply using a stochastically-gated time-dependent rate coefficient, k(sg)(t). However, if gating is due to the protein, this is no longer true, except when the gating dynamics is sufficiently fast or the Ligand concentration is very low. The dynamics of ail the ligands around a protein become correlated even when they diffuse independently. An approximate theory for the kinetics of protein-gated reactions that is exact in both the fast and slow gating limits is developed. In order to test this theory, a Brownian dynamics simulation algorithm based on a path-integral formulation is introduced to calculate both k(sg)(t) and the time dependence of the protein concentration. Illustrative simulations using a simple model are carried out for a variety of gating rates. The results are in good agreement with the approximate theory. C1 NIDDK, NIH, CHEM PHYS LAB, BETHESDA, MD 20892 USA. RP Zhou, HX (reprint author), HONG KONG UNIV SCI & TECHNOL, DEPT BIOCHEM, CLEAR WATER BAY, KOWLOON, HONG KONG. RI Szabo, Attila/H-3867-2012; Zhou, Huan-Xiang/M-5170-2016 OI Zhou, Huan-Xiang/0000-0001-9020-0302 NR 18 TC 54 Z9 54 U1 0 U2 7 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3654 J9 J PHYS CHEM-US JI J. Phys. Chem. PD FEB 15 PY 1996 VL 100 IS 7 BP 2597 EP 2604 DI 10.1021/jp952376i PG 8 WC Chemistry, Physical SC Chemistry GA TV694 UT WOS:A1996TV69400019 ER PT J AU Moreira, JE Reese, TS Kachar, B AF Moreira, JE Reese, TS Kachar, B TI Freeze-substitution as a preparative technique for immunoelectronmicroscopy: Evaluation by atomic force microscopy SO MICROSCOPY RESEARCH AND TECHNIQUE LA English DT Article DE fixation; freeze-substitution; immunoelectronmicroscopy; etching; atomic force microscopy ID RAT SUBMANDIBULAR-GLAND; SECTIONS; CRYOSUBSTITUTION; PROTEINS AB Cryofixation followed by freeze substitution in osmium tetroxide was evaluated as a method for preparing biological specimens for immunoelectronmicroscopy. Samples were rapidly frozen by impact onto a sapphire block cooled with liquid nitrogen, substituted at -80 degrees C in acetone containing osmium tetroxide, and embedded in epoxy resin. With this protocol, excellent ultrastructure can be combined with localization of antigens that otherwise would be inactivated by the osmium, but labeling may need to be enhanced by chemically etching the sections prior to staining. The effects of etching on various structures in the sections were investigated by examining the sections with atomic force microscopy, an approach that yields three-dimensional views of the surface of the section. A considerable part of the section was removed or collapsed by the etching, and these effects occurred differentially in several components of the tissue and with different etching protocols. Nevertheless, the results suggest that the partial removal of the plastic by etching of freeze-substituted tissue can be explored as a method for exposing fine biological structures for observation with atomic force microscopy. (C) 1996 Wiley-Liss, Inc.* C1 NIDOCD,LAB CELLULAR BIOL,BETHESDA,MD 20892. RP Moreira, JE (reprint author), NINCDS,NEUROBIOL LAB,36 CONVENT DR,BETHESDA,MD 20892, USA. NR 28 TC 12 Z9 12 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-910X J9 MICROSC RES TECHNIQ JI Microsc. Res. Tech. PD FEB 15 PY 1996 VL 33 IS 3 BP 251 EP 261 DI 10.1002/(SICI)1097-0029(19960215)33:3<251::AID-JEMT2>3.0.CO;2-T PG 11 WC Anatomy & Morphology; Biology; Microscopy SC Anatomy & Morphology; Life Sciences & Biomedicine - Other Topics; Microscopy GA TQ372 UT WOS:A1996TQ37200002 PM 8652883 ER PT J AU Bassett, DE Boguski, MS Hieter, P AF Bassett, DE Boguski, MS Hieter, P TI Yeast genes and human disease SO NATURE LA English DT Letter C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. RP Bassett, DE (reprint author), NIH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BETHESDA,MD 20894, USA. NR 9 TC 97 Z9 101 U1 0 U2 4 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 15 PY 1996 VL 379 IS 6566 BP 589 EP 590 DI 10.1038/379589a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TV688 UT WOS:A1996TV68800030 PM 8628392 ER PT J AU Martin, A Wiggs, CL Ungerleider, LG Haxby, JV AF Martin, A Wiggs, CL Ungerleider, LG Haxby, JV TI Neural correlates of category-specific knowledge SO NATURE LA English DT Article ID MENTAL-IMAGERY; VISUAL-CORTEX; RECOGNITION; IMPAIRMENT; PICTURES AB AN intriguing and puzzling consequence of damage to the human brain is selective loss of knowledge about a specific category of objects, One patient may be unable to identify or name living things(1-3), whereas another may have selective difficulty identifying man-made objects(4-6). To investigate the neural correlates of this remarkable dissociation, we used positron emission tomography to map regions of the normal brain that are associated with naming animals and tools. We found that naming pictures of animals and tools was associated with bilateral activation of the ventral temporal lobes and Broca's area, In addition, naming animals selectively activated the left medial occipital lobe-a region involved in the earliest stages of visual processing. In contrast, naming tools selectively activated a left premotor area also activated by imagined hand movements(7), and an area in the left middle temporal gyrus also activated by the generation of action words(8-10). Thus the brain regions active during object identification are dependent, in part, on the intrinsic properties of the object presented. RP Martin, A (reprint author), NIMH,PSYCHOL & PSYCHOPATHOL LAB,BLDG 10,ROOM 3D-41,BETHESDA,MD 20892, USA. RI martin, alex/B-6176-2009 NR 26 TC 1052 Z9 1071 U1 1 U2 33 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 15 PY 1996 VL 379 IS 6566 BP 649 EP 652 DI 10.1038/379649a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TV688 UT WOS:A1996TV68800055 PM 8628399 ER PT J AU Goldstein, AM Tucker, MA AF Goldstein, AM Tucker, MA TI Familial melanoma and pancreatic cancer - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP Goldstein, AM (reprint author), NCI,BETHESDA,MD 20892, USA. RI Tucker, Margaret/B-4297-2015 NR 2 TC 4 Z9 4 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 15 PY 1996 VL 334 IS 7 BP 471 EP 471 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA TU696 UT WOS:A1996TU69600022 ER PT J AU Chen, SL Maroulakou, IG Green, JE RomanoSpica, V Modi, W Lautenberger, J Bhat, NK AF Chen, SL Maroulakou, IG Green, JE RomanoSpica, V Modi, W Lautenberger, J Bhat, NK TI Isolation and characterization of a novel gene expressed in multiple cancers SO ONCOGENE LA English DT Article DE differential display; lung cancer; epithelial cells; leucine zipper; gene expression ID CHAIN; CDNA; CELLS AB Using differential display method, we have isolated and characterized a novel gene, N8, encoding a similar to 24 kDa protein. It is located on human chromosome 8q13 region. N8 gene is expressed at high levels in tumor derived cell lines from multiple cancers. It is also expressed at higher levels in lung tumors than normal lung tissue, NS is also differentially expressed in fetal and adult tissues. In adult, N8 is expressed at high levels in brain, kidney, prostate, pancreas and intestine and at very low levels in lung, liver, hematopoietic cells and gonads. During murine embryonic development N8 is expressed in the epithelium of the intestine, stomach, olfactory epithelium, neuronal layers of retina, kidney and salivary gland. Taken together, these results suggest that N8 may play different roles during embryogenesis and in the adult animals. C1 NCI,FREDERICK CANC RES & DEV CTR,SCI APPLICAT INT CORP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MOLEC ONCOL LAB,FREDERICK,MD 21702. CATHOLIC UNIV,INST HYG,ROME,ITALY. NR 27 TC 52 Z9 57 U1 0 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB 15 PY 1996 VL 12 IS 4 BP 741 EP 751 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA TW686 UT WOS:A1996TW68600005 PM 8632896 ER PT J AU Michieli, P Li, WQ Lorenzi, MV Miki, T Zakut, R Givol, D Pierce, JH AF Michieli, P Li, WQ Lorenzi, MV Miki, T Zakut, R Givol, D Pierce, JH TI Inhibition of oncogene-mediated transformation by ectopic expression of p21(Waf1) in NIH3T3 cells SO ONCOGENE LA English DT Article DE cellular transformation; oncogenes; tumor suppressor genes; p53 effectors; cyclin-dependent kinase inhibitors ID PROTEIN; FIBROBLASTS; RAS; P21; DIFFERENTIATION; LOCALIZATION; KINASES; P53 AB The p53-regulated p21(Waf1) protein is a universal inhibitor of cyclin-dependent kinases (CDKs). To study the potential tumor-suppressive properties of CDK inhibitors, the ability of p21(Waf1) to interfere with oncogene-mediated cellular transformation was analysed in the NIH3T3 cell system. Cotransfection of waf1 together with activated ras or several other oncogenes into NIH3T3 cells potently inhibited the formation of transformed foci in a dose-dependent manner, Expression of the CDK-binding N-terminal half of p21(Waf1) (N-p21(Waf1)) was necessary and sufficient to inhibit Ras-induced focus formation. In contrast, expression of the C-terminal domain (C-p21(Waf1)) had no effect on Ras-induced focus formation. Immunofluorescence analysis revealed that ectopically expressed p21(Waf1) and C-p21(Waf1) were localized in the nucleus, while N-p21(Waf1) was found in the cytoplasm, with the tendency to accumulate around the nuclear membrane. Surprisingly, stable NIH3T3 transfectants expressing ectopic p21(Waf1) grew at the same rate and displayed similar cell cycle distribution as NIH3T3 cells transfected with the same vector containing no insert. However ectopic p21(Waf1) expression did inhibit Ras-mediated anchorage-independent colony formation, indicating that p21(Waf1) can selectively interfere with oncogene-mediated transformation without affecting NIH3T3 cell growth, at least at the levels of p21(Waf1) expression experiments. Transient NIH3T3 cells inhibited Ras-indnced transcription from a E2F-responsive element but not from a serum-responsive element, indicating that p21(Waf1) acts downstream of early transcriptional events induced by Ras but upstream of E2F-controlled gene transcription. These results provide evidence that p21(Waf1) potently suppresses oncogene-mediated cellular transformation of NIH3T3 cells and that it may do so by inhibiting E2F-driven transcription of S phase genes. C1 WEIZMANN INST SCI,DEPT MOLEC CELL BIOL,IL-76100 REHOVOT,ISRAEL. RP Michieli, P (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,NIH,BLDG 37,BETHESDA,MD 20892, USA. RI Michieli, Paolo/A-2588-2011 NR 49 TC 39 Z9 39 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB 15 PY 1996 VL 12 IS 4 BP 775 EP 784 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA TW686 UT WOS:A1996TW68600008 PM 8632899 ER PT J AU Cohen, DJ Tian, Y Ooi, BS Henkart, PA AF Cohen, DJ Tian, Y Ooi, BS Henkart, PA TI Differential effects of costimulator signals and interleukin-2 on T cell receptor-mediated cell death of resting and activated CD4(+) murine splenic T cells SO TRANSPLANTATION LA English DT Article ID LYMPHOCYTES-T; IL-2 PRODUCTION; APOPTOSIS; CD28; PROLIFERATION; ANTIGEN; THYMOCYTES; PATHWAY; LIGAND; OCCURS AB Postthymic T cell receptor (TCR)-mediated cell death offers the potential for creating antigen-specific transplant tolerance analogous to thymic clonal deletion. Murine splenic CD4(+) T cells were rigorously purified by: (a) adherent cell depletion and (b) magnetic bead/monoclonal antibody (mAb) depletion of macrophages, Ia(+) cells, mu-chain(+) cells, NR cells, and CD8(+) T cells, CD4(+)s were typically >95% pure by flow cytometry. Resting CD4(+)s stimulated by plastic-immobilized anti-TCR/CD3 mAb were shown to die in the absence of exogenous interleukin (IL)-2. Blasting CD4(+)s showed dose-dependent cell death upon religation of TCR/CD3 in the presence of IL-2; however, withdrawal of IL-2 from blasting CD4(+)s also resulted in cell death. Cell death was shown to be apoptotic by flow cytometry DNA content analysis. Anti-CD28 mAb, co-immobilized with anti-TCR/CD3 mAb, inhibited cell death of resting CD4(+)s in the absence of exogenous IL-2; however, anti-CD28 mAb showed minimal cell death inhibition of CD4(+) blasts when TCR/CD3 was religated. In contrast, splenic adherent cells effectively inhibited cell death of blasting CD4(+)s induced by TCR/CD3 mAb religation. We conclude that TCR-mediated programmed cell death of highly purified splenic CD4(+)s is dependent upon activation state, availability of IL-2, and accessory cell or CD28 costimulator signals. Furthermore, IL-2 acts to protect against cell death in both resting and activated CD4(+) T cells. IL-2 protection could be overcome by high concentrations of anti-TCR/CD3 mAb, which results in cell death of CD4(+) blasts. In the effort to understand potential mechanisms of peripheral tolerance induction, these findings assist to distinguish and define conditions for antigen receptor-mediated programmed cell death of mature CD4(+) T cells. C1 GEORGE WASHINGTON UNIV,WASHINGTON,DC 20422. NCI,NIH,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP Cohen, DJ (reprint author), VET AFFAIRS MED CTR,RENAL SECT,50 IRVING ST NW,ROOM 4B202,WASHINGTON,DC 20422, USA. NR 35 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD FEB 15 PY 1996 VL 61 IS 3 BP 486 EP 491 DI 10.1097/00007890-199602150-00029 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA TW446 UT WOS:A1996TW44600029 PM 8610365 ER PT J AU Breen, N Kessler, L AF Breen, N Kessler, L TI Trends in cancer screening - United States, 1987 and 1992 (Reprinted from MMWR, vol 45, pg 57-61, 1996) SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Reprint ID COLORECTAL-CANCER; MORTALITY; SIGMOIDOSCOPY C1 CDC,NATL CTR HLTH STAT,CTR CHRON DIS PREVENT & HLTH PROMOT,DIV CANC PREVENT & CONTROL,ATLANTA,GA. RP Breen, N (reprint author), NCI,APPL RES BRANCH,BETHESDA,MD 20892, USA. NR 9 TC 2 Z9 2 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 14 PY 1996 VL 275 IS 6 BP 428 EP 429 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA TU638 UT WOS:A1996TU63800009 ER PT J AU Walker, DH Barbour, AG Oliver, JH Lane, RS Dumler, JS Dennis, DT Persing, DH Azad, AF McSweegan, E AF Walker, DH Barbour, AG Oliver, JH Lane, RS Dumler, JS Dennis, DT Persing, DH Azad, AF McSweegan, E TI Emerging bacterial zoonotic and vector-borne diseases - Ecological and epidemiological factors SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID CAT-SCRATCH DISEASE; FEVER GROUP RICKETTSIOSIS; SPOTTED-FEVER; HUMAN EHRLICHIOSIS; LYME-DISEASE; BORRELIA-BURGDORFERI; TRANSOVARIAL TRANSMISSION; SEROLOGIC SURVEY; ETIOLOGIC AGENT; INNER-MONGOLIA AB Among the etiologic agents of emerging infectious diseases are several bacterial organisms that naturally reside in animal and arthropod hosts. The most compelling emerging bacterial zoonotic and vector-borne diseases in the United States are Lyme disease; a Southern erythema migrans-like illness; human monocytic ehrlichiosis; human granulocytic ehrlichiosis; a novel cat flea-associated typhus group rickettsiosis; bartonelloses of immunocompetent and immunocompromised persons, particularly with AIDS; and sylvatic plague. Some of these antimicrobial-treatable infections are life threatening. During the acute stage of illness when antimicrobial agents are most effective, the flulike clinical signs and symptoms and available laboratory tests frequently do not point to a particular diagnosis. Epidemiological factors determined by the ecology of the bacteria are often the most useful diagnostic clues. The recognition of these evolving problems emphasizes the need for development of better laboratory diagnostic methods, for surveillance for and tracking of disease, and for continued research into factors contributing to transmission of the organisms. The continual appearance of previously unidentified bacterial infections requires prospective national strategies for timely recognition of the syndrome, identification of the agent, establishment of criteria and methods for diagnosis, optimization of the treatment regimen, and determination of successful approaches to prevention and control. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MICROBIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. GEORGIA SO UNIV,DEPT BIOL,STATESBORO,GA 30460. UNIV CALIF BERKELEY,DEPT ENVIRONM SCI POLICY & MANAGEMENT,BERKELEY,CA. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT MICROBIOL & IMMUNOL,BALTIMORE,MD 21201. CTR DIS CONTROL & PREVENT,DIV VECTOR BORNE INFECT DIS,FT COLLINS,CO. MAYO CLIN & MAYO FDN,DEPT LAB MED & PATHOL,ROCHESTER,MN. NIAID,BETHESDA,MD 20892. RP Walker, DH (reprint author), UNIV TEXAS,MED BRANCH,DEPT PATHOL,301 UNIV BLVD,GALVESTON,TX 77555, USA. RI Barbour, Alan/B-3160-2009 OI Barbour, Alan/0000-0002-0719-5248 FU NIAID NIH HHS [AI21242, AI31431] NR 92 TC 82 Z9 88 U1 2 U2 8 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 14 PY 1996 VL 275 IS 6 BP 463 EP 469 DI 10.1001/jama.275.6.463 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA TU638 UT WOS:A1996TU63800035 PM 8627968 ER PT J AU Bilski, P Reszka, K Bilska, M Chignell, CF AF Bilski, P Reszka, K Bilska, M Chignell, CF TI Oxidation of the spin trap 5,5-dimethyl-1-pyrroline N-oxide by singlet oxygen in aqueous solution SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID DYE-SENSITIZED PHOTOOXYGENATION; ROSE-BENGAL; HYDROPEROXIDE-HEMATIN; MOLECULAR-OXYGEN; SUPEROXIDE; NITRONES; PHOTOSENSITIZATION; PHOTOOXIDATION; ADDUCTS; STATE AB The spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) is frequently used to identify free radicals that are generated photochemically using dyes as photosensitizers. When oxygen is present in such systems, singlet oxygen (O-1(2)) may be produced and can react with DMPO. We have studied the reaction of DMPO with O-1(2) in aqueous solutions over a wide range of pH, using micellar Rose Bengal (pH 2-13) and anthrapyrazole (pH < 2) as photosensitizers. We found that DMPO quenches O-1(2) phosphorescence (k(q) = 1.2 x 10(6) M(-1) s(-1)), thereby initiating oxygen consumption that is slow at pH 10 but increases about 10-fold at pH < 6. This oxygen consumption is a composite process that includes efficient oxidation of both DMPO and its degradation products. The oxidation products include both products in which the DMPO pyrroline ring remains intact (DMPO/(OH)-O-. and 5,5-dimethyl-2-oxo-pyrroline-1-oxyl (DMPOX) radicals) and those in which it becomes opened (nitro and nitroso products). The nitroso product itself strongly quenched O-1(2) phosphorescence, while (photo)decomposition of the nitroso group, presumably to nitric oxide (NO.), produced nitrite as a minor product. We propose that O-1(2) adds to the >C=N(O) bond in DMPO, producing a biradical, >C(OO.)-N-.(O). This biradical may follow one of two pathways: (i) It may be protonated and rearrange to a strongly oxidizing nitronium-like moiety, which could be reduced to the DMPO hydroperoxide radical DMPO/(O2H)-O-. while oxidizing another DMPO moiety to ultimately form DMPOX. The DMPO/ (O2H)-O-. could undergo further redox decomposition, e.g. via the known Fenton-like reaction, to produce both free (OH)-O-. radical and the DMPO/(OH)-O-. radical. (ii) The biradical >C(OO.)-N-.(O) may cyclize to a 1,2,3-trioxide (ozonide), which could open the pyrroline ring to form 4-methyl-4-nitropentan-1-al and 4-methyl-4-nitrosopentanoic acid. Because the oxidation of DMPO by O-1(2) leads to both rapid O-2 depletion and the formation of transients and products that might interfere with trapping and identification of free radicals, DMPO should be used with caution in systems where O-1(2) is produced. RP Bilski, P (reprint author), NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 41 TC 64 Z9 64 U1 9 U2 38 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD FEB 14 PY 1996 VL 118 IS 6 BP 1330 EP 1338 DI 10.1021/ja952140s PG 9 WC Chemistry, Multidisciplinary SC Chemistry GA TV706 UT WOS:A1996TV70600011 ER PT J AU Peracchi, A Bettati, S Mozzarelli, A Rossi, GL Miles, EW Dunn, MF AF Peracchi, A Bettati, S Mozzarelli, A Rossi, GL Miles, EW Dunn, MF TI Allosteric regulation of tryptophan synthase: Effects of pH, temperature, and alpha-subunit ligands on the equilibrium distribution of pyridoxal 5'-phosphate-L-serine intermediates SO BIOCHEMISTRY LA English DT Article ID ULTRAVIOLET VISIBLE SPECTROSCOPY; SITE-DIRECTED MUTAGENESIS; ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; BIENZYME COMPLEX; L-SERINE; BETA-SUBUNIT; ACTIVE-SITE; ACETOACETATE DECARBOXYLASE; SUBSTRATE-SPECIFICITY AB The equilibrium distribution of catalytic intermediates formed in the reaction of L-serine with the tryptophan synthase alpha(2) beta(2)-complex from Salmonella typhimurium has been investigated by absorption and fluorescence spectroscopy as a function of pH, temperature, and alpha-subunit ligands. The novel result of this study is that the equilibrium between the two major catalytic species, the external aldimine and the alpha-aminoacrylate, is modulated by the ionization of two groups with apparent pK values of 7.8 +/- 0.3 and 10.3 +/- 0.2. Protonation of these groups stabilizes the alpha-aminoacrylate Schiff base by an estimated 100-fold with respect to the external aldimine. Furthermore, the formation of the alpha-aminoacrylate from the external aldimine is an endothermic process. Temperature slightly affects the apparent pK values but remarkably influences the amplitude of the phase associated with the ionization of each group. At 20 degrees C, each phase accounts for nearly half of the titration. Since the isolated beta(2)-dimer does not exhibit a pH-dependent distribution of intermediates, the alpha-beta-subunit interactions seem critical to the onset of this functional property of the beta-subunit. The modulation of intersubunit interactions by the a-subunit ligands DL-alpha-glycerol 3-phosphate and phosphate leads to significant changes in the pH-dependent distribution of intermediates. At saturating concentrations of either of these alpha-subunit ligands, the alpha-aminoacrylate Schiff base is the predominant species over a wide pH range while the apparent pK values of the groups that control the equilibrium are not significantly affected. The pH-dependent interconversion of catalytic intermediates here reported has not been previously detected because phosphate buffers have usually been employed in the studies of this enzyme. Our findings are discussed in the light of a model in which specific protein conformations are associated with the external aldimine and the alpha-aminoacrylate Schiff bases, the latter being stabilized by temperature, protons, and alpha-subunit ligands. C1 UNIV PARMA, IST SCI BIOCHIM, I-43100 PARMA, ITALY. NIDDKD, NIH, LAB BIOCHEM PHARMACOL, BETHESDA, MD 20892 USA. UNIV CALIF RIVERSIDE, DEPT BIOCHEM, RIVERSIDE, CA 92521 USA. RI Peracchi, Alessio/G-5167-2012; Mozzarelli, Andrea/C-3615-2014 OI Peracchi, Alessio/0000-0003-3254-4099; Mozzarelli, Andrea/0000-0003-3762-0062 NR 52 TC 65 Z9 65 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 13 PY 1996 VL 35 IS 6 BP 1872 EP 1880 DI 10.1021/bi951889c PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TV600 UT WOS:A1996TV60000021 PM 8639669 ER PT J AU Robinson, JK Zocchi, A Pert, A Crawley, JN AF Robinson, JK Zocchi, A Pert, A Crawley, JN TI Galanin microinjected into the medial septum inhibits scopolamine-induced acetylcholine overflow in the rat ventral hippocampus SO BRAIN RESEARCH LA English DT Article DE activity; receptor antagonist; behavior; microdialysis; neuropeptide ID BASAL FOREBRAIN; IMMUNOREACTIVITY; NEURONS; MEMORY; RELEASE; INVIVO AB Galanin-like immunoreactive terminals hyperinnervate the basal forebrain cholinergic neurons in Alzheimer's disease. To investigate the hypothesis that galanin acts directly on basal forebrain cell bodies, in vivo microdialysis studies were conducted in awake rats which analyzed the actions of galanin on acetylcholine release. Microinjection of galanin into the cholinergic cell body region of the medial septum-diagonal band (MS-DBB) inhibited acetylcholine release in the ventral hippocampus. These results are consistent with an interpretation that galanin terminals synapsing on cholinergic cell bodies of the basal forebrain may serve to inhibit the release of acetylcholine in the terminal fields of the cholinergic neurons. C1 NIMH, EXPTL THERAPEUT BRANCH, SECT BEHAV NEUROPHARMACOL, BETHESDA, MD 20892 USA. NIMH, BIOL PSYCHIAT BRANCH, UNIT BEHAV PHARMACOL, BETHESDA, MD 20892 USA. NR 26 TC 36 Z9 36 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 EI 1872-6240 J9 BRAIN RES JI Brain Res. PD FEB 12 PY 1996 VL 709 IS 1 BP 81 EP 87 DI 10.1016/0006-8993(95)01307-5 PG 7 WC Neurosciences SC Neurosciences & Neurology GA TX909 UT WOS:A1996TX90900010 PM 8869559 ER PT J AU Ido, A Miura, Y Watanabe, M Sakai, M Inoue, Y Miki, T Hashimoto, T Morinaga, T Nishi, S Tamaoki, T AF Ido, A Miura, Y Watanabe, M Sakai, M Inoue, Y Miki, T Hashimoto, T Morinaga, T Nishi, S Tamaoki, T TI Cloning of the cDNA encoding the mouse ATBF1 transcription factor SO GENE LA English DT Article DE homeodomain; zinc finger; brain; RNase protection assay ID ZINC-FINGER; HOMEODOMAIN; DROSOPHILA; EXPRESSION; ZFH-2; PROTEINS; RECEPTOR; MOTIFS; GENE AB We have isolated a mouse ATBF1 cDNA which is 12-kb long and capable of encoding a 406-kDa protein containing four homeodomains and 23 zinc-finger motifs. Mouse ATBF1 is 94% homologous to the human ATBF1-A transcription factor. Northern blot and RNase protection analysis showed that levels of ATBF1 transcripts were low in adult mouse tissues, but high in developing brain, consistent with a role for ATBF1 in neuronal differentiation. C1 UNIV CALGARY,DEPT MED BIOCHEM,CALGARY,AB T2N 4N1,CANADA. HOKKAIDO UNIV,SCH MED,DEPT ANAT,SAPPORO,HOKKAIDO 060,JAPAN. HOKKAIDO UNIV,DEPT BIOCHEM,SAPPORO,HOKKAIDO 060,JAPAN. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. HYOGO MED UNIV,DEPT GENET,NISHINOMIYA,HYOGO 663,JAPAN. SNOW BRAND MILK PROD CO LTD,LIFE SCI RES INST,ISHIBASHI,TOCHIGI 32905,JAPAN. RI WATANABE, Masahiko/A-4055-2012; Sakai, Masaharu/A-4773-2012 NR 16 TC 29 Z9 31 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD FEB 12 PY 1996 VL 168 IS 2 BP 227 EP 231 DI 10.1016/0378-1119(95)00740-7 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA TW664 UT WOS:A1996TW66400018 PM 8654949 ER PT J AU Schwabe, W Brennan, MB Hochgeschwender, U AF Schwabe, W Brennan, MB Hochgeschwender, U TI Isolation and characterization of the mouse (Mus musculus) somatostatin receptor type-4-encoding gene (mSSTR4) SO GENE LA English DT Article DE gene cloning; oligodeoxynucleotide hybridization; nucleotide sequence; expression; RT-PCR ID MOLECULAR-CLONING; RAT-BRAIN; FUNCTIONAL-CHARACTERIZATION; EXPRESSION; FAMILY; SSTR3; CDNA AB We have isolated and sequenced the mouse somatostatin receptor subtype-4-encoding gene (mSSTR4). The mSSTR4 gene encodes 384 amino acids (aa). The deduced mouse SSTR4 has 95 and 89% aa identity with the deduced rat and human SSTR4, respectively, while it has lower aa identity with the other mouse subtypes (mSSTR1, 60%; mSSTR2, 47%; mSSTR3, 42%). Using an RT-PCR technique, we show that the mSSTR4 gene is expressed in brain, but not in liver, heart, spleen or kidney of the adult mouse. C1 NIMH,NSB,MOLEC GENET UNIT,BETHESDA,MD 20892. NR 20 TC 22 Z9 23 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD FEB 12 PY 1996 VL 168 IS 2 BP 233 EP 235 DI 10.1016/0378-1119(95)00748-2 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA TW664 UT WOS:A1996TW66400019 PM 8654950 ER PT J AU Dickie, P AF Dickie, P TI HIV type 1 nef perturbs eye lens development in transgenic mice SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; A-CRYSTALLIN PROMOTER; LONG TERMINAL REPEAT; NF-KAPPA-B; FIBER DIFFERENTIATION; TAT GENE; T-CELLS; EXPRESSION; PROTEIN; INDUCTION AB HIV transgenic mice often display lens cataracts as a consequence of viral-specific expression of HIV gene products in the developing lens, Cataractous mouse lines encoding either HIV-1 proviral DNA, HIV Delta Gag/Pol] proviral DNA, or the HIV-1 nef gene alone were examined to ascertain the effect of Nef on murine lens development, Ocular disease was characterized by a progressive architectural disorganization within the lens fiber cell compartment developing in 100% of HIV-positive mice in five reported transgenic lines. Late embryonic stage transgenic lenses featured a mild microphthalmia, pyknotic nuclei within the lens fiber department, ballooning lens fiber cells, and elongated lens epithelial cells, Increased DNA fragmentation was evident in transgenic embryonic lenses, suggesting that cell death occurred by apoptosis, As studied in HIV Delta Gag/Pol] transgenic mice, HIV transcription was developmentally linked to alpha A- and alpha beta-crystallin gene expression, preceded disease development (in E14.5-E16.5 embryos), and persisted for weeks after birth, HIV-1 Nef was the predominant HIV gene product detected in the lens fiber cells of this line and was expressed almost to the exclusion of other HIV gene products, Nef was implicated as a major determinant of disease because (1) cataracts developed in mice transgenic for Nef alone and (2) the expression of other HIV gene products in wild-type HIV provirus transgenic mice occurred without a concomitant change in lens pathology. C1 NIAID,NIH,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 76 TC 22 Z9 22 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB 10 PY 1996 VL 12 IS 3 BP 177 EP 189 DI 10.1089/aid.1996.12.177 PG 13 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TU746 UT WOS:A1996TU74600001 PM 8835194 ER PT J AU Theodore, TS Englund, G BucklerWhite, A Buckler, CE Martin, MA Peden, KWC AF Theodore, TS Englund, G BucklerWhite, A Buckler, CE Martin, MA Peden, KWC TI Construction and characterization of a stable full-length macrophage-tropic HIV type 1 molecular clone that directs the production of high titers of progeny virions SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; MONONUCLEAR PHAGOCYTES; BRAIN-TISSUE; HTLV-III; MONOCYTES; INFECTION; IDENTIFICATION; DETERMINANTS; REPLICATION; DISEASE C1 GEORGETOWN UNIV,DIV MOLEC VIROL & IMMUNOL,ROCKVILLE,MD 20852. RP Theodore, TS (reprint author), NIAID,MOLEC MICROBIOL LAB,NIH,BLDG 4,ROOM 316,4 CTR DR,BETHESDA,MD 20892, USA. NR 25 TC 103 Z9 103 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB 10 PY 1996 VL 12 IS 3 BP 191 EP 194 DI 10.1089/aid.1996.12.191 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TU746 UT WOS:A1996TU74600002 PM 8835195 ER PT J AU Cooper, PJ AF Cooper, PJ TI Autoimmunity and onchocerciasis SO LANCET LA English DT Letter ID AUTOANTIBODIES RP Cooper, PJ (reprint author), NIH,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD FEB 10 PY 1996 VL 347 IS 8998 BP 404 EP 404 DI 10.1016/S0140-6736(96)90586-3 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA TU695 UT WOS:A1996TU69500064 PM 8598734 ER PT J AU Omar, RF Gelboin, HV Rahimtula, AD AF Omar, RF Gelboin, HV Rahimtula, AD TI Effect of cytochrome p450 induction on the metabolism and toxicity of ochratoxin A SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE ochratoxin A; metabolism; P450; inducers; inhibitors; monoclonal antibodies; toxicity ID LIVER MICROSOMAL CYTOCHROME-P-450; RAT-LIVER; RENAL-FUNCTION; ISOZYMES; ENZYMES; DEBRISOQUINE; OXIDATION; URINARY; TISSUES; INVIVO AB Liver microsomes from rats treated with various P450 inducers were examined for their ability to metabolize the mycotoxin ochratoxin A (OTA) to 4(R)-4-hydroxyochratoxin A (4R), the major metabolite, and 4(S)-4-hydroxyochratoxin A (4S), the minor metabolite. Pretreatment of rats with phenobarbital (PB), dexamethasone (DXM), 3-methylcolcanthrene (3MC) and isosafrole (ISF) greatly induced 4R formation. PB, DXM, 3MC, clofibrate (CLF) and ISF treatments also induced 4S formation. Isoniazid (INH) pretreatment primarily induced 4S formation. The pH optimum for 4R formation was found to be 6.0 with 3MC microsomes, and 6.5 with PB and DXM microsomes. For 4S formation, the pH optimum was 7.0. At the optimum pH (compared with pH 7.4), 4R formation increased 40-50% with PB and DXM microsomes but 8.0-fold with 3MC microsomes. Studies using the inhibitors metyrapone and alpha-naphthoflavone as well as monoclonal antibodies against various P450s suggested that at least the P450 isoforms IA1/IA2, IIB1 and IIIA1/IIIA2 are involved in 4R formation. Using urinary excretion of the enzymes alkaline phosphatase and gamma-glutamyl transferase as an index of renal damage, we observed that pretreatment of rats with PB, which induced hepatic P450 (P450II2B1), protected against OTA nephrotoxicity, whereas cobalt-protoporphyrin IX pretreatment, which decreased P450 levels, exacerbated OTA nephrotoxicity. Our results suggest that at least P450IIB1-dependent metabolism of OTA leads to its detoxication and that OTA itself may be toxic in some circumstances or that other pathways are responsible for its activation. C1 MEM UNIV NEWFOUNDLAND, DEPT BIOCHEM, ST JOHNS, NF A1B 3X9, CANADA. NCI, MOLEC CARCINOGENESIS LAB, BETHESDA, MD 20892 USA. NR 56 TC 35 Z9 35 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD FEB 9 PY 1996 VL 51 IS 3 BP 207 EP 216 DI 10.1016/0006-2952(95)02194-9 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TR741 UT WOS:A1996TR74100002 PM 8573185 ER PT J AU Jenkins, AJ Llosa, T Montoya, I Cone, EJ AF Jenkins, AJ Llosa, T Montoya, I Cone, EJ TI Identification and quantitation of alkaloids in coca tea SO FORENSIC SCIENCE INTERNATIONAL LA English DT Article DE coca tea bags; cocaine; benzoylecgonine ID HERBAL TEA; LEAVES AB The consumption of coca tea is a common occurrence in many South American countries. The tell is often packaged in individual servings as tea bags which contain approximately 1 g of plant material. The consumption of coca tea leads to ingestion of cocaine and other alkaloids; however, there is little information available regarding the pharmacological or toxicological effects that result from consumption of coca tea. We performed a series of studies with coca tea bags from two South American countries! Peru and Bolivia. The alkaloidal content of the 'coca leaf in coca tea bags was determined by two different extraction methods: Soxhlet extraction with methanol (exhaustive extraction), and mechanical agitation with methanol. Extracts were purified by solid-phase extraction (SPE) followed by analysis by gas chromatography/mass spectrometry (GC/MS). Coca tea prepared from Peruvian and Bolivian coca tea bags was also analyzed by SPE-GC/MS assay. In addition, urine specimens were analyzed from an individual who consumed one cup of Peruvian coca tea and one cup of Bolivian coca tea on separate occasions. Urine samples were analyzed by immunoassay (TDx(R)) and SPE-GC/MS. Analysis of coca tea bags and coca tea indicated that cocaine, benzoylecgonine, ecgonine methyl ester and trans-cinnamoylcocaine were present in varying quantities. With exhaustive extraction, an average of 5.11 mg, and 4.86 mg of cocaine per tea bag were found in coca leaf from Peru and Bolivia, respectively. The average amounts of benzoylecgonine and ecgonine methyl ester in Peruvian coca leaf were 0.11 and 1.15 mg, and in Bolivian coca leaf were 0.12 and 2.93 mg pet tea bag, respectively. trans-Cinnamoylcocaine was found in trace amounts in Peruvian tea bags and 0.16 mg/tea bag of Bolivian tea. When tea was prepared, an average of 4.14 mg of cocaine was present in a cup of Peruvian coca tea and 4.29 mg of cocaine was present in Bolivian tea. Following the consumption of a cup of Peruvian tea by one individual, a peak urine benzoylecgonine concentration of 3940 ng/ml occurred 10 h after ingestion. Consumption of Bolivian coca tea resulted in a peak benzoylecgronine concentration of 4979 ng/ml at 3.5 h. The cumulative urinary excretion of benzoylecgonine after approximately 48 h, determined by GC/MS, was 3.11 mg and 2.69 mg after consumption of Peruvian and Bolivian coca tea, respectively. This study demonstrated that coca tea bags and coca tea contain a significant amount of cocaine and cocaine-related alkaloids and the consumption of a single cup of Peruvian or Bolivian coca tea produces positive drug test results for cocaine metabolites. C1 NIDA,NIH,ADDICT RES CTR,BALTIMORE,MD 21224. FU Intramural NIH HHS [Z99 DA999999] NR 19 TC 27 Z9 29 U1 0 U2 10 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0379-0738 J9 FORENSIC SCI INT JI Forensic Sci.Int. PD FEB 9 PY 1996 VL 77 IS 3 BP 179 EP 189 DI 10.1016/0379-0738(95)01860-3 PG 11 WC Medicine, Legal SC Legal Medicine GA TZ206 UT WOS:A1996TZ20600006 PM 8819993 ER PT J AU Chertov, O Michiel, DF Xu, LL Wang, JM Tani, K Murphy, WJ Longo, DL Taub, DD Oppenheim, JJ AF Chertov, O Michiel, DF Xu, LL Wang, JM Tani, K Murphy, WJ Longo, DL Taub, DD Oppenheim, JJ TI Identification of defensin-1, defensin-2, and CAP37/azurocidin as T-cell chemoattractant proteins released from interleukin-8-stimulated neutrophils SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; CHEMOTACTIC FACTOR; PURIFICATION; RECEPTOR; PEPTIDE; EXPRESSION; CYTOKINES; SEQUENCE; ADHESION; PRODUCE AB Reports that interleukin-8 (IL-8) induces the infiltration of neutrophils followed by T-cells into injection sites led us to postulate that by stimulation of neutrophil degranulation IL-8 may cause the release of factors with chemoattractant activity for T-lymphocytes. Extracts of human neutrophil granules were chromatographed to isolate and purify T-lymphocyte chemoattractant factors. Two major peaks of T-cell chemotactic activity were purified by C18 reversed phase high pressure liquid chromatography (HPLC). The first peak was resolved further by C4 reversed phase HPLC and yielded an active fraction shown by NH2-terminal amino acid sequence analysis to contain defensins HNP-1, HNP-2, and HNP-3. Purified defensins HNP-1 and HNP-2 (kindly provided by Dr. R. I. Lehrer, UCLA) were also potent chemoattractants for human T-cells, while HNP-3 was inactive. The second peak of T-cell chemoattractant activity was also further purified to homogeneity by C4 reversed phase HPLC and identified by NH2-terminal sequence analysis as CAP37/azurocidin, a protein with sequence homology to serine proteases, 0.1-100 ng of defensins and 1.0-100 ng/ml CAP37 were able to stimulate in vitro T-cell chemotaxis. Neutrophil activating factors, i.e. IL-8, phorbol 12-myristate 18-acetate/ionomycin, and formylmethionylleucylphenylalanine each induced the release of CAP37 and defensins from neutrophil granules. Subcutaneous administration of defensins or CAP37/azurocidin into BALB/c mice resulted in a moderate neutrophil and mononuclear cell infiltrate by 4 h, which was greater by 24 h at the site of injection. Additionally, subcutaneous injection of defensins into chimeric huPBL-SCID mice resulted in significant infiltration by human CD3+ cells within 4 h. These results identify the antimicrobial proteins, CAP37/azurocidin and defensins HNP-1 and HNP-8, as potent neutrophil-derived chemoattractants for T-cells. These proteins represent primordial antimicrobial peptides which may have evolved into acute inflammatory cell-derived signals that mobilize immunocompetent T-cells and other inflammatory cells. C1 NCI,FREDERICK CANC RES & DEV CTR,MOLEC IMMUNOREGULAT LAB,NIH,DIV CANC TREATMENT,FREDERICK,MD 21702. SCI APPLICAT INT CORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. SCI APPLICAT INT CORP,CLIN SERV PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74102] NR 37 TC 398 Z9 416 U1 3 U2 9 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 9 PY 1996 VL 271 IS 6 BP 2935 EP 2940 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TU691 UT WOS:A1996TU69100012 PM 8621683 ER PT J AU Johnson, AC AF Johnson, AC TI Activation of epidermal growth factor receptor gene transcription by phorbol 12-myristate 13-acetate is mediated by activator protein 2 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANS-ACTING FACTOR; HUMAN-BRAIN TUMORS; CANCER CELL-LINE; EGF-RECEPTOR; MESSENGER-RNA; ENHANCED EXPRESSION; HUMAN-FIBROBLASTS; CARCINOMA-CELLS; BINDING-SITES; OWN RECEPTOR AB The response of the epidermal growth factor (EGF) receptor gene to phorbol 12-myristate 13-acetate (PMA) was analyzed using nuclei and nuclear extracts prepared from PMA-treated KB cells. Transient transfection assays and nuclear run-off experiments showed that PMA increased EGF receptor gene transcription. Cell-free transcription with promoter mutants revealed that the region of the promoter containing nucleotides -150 to -16 was sufficient for PMA inducibility. A promoter fragment containing nucleotides -167 to -105 showed increased binding of a factor present in extracts prepared from PMA-treated cells. When this factor was partially purified by column chromatography, it showed specific PIMA-dependent binding to an EGF receptor promoter fragment. This binding was competed by an SV40 fragment containing binding sites for Sp1, AP1, and AP2. Purified AP2 was used in DNase I footprinting experiments to show that this factor can bind to the EGF receptor promoter. Oligonucleotides corresponding to the AP2 binding sites found in the EGF receptor promoter showed the ability to bind AP2 and compete for the binding of a factor induced by PMA treatment. The addition of AP2 to nuclear extract resulted in increased transcription from the EGF receptor promoter. These results demonstrate that AP2 can activate EGF receptor gene expression and may mediate the PMA response of this gene. RP Johnson, AC (reprint author), NCI,MOLEC BIOL LAB,DIV BASIC SCI,NIH,37-2D18,37 CONVENT DR,MSC 4255,BETHESDA,MD 20892, USA. NR 52 TC 40 Z9 40 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 9 PY 1996 VL 271 IS 6 BP 3033 EP 3038 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TU691 UT WOS:A1996TU69100026 PM 8621697 ER PT J AU Aznavoorian, S Stracke, ML Parsons, J McClanahan, J Liotta, LA AF Aznavoorian, S Stracke, ML Parsons, J McClanahan, J Liotta, LA TI Integrin alpha(v)beta(3), mediates chemotactic and haptotactic motility in human melanoma cells through different signaling pathways SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MANNOSE 6-PHOSPHATE RECEPTOR; TYROSINE PHOSPHORYLATION; EXTRACELLULAR-MATRIX; PHOSPHATIDYLINOSITOL TRISPHOSPHATE; VITRONECTIN RECEPTOR; FIBRONECTIN RECEPTOR; ENDOTHELIAL-CELLS; HUMAN-NEUTROPHILS; TUMOR-CELLS; GI-PROTEIN AB Distinctions between chemotaxis and haptotaxis of cells to extracellular matrix proteins have not been defined in terms of mechanisms or signaling pathways. Migration of A2058 human melanoma cells to soluble (chemotaxis) and substratum-bound (haptotaxis) vitronectin, mediated by alpha(v) beta(3) provided a system with which to address these questions. Both chemotaxis and haptotaxis were completely inhibited by treatment with RGD-containing peptides. Chemotaxis was abolished by a blocking antibody to alpha(v) beta(3) (LM609), whereas haptotaxis was inhibited only by approximately 50%, suggesting involvement of multiple receptors and/or signaling pathways. However, blocking antibodies to alpha(v) beta(3) also present on A2058 cells, did not inhibit. Pertussis toxin treatment of cells inhibited chemotaxis by > 80%, but did not inhibit haptotaxis. Adhesion and spreading over vitronectin induced the phosphorylation of paxillin on tyrosine. In cells migrating over substratum-bound vitronectin, tyrosine phosphorylation of paxillin increased 5-fold between 45 min and 5 h. Dilutions of anti-alpha(v) beta(3) that inhibited haptotaxis also inhibited phosphorylation of paxillin (by alpha 50%) and modestly reduced cell spreading. In contrast, soluble vitronectin (50-100 mu g/ ml) did not induce tyrosine phosphorylation of paxillin. The data suggest that soluble vitronectin stimulates chemotaxis predominantly through a G protein-mediated pathway that is functionally linked to alpha(v) beta(3). Haptotaxis is analogous to directional cell spreading and requires alpha v beta 3-mediated tyrosine phosphorylation of paxillin. RP Aznavoorian, S (reprint author), NCI,PATHOL LAB,NIH,BLDG 10,RM 2A33,BETHESDA,MD 20892, USA. NR 67 TC 70 Z9 75 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 9 PY 1996 VL 271 IS 6 BP 3247 EP 3254 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TU691 UT WOS:A1996TU69100056 PM 8621727 ER PT J AU Werner, MH Gronenborn, AM Clore, GM AF Werner, MH Gronenborn, AM Clore, GM TI Intercalation, DNA kinking, and the control of transcription SO SCIENCE LA English DT Article ID MOLECULAR-DYNAMICS SIMULATIONS; CO-CRYSTAL STRUCTURE; TATA-BOX COMPLEX; NUCLEIC-ACIDS; TRANSACTIVATION DOMAIN; BINDING-AFFINITY; PROTEIN-BINDING; FORCE-FIELD; B-DNA; HELIX AB Biological processes involved in the control and regulation of transcription are dependent on protein-induced distortions in DNA structure that enhance the recruitment of proteins to their specific DNA targets. This function is often accomplished by accessory factors that bind sequence specifically and locally bend or kink the DNA. The recent determination of the three-dimensional structures of several protein-DNA complexes, involving proteins that perform such architectural tasks, brings to light a common theme of side chain intercalation as a mechanism capable of driving the deformation of the DNA helix. The protein scaffolds orienting the intercalating side chain (or side chains) are structurally diverse, presently comprising four distinct topologies that can accomplish the same task. The intercalating side chain (or side chains), however, is exclusively hydrophobic. Intercalation can either kink or bend the DNA, unstacking one or more adjacent base pairs and locally unwinding the DNA over as much as a full turn of helix. Despite these distortions, the return to B-DNA helical parameters generally occurs within the adjacent half-turns of DNA. C1 NIDDKD, CHEM PHYS LAB, BETHESDA, MD 20892 USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 100 TC 230 Z9 230 U1 0 U2 17 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD FEB 9 PY 1996 VL 271 IS 5250 BP 778 EP 784 DI 10.1126/science.271.5250.778 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU694 UT WOS:A1996TU69400038 PM 8628992 ER PT J AU Yannelli, JR Hyatt, C McConnell, S Hines, K Jacknin, L Parker, L Sanders, M Rosenberg, SA AF Yannelli, JR Hyatt, C McConnell, S Hines, K Jacknin, L Parker, L Sanders, M Rosenberg, SA TI Growth of tumor-infiltrating lymphocytes from human solid cancers: Summary of a 5-year experience SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID RENAL-CELL CARCINOMA; ADOPTIVE IMMUNOTHERAPY; RECOMBINANT INTERLEUKIN-2; METASTATIC MELANOMA; CYTOKINE SECRETION; AUTOLOGOUS TUMOR; COLON CARCINOMAS; ALPHA; TRANSDUCTION; RECOGNITION AB Between 1989 and 1993, 255 tumor biopsies representing 4 tumor histologies (melanoma, breast cancer, colon cancer and renal cell cancer) were received by the Surgery Branch of the National Cancer Institute. Tumor-infiltrating lymphocytes (TIL) were grown from single-cell suspensions of tumor biopsies over the course of 30-45 days. The TIL were grown in medium containing IL-2. To obtain numbers suitable for therapy (> 10(11)), TIL were expanded using a large-scale system of cell culture and harvesting. While the largest number of biopsies was obtained from melanoma patients, TIL were successfully grown from 160 of 255 tumor biopsies representing all 4 histologies. Under the culture conditions employed, several characteristics of TIL expansion were observed. The cell surface phenotype of TIL which grew out from the tumor biopsies was generally a mix of CD3(+)/CD4(+) or CD3(+)/CD8(+) lymphocytes. Only TIL from melanoma biopsies were found to be consistently cytolytic and, in many cases, lysed autologous tumor cells preferentially. Interestingly, TIL derived from extra-nodal sites of metastatic melanoma biopsies (subcutaneous, lung, bowel; 36 of 67, 54%) were more likely to have these cytolytic characteristics than TIL derived from tumor-involved lymph node biopsies (7 of 39, 18%). The present study summarizes 5 years of laboratory effort and validates the technologies developed for the large-scale growth and harvesting of TIL. In addition, it summarizes the laboratory effort supporting previously published clinical reports on TIL from our group. (C) 1996 Wiley-Liss, Inc.* C1 NCI,NIH,SURG BRANCH,BETHESDA,MD 20892. NR 45 TC 106 Z9 112 U1 1 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD FEB 8 PY 1996 VL 65 IS 4 BP 413 EP 421 DI 10.1002/(SICI)1097-0215(19960208)65:4<413::AID-IJC3>3.0.CO;2-# PG 9 WC Oncology SC Oncology GA TX087 UT WOS:A1996TX08700003 PM 8621219 ER PT J AU Hsing, AW Nam, JM Chien, HTC McLaughlin, JK Fraumeni, JF AF Hsing, AW Nam, JM Chien, HTC McLaughlin, JK Fraumeni, JF TI Risk factors for adrenal cancer: An exploratory study SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID RESPIRATORY-TRACT TUMORS; ORAL-CONTRACEPTIVE USE; DEAD CONTROLS; RATS; HAMSTERS AB Adrenal cancer is a heterogeneous group of neoplasms with unknown etiology. In search of risk factors, we conducted a case-control study based on data from the 1986 National Mortality Followback Survey, which included a questionnaire sent to the next of kin of almost 20,000 deceased adults (age greater than or equal to 25 years) in the United States. Information was obtained on a large number of items, including use of cigarettes, alcohol, oral contraceptives (OCs), height and weight and food consumption patterns. A total of 176 subjects who died of adrenal cancer (88 men and 88 women) and 352 controls (176 men and 176 women) who died of causes unrelated to smoking, drinking or OCs (for female controls) were included in the study. Although information on histologic type was not available, most cases were estimated from incidence surveys to be adrenocortical carcinoma, with a small percentage being malignant pheochromocytoma or neuroblastoma. An increased risk was associated with heavy smoking (greater than or equal to 25 cigarettes/day) among men (odds ratio [OR] = 2.0, 95% confidence interval [CI] 1.0-4.4) but not women. No clear association was seen for alcohol use, height and weight or food consumption patterns in either sex. Among women, increased risks were found for ever users of OCs (OR = 1.8, 95% CI 1.0-3.2) and especially those who used them before age 25 (OR = 2.5, 95% CI 1.2-5.5). When the analysis was restricted to subjects with spousal respondents, more pronounced risks were seen for ever users of OCs and for those who used OCs before age 25. Our findings suggest that cigarette smoking and use of OCs may increase the risk of adrenal cancer, but additional studies are needed with more detailed information on risk factors and histologic type of adrenal cancer. (C) 1996 Wiley-Liss, Inc.* C1 WESTAT CORP,ROCKVILLE,MD. INT EPIDEMIOL INST,ROCKVILLE,MD. RP Hsing, AW (reprint author), NCI,DIV CANC EPIDEMIOL & GENET,EPN 415,6130 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 30 TC 30 Z9 31 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD FEB 8 PY 1996 VL 65 IS 4 BP 432 EP 436 DI 10.1002/(SICI)1097-0215(19960208)65:4<432::AID-IJC6>3.0.CO;2-Y PG 5 WC Oncology SC Oncology GA TX087 UT WOS:A1996TX08700006 PM 8621222 ER PT J AU Greco, D Salmaso, S Mastrantonio, P Giuliano, M Tozzi, AE Anemona, A Atti, MLCD Giammanco, A Panei, P Blackwelder, WC Klein, DL Wassilak, SGF Stefanelli, P Bottone, M Sofia, T Luzi, S Bellomi, G Cobianchi, F Canganella, G Meduri, F Scuderi, G Chiarini, A Maggio, M Taormina, S Genovese, M Moiraghi, A Barale, A DiTommaso, S Malaspina, S Vasile, E Ferraro, P DalLago, P DeMarzi, L Robino, L Giraldo, E Coppola, N Materassi, P Castellani, GT Basso, F Barbuti, S Quarto, M Lopalco, P DOrazio, P Sanguedolce, A AF Greco, D Salmaso, S Mastrantonio, P Giuliano, M Tozzi, AE Anemona, A Atti, MLCD Giammanco, A Panei, P Blackwelder, WC Klein, DL Wassilak, SGF Stefanelli, P Bottone, M Sofia, T Luzi, S Bellomi, G Cobianchi, F Canganella, G Meduri, F Scuderi, G Chiarini, A Maggio, M Taormina, S Genovese, M Moiraghi, A Barale, A DiTommaso, S Malaspina, S Vasile, E Ferraro, P DalLago, P DeMarzi, L Robino, L Giraldo, E Coppola, N Materassi, P Castellani, GT Basso, F Barbuti, S Quarto, M Lopalco, P DOrazio, P Sanguedolce, A TI A controlled trial of two acellular vaccines and one whole-cell vaccine against pertussis SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID BORDETELLA-PERTUSSIS; ANTIBODY-RESPONSE; EFFICACY; EPIDEMIOLOGY; IMMUNIZATION; CHILDREN; TOXIN; PARAPERTUSSIS; EXPERIENCE; DIPHTHERIA AB Background. Concern about both safety and efficacy has made the use of whole-cell pertussis vaccines controversial. In some European countries, including Italy, the rate of vaccination against pertussis is low. Methods. We conducted a double-blind trial in Italy in which infants were randomly assigned to vaccination at two, four, and six months of age with an acellular pertussis vaccine together with diphtheria and tetanus toxoids (DTP); a DTP vaccine containing whole-cell pertussis (manufactured by Connaught Laboratories); or diphtheria and tetanus toxoids without pertussis (DT). The acellular DTP vaccine was either one containing filamentous hemagglutinin, pertactin, and pertussis toxin inactivated with formalin and glutaraldehyde (SmithKline Beecham) or one with filamentous hemagglutinin, pertactin, and genetically detoxified pertussis toxin (Chiron Biocine). Pertussis was defined as 21 days or more of paroxysmal cough, with infection confirmed by culture or serologic testing. Results. The efficacy of each vaccine, given in three doses, against pertussis was determined for 14,751 children over an average of 17 months, with cases included in the analysis if cough began 30 days or more after the completion of immunization. For both of the acellular DTP vaccines, the efficacy was 84 percent (95 percent confidence intervals, 76 to 89 percent for SmithKline DTP and 76 to 90 percent for Biocine DTP), whereas the efficacy of the whole-cell DTP vaccine was only 36 percent (95 percent confidence interval, 14 to 52 percent). The antibody responses were greater to the acellular vaccines than to the whole-cell vaccine. Local and systemic adverse events were significantly more frequent after the administration of the whole-cell vaccine. For the acellular vaccines, the frequency of adverse events was similar to that in the control (DT) group. Conclusions. The two acellular DTP vaccines we studied were safe, immunogenic, and efficacious against pertussis, whereas the efficacy of the whole-cell DTP vaccine was unexpectedly low. C1 IST SUPER SANITA,LAB BACTERIOL & MED MYCOL,I-00161 ROME,ITALY. UNIV PALERMO,DEPT HYG & MICROBIOL,PALERMO,ITALY. NIAID,BETHESDA,MD 20892. RP Greco, D (reprint author), IST SUPER SANITA,EPIDEMIOL & BIOSTAT LAB,VIALE REGINA ELENA 299,I-00161 ROME,ITALY. RI Tozzi, Alberto Eugenio/F-9494-2012; STEFANELLI, PAOLA/B-8729-2016 OI Tozzi, Alberto Eugenio/0000-0002-6884-984X; STEFANELLI, PAOLA/0000-0003-1620-4385 FU NIAID NIH HHS [N01-AI-25138] NR 40 TC 486 Z9 491 U1 1 U2 12 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 8 PY 1996 VL 334 IS 6 BP 341 EP 348 DI 10.1056/NEJM199602083340601 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA TT487 UT WOS:A1996TT48700001 PM 8538704 ER PT J AU Rosenberg, SA AF Rosenberg, SA TI Secrecy in medical research SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material RP Rosenberg, SA (reprint author), NCI,BETHESDA,MD 20892, USA. NR 2 TC 50 Z9 51 U1 1 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 8 PY 1996 VL 334 IS 6 BP 392 EP 394 DI 10.1056/NEJM199602083340610 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA TT487 UT WOS:A1996TT48700010 PM 8538713 ER PT J AU Sax, CM Ilagan, JG Haynes, JI AF Sax, CM Ilagan, JG Haynes, JI TI Lens-preferred activity of the -1809/+46 mouse alpha A-crystallin promoter in stably integrated chromatin SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE crystallin; eye; gene expression; lens; transgenic mouse ID CHLORAMPHENICOL ACETYLTRANSFERASE; TRANSGENIC MICE; GENE; EXPRESSION; TRANSCRIPTION; EVOLUTION; SEQUENCES; PROTEIN; CELLS AB The alpha A-crystallin gene is expressed in a highly lens preferred manner. Here we show that the mouse alpha A-crystallin - 1809/+46 promoter fragment displays lens-preferred activity in transgenic mice and in stably transfected lens cells. These findings are in contrast to the lack of activity of this promoter previously reported in transiently transfected lens cells. Our current findings suggest that the -1809/+46 mouse alpha A-crystallin promoter functions in a lens preferred manner when stably integrated into chromatin. C1 HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,BETHESDA,MD 20817. RP Sax, CM (reprint author), NEI,MOLEC & DEV BIOL LAB,NIH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 26 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD FEB 7 PY 1996 VL 1305 IS 1-2 BP 49 EP 53 DI 10.1016/0167-4781(95)00202-2 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TW616 UT WOS:A1996TW61600011 PM 8605249 ER PT J AU Hatch, CL Bonner, WM AF Hatch, CL Bonner, WM TI An upstream region of the H2AZ gene promoter modulates promoter activity in different cell types SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE H2AZ gene; promoter; promoter activity; (human) ID TRANSCRIPTION AB Human H2AZ gene promoter fragments that included sequences upstream from the core promoter resulted in decreased activity of reporter constructs transfected into several human cell lines, but increased activity in the undifferentiated human embryonal carcinoma cell line Tera-2, Differentiation of Tera-2 cells in media containing retinoic acid restored the ability of the upstream region to downregulate H2AZ gene promoter activity. Levels of endogenous H2AZ mRNA were also found to be 2.5-fold higher in undifferentiated Tera-2 cells than in differentiated Tera-2 cells. A 128 bp region located 234 to 361 bp upstream from the transcription start site of the H2AZ gene was found to be responsible for the modulation of reporter activity. The upstream region also functioned similarly when removed from the H2AZ gene promoter and inserted upstream of the SV40 promoter in reporter constructs. Gel mobility shift studies of fragments of this region revealed two sequence elements, CTCCTCC and CACGTG, that bound nuclear factors in vitro. C1 NCI,MOLEC PHARMACOL LAB,NIH,DCT,DTP,BETHESDA,MD 20892. NR 11 TC 6 Z9 6 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD FEB 7 PY 1996 VL 1305 IS 1-2 BP 59 EP 62 DI 10.1016/0167-4781(95)00223-5 PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TW616 UT WOS:A1996TW61600013 PM 8605251 ER PT J AU Jackers, P Clausse, N Fernandez, MT Berti, A Princen, F Wewer, U Sobel, ME Castronovo, V AF Jackers, P Clausse, N Fernandez, MT Berti, A Princen, F Wewer, U Sobel, ME Castronovo, V TI Seventeen copies of the human 37 kDa laminin receptor precursor/p40 ribosome-associated protein gene are processed pseudogenes arisen from retropositional events SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE processed pseudogene; laminin receptor precursor, 37 kDa; retroposon; p40 ribosome-associated protein; ribosome-associated protein ID EMBRYONIC RETINA; GENOMIC ANALYSIS; BINDING-PROTEIN; SEQUENCE; FAMILY; METASTASIS; CELLS; RNA AB A cDNA coding for a 37 kDa polypeptide has been identified in several species as both the potential precursor of the 67 kDa laminin receptor (37LRP) and a putative ribosome-associated protein (p40). Interestingly, increased expression of this polypeptide (37LRP/p40) is consistently observed in invasive and metastatic cancer cells and is associated with poor prognosis. Southern-blot analysis of human genomic DNA predicted multiple copies of the 37LRP/p40 gene. In this study, we report that the number of copies of this sequence in the human genome is 26 +/- 2. We have sequenced and analyzed 19 genomic clones corresponding to the 37LRP/p40 gene and found that they were all processed pseudogenes. They all lack intronic sequences and show multiple genetic alterations leading in some cases to the appearance of stop codons. Moreover, they all bear characteristic features of retroposons as the presence of a poly(A)-tail at their 3' end and short direct repeated flanking DNA sequences. None of the pseudogenes analyzed present cis-elements in their 5' flanking region such as TATA or GC boxes. Our data reveal that over 50% of the 37LRP/p40 gene copies are pseudogenes most probably generated by retropositional events. The finding of multiple pseudogenes for the 37LRP/p40 gene suggests that the accumulation of several copies of this gene might have given a survival advantage to the cell in the course of evolution. C1 NCI,NIH,MOLEC PATHOL SECT,BETHESDA,MD 20892. RP Jackers, P (reprint author), UNIV LIEGE,MAT RES LAB,LIEGE,BELGIUM. RI Fernandez-Sanchez, Maria Teresa/Q-1673-2015 OI Fernandez-Sanchez, Maria Teresa/0000-0003-4800-9517 NR 24 TC 16 Z9 19 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD FEB 7 PY 1996 VL 1305 IS 1-2 BP 98 EP 104 DI 10.1016/0167-4781(95)00206-5 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TW616 UT WOS:A1996TW61600018 PM 8605257 ER PT J AU Lei, PS Ogawa, Y Kovac, P AF Lei, PS Ogawa, Y Kovac, P TI Synthesis of the methyl alpha-glycosides of a di-, tri-, and a tetra-saccharide fragment mimicking the terminus of the O-polysaccharide of Vibrio cholerae O:1, serotype Ogawa SO CARBOHYDRATE RESEARCH LA English DT Article DE polysaccharide; Vibrio cholerae; glycoside, alpha-linked; synthesis; oligosaccharides ID BETA-GLYCOSIDES; O-(3-DEOXY-3-FLUORO-BETA-D-GALACTOPYRANOSYL)-(1->6)-O-BETA-D-GALACTOPYRA NOSYL-(. AB Methyl 4-(3-deoxy-L-glycero-tetronamido)-4,6-dideoxy-2-O-methyl-alpha-D-mannopyranoside was acetylated, and the fully protected methyl glycoside was treated with dichloromethyl methyl ether-ZnCl2 (DCMME-ZnCl2) reagent to give 3-O-acetyl-4-(2,4-di-O-acetyl-3-deoxy-L-glycero-tetronamido)-4,6-dideoxy-2-O-methyl-alpha-D-mannopyranosyl chloride (3). Condensation of 3 with methyl 3-O-acetyl-4-(2,4-di-O-acetyl-3-deoxy-L-glycero-tetronamido)-4,6-dideoxy-alpha-D-mannopyranoside (4) gave the fully acetylated disaccharide 5, which was deacetylated yielding the methyl cr-glycoside of title disaccharide, The disaccharide glycosyl donor required for the blockwise synthesis of the title tri- and the tetra-saccharide, 3-O-acetyl-3-(2,4-di-O-acetyl-3-deoxy-L-glycero-tetronamido)-4,6-dideoxy-2-O-methyl-alpha-D-mannopyranosyl-( 1 --> 2)-3-O-acetyl-4-(2,4-di-O-acetyl-3-deoxy-L-glycero-tetronamido)-4,6-dideoxy-alpha-D-mannopyranosyl chloride (12), was obtained by condensation of 3 with the 1-O-acetyl analog of 4, followed by treatment of the disaccharide formed with DCMME-ZnCl2. The synthesis of the methyl alpha-glycoside of the title trisaccharide involved a condensation of 12 with 4, followed by deacetylation. Similarly, the condensation of 12 with 15, the latter being the analog of 5 having a free HO-2, followed by deacetylation, gave the methyl alpha-glycoside of the title tetrasaccharide. All glycosylation reactions were mediated by silver trifluoromethanesulfonate in the presence of 2,4,6-trimethylpyridine. 4-(3-Deoxy-L-glycero-tetronamido)-4,6-dideoxy-2-O-methyl-alpha,beta-D-mannopyranose was prepared for the first time, It was characterized by NMR spectroscopy, and via its crystalline per-O-acetyl derivative. It is the saccharide whose alpha-form constitutes the terminal, non-reducing end-group of the O-PS of V. cholerea O:1, serotype Ogawa. C1 NIDDK,NIH,BETHESDA,MD 20892. NR 16 TC 25 Z9 26 U1 1 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD FEB 7 PY 1996 VL 281 IS 1 BP 47 EP 60 DI 10.1016/0008-6215(95)00331-2 PG 14 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA TV933 UT WOS:A1996TV93300004 PM 8839176 ER PT J AU Klein, HG Sloand, EM AF Klein, HG Sloand, EM TI Transfusion vs anesthesia-related hepatitis - Reply SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP Klein, HG (reprint author), NIH,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 7 PY 1996 VL 275 IS 5 BP 361 EP 362 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA TT303 UT WOS:A1996TT30300025 ER PT J AU Judd, HL Wasilauskas, C Johnson, S Merino, M BarrettConnor, E Trabal, J Miller, VT Barnabei, V Levin, G Bush, T Foster, D Zacur, H Woodruff, JD Stefanick, M Akana, A Heinrichs, WL OHanlan, K Buyalos, RP Greendale, G Lozano, K CarrionPetersen, L Cavero, C Langer, R Schrott, HG Benda, JA deProsse, C Fedderson, D Johnson, SR Ahmad, MM Brown, HP Schenken, RS RodriguezSifuentes, M Valente, PT Espeland, M Lane, K Legault, C MebaneSims, IL Kelaghan, J McGowan, J Fradkin, J Sherman, S Scully, R AF Judd, HL Wasilauskas, C Johnson, S Merino, M BarrettConnor, E Trabal, J Miller, VT Barnabei, V Levin, G Bush, T Foster, D Zacur, H Woodruff, JD Stefanick, M Akana, A Heinrichs, WL OHanlan, K Buyalos, RP Greendale, G Lozano, K CarrionPetersen, L Cavero, C Langer, R Schrott, HG Benda, JA deProsse, C Fedderson, D Johnson, SR Ahmad, MM Brown, HP Schenken, RS RodriguezSifuentes, M Valente, PT Espeland, M Lane, K Legault, C MebaneSims, IL Kelaghan, J McGowan, J Fradkin, J Sherman, S Scully, R TI Effects of hormone replacement therapy on endometrial histology in postmenopausal women - The Postmenopausal Estrogen Progestin Interventions (PEPI) trial SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID CONJUGATED ESTROGENS; MENOPAUSAL WOMEN; CANCER; RISK; CARCINOMA; ASSOCIATION; DISEASE AB Objective.-To report the histological findings of the endometrium of postmenopausal women who were randomized to receive placebo, estrogen only, or one of three estrogen plus progestin (EI-P) regimens in the Postmenopausal Estrogen/ Progestin Interventions (PEPI) Trial. Design.-A 3-year multicenter, randomized, double-masked, placebo-controlled trial. Participants-A total of 596 postmenopausal women aged 45 through 64 years without contraindication to hormone therapy. Intervention.-Participants were randomized and stratified in equal numbers to one of the following treatments in 28-day cycles: placebo, 0.625 mg/d of conjugated equine estrogens (GEE), 0.625 mg/d of CEE plus 10 mg/d of medroxyprogesterone acetate (MPA)for the first 12 days, 0.625 mg/d of CEE plus 2.5 mg/d of MPA, or 0.625 mg/d of CEE plus 200 mg/d of micronized progesterone (MP) for the first 12 days. Outcome Measure.-Histology of endometrium collected at baseline, annual, or unscheduled Visits by biopsy, curettage, or hysterectomy. Analysis.-Intention to treat. Results.-During follow-up women assigned to estrogen atone were more likely to develop simple (cystic), complex (adenomatous), or atypical hyperplasia than those given placebo (27.7% vs 0.8%, 22.7% vs 0.8%, and 11.8% vs 0%, respectively) for the same types of hyperplasia (P<.001). Participants administered one of the three E+P regimens had similar rates of hyperplasia as those given placebo (P=.16). The occurrence of hyperplasia was distributed evenly across the 3 years of the trial. Women taking estrogens alone also had more unscheduled biopsies (66.4% vs 8.4%; P<.001) and curettages (17.6% vs 0.8%; P<.001) than women receiving placebo. The number of surgical procedures was similar for women receiving placebo and women receiving the E+P regimens (P=.38). Of the 45 women with complex (adenomatous) or atypical hyperplasia, study medications were discontinued in all, and the biopsy results of 34 (94%) of 36 women with hyperplasia reverted to normal with progestin therapy. The remainder had dilatation and curettage (n=2) or hysterectomy with (n=2) or without (n=6) prior medical therapy, or refused further biopsies (n=1). One woman developed adenocarcinoma of the endometrium while receiving placebo. Conclusions.-At a dosage of 0.625 mg, the daily administration of CEE enhanced the development of endometrial hyperplasia. Combining CEE with cyclic or continuous MPA or cyclic MP protected the endometrium from hyperplastic changes associated with estrogen-only therapy. RP Judd, HL (reprint author), NHLBI,2 ROCKLEDGE CTR,SUITE 10193,6701 ROCKLEDGE DR,MSC,BETHESDA,MD 20892, USA. NR 34 TC 342 Z9 351 U1 1 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 7 PY 1996 VL 275 IS 5 BP 370 EP 375 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA TT303 UT WOS:A1996TT30300030 ER PT J AU Clemens, J Brenner, R Rao, M Tafari, N Lowe, C AF Clemens, J Brenner, R Rao, M Tafari, N Lowe, C TI Evaluating new vaccines for developing countries - Efficacy or effectiveness? SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID VI-CAPSULAR POLYSACCHARIDE; BOVINE ROTAVIRUS VACCINE; ENTERIC-COATED CAPSULES; TITER MEASLES-VACCINES; CONTROLLED FIELD TRIAL; ORAL CHOLERA VACCINES; CHILDHOOD TUBERCULOSIS; CONJUGATE VACCINE; TYPHOID VACCINE; ANTIBODY-RESPONSE AB Despite the profusion of promising new vaccines against illnesses prevalent in developing countries, uncertainties about the balance between costs and benefits of new vaccines have retarded their use in public health practice. Conventional prelicensure trials of vaccine protection exacerbate these uncertainties by focusing on measurement of vaccine efficacy-the performance of a vaccine under idealized conditions. Vaccine effectiveness trials provide a more pragmatic perspective by addressing the performance of a vaccine under the ordinary conditions of a public health program, by capturing direct as well as indirect effects of vaccination, and by comprehensively addressing outcomes of public health concern. The use of effectiveness trials should enable more rational triaging of new vaccines for developing countries and may accelerate the introduction of new vaccines into public health practice by resolving speculative debates about practical costs and benefits. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. NICHHD,OFF DIRECTOR,BETHESDA,MD 20892. NR 87 TC 116 Z9 119 U1 0 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 7 PY 1996 VL 275 IS 5 BP 390 EP 397 DI 10.1001/jama.275.5.390 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA TT303 UT WOS:A1996TT30300033 PM 8569019 ER PT J AU Bates, AD ODea, MH Gellert, M AF Bates, AD ODea, MH Gellert, M TI Energy coupling in Escherichia coli DNA gyrase: The relationship between nucleotide binding, strand passage, and DNA supercoiling SO BIOCHEMISTRY LA English DT Article ID N-TERMINAL FRAGMENT; TOPOISOMERASE-IV; SUPERHELICAL TURNS; NALIDIXIC-ACID; DOUBLE HELIX; PLASMID DNA; B-PROTEIN; A-PROTEIN; PURIFICATION; SITE AB Binding of the nonhydrolyzable ATP analogue 5'-adenylyl-beta,gamma-imidodiphosphate (ADPNP) to Escherichia coli DNA gyrase can lead to a limited noncatalytic supercoiling of DNA, Here we examine the efficiency of coupling between ADPNP binding and the change in linking number either of positively or negatively supercoiled plasmid DNA or of small DNA circles, The coupling efficiency varies from 100% (Delta Lk = -2 per gyrase tetramer, a stoichiometry of I) with positively supercoiled substrates under certain reaction conditions to an undetectably low value with moderately negatively supercoiled substrates (sigma = -0.046) or small circular substrates. Furthermore, the rate of ADPNP binding to the gyrase-DNA complex is also dependent on the topological state of the DNA; the previously observed slow binding of ADPNP to the complex of gyrase with linear DNA is accelerated 16-fold when the substrate DNA is negatively supercoiled, suggesting a functional interaction between the nucleotide-binding and DNA-binding domains which is independent of the strand-passage process. The implications for the normal ATP-dependent supercoiling reaction of the enzyme are considered and the results discussed in terms of current mechanistic models for DNA gyrase action and the possible in vivo roles of the enzyme. C1 NIDDKD,NIH,MOLEC BIOL LAB,BETHESDA,MD 20892. RP Bates, AD (reprint author), UNIV LIVERPOOL,DEPT BIOCHEM,POB 147,LIVERPOOL L69 3BX,MERSEYSIDE,ENGLAND. FU Wellcome Trust NR 34 TC 46 Z9 46 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 6 PY 1996 VL 35 IS 5 BP 1408 EP 1416 DI 10.1021/bi952433y PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TU586 UT WOS:A1996TU58600010 PM 8634270 ER PT J AU vanderGeer, P Wiley, S Gish, GD Lai, VKM Stephens, R White, MF Kaplan, D Pawson, T AF vanderGeer, P Wiley, S Gish, GD Lai, VKM Stephens, R White, MF Kaplan, D Pawson, T TI Identification of residues that control specific binding of the Shc phosphotyrosine-binding domain to phosphotyrosine sites SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE tyrosine phosphorylation; signal transduction ID TYROSINE KINASE-ACTIVITY; INSULIN-RECEPTOR; MONOCLONAL-ANTIBODIES; SIGNAL TRANSDUCTION; NUCLEOTIDE EXCHANGE; EGF RECEPTOR; GRB2; PROTEIN; RAS; PHOSPHORYLATION AB The She adaptor protein contains two phosphotyrosine [Tyr(P)]binding modules-an N-terminal Tyr(P) binding (PTB) domain and a C-terminal Src homology 2 (SH2) domain, We have compared the ability of the She PTB domain to bind the receptors for nerve growth factor and insulin, both of which contain juxtamembrane Asn-Pro-Xaa-Tyr(P) motifs implicated in PTB binding, The She PTB domain binds with high affinity to a phosphopeptide corresponding to the nerve growth factor receptor Tyr-490 autophosphorylation site, Analysis of individual residues within this motif indicates that the Asn at position -3 [with respect to Tyr(P)], in addition to Tyr(P), is critical for PTB binding, while the Pro at position -2 plays a less significant role. A hydrophobic amino acid 5 residues N-terminal to the Tyr(P) is also essential for high-affinity binding, In contrast, the She PTB domain does not bind stably to the Asn-Pro-Xaa-Tyr(P) site at Tyr-960 in the activated insulin receptor, which has a polar residue (Ser) at position -5. Substitution of this Ser at position -5 with Ile markedly increased binding of the insulin receptor Tyr-960 phosphopeptide to the PTB domain, These results suggest that while the She PTB domain recognizes a core sequence of Asn-Pro-Xaa-Tyr(P), its binding affinity is modulated by more N-terminal residues in the ligand, which therefore contribute to the specificity of PTB-receptor interactions, An analysis of residues in the She PTB domain required for binding to Tyr(P) sites identified a specific and evolutionarily conserved Arg (Arg-175) that is uniquely important for ligand binding and is potentially involved in Tyr(P) recognition. C1 MT SINAI HOSP,SAMUEL LUNENFELD RES INST,PROGRAMME MOLEC BIOL & CANC,TORONTO,ON M5G 1X5,CANADA. MT SINAI HOSP,SAMUEL LUNENFELD RES INST,PROT ENGN NETWORK CTR EXCELLENCE,TORONTO,ON M5G 1X5,CANADA. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. JOSLIN DIABET CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Pawson, Tony/E-4578-2013; Gish, Gerald/C-7228-2017 NR 49 TC 94 Z9 94 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 6 PY 1996 VL 93 IS 3 BP 963 EP 968 DI 10.1073/pnas.93.3.963 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU640 UT WOS:A1996TU64000001 PM 8577769 ER PT J AU Kuan, CT Pastan, I AF Kuan, CT Pastan, I TI Improved antitumor activity of a recombinant anti-Lewis(y) immunotoxin not requiring proteolytic activation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE cancer therapy; Pseudomonas exotoxin; monoclonal antibody B1 Fv fragment; disulfide-stabilized Fv fragment; protein engineering ID PSEUDOMONAS EXOTOXIN; MONOCLONAL-ANTIBODIES; FORM; FRAGMENT; DOMAIN; FV; B3 AB B1(dsFv)-PE33 is a recombinant immunotoxin composed of a mutant form of Pseudomonas exotoxin (PE) that does not need proteolytic activation and a disulfide-stabilized Fv fragment of the anti-Lewis(y) monoclonal antibody B1, which recognizes a carbohydrate epitope on human carcinoma cells, In this molecule, amino acids 1-279 of PE are deleted and domain Ib (amino acids 365-394) is replaced by the heavy chain variable region (VH) domain of monoclonal antibody B1, The light chain (VL) domain is connected to the VH domain by a disulfide bond. This recombinant toxin, termed B1(dsFv)-PE33, does not require proteolytic activation and it is smaller than other immunotoxins directed at Lewis(y), all of which require proteolytic activation, Furthermore, it is more cytotoxic to antigen-positive cell lines, B1(dsFv)-PE38 has the highest antitumor activity of anti-Lewis(y) immunotoxins previously constructed, B1(dsFv)-PE33 caused complete regression of tumors when given at 12 mu g/kg (200 pmol/kg) every other day for three doses, whereas B1(dsFv)-PE38 did not cause regressions at 13 mu g/kg (200 pmol/kg). By bypassing the need for proteolytic activation and decreasing molecular size we have enlarged the therapeutic window for the treatment of human cancers growing in mice, so that complete remissions are observed at 2.5% of the LD(50). C1 NCI,DIV BASIC SCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 31 TC 27 Z9 29 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 6 PY 1996 VL 93 IS 3 BP 974 EP 978 DI 10.1073/pnas.93.3.974 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU640 UT WOS:A1996TU64000003 PM 8577771 ER PT J AU Li, BQ Subleski, M Fusaki, N Yamamoto, T Copeland, T Princler, GL Kung, HF Kamata, T AF Li, BQ Subleski, M Fusaki, N Yamamoto, T Copeland, T Princler, GL Kung, HF Kamata, T TI Catalytic activity of the mouse guanine nucleotide exchanger mSOS is activated by Fyn tyrosine protein kinase and the T-cell antigen receptor in T cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE guanine nucleotide exchange activity; signal transduction; Ras ID INSULIN-RECEPTOR; RAS; GRB2; SRC; RESPONSIVENESS; IDENTIFICATION; ASSOCIATION; STIMULATION; SEVENLESS; PATHWAYS AB mSOS, a guanine nucleotide exchange factor, is a positive regulator of Ras, Fyn tyrosine protein kinase is a potential mediator in T-cell antigen receptor signal transduction in subsets of T cells, We investigated the functional and physical interaction between mSOS and Fyn in T-cell hybridoma cells, Stimulation of the T-cell antigen receptor induced the activation of guanine nucleotide exchange activity in mSOS immunoprecipitates. Overexpression of Fyn mutants with an activated kinase mutation and with a Src homology 2 deletion mutation resulted in a stimulation and suppression of the mSOS activity, respectively, The complex formations of Fyn-Shc, Shc-Grb2, and Grb2-mSOS were detected in the activated Fyn-transformed cells, whereas the SH2 deletion mutant of Fyn failed to form a complex with mSOS. Moreover, tyrosine phosphorylation of She was induced by the overexpression of the activated Fyn. These findings support the idea that Fyn activates the activity of mSOS bound to Grb2 through tyrosine phosphorylation of She. Unlike the current prevailing model, Fyn-induced activation of Ras might involve the stimulation of the catalytic guanine nucleotide exchange activity of mSOS. C1 NCI,FREDERICK CANC RES & DEV CTR,LAB BIOCHEM PHYSIOL,DIV BASIC SCI,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,SAIC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LAB,BRI,FREDERICK,MD 21702. UNIV TOKYO,INST MED SCI,MINATO KU,TOKYO 108,JAPAN. NR 32 TC 38 Z9 39 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 6 PY 1996 VL 93 IS 3 BP 1001 EP 1005 DI 10.1073/pnas.93.3.1001 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU640 UT WOS:A1996TU64000008 PM 8577703 ER PT J AU Tamura, T Stadtman, TC AF Tamura, T Stadtman, TC TI A new selenoprotein from human lung adenocarcinoma cells: Purification, properties, and thioredoxin reductase activity SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE selenocysteine; selenium-75; flavoprotein; selenoenzyme ID SELENIUM; PROTEINS; LIVER; SELENOCYSTEINE; IDENTIFICATION; BINDING; SYSTEM AB We report the isolation and characterization of a new selenoprotein from a human lung adenocarcinoma cell line, NCI-H441. Cells were grown in RPMI 1640 medium containing 10% (vol/vol) fetal bovine serum and 0.1 mu M [Se-75]selenite. A Se-75-labeled protein was isolated from sonic extracts of the cells by chromatography on DE-23, phenyl-Sepharose, heparin-agarose, and butyl-Sepharose, The protein, a homodimer of 57-kDa subunits, was shown to contain selenium in the form of selenocysteine; hydrolysis of the protein alkylated with either iodoacetate or 3-bromopropionate yielded Se-carboxy methyl - selenocysteine or Se-carboxyethyl-selenocysteine, respectively. The selenoprotein showed two isoelectric points at pH 5.2 and pH 5.3. It was distinguished from selenoprotein P by N-glycosidase assay and by the periodate-dansylhydrazine test, which indicated no detectable amounts of glycosyl groups on the protein, The selenoprotein contains FAD as a prosthetic group and catalyzes NADPH-dependent reduction of 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB), and reduction of insulin in the presence of thioredoxin (Trx), The specific activity was determined to be 31 units/mg by DTNB assay, Apparent K-m, values for DTNB, Escherichia coli Trx, and rat Trx were 116, 34, and 3.7 mu M, respectively. DTNB reduction was inhibited by 0.2 mM arsenite, Although the subunit composition and catalytic properties are similar to those of mammalian thioredoxin reductase (TR), the human lung selenoprotein failed to react with anti-rat liver TR polyclonal antibody in immunoblot assays, The selenocysteine-containing TR from the adenocarcinoma cells may be a variant form distinct from rat liver TR. C1 NHLBI,NIH,IR,BIOCHEM LAB,BETHESDA,MD 20892. OKAYAMA UNIV,FAC AGR,OKAYAMA 700,JAPAN. NR 36 TC 359 Z9 373 U1 3 U2 27 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 6 PY 1996 VL 93 IS 3 BP 1006 EP 1011 DI 10.1073/pnas.93.3.1006 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU640 UT WOS:A1996TU64000009 PM 8577704 ER PT J AU Wu, YM Kirkman, LA Wellems, TE AF Wu, YM Kirkman, LA Wellems, TE TI Transformation of Plasmodium falciparum malaria parasites by homologous integration of plasmids that confer resistance to pyrimethamine SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE transfection; dihydrofolate reductase thymidylate synthase; episomes; drug resistance ID THYMIDYLATE SYNTHASE GENE; TRYPANOSOMA-BRUCEI; TOXOPLASMA-GONDII; MOLECULAR-BASIS; TRANSFECTION; MUTATIONS; RECOMBINATION; REPLACEMENT; CYCLOGUANIL; EXPRESSION AB Plasmodium falciparum malaria parasites were transformed with plasmids containing P, falciparum or Toxoplasma gondii dihydrofolate reductase-thymidylate synthase (dhfr-ts) coding sequences that confer resistance to pyrimethamine, Under pyrimethamine pressure, transformed parasites were obtained that maintained the transfected plasmids as unrearranged episomes for several weeks, These parasite populations were replaced after 2 to 3 months by parasites that had incorporated the transfected DNA into nuclear chromosomes, Depending upon the particular construct used for transformation, homologous integration was detected in the P, falciparum dhfr-ts locus (chromosome 4) or in hrp3 and hrp2 sequences that were used in the plasmid constructs as gene control regions (chromosomes 13 and 8, respectively), Transformation by homologous integration sets the stage for targeted gene alterations and knock-outs that will advance understanding of P, falciparum. RP Wu, YM (reprint author), NIAID,NIH,PARASIT DIS LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 30 TC 299 Z9 304 U1 1 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 6 PY 1996 VL 93 IS 3 BP 1130 EP 1134 DI 10.1073/pnas.93.3.1130 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU640 UT WOS:A1996TU64000032 PM 8577727 ER PT J AU Clubb, RT Mizuuchi, M Huth, JR Omichinski, JG Savilahti, H Mizuuchi, K Clore, GM Gronenborn, AM AF Clubb, RT Mizuuchi, M Huth, JR Omichinski, JG Savilahti, H Mizuuchi, K Clore, GM Gronenborn, AM TI The wing of the enhancer-binding domain of Mu phage transposase is flexible and is essential for efficient transposition SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE helix-turn-helix; mutagenesis; NMR; heteronuclear relaxation ID MODEL-FREE APPROACH; BACKBONE DYNAMICS; BACTERIOPHAGE-MU; NMR-SPECTROSCOPY; DNA; RELAXATION; PROTEINS; CLEAVAGE; ENDS AB A tetramer of the Mu transposase (MuA) pairs the recombination sites, cleaves the donor DNA, and joins these ends to a target DNA by strand transfer, Juxtaposition of the recombination sites is accomplished by the assembly of a stable synaptic complex of MuA protein and Mu DNA, This initial critical step is facilitated by the transient binding of the N-terminal domain of MuA to an enhancer DNA element within the Mu genome (called the internal activation sequence, IAS). Recently we solved the three-dimensional solution structure of the enhancer-binding domain of Mu phage transposase (residues 1-76, MUA(76)) and proposed a model for its interaction with the IAS element, Site-directed mutagenesis coupled with an in vitro transposition assay has been used to assess the validity of the model, We have identified five residues on the surface of MuA that are crucial for stable synaptic complex formation but dispensable for subsequent events in transposition. These mutations are located in the loop (wing) structure and recognition helix of the MUA(76) domain of the transposase and do not seriously perturb the structure of the domain, Furthermore, in order to understand the dynamic behavior of the MUA(76) domain prior to stable synaptic complex formation, we have measured heteronuclear N-15 relaxation rates for the unbound MUA(76) domain, In the DNA free state the backbone atoms of the helix-turn-helix motif are generally immobilized whereas the residues in the wing are highly flexible on the pico- to nanosecond time scale, Together these studies define the surface of MuA required for enhancement of transposition in vitro and suggest that a flexible loop in the MuA protein required for DNA recognition may become structurally ordered only upon DNA binding. C1 NIDDKD,NIH,CHEM PHYS LAB,BETHESDA,MD 20892. NIDDKD,NIH,MOLEC BIOL LAB,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 26 TC 15 Z9 16 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 6 PY 1996 VL 93 IS 3 BP 1146 EP 1150 DI 10.1073/pnas.93.3.1146 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU640 UT WOS:A1996TU64000035 PM 8577730 ER PT J AU Wersto, RP Rosenthal, ER Crystal, RG Spring, KR AF Wersto, RP Rosenthal, ER Crystal, RG Spring, KR TI Uptake of fluorescent dyes associated with the functional expression of the cystic fibrosis transmembrane conductance regulator in epithelial cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE gene therapy ID CFTR CHLORIDE CHANNEL; MULTIDRUG-RESISTANCE; PLASMA-MEMBRANE; PORE BEHAVIOR; GENE; CL; TRANSPORT; PATTERNS; PROTEIN AB Specific mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), the most common autosomal recessive fatal genetic disease of Caucasians, result in the loss of epithelial cell adenosine 3',5'-cyclic-monophosphate (cAMP)-stimulated Cl- conductance. We show that the influx of a fluorescent dye, dihydrorhodamine 6G (dR6G), is increased in cells expressing human CFTR after retrovirus- and adenovirus-mediated gene transfer. dR6G influx is stimulated by cAMP and is inhibited by antagonists of cAMP action, Dye uptake is ATP-dependent and inhibited by Cl- removal or the addition of 10 mM SCN-. Increased staining is associated with functional activation of CFTR Cl- permeability, dR6G staining enables both the fluorescent assessment of CFTR function and the identification of successfully corrected cells after gene therapy. C1 NHLBI,NIH,PULM BRANCH,BETHESDA,MD 20892. NHLBI,NIH,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. NR 33 TC 14 Z9 16 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 6 PY 1996 VL 93 IS 3 BP 1167 EP 1172 DI 10.1073/pnas.93.3.1167 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU640 UT WOS:A1996TU64000039 PM 8577734 ER PT J AU Segal, ED Falkow, S Tompkins, LS AF Segal, ED Falkow, S Tompkins, LS TI Helicobacter pylori attachment to gastric cells induces cytoskeletal rearrangements and tyrosine phosphorylation of host cell proteins SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CAMPYLOBACTER-PYLORI; EPITHELIAL-CELLS; GNOTOBIOTIC PIGLETS; EUKARYOTIC CELLS; BACTERIAL UPTAKE; ADHERENCE; INTERNALIZATION; PHAGOCYTOSIS; ADHESION; INVASION AB The consequences of Helicobacter pylori attachment to human gastric cells were examined by transmission electron microscopy and immunofluorescence microscopy, H. pylori attachment resulted in (i) effacement of microvilli at the site of attachment, (ii) cytoskeletal rearrangement directly beneath the bacterium, and (iii) cup/pedestal formation at the site of attachment, Double-immunofluorescence studies revealed that the cytoskeletal components actin, alpha-actinin, and talin are involved in the process, Immunoblot analysis showed that binding of H. pylori to AGS cells induced tyrosine phosphorylation of two host cell proteins of 145 and 105 kDa. These results indicate that attachment of H. pylori to gastric epithelial cells resembles that of enteropathogenic Escherichia coli, Coccoid H. pylori, which are thought to be terminally differentiated bacterial forms, are capable of binding and inducing cellular changes of the same sort as spiral H. pylori, including tyrosine phosphorylation of host proteins. C1 STANFORD UNIV, SCH MED, CTR DIGEST DIS, STANFORD, CA 94305 USA. STANFORD UNIV, SCH MED, DEPT MED, STANFORD, CA 94305 USA. NIAID, NIH, ROCKY MT LAB, HAMILTON, MT 59840 USA. RP Segal, ED (reprint author), STANFORD UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA. FU NIAID NIH HHS [AI23796]; NIDDK NIH HHS [DK 38707] NR 32 TC 224 Z9 233 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 6 PY 1996 VL 93 IS 3 BP 1259 EP 1264 DI 10.1073/pnas.93.3.1259 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TU640 UT WOS:A1996TU64000056 PM 8577751 ER PT J AU Balow, JP Kearse, KP AF Balow, JP Kearse, KP TI Isolation of newly expressed surface T cell antigen receptor complexes by serial precipitation with anti-TCR antibodies and immobilized streptavidin SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE T cell antigen receptor complex; surface transport; streptavidin; biotinylation ID PROTEIN AB Expression of the multisubunit T cell antigen receptor (TCR) complex is an enigmatic process requiring coordinated regulation of at least six different gene products (alpha, beta, gamma, delta, epsilon, and zeta), the ordered pairing of partner chains within the endoplasmic reticulum (ER), and intracellular transport of complete, but not incomplete, TCR complexes to the cell surface. Movement of nascent TCR glycoproteins from the ER to the Golgi compartment is easily studied using various lectins and/or glycosidases specific for oligosaccharide modifications that occur within the Golgi system. In contrast, cell surface transport of TCR complexes is relatively difficult to assess, since this requires physical separation of intracellular complexes from surface TCR complexes. In the current report we describe a method for the isolation of newly transported surface TCR complexes which utilizes metabolic and surface labeling techniques in conjunction with serial precipitation methods. Specifically, we describe the use of anti-TCR antibodies and immobilized streptavidin to isolate nascent TCR alpha proteins localized on the plasma membrane. This technique is rapid, specific, and provides a novel approach for studying the intracellular transport of nascent immune receptor molecules to the cell surface. C1 NCI,EXPTL IMMUNOL BRANCH,NIH,BETHESDA,MD 20892. NR 23 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD FEB 5 PY 1996 VL 189 IS 2 BP 251 EP 258 DI 10.1016/0022-1759(95)00255-3 PG 8 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA TY911 UT WOS:A1996TY91100010 PM 8613676 ER PT J AU Butler, AA Funk, B Breier, BH LeRoith, D Roberts, CT Gluckman, PD AF Butler, AA Funk, B Breier, BH LeRoith, D Roberts, CT Gluckman, PD TI Growth hormone (GH) status regulates GH receptor and GH binding protein mRNA in a tissue- and transcript-specific manner but has no effect on insulin-like growth factor-I receptor mRNA in the rat SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE GH; (GH binding protein); (GH receptor); (IGF-I receptor); mRNA; rat ID GENE-EXPRESSION; IGF-I; MESSENGER-RNA; DOWN-REGULATION; SOMATOMEDIN-C; LIVER; SERUM; SECRETION; SITES; ACID AB The effect of growth hormone-deficiency (GHD) and treatment with recombinant bovine GH (bGH) or human IGF-I (hIGF-I) for 10 days on the expression of GH receptor (GHR), GH binding protein (GHBP) and of insulin-like growth factor-I receptor (IGF-IR) mRNA was examined using dw/dw and normal Lewis rats. Hepatic GHR and GHBP mRNA expression was significantly lower in dw/dw rats in comparison to Lewis rats (P < 0.01) while specific I-125-bGH binding to hepatic microsomal membranes was significantly higher (P < 0.01), suggesting a reduction in hepatic GHR turnover with GHD. Treatment with bGH reduced hepatic specific I-125-bGH binding in dw/dw rats, but had no effect in Lewis rats. Treatment with hIGF-I increased hepatic specific I-125-bGH binding in Lewis rats. Hepatic GHR and GHBP mRNA expression was not changed by bGH or hIGF-I treatment, suggesting that differences in hepatic specific I-125-bGH binding may be due to posttranscriptional mechanisms. GHBP mRNA expression was higher in kidney, heart, and muscle of dw/dw rats in comparison to Lewis rats (P < 0.01), while GHR mRNA abundance was not changed. Treatment of dw/dw rats with hIGF-I or bGH resulted in a coordinate reduction of GHR and GHBP mRNAs in kidney (P < 0.01). IGF-IR mRNA was nor detected in liver and despite reduced plasma IGF-I levels and IGF-I mRNA expression IGF-IR mRNA abundance was not changed in nonhepatic tissues by GHD. Our data suggest that changes in plasma IGF-I levels and local IGF-I mRNA do not influence IGF-IR mRNA expression, while GHR and GHBP mRNA expression in different rat tissues are regulated independently. The increased nonhepatic GHBP mRNA expression with GHD suggests that nonhepatic GHBP may have an important physiological function distinct from that of GHBP in liver or in plasma. C1 UNIV AUCKLAND,SCH MED,RES CTR DEV MED & BIOL,AUCKLAND,NEW ZEALAND. NIDDKD,DIABET BRANCH,NIH,BETHESDA,MD 20892. RI Breier, Bernhard/D-1176-2009; OI Roberts, Charles/0000-0003-1756-5772 NR 44 TC 20 Z9 21 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0303-7207 J9 MOL CELL ENDOCRINOL JI Mol. Cell. Endocrinol. PD FEB 5 PY 1996 VL 116 IS 2 BP 181 EP 189 DI 10.1016/0303-7207(95)03713-6 PG 9 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA TW846 UT WOS:A1996TW84600007 PM 8647318 ER PT J AU Kraemer, KH AF Kraemer, KH TI Xeroderma pigmentosum knockouts SO LANCET LA English DT Editorial Material RP Kraemer, KH (reprint author), NCI,MOLEC CARCINOGENESIS LAB,BLDG 37,BETHESDA,MD 20892, USA. FU Intramural NIH HHS [Z01 BC004517-31] NR 12 TC 9 Z9 9 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD FEB 3 PY 1996 VL 347 IS 8997 BP 278 EP 279 DI 10.1016/S0140-6736(96)90462-6 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA TT485 UT WOS:A1996TT48500005 PM 8569358 ER PT J AU Chen, HW Sandler, DP Taylor, JA Shore, DL Liu, E Bloomfield, CD Bell, DA AF Chen, HW Sandler, DP Taylor, JA Shore, DL Liu, E Bloomfield, CD Bell, DA TI Increased risk for myelodysplastic syndromes in individuals with glutathione transferase theta 1 (GSTT1) gene defect SO LANCET LA English DT Article ID EXPOSURE; CARCINOGENESIS; SUSCEPTIBILITY; CANCER AB Background The glutathione S-transferases (GST) mediate exposure to various cytotoxic and genotoxic agents, including those associated with increased risk of the myelodysplastic syndromes (MDS). Both GST M1 (GSTM1) and GST theta 1 (GSTT1) genes have a ''null'' variant allele, in which the entire gene is absent. We tested whether the homozygous null genotype of GSTM1 and GSTT1 altered the risk for MDS. Methods In a hospital-based case-control study we analysed lymphocyte or bone-marrow DNA samples from 96 patients with MDS and 201 cancer-free controls of similar, age, race, and sex. We have restricted our report to the 92 white MDS patients. We analysed GSTM1 and GSTT1 genotypes by PCR. Findings The frequency of the GSTT1 null genotype was higher among MDS cases (46%) than among controls (16%). Inheritance of the GSTT1 null genotype conferred a 4.3-fold risk of MDS (odds ratio 4.3, 95% CI 2.5-7.4, p<0.00001). The GSTM1 null genotype was not associated with increased risk of MDS (odds ratio 0.8, 0.5-1.3). Interpretation Individuals with the GSTT1 null genotype may have enhanced susceptibility to MDS. The mechanism might involve decreased detoxification of environmental or endogenous carcinogens. C1 NIEHS,RES TRIANGLE PK,NC 27709. WESTAT CORP,RES TRIANGLE PK,NC. UNIV N CAROLINA,CHAPEL HILL,NC. ROSWELL PK CANC INST,BUFFALO,NY 14263. CANC & LEUKEMIA GRP B,DURHAM,NC. RI Liu, Edison/C-4141-2008; OI taylor, jack/0000-0001-5303-6398; Sandler, Dale/0000-0002-6776-0018 NR 20 TC 243 Z9 255 U1 0 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD FEB 3 PY 1996 VL 347 IS 8997 BP 295 EP 297 DI 10.1016/S0140-6736(96)90468-7 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA TT485 UT WOS:A1996TT48500011 PM 8569364 ER PT J AU Wu, T Ikezono, T Angus, CW Shelhamer, JH AF Wu, T Ikezono, T Angus, CW Shelhamer, JH TI Tumor necrosis factor-alpha induces the 85-kDa cytosolic phospholipase A(2) gene expression in human bronchial epithelial cells SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE tumor necrosis factor; phospholipase A(2); arachidonic acid; airway epithelial cell ID PROTEIN-KINASE-C; STIMULATES EICOSANOID PRODUCTION; PLATELET-ACTIVATING-FACTOR; ARACHIDONIC-ACID; HUMAN-FIBROBLASTS; GROWTH-FACTOR; CALPHOSTIN-C; RELEASE; PROSTAGLANDIN-E(2); BIOSYNTHESIS AB Phospholipase A(2) (PLA(2)) activity has been suggested to mediate some of the tumor necrosis factor (TNF) induced cellular responses including cytotoxicity. We evaluated the induction of both the 85-kDa cytosolic phospholipase A(2) (cPLA(2)) and non-pancreatic group IT PLA(2) gene expression by TNF-alpha in a human bronchial epithelial cell line (BEAS 2B cell). TNF-alpha (20 ng/ml) induced a significantly increased release of prelabeled [H-3]arachidonic acid (AA) following 4-24 h incubation. Calcium ionophore A23187 (10(-5) M) further increased the [H-3]AA release from the TNF-alpha-treated cells. In vitro activity assay revealed that TNF-alpha increased the dithiothreitol (DTT)-resistant PLA(2) activity which was blocked by the cPLA(2) inhibitor AACOCF(3). Treatment with TNF-alpha for 4-24 h increased the cPLA(2) protein and mRNA levels which were blocked by the broad inhibitor of protein kinases staurosporine, the protein kinase C (PKC) inhibitor calphostin C, and to a lesser extent the calcium/calmodulin-dependent protein kinase inhibitor W-7. Reverse transcription and polymerase chain reaction amplification of the group II PLA(2) mRNA showed that it is expressed in human lung but not in the bronchial epithelial cell line. TNF-alpha failed to induce the expression of group II PLA(2) in the BEAS 2B cells. These results demonstrate that the cPLA(2) gene expression is up-regulated by TNF-alpha and this effect may contribute to the TNF-alpha stimulated AA release in airway epithelial cells. C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 53 TC 53 Z9 53 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4889 J9 BBA-MOL CELL RES JI Biochim. Biophys. Acta-Mol. Cell Res. PD FEB 2 PY 1996 VL 1310 IS 2 BP 175 EP 184 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TX416 UT WOS:A1996TX41600001 PM 8611631 ER PT J AU Pato, MD Sellers, JR Preston, YA Harvey, EV Adelstein, RS AF Pato, MD Sellers, JR Preston, YA Harvey, EV Adelstein, RS TI Baculovirus expression of chicken nonmuscle heavy meromyosin II-B - Characterization of alternatively spliced isoforms SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MYOSIN LIGHT CHAIN; PROTEIN-KINASE-C; SMOOTH-MUSCLE; PHOSPHORYLATION; REGION; ACTIN; CDNA; SUBFRAGMENT-1; NUCLEOTIDE; DIVERSITY AB We have expressed two truncated isoforms of chicken nonmuscle myosin II-B using the baculovirus expression system, One of the expressed heavy meromyosins (HMM(exp)) consists of two 150-kDa myosin heavy chains (MHCs), comprising amino acids 1-1231 as well as two pairs of 20-kDa and 17-kDa myosin light chains (MLCs) in a 1:1:1 molar ratio, The second HMM(exp) was identical except that it contained an insert of 10 amino acids (PESPKPVKHQ) at the 25-50-kDa domain boundary in the subfragment-1 region of the MHC. These 10 amino acids include a consensus sequence (SPK) for proline directed kinases, Expressed HMMs were soluble at low ionic strength and bound to rabbit skeletal muscle actin in an ATP-dependent manner, These properties afforded a rapid purification of milligram quantities of expressed protein, Both isoforms were capable of moving actin filaments in an in vitro motility assay and manifested a greater than 20-fold activation of actin-activated MgATPase activity following phosphorylation of the 20-kDa MLC. HMM(exp) with the 10-amino acid insert was phosphorylated by Cdc2, Cdk5, and mitogen-activated protein kinase in vitro to 0.3-0.4 mol of PO4/mol of MHC The site phosphorylated in the MHC was identified as the serine residue present in the 10-amino acid insert and its presence was confirmed in bovine brain MHCs. Characterization of the baculovirus expressed noninserted and inserted MHC isoforms with respect to actin-activated MgATPase activity and ability to translocate actin filaments in an in vitro motility assay produced the following average values following MLC phosphorylation: noninserted HMM(exp), V-max 0.28 s(-1), K-m = 12.7 mu M; translocation rate = 0.077 mu m/s; inserted HMM(exp) V-max = 0.37 s(-1), K-m = 15.1 mu M; translocation rate = 0.092 mu m/s. C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. OI Adelstein, Robert/0000-0002-8683-2144 NR 44 TC 54 Z9 54 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 2 PY 1996 VL 271 IS 5 BP 2689 EP 2695 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TT488 UT WOS:A1996TT48800056 PM 8576242 ER PT J AU Oka, H Ikai, Y Hayakawa, J Harada, K Suzuki, M Shimizu, A Hayashi, T Takeba, K Nakazawa, H Ito, Y AF Oka, H Ikai, Y Hayakawa, J Harada, K Suzuki, M Shimizu, A Hayashi, T Takeba, K Nakazawa, H Ito, Y TI Separation of ivermectin components by high-speed counter-current chromatography SO JOURNAL OF CHROMATOGRAPHY A LA English DT Article ID COIL PLANET CENTRIFUGE AB High-speed counter-current chromatography (HSCCC) has been successfully applied to the separation of the ivermectin components. A 25-mg quantity of the sample was separated using a two-phase solvent system of n-hexane-ethyl acetate-methanol-water (19:1:10:10, v/v). The fractions were analyzed by high-performance liquid chromatography, nuclear magnetic resonance, and fast-atom bombardment mass spectrometry. The separation yielded 18.7 mg of 99.9% pure ivermectin Bla, 1.0 mg of 96.0% pure ivermectin Bib, and 0.3 mg of 98.0% pure avermectin Bla (precursor of ivermectin). C1 MEIJO UNIV,FAC PHARM,TEMPAKU KU,NAGOYA,AICHI 468,JAPAN. ICHIMIYA PUBL HLTH CTR,ICHIMIYA,AICHI 491,JAPAN. TOKYO METROPOLITAN RES LAB PUBL HLTH,SHINJUKU KU,TOKYO 169,JAPAN. HOSHI UNIV,FAC PHARMACEUT SCI,SHINAGAWA KU,TOKYO 142,JAPAN. NHLBI,NIH,BIOPHYS CHEM LAB,BETHESDA,MD 20892. RP Oka, H (reprint author), AICHI PREFECTURAL INST PUBL HLTH,KITA KU,TSUJI MACHI,NAGOYA,AICHI 462,JAPAN. NR 11 TC 13 Z9 15 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 J9 J CHROMATOGR A JI J. Chromatogr. A PD FEB 2 PY 1996 VL 723 IS 1 BP 61 EP 68 DI 10.1016/0021-9673(95)00803-9 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA TW152 UT WOS:A1996TW15200008 ER PT J AU Viswanadhan, VN Reddy, MR Wlodawer, A Varney, MD Weinstein, JN AF Viswanadhan, VN Reddy, MR Wlodawer, A Varney, MD Weinstein, JN TI An approach to rapid estimation of relative binding affinities of enzyme inhibitors: Application to peptidomimetic inhibitors of the human immunodeficiency virus type 1 protease SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID FREE-ENERGY PERTURBATION; ATOMIC SOLVATION PARAMETERS; SYNTHETIC HIV-1 PROTEASE; MOLECULAR-DYNAMICS; DIHYDROFOLATE-REDUCTASE; QUANTITATIVE STRUCTURE; CRYSTAL-STRUCTURE; NUCLEIC-ACIDS; SURFACE-AREA; PROTEINS AB This report describes a method for rapid assessment of the binding affinities of a series of analogous ligands to an enzyme. This approach is based on two variables (scores), representing (i) the enthalpy of binding and (ii) the strength of hydrophobic interaction. The method is then used to evaluate the binding of 11 different peptidomimetic inhibitors to the HIV-1 protease. Three-dimensional structures of these enzyme-inhibitor complexes are modeled based on the crystal structures of HIV-1 protease complexes with the known inhibitors. These structures are minimized using the AMBER force field, and the scores of binding enthalpy for each of the ligands are calculated. A second score to represent the hydrophobic interaction between a pair of atoms uses an exponential function of distance between the atoms and the product of their atomic hydrophobicity constants. This exponential function is used to assess the hydrophobic interaction energy between an enzyme and its inhibitor and also to compute and display a 'molecular hydrophobicity map' as a 3D visualization tool. These methods are then applied to obtain trends in relative binding affinities of pairs of analogous inhibitors. Calculated scores agree well with corresponding results from thermodynamic cycle perturbation (TCP) simulations as well as experimental binding data. Since the proposed calculations are computationally cheaper and faster than TCP calculations, it is suggested that these scores can farm the basis for rapid, preliminary theoretical screening of proposed derivatives of an inhibitor prior to TCP analysis, synthesis, and testing. C1 AGOURON PHARMACEUT INC,SAN DIEGO,CA 92121. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD 21702. RP Viswanadhan, VN (reprint author), NCI,DEV THERAPEUT PROGRAM,NATL INST HLTH,MOLEC PHARMACOL LAB,BETHESDA,MD 20892, USA. NR 57 TC 35 Z9 36 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD FEB 2 PY 1996 VL 39 IS 3 BP 705 EP 712 DI 10.1021/jm940778t PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA TT921 UT WOS:A1996TT92100010 PM 8576913 ER PT J AU Breveglieri, A Guerrini, R Salvadori, S Bianchi, C Bryant, SD Attila, M Lazarus, LH AF Breveglieri, A Guerrini, R Salvadori, S Bianchi, C Bryant, SD Attila, M Lazarus, LH TI Design and synthesis of 1-aminocycloalkane-1-carboxylic acid-substituted deltorphin analogues: Unique delta and mu opioid activity in modified peptides SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID HIGH-AFFINITY; CONFORMATIONAL PROPERTIES; RECEPTOR SELECTIVITY; AMPHIBIAN SKIN; BINDING; DERMENKEPHALIN; DERMORPHIN; REQUIREMENTS; SEQUENCE; FEATURES AB Deltorphin analogues were substituted by a series of achiral C-alpha,C-alpha-dialkyl cyclic alpha-amino acids (1-aminocycloalkane-1-carbaxylic acids, Ac(x)c, where (x) = a hexane, pentane, or propane cycloalkane ring) in position 2, 3, 4, or 2 and 3 in deltorphin C, and in position 2 in [Ac(6)(c)2,- des-Phe(3)]deltorphin C hexapeptide. Receptor assays indicated that even though Ac(6)c(2) and Ac(6)c(3) exhibited a diminished K-i delta by ca. 20-fold (2.5-3.3 nM) relative to deltorphin C (K-i delta = 0.15 nM), selectivity was marginally elevated (K-i mu/K-i delta = 1250) or enhanced by about 70%, and both peptides fitted stringent iterative calculations for a two-site binding model (eta = 0.625 and 0.766, respectively, P < 0.0001). The disubstituted [Ac(6)c(2,3)]- or [Ac(6)c(2),des-Phe(3)]deltorphin analogues yielded peptides with decreased K-i delta, such that the latter peptide was essentially inactive. The presence of Ac(5)c or Ac(3)c in place of Phe(3) further diminished K-i delta (15.4 to 19.0 nM), yet delta selectivity only fell about one-half(K-i mu/K-i delta = 440 and 535, respectively), and only the former peptide fitted a two-site binding model (eta = 0.799). The replacement of Asp(4) by Ac(6)c, Ac5c, or Ac(3)c produced essentially nonselective analogues through the acquisition of high mu affinities (2.5, 0.58, and 0.27 nM, respectively) while maintaining high delta affinities (K-i delta = 0.045-0;054 nM) which were about 3 fold greater than that of deltorphin C. Using pharmacological assays in vitro (mouse vas deferens and guinea pig ileum), position 3-substituted analogues all indicated substantial losses in bioactivity, whereas substitution by 1-aminocycloalkanes at the fourth position retained high delta activity. In fact, the bioactivity of [Ac(3)c(4)]deltorphin C indicated a peptide with relatively weak delta selectivity, which was comparable to the observations with the receptor binding data. In summary, the data confirmed that (i) delta selectivity occurs in the absence of D-chirality at position 2, (ii) the aromaticity of Phe(3) is replaceable by an achiral residue with a hydrophobic ring-saturated side chain, and (iii) the acquisition of dual high-affinity analogues occurs through the elimination of the anionic function at position 4 and replacement by an amino acid with a hydrophobic side chain. C1 NIEHS,PEPTIDE NEUROCHEM SECT,RES TRIANGLE PK,NC 27709. UNIV FERRARA,DEPT PHARMACEUT SCI,I-44100 FERRARA,ITALY. UNIV FERRARA,INST PHARMACOL,I-44100 FERRARA,ITALY. UNIV HELSINKI,DEPT PHARM,DIV PHARMACOL & TOXICOL,SF-00014 HELSINKI,FINLAND. OI Guerrini, Remo/0000-0002-7619-0918 NR 51 TC 31 Z9 31 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD FEB 2 PY 1996 VL 39 IS 3 BP 773 EP 780 DI 10.1021/jm950490j PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA TT921 UT WOS:A1996TT92100017 PM 8576920 ER PT J AU Ji, XD Melman, N Jacobson, KA AF Ji, XD Melman, N Jacobson, KA TI Interactions of flavonoids and other phytochemicals with adenosine receptors SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID MOLECULAR-CLONING; RAT-BRAIN; ANTAGONISTS; ADENOSINE-A1-RECEPTOR; INHIBITION AB Flavone derivatives and other phytochemicals were found to bind to three subtypes of adenosine receptors in the micromolar range. Affinity was determined in radioligand binding assays at rat brain A(1) and A(2A) receptors using [H-3]-N-6-PIA ([H-3]-(R)-N-6-phenylisopropyladenosine) and [H-3]CGS21680 ([H-3]-2-[[4-(2-carboxyethyl)phenyl]ethyl respectively. Affinity was determined at cloned human and rat brain A(3) receptors using [I-125]-AB-MECA [N-6-(4-amino-3-iodobenzyl)adenosine-5'(N-methyluronamide)]. A structure-activity analysis indicated that the hydroxyl groups of naturally occurring flavones are not essential for affinity at adenosine receptors. Galangin, 14, displayed K-i values of 1 mu M at both rat A(1) and A(2A) receptors and 3 mu M at human A(3) receptors. Methylation but not acetylation of the hydroxyl groups of galangin enhanced A(3) affinity. Pentamethylmorin, 20, appeared to bind with 14-17-fold selectivity for human A(3) receptors vs rat A(1) and A(2A) receptors, with a K-i value of 2.65 mu M. Two flavone derivatives (14 and 15) showed 14-fold greater affinity at human vs rat A(3) receptors. Reduction of the 2,3-olefinic bond, as in (+/-)-dihydroquercetin, or glycosidation, as in robinin, greatly diminished affinity. An isoflavone, genistein, also bound only very weakly at 47 receptors. alpha-Naphthoflavone had greater receptor affinity (0.79 mu M at A(1) receptors) than the beta-isomer. Other natural products of plant origin, including oxogalanthine lactam, hematoxylin, and arborinine were found to bind to A(1) adenosine receptors with K-i values of 3-13 mu M. These findings indicate that the flavones, flavonols, flavanones, and other phytochemicals may provide leads for the development of novel adenosine antagonists. The unexpected finding of considerable affinity of flavones at both rat and human A(3) receptors may explain some of the previously observed biological effects of these compounds. C1 NIDDK,MOLEC RECOGNIT SECT,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999] NR 51 TC 79 Z9 81 U1 0 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD FEB 2 PY 1996 VL 39 IS 3 BP 781 EP 788 DI 10.1021/jm950661k PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA TT921 UT WOS:A1996TT92100018 PM 8576921 ER PT J AU Baraldi, PG Cacciari, B Spalluto, G Ji, XD Olah, ME Stiles, G Dionisotti, S Zocchi, C Ongini, E Jacobson, KA AF Baraldi, PG Cacciari, B Spalluto, G Ji, XD Olah, ME Stiles, G Dionisotti, S Zocchi, C Ongini, E Jacobson, KA TI Novel N-6-(substituted-phenylcarbamoyl)adenosine-5'-uronamides as potent agonists for A(3) adenosine receptors SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID MOLECULAR-CLONING; ANTAGONISTS; DERIVATIVES; A2-RECEPTORS; A1-ADENOSINE; EXPRESSION; SUBCLASSES; BRAIN; CDNA; A1 AB A series of adenosine-5'-uronamide derivatives bearing N-6-phenylurea groups have been synthesized and tested for their affinity at A(1) and A(2A) adenosine receptors in rat brain membranes and at cloned rat A(3) receptors from stably transfected CHO cells. Some N-6-arylcarbamoyl derivatives, N-6-((2-chlorophenyl)carbamoyl)-, N-6-((3-chlorophenyl)carbarmoyl)-, and N-6-((4-methoxyphenyl)carbamoyl)adenosine-5'-ethyluronamide (41-n), were found to have affinity at A(3) receptors in the low nanomolar range (K-i values < 10 nM). In CHO cells stably transfected with the rat A(3) receptor, compound 4n was found to be a full agonist in inhibiting adenylate cyclase activity. The present study represents the first example of N-6-acyl-substituted adenosine analogs having high affinity at adenosine receptors and, in particular, at the A(3) receptor subtype. C1 NIDDKD,BIOORGAN CHEM LAB,MOLEC RECOGNIT SECT,NATL INST HLTH,BETHESDA,MD 20892. SCHERING PLOUGH SPA,RES LABS,I-20060 COMAZZO,ITALY. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT PHARMACOL,DURHAM,NC 27710. RP Baraldi, PG (reprint author), UNIV FERRARA,DIPARTIMENTO SCI FARMACEUT,VIA FOSSATO MORTARA 17-19,I-44100 FERRARA,ITALY. RI Jacobson, Kenneth/A-1530-2009; Baraldi, Pier Giovanni/B-7933-2017 OI Jacobson, Kenneth/0000-0001-8104-1493; FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999] NR 42 TC 46 Z9 46 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD FEB 2 PY 1996 VL 39 IS 3 BP 802 EP 806 DI 10.1021/jm950518r PG 5 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA TT921 UT WOS:A1996TT92100021 PM 8576924 ER PT J AU Troncoso, JC Kawas, CH Chang, CK Folstein, MF Hedreen, JC AF Troncoso, JC Kawas, CH Chang, CK Folstein, MF Hedreen, JC TI Lack of association of the apoE4 allele with hippocampal sclerosis dementia SO NEUROSCIENCE LETTERS LA English DT Article DE aging; Alzheimer's disease; frontal lobe dementia; neurodegeneration ID APOLIPOPROTEIN-E GENOTYPE; ALZHEIMERS-DISEASE; EPSILON-4 AB We determined the apolipoprotein E4 (apoE) genotype in 12 cases of autopsy-confirmed hippocampal sclerosis dementia (HSD), a disorder characterized pathologically by neuronal degeneration, predominantly of temporal lobe structures, without senile plaques or neurofibrillary tangles. The frequency of the apoE4 allele in HSD was 12.5%, similar to that of a control population and significantly different from the similar to 40% found in Alzheimer's disease (AD) (P < 0.001). These observations suggest that apoE4 is not a risk factor for HSD. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,NIA,CTR GERONTOL RES,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,RUSH ALZHEIMERS DIS CTR,BALTIMORE,MD 21205. MIT,CAMBRIDGE,MA 02139. RP Troncoso, JC (reprint author), JOHNS HOPKINS UNIV,SCH MED,NEUROPATHOL LAB,558 ROSS RES BLDG,720 RUTLAND AVE,BALTIMORE,MD 21205, USA. FU NIA NIH HHS [AG07914, AG08325, AG05146] NR 24 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD FEB 2 PY 1996 VL 204 IS 1-2 BP 138 EP 140 DI 10.1016/0304-3940(96)12331-4 PG 3 WC Neurosciences SC Neurosciences & Neurology GA TV439 UT WOS:A1996TV43900035 PM 8929997 ER PT J AU Muller, DC Elahi, D Tobin, JD Andres, R AF Muller, DC Elahi, D Tobin, JD Andres, R TI Insulin response during the oral glucose tolerance test: The role of age, sex, body fat and the pattern of fat distribution SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE tolerance test; insulin; obesity; fat distribution ID DEPENDENT DIABETES-MELLITUS; CARDIOVASCULAR RISK-FACTORS; OBESITY; INTOLERANCE; RESISTANCE; MEN; HYPERINSULINEMIA; DENSITY AB To clarify their primary roles on insulin response to oral glucose, age and sex differences in body composition should be taken into account. Oral glucose tolerance rests were performed on 472 men and 299 women of the Baltimore Longitudinal Study of Aging, ranging in age from 20 to 96 years. Subjects who were taking medications or had any diseases which could affect glucose tolerance were excluded. In addition to insulin and glucose values for the glucose tolerance test, we calculated body mass index (BMI), percentage body fat from skinfolds (% Body Fat), waist hip ratio (WHR), mean glucose level over the 2-hour test (G(M)), the basal insulin (I-o), and the mean insulin response over the 2-hour test (I-M). There was no significant sex difference in mean age, but men had significantly higher BMI (25.6 vs 24.0 kg/m(2)), WHR (0.93 vs 0.76), and G(M) (8.5 vs 7.7 mM), while % Body Fat was lower (25% vs 33%). Unadjusted I-o and I-M levels were significantly higher in men than in women (51 vs 44 and 303 vs 231 pM - antilogs of log-normalized values). Insulin levels, adjusted for differences in age, % Body Fat, WHR, and G(M) by analysis of covariance, however, showed no sex differences (49 vs 46 and 282 vs 257 pM). Adjusted insulin levels declined significantly with age; I-M fell progressively from 323 pM in 20 to 39-year olds, 267 pM in 40 to 59-year, 253 pM in 60 to 79-years, and 228 pM in 80 to 96-year olds (p<0.01). We conclude that the sex differences in insulin levels are explained by differences in body habitus and post-load glucose levels, but that insulin levels decline with age per se. RP Muller, DC (reprint author), NIA,GERONTOL RES CTR,NIH,LAB CLIN PHYSIOL,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 33 TC 36 Z9 37 U1 0 U2 1 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD FEB PY 1996 VL 8 IS 1 BP 13 EP 21 PG 9 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA TZ831 UT WOS:A1996TZ83100002 PM 8695671 ER PT J AU Espey, MG Tang, Y Morse, HC Moffett, JR Namboodiri, MAA AF Espey, MG Tang, Y Morse, HC Moffett, JR Namboodiri, MAA TI Localization of quinolinic acid in the murine AIDS model of retrovirus-induced immunodeficiency: Implications for neurotoxicity and dendritic cell immunopathogenesis SO AIDS LA English DT Article DE AIDS; AIDS dementia complex; excitotoxicity; immunohistochemistry; interdigitating dendritic cell; murine leukemia virus; spleen ID INDOLEAMINE 2,3-DIOXYGENASE; TRYPTOPHAN DEGRADATION; HIV-1 INFECTION; SYNDROME MAIDS; RAT-BRAIN; MICE; METABOLISM; ACTIVATION; FLUID; MOUSE AB Objective and design: Using murine AIDS (MAIDS) as a model of retrovirus-induced immunodeficiency, the aims of this study were (1) to determine the cellular source(s) of quinolinic acid (Quin) with regard to its significance as a potential neuroexcitotoxin in AIDS dementia complex, and (2) to characterize the relationship between dendritic cell Quin immunoreactivity and the histopathological changes associated with the progression of disease. Methods: Mice with MAIDS were sacrificed from 1 to 16 weeks post-infection. Temporal and spatial changes in the in vivo distribution of Quin at the cellular level were determined by carbodiimide-based immunohistochemical methods. Results: Cellular Quin immunoreactivity was chronically elevated in lymphoid tissues of mice with MAIDS. In contrast, no cellular Quin immunoreactivity was visible in the brain parenchyma at any timepoint studied. Conclusion: These findings are consistent with the view that select immune cells in the peripheral lymphoid tissues may be the primary source of Quin, which may contribute to neurotoxic complications in retrovirus-induced immunodeficiency syndromes. The predominant Quin immunoreactive cell types changed with the progression of disease. A significant finding was the marked increase in the number of Quin immunoreactive dendritic cells in the early phase of MAIDS, suggesting a relationship between dendritic cells and Quin in retroviral infection. C1 NIAID,NIH,IMMUNOPATHOL LAB,BETHESDA,MD 20892. RP Espey, MG (reprint author), GEORGETOWN UNIV,DEPT BIOL,402 REISS BLDG,37TH & O ST NW,WASHINGTON,DC 20057, USA. OI Morse, Herbert/0000-0002-9331-3705 FU NIDDK NIH HHS [DK37024] NR 47 TC 24 Z9 25 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD FEB PY 1996 VL 10 IS 2 BP 151 EP 158 DI 10.1097/00002030-199602000-00004 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TW205 UT WOS:A1996TW20500004 PM 8838702 ER PT J AU Johnson, EO vandenBree, MBM Pickens, RW AF Johnson, EO vandenBree, MBM Pickens, RW TI Indicators of genetic and environmental influence in alcohol-dependent individuals SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE genetics; twins; alcohol dependence; males ID TWIN; INHERITANCE; ABUSE; RISK; AGE AB Although much is known about genetic and environmental influences in alcohol dependence at the population level, little is known about the relative contribution of such influences on individuals. As an initial step toward individual assessment, concordance for the Diagnostic Interview Schedule, version III alcohol symptoms was determined in a sample (n = 113) of male monozygotic (MZ) and dizygotic (DZ) twins. Items were assigned to a genetic or environmental scale on the basis of significant MZ/DZ differences in proband-wise concordance rates. Weights were assigned to items based on factor analyses. For the genetic scale, significant differences were found between MZ and DZ intraclass correlations. No significant differences were found between MZ and DZ correlations on the environmental scale. When scores on the environmental scale were controlled, genetic scale scores were correlated with earlier age of onset of alcohol problems and a shorter interval between first intoxication and onset of alcohol problems. When scores on the genetic scale were controlled, environmental scale scores were correlated with later age of onset of alcohol problems and a longer interval between first intoxication and onset of alcohol problems. These results suggest it is possible to assess relative influence of genetic and environmental factors in individual cases of alcohol dependence. C1 JOHNS HOPKINS UNIV,DEPT MENTAL HYG,BALTIMORE,MD 21218. RP Johnson, EO (reprint author), NATL INST DRUG ABUSE,DIV INTRAMURAL RES,POB 5180,BALTIMORE,MD 21224, USA. FU NIAAA NIH HHS [AA 06500]; NIDA NIH HHS [DA 07292] NR 34 TC 29 Z9 30 U1 1 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD FEB PY 1996 VL 20 IS 1 BP 67 EP 74 DI 10.1111/j.1530-0277.1996.tb01046.x PG 8 WC Substance Abuse SC Substance Abuse GA TX852 UT WOS:A1996TX85200014 PM 8651465 ER PT J AU Termanini, B Gibril, F Stewart, CA Weber, HC Jensen, RT AF Termanini, B Gibril, F Stewart, CA Weber, HC Jensen, RT TI A prospective study of the effectiveness of low dose omeprazole as initial therapy in Zollinger-Ellison syndrome SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS LA English DT Article ID GASTRIC-ACID SECRETION; REFLUX ESOPHAGITIS; MANAGEMENT; EFFICACY; LANSOPRAZOLE; RANITIDINE; CIMETIDINE; SAFETY; STATES AB Background: The proton pump inhibitors (omeprazole and lansoprazole) are the drugs of choice for the medical management of gastric acid hypersecretion in Zollinger-Ellison syndrome (ZES), These drugs are safe for long-term therapy but are acid-labile and high doses are expensive, The recommended starting dose of omeprazole is 60 mg/day. However, it has been shown in recent studies that the maintenance dose of omeprazole could be safely reduced to 20 mg once or twice a day in more than two-thirds of patients with ZES. The purpose of this study is to determine if an initial starting dose of omeprazole 20 mg/day is safe and effective in patients with ZES, Methods: Forty-nine consecutive patients with ZES being treated with ranitidine for at least 2 weeks were admitted to the NIH. Omeprazole 20 mg was started on day 1 of the admission and ranitidine discontinued 4 h after the first dose. Gastric acid output was measured for 1 h prior to the next omeprazole dose on day 2, then on day 3 if the value was > 10 mmol/h on the previous day. If acid-peptic symptoms developed or the gastric acid output remained > 10 mmol/h on day 3, the patient was considered to have failed omeprazole 20 mg/day initial therapy and the dose titrated daily to achieve adequate control of acid-peptic symptoms and gastric secretion. Results: In 33 of the 49 patients (68%) omeprazole 20 mg/day was successful as initial therapy. Sixteen patients (32%) failed this initial omeprazole dose (eight patients owing to persistent peptic symptoms and eight patients owing to inadequate acid control). The final daily omeprazole dose required in these patients was 40 mg in eight patients (16%), 60 mg in one patient (2%) and 80 mg in seven patients (14%), Basal acid output (BAO) was the only clinical or laboratory feature that was significantly different between the two groups in which low dose initial omeprazole therapy was or was not successful; all patients with basal acid output < 20 mmol/h had a successful outcome. Conclusions: Because of the need to rapidly control gastric acid hypersecretion owing to the high risk of complications from peptic ulcer disease, patients with ZES should continue to be started on omeprazole 60 mg/day and the dose adjusted by acute titration methods as is currently recommended. After a maintenance dose is established, attempts should be undertaken to reduce the dose to 20 mg/day once or twice a day. Only the minority of patients with ZES in whom basal acid output is known to be < 20 mmol/h (20% of patients) should be started on a low initial omeprazole dose. C1 NIDDK,NIH,DDB,BETHESDA,MD 20892. NR 44 TC 12 Z9 12 U1 0 U2 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-2813 J9 ALIMENT PHARM THERAP JI Aliment. Pharmacol. Ther. PD FEB PY 1996 VL 10 IS 1 BP 61 EP 71 PG 11 WC Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Gastroenterology & Hepatology; Pharmacology & Pharmacy GA TX821 UT WOS:A1996TX82100006 PM 8871445 ER PT J AU Kostis, JB Shelton, B Gosselin, G Goulet, C Hood, WB Kohn, RM Kubo, SH Schron, E Weiss, MB Willis, PW Young, JB Probstfield, J AF Kostis, JB Shelton, B Gosselin, G Goulet, C Hood, WB Kohn, RM Kubo, SH Schron, E Weiss, MB Willis, PW Young, JB Probstfield, J TI Adverse effects of enalapril in the studies of left ventricular dysfunction (SOLVD) SO AMERICAN HEART JOURNAL LA English DT Article ID CONGESTIVE-HEART-FAILURE; CONVERTING-ENZYME-INHIBITION; MYOCARDIAL-INFARCTION; CAPTOPRIL; THERAPY; TRIAL AB In the Studies of Left Ventricular Dysfunction (LVD), enalapril or placebo was administered in a double-blind fashion to 6797 participants with ejection fraction less than or equal to 0.35. During 40 months' average follow-up, 28.1% of participants randomized to enalapril reported side effects compared with 16.0% in the placebo group (p < 0.0001). Enalapril use was associated with a higher rate of symptoms related to hypotension (14.8% vs 7.1%, p < 0.0001), azotemia (3.8% vs 1.6%, p < 0.0001), cough (5.0% vs 2.0%, p < 0.0001), fatigue (5.8% vs 3.5%, p < 0.0001), hyperkalemia (1.2% vs 0.4%, p = 0.0002), and angioedema (0.4% vs 0.1%, p < 0.05). Side effects resulted in discontinuation of blinded therapy in 15.2% of the enalapril group compared with 8.6% in the placebo group (p < 0.0001). Thus enalapril is well tolerated by patients with LVD; however, hypotension, azotemia, cough, fatigue, and other side effects result in discontinuation of therapy in a significant minority of patients. C1 UNIV N CAROLINA,CHAPEL HILL,NC. MONTREAL HEART INST,MONTREAL,PQ H1T 1C8,CANADA. UNIV ROCHESTER,SCH MED & DENT,ROCHESTER,NY 14627. SUNY BUFFALO,BUFFALO,NY. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. NEW YORK MED COLL,VALHALLA,NY 10595. MICHIGAN STATE UNIV,E LANSING,MI 48824. BAYLOR COLL MED,HOUSTON,TX 77030. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. RP Kostis, JB (reprint author), UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,1 ROBERT WOOD JOHNSON PL,CN19,NEW BRUNSWICK,NJ 08903, USA. NR 26 TC 85 Z9 87 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD FEB PY 1996 VL 131 IS 2 BP 350 EP 355 DI 10.1016/S0002-8703(96)90365-8 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA TV307 UT WOS:A1996TV30700023 PM 8579032 ER PT J AU Jaffe, ES AF Jaffe, ES TI Primary body cavity-based AIDS-related lymphomas - Evolution of a new disease entity SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Editorial Material ID EPSTEIN-BARR-VIRUS; EXPRESSION RP Jaffe, ES (reprint author), NCI,NIH,DIV CLIN SCI,LAB PATHOL,HEMATOPATHOL SECT,BETHESDA,MD 20892, USA. NR 24 TC 65 Z9 65 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD FEB PY 1996 VL 105 IS 2 BP 141 EP 143 PG 3 WC Pathology SC Pathology GA TU716 UT WOS:A1996TU71600002 PM 8607435 ER PT J AU Cavazza, A Colby, TV Tsokos, M Rush, W Travis, WD AF Cavazza, A Colby, TV Tsokos, M Rush, W Travis, WD TI Lung tumors with a rhabdoid phenotype SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE rhabdoid tumors; carcinoma; lung neoplasms ID NATIONAL-WILMS-TUMOR; CENTRAL-NERVOUS-SYSTEM; STUDY-PATHOLOGY-CENTER; SOFT-TISSUE; ULTRASTRUCTURAL EVIDENCE; EPITHELIOID SARCOMA; HISTIOCYTIC ORIGIN; FEATURES; LIVER; KIDNEY AB Six malignant tumors of the lung with a rhabdoid phenotype are described. All presented as lung masses in middle-aged to elderly adults (mean age 51 years), with no sex predilection. The tumors ranged from 1.3 cm to 8.0 cm in size and were generally associated with locally advanced disease. The distinctive (and defining) histologic feature was the presence of macronucleolated tumor cells with a large eosinophilic globular cytoplasmic inclusion. These ''rhabdoid'' elements comprised at least 10% of the neoplastic population. Immunohistochemistry revealed diffuse vimentin positivity in all cases. Epithelial and neuroen-docrine markers were at least focally positive in five and in all six cases, respectively. Electron microscopy was performed in one case and it showed paranuclear aggregates of intermediate filaments, dense core granules, and intercellular attachments. Malignant tumors of the lung with a rhabdoid phenotype are very rare. The majority are poorly differentiated carcinomas, and they frequently show features suggesting a neuroendocrine differentiation. C1 MAYO CLIN SCOTTSDALE,DEPT PATHOL & LAB MED,SCOTTSDALE,AZ 85259. NCI,NIH,PATHOL LAB,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,DEPT PULM & MEDIASTINAL PATHOL,WASHINGTON,DC 20306. NR 78 TC 51 Z9 54 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD FEB PY 1996 VL 105 IS 2 BP 182 EP 188 PG 7 WC Pathology SC Pathology GA TU716 UT WOS:A1996TU71600009 PM 8607442 ER PT J AU Schramm, WF Stockbauer, JW Hoffman, HJ AF Schramm, WF Stockbauer, JW Hoffman, HJ TI Exercise, employment, other daily activities, and adverse pregnancy outcomes SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE birth weight; employment; exercise; pregnancy outcome ID MATERNAL EXERCISE; PHYSICAL-ACTIVITY; BIRTH-WEIGHT; LABOR; HEALTH AB The relations of exercise, employment, and other daily activities during pregnancy with pregnancy outcomes were examined using data from the Missouri Maternal and Infant Health Survey. Maternal surveys were available for the following singleton birth categories: 450 fetal deaths; 782 very low birth weight (VLBW, <1,500 g); 802 moderately low birth weight (MLBW, 1,500-2,499 g); and 794 normal birth weight (NBW, greater than or equal to 2,500 g). All mothers were Missouri residents at the time of their December 1989 to March 1991 deliveries. It was found that VLBW mothers had exercised during pregnancy significantly less than NEW mothers. When compared with NEW mothers before pregnancy, VLBW mothers had been just as likely not to exercise as NEW mothers (odds ratio (OR) = 0.88, 95% confidence interval (CI) 0.69-1.12). During the first, second, and third trimesters, the odds ratios decreased to 0.70 (95% CI 0.53-0.92), 0.54 (95% CI 0.40-0.74), and 0.33 (95% CI 0.20-0.53), respectively. The VLBW mothers also were less likely to exercise during the third trimester than MLBW mothers (OR = 0.34, 95% CI 0.21-0.54) or mothers with fetal deaths (OR = 0.36, 95% CI 0.19-0.67), During the 3 months after pregnancy, none of the exercise odds ratios were statistically significant between groups. No significantly increased risks were found between employment during pregnancy or other daily activities and adverse pregnancy outcome. The study supports the recently relaxed guidelines of exercise during pregnancy. C1 NATL INST DEAFNESS & OTHER COMMUN DISORDERS,BETHESDA,MD. RP Schramm, WF (reprint author), BUR HLTH DATA ANAL,POB 570,JEFFERSON CITY,MO 65102, USA. FU NICHD NIH HHS [N01-HD-6-2916] NR 16 TC 40 Z9 43 U1 2 U2 3 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 1 PY 1996 VL 143 IS 3 BP 211 EP 218 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TR349 UT WOS:A1996TR34900001 PM 8561154 ER PT J AU Gallagher, D Visser, M Sepulveda, D Pierson, RN Harris, T Heymsfield, SB AF Gallagher, D Visser, M Sepulveda, D Pierson, RN Harris, T Heymsfield, SB TI How useful is body mass index for comparison of body fatness across age, sex, and ethnic groups? SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE aging; body composition; body mass index; ethnic groups ID FAT; OBESITY; WEIGHT; HEIGHT; TOMOGRAPHY; STATURE; TISSUE; HEALTH AB This study tested the hypothesis that body mass index (BMI) is representative of body fatness independent of age, sex, and ethnicity, Between 1986 and 1992, the authors studied a total of 202 black and 504 white men and women who resided in or near New York City, were ages 20-94 years, and had BMIs of 18-35 kg/m(2)., Total body fat, expressed as a percentage of body weight (BF%), was assessed using a four-compartment body composition model that does not rely on assumptions known to be age, sex, or ethnicity dependent, Statistically significant age dependencies were observed in the BF%-BMI relations in all four sex and ethnic groups (p values < 0.05-0.001) with older persons showing a higher BF% compared with younger persons with comparable BMIs, Statistically significant sex effects were also observed in BF%-BMI relations within each ethnic group (p values < 0.001) after controlling first for age, For an equivalent BMI, women have significantly greater amounts of total body fat than do men throughout the entire adult life span, Ethnicity did not significantly influence the BF%-BMI relation after controlling first for age and sex even though both black women and men had longer appendicular bone lengths relative to stature (p values < 0.001 and 0.02, respectively) compared with white women and men, Body mass index alone accounted for 25% of between-individual differences in body fat percentage for the 706 total subjects; adding age and sex as independent variables to the regression model increased the variance (r(2)) to 67%. These results suggest that BMI is age and sex dependent when used as an indicator of body fatness, but that it is ethnicity independent in black and white adults. C1 AGR UNIV WAGENINGEN, DEPT HUMAN NUTR, WAGENINGEN, NETHERLANDS. NIA, BETHESDA, MD 20892 USA. RP Gallagher, D (reprint author), COLUMBIA UNIV, ST LUKES ROOSEVELT HOSP CTR, OBES RES CTR, COLL PHYSICIANS & SURGEONS, DEPT MED, NEW YORK, NY 10025 USA. OI Gallagher, Dympna/0000-0003-1769-9754 FU NIDDK NIH HHS [P01-DK37352] NR 49 TC 674 Z9 693 U1 7 U2 47 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 EI 1476-6256 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 1 PY 1996 VL 143 IS 3 BP 228 EP 239 PG 12 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TR349 UT WOS:A1996TR34900003 PM 8561156 ER PT J AU Bergasa, NV Jones, EA Kleiner, DE Rabin, L Park, Y Wells, MC Hoofnagle, JH AF Bergasa, NV Jones, EA Kleiner, DE Rabin, L Park, Y Wells, MC Hoofnagle, JH TI Pilot study of low dose oral methotrexate treatment for primary biliary cirrhosis SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID CONTROLLED TRIAL; RHEUMATOID-ARTHRITIS; PREDNISOLONE TREATMENT; AZATHIOPRINE; CYCLOSPORINE; DISEASE; THERAPY AB Objective: To assess the efficacy of low doses of oral methotrexate as therapy for primary biliary cirrhosis. Methods: Ten symptomatic patients with this disease were treated with methotrexate at a dose of 15 mg/wk in an open label trial. Results: Eight patients completed 1 yr of treatment and six completed 2. Pruritus and fatigue decreased in all patients treated for at least 1 yr. Mean levels of serum alkaline phosphatase, ALT, and IgM were less at 1 and 2 yr than corresponding baseline means. Total serum bilirubin increased in three patients during treatment. Serum aminotransferases and alkaline phosphatase became normal in one patient with stage I disease. Although liver biopsies at 1 and 2 yr revealed a decrease in the intensity of the inflammatory infiltrate, they also showed an increase in fibrosis suggestive of disease progression. Methotrexate was discontinued in five patients: for disease progression in four (one at 4 months, one at 1 yr, and two at 2 Sr) and for intractable pruritus in one (at 4 months). All patients experienced transient mucositis and intermittent dyspepsia. Conclusions: These findings suggest that methotrexate treatment in patients with primary biliary cirrhosis is not beneficial in patients with advanced disease; in patients with early disease, methotrexate may be associated with amelioration of symptoms, reduction in serum biochemical indices of liver disease, and reduction in hepatic inflammation. However, prospective, randomized, controlled trials will be necessary for definitive evaluation of the effects of methotrexate on the quality of life and survival of patients with primary biliary cirrhosis. C1 NCI,NIH,DEPT PATHOL,NIDDKD,LIVER DIS SECT,BETHESDA,MD. ARMED FORCES INST PATHOL,DEPT HEPAT PATHOL,WASHINGTON,DC 20306. OI Kleiner, David/0000-0003-3442-4453 NR 28 TC 24 Z9 24 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD FEB PY 1996 VL 91 IS 2 BP 295 EP 299 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA TV544 UT WOS:A1996TV54400017 PM 8607496 ER PT J AU Tisdale, JF Figg, WD Reed, E McCall, NA Alkins, BR Horne, MK AF Tisdale, JF Figg, WD Reed, E McCall, NA Alkins, BR Horne, MK TI Severe thrombocytopenia in patients treated with suramin: Evidence for an immune mechanism in one SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE suramin; thrombocytopenia; immune ID DRUG AB Although suramin has long been used to treat human trypanosomiasis, recent clinical trials have tested its efficacy against the acquired immunodeficiency syndrome (AIDS) and various malignancies, Thrombocytopenia was observed in early trials with suramin in AIDS, but has been uncommon in patients treated for solid tumors. Here we describe 5 patients out of a total of 67 (7%) who developed severe thrombocytopenia while receiving suramin as part of a phase II clinical trial for metastatic prostate carcinoma refractory to hormonal therapy. IgG purified from one patient's plasma caused suramin-dependent platelet aggregation, There was also evidence of crossreactivity between suramin and heparin in this system, An immune mechanism, however, could not be documented in the other cases, suggesting that multiple mechanisms may he responsible for severe thrombocytopenia in this patient population. (C) 1996 Wiley-Liss, Inc. C1 NIH,CTR CLIN,DEPT CLIN PATHOL,SERV HEMATOL,BETHESDA,MD 20892. NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. RI Figg Sr, William/M-2411-2016 NR 20 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD FEB PY 1996 VL 51 IS 2 BP 152 EP 157 PG 6 WC Hematology SC Hematology GA TT553 UT WOS:A1996TT55300010 PM 8579057 ER PT J AU McKeown, LP Connaghan, G Wilson, O Hansmann, K Merryman, P Gralnick, HR AF McKeown, LP Connaghan, G Wilson, O Hansmann, K Merryman, P Gralnick, HR TI 1-desamino-8-arginine-vasopressin corrects the hemostatic defects in type 2B von Willebrand's disease SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE DDAVP; type 2B von Willebrand's disease; thrombocytopenia ID IIB VONWILLEBRANDS DISEASE; 1-DESAMINO-8-D-ARGININE VASOPRESSIN DDAVP; IB-BINDING DOMAIN; PLATELET-AGGREGATION; GLYCOPROTEIN-IB; MISSENSE MUTATIONS; FACTOR GENE; DESMOPRESSIN; HEMOPHILIA; SUBSTITUTION AB DDAVP is effective treatment in most types of von Willebrand's disease; however, in type 2B von Willebrand's disease the use of DDAVP has been contraindicated due to DDAVP-induced thrombocytopenia. Several reports have confirmed the thrombocytopenic effects of DDAVP and the presence of circulating platelet aggregates in type 2B von Willebrand's disease, We have infused three type 2B patients with DDAVP, The three patients had different mutations of their vWf, All three patients had a missense mutation which resulted in a single amino acid substitution in the disulfide loop of the Al domain. Administration of 20 mu g of DDAVP resulted in significant elevations of factor VIII, vWf antigen, and ristocetin cofactor levels, In contrast to other studies, DDAVP did not induce or enhance thrombocytopenia in these three patients, When blood was obtained by fingerstick and diluted into sodium oxalate (Unopette(R)) or EDTA (Microvette(R)), the platelet counts did not change over 4 hr. In contrast, blood collected directly into evacuated tubes containing sodium citrate, lithium heparin, or EDTA consistently demonstrated varying degrees of thrombocytopenia and platelet clumping; We also observed a shortening of the preinfusion bleeding time over the 4 hr period. All three patients have been studied twice and each has shown consistent results. DDAVP appears to be a useful form of treatment in type 2B vWd. (C) 1996 Wiley-Liss, Inc. C1 NIH,CTR CLIN,SERV HEMATOL,BETHESDA,MD 20892. NR 33 TC 22 Z9 22 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD FEB PY 1996 VL 51 IS 2 BP 158 EP 163 DI 10.1002/(SICI)1096-8652(199602)51:2<158::AID-AJH11>3.0.CO;2-E PG 6 WC Hematology SC Hematology GA TT553 UT WOS:A1996TT55300011 PM 8579058 ER PT J AU Neuhausen, SL Mazoyer, S Friedman, L Stratton, M Offit, K Caligo, A Tomlinson, G CannonAlbright, L Bishop, T Kelsell, D Solomon, E Weber, B Couch, F Struewing, J Tonin, P Durocher, F Narod, S Skolnick, MH Lenoir, G Serova, O Ponder, B StoppaLyonnet, D Easton, D King, MC Goldgar, DE AF Neuhausen, SL Mazoyer, S Friedman, L Stratton, M Offit, K Caligo, A Tomlinson, G CannonAlbright, L Bishop, T Kelsell, D Solomon, E Weber, B Couch, F Struewing, J Tonin, P Durocher, F Narod, S Skolnick, MH Lenoir, G Serova, O Ponder, B StoppaLyonnet, D Easton, D King, MC Goldgar, DE TI Haplotype and phenotype analysis of six recurrent BRCA1 mutations in 61 families: Results of an international study SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID CANCER AB Several BRCA1 mutations have now been found to occur in geographically diverse breast and ovarian cancer families. To investigate mutation origin and mutation-specific phenotypes due to BRCA1, we constructed a haplotype of nine polymorphic markers within or immediately flanking the BRCA1 locus in a set of 61 breast/ovarian cancer families selected for having one of six recurrent BRCA1 mutations. Tests of both mutations and family-specific differences in age at diagnosis were not significant. A comparison of the six mutations in the relative proportions of cases of breast and ovarian cancer was suggestive of an effect (P = .069), with 57% of women presumed affected because of the 1294 del 40 BRCA1 mutation having ovarian cancer, compared with 14% of affected women with the splice-site mutation in intron 5 of BRCA1. For the BRCA1 mutations studied here, the individual mutations are estimated to have arisen 9-170 generations ago. In general, a high degree of haplotype conservation across the region was observed, with haplotype differences most often due to mutations in the short-tandem-repeat markers, although some likely instances of recombination also were observed. For several of the instances, there was evidence for multiple, independent, BRCA1 mutational events. C1 UNIV UTAH,SCH MED,DEPT MED INFORMAT,GENET EPIDEMIOL GRP,SALT LAKE CITY,UT 84108. UNIV UTAH,SCH MED,DEPT INTERNAL MED,SALT LAKE CITY,UT. MYRIAD GENET,SALT LAKE CITY,UT. UNIV CAMBRIDGE,DEPT PATHOL,CRC,HUMAN CANC GENET RES GRP,CAMBRIDGE,ENGLAND. UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720. UNIV CALIF BERKELEY,SCH PUBL HLTH,BERKELEY,CA 94720. INST CANC RES,SECT MOLEC CARCINOGENESIS,SUTTON,SURREY,ENGLAND. INST CANC RES,EPIDEMIOL SECT,SUTTON,SURREY,ENGLAND. MEM SLOAN KETTERING CANC CTR,DEPT HUMAN GENET,NEW YORK,NY 10021. INST ANAT PATOL,PISA,ITALY. SW TEXAS STATE UNIV,DEPT PEDIAT,DALLAS,TX. IMPERIAL CANC RES FUND,GENET EPIDEMIOL LAB,LEEDS,W YORKSHIRE,ENGLAND. IMPERIAL CANC RES FUND,CLARE HALL LABS,LONDON,ENGLAND. IMPERIAL CANC RES FUND,LINCOLNS INN FIELDS,LONDON,ENGLAND. UNIV PENN,DEPT HEMATOL ONCOL,PHILADELPHIA,PA 19104. NATL CANC INST,GENET EPIDEMIOL BRANCH,BETHESDA,MD. NIH,BETHESDA,MD. MCGILL UNIV,DEPT MED GENET,MONTREAL,PQ,CANADA. CHU LAVAL,RES CTR,DEPT MOLEC ENDOCRINOL,QUEBEC CITY,PQ,CANADA. UNIV LAVAL,QUEBEC CITY,PQ,CANADA. INT AGCY RES CANC,F-69372 LYON,FRANCE. INST CURIE,UNITE GENET ONCOL,PARIS,FRANCE. RI Struewing, Jeffery/C-3221-2008; Struewing, Jeffery/I-7502-2013; OI Struewing, Jeffery/0000-0002-4848-3334; Bishop, Tim/0000-0002-8752-8785; albright, lisa/0000-0003-2602-3668 FU NCI NIH HHS [CA-55914] NR 22 TC 213 Z9 215 U1 0 U2 4 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD FEB PY 1996 VL 58 IS 2 BP 271 EP 280 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA TR791 UT WOS:A1996TR79100003 PM 8571953 ER PT J AU Reynolds, JE Marazita, ML Meyer, JM Stevens, CA Eaves, LJ Arnos, KS Ploughman, LM MacLean, C Nance, WE Diehl, SR AF Reynolds, JE Marazita, ML Meyer, JM Stevens, CA Eaves, LJ Arnos, KS Ploughman, LM MacLean, C Nance, WE Diehl, SR TI Major-locus contributions to variability of the craniofacial feature dystopia canthorum in waardenburg syndrome SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID MOUSE AB We used segregation analysis to investigate the genetic basis of variation in dystopia canthorum, one of the key diagnostic features of Waardenburg syndrome type 1 (WS1). We sought to determine whether the W-index, a quantitative measure of this craniofacial feature, is influenced primarily either by allelic variation in the PAX3 disease gene or other major loci, by polygenic background effects, or by all of these potential sources of genetic variation. We studied both WS1-affected individuals and their WS1-unaffected relatives. After adjustment of the W-index for WS1 disease status, segregation analyses by the regression approach indicated major-locus control of this variation, although residual parent-offspring and sib-sib correlations are consistent with additional (possibly polygenic) effects. Separate analyses of WS1-affected and WS1-unaffected individuals suggest that epistatic interactions between disease alleles at the PAX3 WS1 locus and a second major locus influence variation in dystopia canthorum. Our approach should be applicable for assessing the genetic architecture of variation associated with other genetic diseases. C1 NIDR,DEODP,MOLEC EPIDEMIOL & DIS INDICATORS BRANCH,BETHESDA,MD 20892. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT HUMAN GENET,RICHMOND,VA 23284. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PSYCHIAT,RICHMOND,VA 23284. UNIV PITTSBURGH,CLEFT PALATE CRANIOFACIAL CTR,PITTSBURGH,PA. GALLAUDET UNIV,WASHINGTON,DC 20002. FU NCRR NIH HHS [RR03655]; NIDCD NIH HHS [DC00038] NR 23 TC 3 Z9 3 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD FEB PY 1996 VL 58 IS 2 BP 384 EP 392 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA TR791 UT WOS:A1996TR79100015 PM 8571965 ER PT J AU Popescu, NC Zimonjic, DB AF Popescu, NC Zimonjic, DB TI Alterations of chromosome 11q13 in cervical carcinoma cell lines SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Letter ID HELA-CELLS; TUMORIGENICITY; HYBRIDS; EXPRESSION; GENE RP Popescu, NC (reprint author), NCI,DIV CANC ETIOL,BIOL LAB,37 CONVENT DR,MSC 4255,BETHESDA,MD 20892, USA. NR 18 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD FEB PY 1996 VL 58 IS 2 BP 422 EP 424 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA TR791 UT WOS:A1996TR79100020 PM 8571970 ER PT J AU Figg, WD Middleman, MN Sartor, O AF Figg, WD Middleman, MN Sartor, O TI Therapeutic options in patients with hormone-refractory prostate cancer - Reply SO AMERICAN JOURNAL OF MEDICINE LA English DT Letter C1 LOUISIANA STATE UNIV,SHREVEPORT,LA 71105. RP Figg, WD (reprint author), NCI,BETHESDA,MD 20892, USA. RI Figg Sr, William/M-2411-2016 NR 8 TC 2 Z9 2 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD FEB PY 1996 VL 100 IS 2 BP 243 EP 244 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA TV798 UT WOS:A1996TV79800022 ER PT J AU Vymazal, J Babis, M Brooks, RA Filip, K Dezortova, M Hrncarkova, H Hajek, M AF Vymazal, J Babis, M Brooks, RA Filip, K Dezortova, M Hrncarkova, H Hajek, M TI T1 and T2 alterations in the brains of patients with hepatic cirrhosis SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE liver; brain, magnetic resonance ID ACQUIRED HEPATOCEREBRAL DEGENERATION; MR IMAGES; SCAN ABNORMALITIES; GLOBUS-PALLIDUS; BASAL GANGLIA; DISEASE; HYPERINTENSITY; RELAXATION; FAILURE; SIGNAL AB PURPOSE: To determine whether previously reported T1-weighted MR hyperintensities in the brains of patients with hepatic cirrhosis are accompanied by changes in T2. METHODS: We measured T1 and T2 in the brains of 10 patients with chronic liver disease and 7 age-matched healthy volunteers, using classic spin-echo sequences with multiple saturation recovery limes and multiple echoes. RESULTS: Both T1 and T2 were shortened in the basal ganglia, cortex, and white matter of the patients, with the greatest shortening in the globus pallidus, where 1/T1 was increased by 0.76 s(-1) or 74%, and 1/T2 by 1.45 s(-1) or 11%. CONCLUSIONS: The T1 changes were accompanied by T2 changes of greater magnitude that were not as visible because T2 is normally much shorter than T1, especially in the globus pallidus. C1 NINCDS,NIH,NEUROIMAGING BRANCH,BETHESDA,MD 20892. INST CLIN & EXPTL MED,PRAGUE,CZECH REPUBLIC. CHARLES UNIV,MR UNIT,CLIN RADIOL,THIRD MED SCH 10000,PRAGUE,CZECH REPUBLIC. NR 19 TC 37 Z9 40 U1 1 U2 2 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD FEB PY 1996 VL 17 IS 2 BP 333 EP 336 PG 4 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA TW234 UT WOS:A1996TW23400028 PM 8938307 ER PT J AU DiChiro, G AF DiChiro, G TI Gloves and memos SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Letter RP DiChiro, G (reprint author), NIH,NEUROIMAGING BRANCH,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD FEB PY 1996 VL 17 IS 2 BP 399 EP 400 PG 2 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA TW234 UT WOS:A1996TW23400047 PM 8938322 ER PT J AU Basti, S Hejtmancik, JF Padma, T Ayyagari, R KaiserKupfer, MI Murty, JS Rao, GN AF Basti, S Hejtmancik, JF Padma, T Ayyagari, R KaiserKupfer, MI Murty, JS Rao, GN TI Autosomal dominant zonular cataract with sutural opacities in a four-generation family SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID CONGENITAL CATARACT; LINKAGE; GENE AB PURPOSE: We identified and examined four generations of a family with coexisting autosomal dominant zonular cataracts and sutural opacities and sought to determine their genetic basis. METHODS: Twenty-four of the 48 members in the family were examined, Systemic and ocular histories were obtained, and a detailed ophthalmic examination was performed, From each individual, 20 mi of blood was drawn for linkage studies with microsatellite markers in regions to which zonular cataracts had previously been localized (chromosomes 1, 2, and 16). RESULTS: Individuals of the first generation were reportedly asymptomatic, Several members of the second generation had morphologically identical zonular cataracts, Affected members of the third generation showed morphologic heterogeneity, with the zonular opacity varying from a uniform lamella to a segregation of dots, A high degree of consanguinity in the second generation suggested recessive inheritance with a pseudodominant inheritance pattern, However, examination of one member of the asymptomatic first generation disclosed senile cataractous changes superimposed on a faint zonular cataract enclosing sutural opacities and a pulverulent fetal nucleus, The latter findings were reconfirmed to be present in affected members of all generations, suggesting an autosomal dominant mode of inheritance, Initial efforts at linkage analysis excluded the gene locus causing this cataract from the Duffy, haptoglobin, and gamma-crystallin regions. CONCLUSIONS: The cataract in this family is both phenotypically and genetically distinct from previously described and mapped cataracts. C1 NEI,BETHESDA,MD 20892. OSMANIA UNIV,DEPT GENET,HYDERABAD 500007,ANDHRA PRADESH,INDIA. RP Basti, S (reprint author), LV PRASAD EYE INST,RD 2,BANJARA HILLS,HYDERABAD 500034,ANDHRA PRADESH,INDIA. NR 29 TC 12 Z9 12 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD FEB PY 1996 VL 121 IS 2 BP 162 EP 168 PG 7 WC Ophthalmology SC Ophthalmology GA TU830 UT WOS:A1996TU83000005 PM 8623885 ER PT J AU Ward, JM Benveniste, RE Fox, CH Battles, JK Gonda, MA Tully, JG AF Ward, JM Benveniste, RE Fox, CH Battles, JK Gonda, MA Tully, JG TI Autoimmunity in chronic active Helicobacter hepatitis of mice - Serum antibodies and expression of heat shock protein 70 in liver SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID PRIMARY BILIARY-CIRRHOSIS; DELTA T-CELLS; MOLECULAR MIMICRY; PYLORI; STRESS; AUTOANTIBODIES; BACTERIAL; IMMUNITY; HOMOLOG; DISEASE AB Male A/JCr mice with naturally occurring Helicobacter hepaticus infection develop a progressive chronic active hepatitis and liver tumors, despite the presence of serum antibodies to Helicobacter proteins. A rabbit antiserum prepared against the bacterial proteins immunoreacted with hepatocytes present in liver sections from infection mice with progressive lesions. We found that sera from these mice contained IgG antibodies that reacted in immunoblots with recombinant heat shock protein 70 (DnaK from Escherichia coli) but not with heat shock protein 60 (GroEL) or heat shock protein 10 (GroES). A rabbit antibody to heat shock protein 70 reacted with H. hepaticus in tissue sections and to a H. hepaticus protein (70 kd) in Western blots. Immunohistochemistry and in situ hybridization for heat shock protein 70 revealed that individual hepatocytes and other cells expressed the protein in livers with hepatitis but not usually in normal livers. Liver tumors and preneoplastic lesions in infected mice did not usually express heat shock protein 70 except focally in a few tumors. In situ hybridization for H. hepaticus 16s rRNA showed that the bacteria was found throughout the liver associated with hepatitis but not within tumors. CD3(+) T lymphocytes were found in close association with hepatic lesions. These data suggest a role for autoimmunity in progressive hepatitis and carcinogenesis in livers infected with H. hepaticus. C1 NCI,OFF LAB ANIM SCI,FREDERICK,MD 21702. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NIAID,NIH,MOLEC MICROBIOL LAB,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,LAB CELL & MOLEC STRUCT,SAIC FREDERICK,FREDERICK,MD. MOLEC HISTOL LAB INC,GAITHERSBURG,MD. RP Ward, JM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VET & TUMOR PATHOL SECT,FAIRVIEW 201,FREDERICK,MD 21702, USA. NR 52 TC 44 Z9 46 U1 1 U2 1 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD FEB PY 1996 VL 148 IS 2 BP 509 EP 517 PG 9 WC Pathology SC Pathology GA TU542 UT WOS:A1996TU54200018 PM 8579113 ER PT J AU Ferraris, JD Burg, MB Williams, CK Peters, EM GarciaPerez, A AF Ferraris, JD Burg, MB Williams, CK Peters, EM GarciaPerez, A TI Betaine transporter cDNA cloning and effect of osmolytes on its mRNA induction SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY LA English DT Article DE betaine/gamma-aminobutyric acid transporter; osmoregulation; osmotic stress; aldose reductase ID RENAL MEDULLARY CELLS; KIDNEY ALDOSE REDUCTASE; EXTRACELLULAR NACL; EXPRESSION; RNA; EFFICIENCY; SORBITOL AB Cells generally adapt to long-term hyperosmolality by accumulating compatible organic osmolytes, thereby helping to normalize both volume and intracellular inorganic ion concentration. When organic osmolytes are accumulated, as in renal inner medullary cells, it is the sum of their concentrations that is theoretically important. In effect, when one organic osmolyte rises, the others generally fall to maintain their sum approximately constant. The present study addresses the mechanism controlling betaine accumulation. Hypertonicity induces accumulation of betaine, sorbitol, inositol, and other organic osmolytes in PAP-HT25 cells, a line derived from rabbit renal papilla. Hypertonicity increases the betaine transporter expression in these cells. To obtain a specific probe for betaine transporter mRNA, we cloned from PAP-HT25 cells a cDNA that encodes the full protein. We then examined the effect of betaine, sorbitol, and inositol on betaine transporter mRNA abundance. Increased accumulation of any of these three organic osmolytes reduces betaine transporter mRNA. We previously observed similar results for aldose reductase, the enzyme responsible for osmotically regulated sorbitol accumulation. We conclude that the accumulation of organic osmolytes regulates betaine transporter gene expression. Because the aldose reductase gene is controlled in a similar fashion, we surmise that the two genes share a common signal for induction. RP Ferraris, JD (reprint author), NHLBI, NIH,KIDNEY & ELECTROLYTE METAB LAB,BLDG 10, RM 6N307,10 CTR DR, MSC 1598, BETHESDA, MD 20892 USA. NR 27 TC 17 Z9 18 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6143 J9 AM J PHYSIOL-CELL PH JI Am. J. Physiol.-Cell Physiol. PD FEB PY 1996 VL 270 IS 2 BP C650 EP C654 PG 5 WC Cell Biology; Physiology SC Cell Biology; Physiology GA TV844 UT WOS:A1996TV84400031 PM 8779931 ER PT J AU Wu, AJ Chen, ZJ Baum, BJ Ambudkar, IS AF Wu, AJ Chen, ZJ Baum, BJ Ambudkar, IS TI Interferon-gamma induces persistent depletion of internal Ca2+ stores in a human salivary gland cell line SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY LA English DT Article DE calcium mobilization; thapsigargin; carbachol; serum; cell proliferation; salivary cells ID INTRACELLULAR CALCIUM; ACINAR-CELLS; SJOGRENS-SYNDROME; ACTIVATION; EXPRESSION; GROWTH; PROLIFERATION; STIMULATION; MOLECULES; ENTRY AB Interferon-gamma (IFN-gamma), in the presence of tumor necrosis factor-alpha (TNF-alpha), decreases proliferation of a human salivary gland ductal cell line, HSG (Wu, A., R. Kurrasch, J. Katz, P. Fox, B. Baum, and J. Atkinson. J. Cell. Physiol. 161: 217-226, 1994). We examined the possible effects of these cytokines (1,000 U/ml IFN-gamma +/- 20 U/ml TNF-alpha for 7 days) on Ca2+ mobilization in HSG cells. In HSG cells, fetal bovine serum (10%) or carbachol (100 mu M) stimulated rapid increases in cytosolic Ca2+ concentration ([Ca2+](i)), apparently mobilized from different thapsigargin-sensitive intracellular Ca2+ stores. Serum induced a proliferative effect; on HSG cells, which was suppressed (>90%) by treatment with IFN-gamma +/- TNF-alpha, but not with TNF-alpha. alone. Serum-, carbachol-, and thapsigargin-stimulated [Ca2+](i) elevations were reduced by 90, 60, and >65%, respectively, in cells treated with IFN-gamma +/- TNF-alpha and 30, 45, and 45%, respectively, in cells treated with TNF-alpha. Removal of the cytokines from the growth medium induced recovery of both cell proliferation and Ca2+ mobilization responses within 7 days. Treatment of HSG cells with thapsigargin (0.02-2 nM) induced a dose-dependent decrease in cell proliferation. Additionally, acute treatment (<10 min) of cells with LFN-gamma did not affect [Ca2+](i) or alter carbachol-, thapsigargin-, or serum-induced changes in [Ca2+](i). These data demonstrate that prolonged treatment of HSG cells with IFN-gamma +/- TNF-alpha leads to a persistent depletion of intracellular Ca2+ stores. We suggest that this may have a role in cell growth. C1 NIDR, NIH, ORAL MED LAB, BETHESDA, MD 20892 USA. RP Wu, AJ (reprint author), NIDR, NIH,CLIN INVEST & PATIENT CARE BRANCH,BLDG 10, 1N-113,10 CTR DR, MSC1190, BETHESDA, MD 20892 USA. NR 32 TC 15 Z9 15 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6143 J9 AM J PHYSIOL-CELL PH JI Am. J. Physiol.-Cell Physiol. PD FEB PY 1996 VL 270 IS 2 BP C514 EP C521 PG 8 WC Cell Biology; Physiology SC Cell Biology; Physiology GA TV844 UT WOS:A1996TV84400014 PM 8779914 ER PT J AU Jones, PP Snitker, S Skinner, JS Ravussin, E AF Jones, PP Snitker, S Skinner, JS Ravussin, E TI Gender differences in muscle sympathetic nerve activity: Effect of body fat distribution SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE hydrodensitometry; waist-to-thigh ratio; abdominal-visceral fat; sympathetic nervous system ID SYSTEM ACTIVITY; OBESITY; AGE; REST; WOMEN; DIET; MEN AB Muscle sympathetic nerve activity (MSNA) has been correlated with percent body fat (%BF) in males. Because MSNA is typically lower and %BF higher in females, we tested whether this relationship could be generalized to females. Because abdominal-visceral body fat in men may be responsible for elevated sympathetic activity, we hypothesized that an estimate [waist-to-thigh ratio (W/T)] would correlate positively with MSNA in both genders and account for higher MSNA in males. Microneurography, hydrodensitometry, and W/T measures were obtained in 14 males and 14 females with a large range of %BF and W/T. Regression analyses revealed positive correlations between MSNA and %BF in males (r = 0.55, P = 0.04) and in females (r = 0.63, P = 0.02), with no difference in the slopes of the regression lines but a higher intercept in males (P < 0.01). When genders were pooled, MSNA and WPT were correlated (r = 0.68, P < 0.0001); this positive correlation was also found in males (r = 0.57, P = 0.04) but not as strongly in females (r = 0.49, P = 0.07). Forward stepwise multiple-regression analysis using %BF, W/T, gender, and age indicated that W/T was the primary factor related to MSNA (R(2) = 0.46); the other factors were not independent predictors. It is concluded that %BF is related to MSNA in both males and females but that the regression line is shifted downward in females because of lower levels of MSNA. W/T is a better correlate of MSNA than %BF and partially explains the higher MSNA in males. These findings may be relevant to the cardiovascular and metabolic disease risk associated with abdominal obesity. C1 NIDDKD, NIH, CLIN DIABET & NUTR SECT, PHOENIX, AZ 85016 USA. ARIZONA STATE UNIV, EXERCISE & SPORT RES INST, TEMPE, AZ 85287 USA. NR 24 TC 80 Z9 81 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD FEB PY 1996 VL 270 IS 2 BP E363 EP E366 PG 4 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA TW100 UT WOS:A1996TW10000022 PM 8779960 ER PT J AU Smolich, JJ Cox, HS Eisenhofer, G Esler, MD AF Smolich, JJ Cox, HS Eisenhofer, G Esler, MD TI Increased spillover and reduced clearance both contribute to rise in plasma catecholamines after birth in lambs SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE fetus; newborn; norepinephrine; epinephrine; radioactive microspheres ID TERM FETAL SHEEP; CHEMICAL SYMPATHECTOMY; POSTNATAL ADAPTATION; BLOOD-FLOW; NORADRENALINE; ADRENALINE; RELEASE; CIRCULATION; APPEARANCE; PRETERM AB We studied the relationship between changes in norepinephrine (NE) and epinephrine (Epi) levels, total body spillover, and total body clearance at birth. Near-term fetal lambs were chronically instrumented under general anesthesia with arterial, venous, and left atrial catheters. One week later, NE and Epi kinetics (isotope dilution methodology) and systemic blood flows (radioactive microspheres) were measured in fetuses and then in the same animals 1 and 4 h after cesarean section delivery. Comparing fetal and l-h lambs I)systemic output fell by 33% (P < 0.005); 2) systemic plasma NE increased by 144% (P < 0.005), and plasma Epi increased sevenfold (P < 0.005); 3)total body NE spillover rose by 63% (P < 0.01) and Epi spillover by fivefold (P < 0.005); and 4) total body NE clearance decreased by 34% (P < 0.005) and Epi clearance by 37% (P < 0.005). Systemic blood flow and kinetic data were similar in 1- and 4-h lambs and were therefore pooled to define the interrelationship among perinatal changes in NE and Epi plasma levels, spillover, and clearance. Between fetal and newborn lambs, plasma NE rose by 1,375 +/- 207 pg/ml, of which 604 +/- 119 pg/ml (similar to 44%) resulted from increased NE total body spillover and 771 +/- 160 pg/ml from reduced NE total body clearance. In the same interval, plasma Epi rose by 292 +/- 30 pg/ml, of which 123 +/- 18 pg/ml (similar to 42%) was due to Epi total body spillover and 169 +/- 19 pg/ml to reduced Epi total body clearance. These findings indicate that 1) sympathoadrenal activity increases with birth, and 2) increased total body spillover and reduced total body clearance contribute a similar portion of the plasma NE and Epi surge at birth. C1 BAKER MED RES INST, PRAHRAN, VIC 3181, AUSTRALIA. NINCDS, NIH, CLIN NEUROSCI BRANCH, BETHESDA, MD 20205 USA. RP Smolich, JJ (reprint author), MONASH UNIV, INST REPROD & DEV, CLAYTON, VIC 3168, AUSTRALIA. NR 34 TC 12 Z9 13 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD FEB PY 1996 VL 270 IS 2 BP H668 EP H677 PG 10 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA TV837 UT WOS:A1996TV83700030 PM 8779844 ER PT J AU Leibenluft, E AF Leibenluft, E TI Women with bipolar illness: Clinical and research issues SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Review ID MANIC-DEPRESSIVE PATIENTS; CYCLING AFFECTIVE-DISORDER; THYROID-FUNCTION; MENSTRUAL-CYCLE; LITHIUM-CARBONATE; ANTITHYROID ANTIBODIES; PSYCHIATRIC-DISORDERS; LIFETIME PREVALENCE; PUERPERAL PSYCHOSIS; CIRCADIAN-RHYTHMS AB Objective: The purpose of this article is to review the literature concerning gender differences in the course of bipolar illness and discuss issues relevant to the treatment of women with the illness. Method: The literature concerning the following topics is reviewed: gender differences in the course of bipolar illness; effects of the female reproductive cycle on the course of bipolar illness; special considerations in the treatment of bipolar women (focusing on the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-thyroid axes); and hypotheses to explain the greater prevalence of rapid cycling among bipolar women than among bipolar men. Results: Data clearly indicate that rapid cycling among bipolar women. Data also suggest that bipolar women may have more depressive episodes (and fewer manic episodes) and may be more likely to suffer from mixed (as opposed to pure) mania than bipolar men. While it is clear that bipolar women are at high risk for postpartum episodes, the effects of other reproductive system events (i.e., puberty, menstrual cycle, pregnancy, menopause, use of oral contraceptives or hormone replacement therapy) on the course of treatment of bipolar illness have received little systematic study. It is unclear whether women are at higher risk than men for developing lithium-induced hypothyroidism. Higher rates of hypothyroidism, greater use of antidepressant, and gonadal steroid effects are possible explanations for the greater prevalence of rapid cycling among bipolar women. Conclusions: Gender differences in bipolar illness and the effects of the female reproductive system on the course and treatment of the illness deserve more study. The importance of a longitudinal approach to these questions is emphasized. RP Leibenluft, E (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,10-4S-239,10 CTR DR MSC 1390,BETHESDA,MD 20892, USA. NR 132 TC 155 Z9 162 U1 6 U2 15 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD FEB PY 1996 VL 153 IS 2 BP 163 EP 173 PG 11 WC Psychiatry SC Psychiatry GA TT557 UT WOS:A1996TT55700004 PM 8561195 ER PT J AU Mann, JJ Malone, KM Diehl, DJ Perel, J Cooper, TB Mintun, MA AF Mann, JJ Malone, KM Diehl, DJ Perel, J Cooper, TB Mintun, MA TI Demonstration in vivo of reduced serotonin responsivity in the brain of untreated depressed patients SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL METABOLIC RESPONSES; AFFECTIVE-DISORDERS; GLUCOSE-UTILIZATION; BLOOD-PLATELETS; MOOD DISORDERS; RECEPTOR-BINDING; FRONTAL-CORTEX; AWAKE RATS; TRYPTOPHAN AB Objective: For over 25 years, it has been hypothesized that major depression is due to a deficiency of available serotonin or subsensitivity of key serotonin receptors in relevant brain regions. Direct evidence supporting this hypothesis has been lacking because of the difficulty in studying regional brain serotonergic function. The authors have developed a method for visualizing in vivo regional brain responses to serotonin release by comparing regional brain glucose metabolism after administration of the serotonin-releasing dl-fenfluramine, relative to placebo. Method: Results with healthy subjects (N=6) were compared to those obtained with drug-free inpatients with moderately severe major depression (N=6). Results: Healthy subjects had several areas of statistically significant increases in metabolism, mostly in the left prefrontal and temporoparietal cortex, and areas of decreased metabolism, such as in the right prefrontal cortex. In contrast, the depressed patients had no areas of increase or decrease in metabolism, differing significantly from healthy subjects. Results with patients resembled those with healthy subjects (N=10) who were scanned twice without active drug on either occasion. Conclusions: This study provides the first direct visualization of blunted regional brain responses to serotonin release in the brain of patients with major depression, a finding that supports the hypothesis of impaired serotonergic transmission in depression. C1 NEW YORK STATE PSYCHIAT INST & HOSP,MENTAL HLTH CLIN RES CTR STUDY SUICIDAL BEHAV,NEW YORK,NY 10032. COLUMBIA UNIV,NEW YORK,NY 10027. UNIV PITTSBURGH,NIMH CTR FUNCT BRAIN IMAGING,PITTSBURGH,PA 15260. RP Mann, JJ (reprint author), NEW YORK STATE PSYCHIAT INST & HOSP,DEPT NEUROSCI,722 W 168TH ST,NEW YORK,NY 10032, USA. FU NIMH NIH HHS [MH-40695, MH-46745, MH-49815] NR 70 TC 160 Z9 162 U1 1 U2 4 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD FEB PY 1996 VL 153 IS 2 BP 174 EP 182 PG 9 WC Psychiatry SC Psychiatry GA TT557 UT WOS:A1996TT55700005 PM 8561196 ER PT J AU Sonnenberg, A Everhart, JE AF Sonnenberg, A Everhart, JE TI The prevalence of self-reported peptic ulcer in the United States SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID HELICOBACTER-PYLORI; DISEASE; SEX AB Objectives. The purpose of this study was to draw a current picture of the sociodemographic characteristics of peptic ulcer in the United States. Methods. During the National Health Interview Survey of 1989, a special questionnaire on digestive diseases was administered to 41 457 randomly selected individuals. Data were retrieved from public use tapes provided by the National Center for Health Statistics. Odds ratios were calculated by logistic regression after adjustment for sample weights in the survey. Results. Of adult US residents, 10% reported having physician-diagnosed ulcer disease, and one third of these individuals reported having an ulcer in the past year. Old age, short education, low family income, being a veteran, and smoking acted as significant and independent risk factors. Gastric and duodenal ulcer occurred in both sexes equally often. Duodenal ulcer was more common in Whites than non-Whites, while gastric ulcer was more common in non-Whites. Conclusions. The age-related rise and socioeconomic gradients of peptic ulcer represent the historic scars of previous infection rates with Heli-cobacter pylori. The racial variations reflect different ages at the time of first infection; younger and older age at the acquisition of H. pylori appear to be associated with gastric and duodenal ulcer, respectively. C1 UNIV NEW MEXICO,ALBUQUERQUE,NM 87131. NIDDKD,BETHESDA,MD 20892. RP Sonnenberg, A (reprint author), DEPT VET AFFAIRS MED CTR,2100 RIDGECREST DR SE,ALBUQUERQUE,NM 87108, USA. NR 24 TC 60 Z9 63 U1 0 U2 1 PU AMER PUBLIC HEALTH ASSN INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD FEB PY 1996 VL 86 IS 2 BP 200 EP 205 DI 10.2105/AJPH.86.2.200 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TU708 UT WOS:A1996TU70800011 PM 8633736 ER PT J AU Sharp, DS Enright, PL Chiu, D Burchfiel, CM Rodriguez, BL Curb, JD AF Sharp, DS Enright, PL Chiu, D Burchfiel, CM Rodriguez, BL Curb, JD TI Reference values for pulmonary function tests of Japanese-American men aged 71 to 90 years SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID RESPIRATORY-DISEASE; UNITED-STATES; SPIROMETRY; HEALTH; MORTALITY AB Pulmonary function was assessed by spirometry in 3,076 elderly Japanese-American men of the Honolulu Heart Program (HHP) cohort. The assessment was done with a stringent quality assurance program that adhered to American Thoracic Society (ATS) recommendations for spirometry. Less than 6% of the participants were unable to perform three acceptable spirometry maneuvers. A ''healthy'' subgroup of 528 men between the ages of 71 and 90 yr was identified by excluding almost all smokers and subjects with lung disease and other factors negatively influencing FEV(1). Reference equations and normal ranges for FEV(1), FVC, and the FEV(1)/FVC ratio were derived from the healthy group. Use of prediction equations from the Cardiovascular Health Study (CHS) of elderly European-American men consistently overpredicted FVC by 0.3 to 0.4 L and FEV(1) by 0.15 L. Men in the HHP were on average 1 1 cm shorter than those in the CHS. Use of a prediction equation derived from the HHP cohort when the men in the cohort were on average 22.6 yr younger consistently overpredicted FEV(1) by 0.2 to 0.3 L. These results underscore the importance of using prediction equations appropriate to the ethnicity, age, and height characteristics of the subjects being studied. C1 UNIV ARIZONA,RESP SCI CTR,TUCSON,AZ. NHLBI,BETHESDA,MD 20892. RP Sharp, DS (reprint author), KUAKINI MED CTR,HONOLULU HEART PROGRAM,347 N KUAKINI ST,HONOLULU,HI 96817, USA. FU NHLBI NIH HHS [N01-HC-02901] NR 19 TC 26 Z9 27 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD FEB PY 1996 VL 153 IS 2 BP 805 EP 811 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA TT884 UT WOS:A1996TT88400051 PM 8564136 ER PT J AU Khalil, N OConnor, RN Flanders, KC Unruh, H AF Khalil, N OConnor, RN Flanders, KC Unruh, H TI TGF-beta(1), but not TGF-beta(2) or TGF-beta(3), is differentially present in epithelial cells of advanced pulmonary fibrosis: An immunohistochemical study SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID GROWTH-FACTOR-BETA; EXTRACELLULAR-MATRIX; COLLAGEN-SYNTHESIS; RESPIRATORY-TRACT; INFLAMMATION; EXPRESSION; FACTOR-BETA-1; LOCALIZATION; MACROPHAGES; RAT AB Although it is recognized that three isoforms of transforming growth factor-beta (TGF-beta) exist in mammals, their expression, distribution, and function in injury and repair are not well characterized. Using immunohistochemistry and antibodies to synthetic peptides of TGF-beta(1), TGF-beta(2), and TGF-beta(3), we determined the distribution of TGF-beta isoforms in lung sections with acute and chronic lesions of idiopathic pulmonary fibrosis (IPF), chronic asbestosis and hypersensitivity pneumonitis, as well as non-specific pneumonitis. In lung sections with advanced pulmonary fibrosis and honeycombing, irrespective of the diagnosis, TGF-beta(1) was prominently expressed in epithelial cells and macrophages and was found to be associated with the extracellular matrix. In lungs with early lesions of IPF and only inflammatory changes, TGF-beta(1) was present in alveolar macrophages but TGF-beta(1) was not present in epithelial cells. Small amounts of matrix-associated TGF-beta(1) were present subepithelially in areas of lung sections from patients with IPF with minimal inflammation and no fibrosis. In normal lungs with no evidence of inflammation or fibrosis TGF-beta(1) was not seen in alveolar macrophages, epithelial cells, or extracellularly, TGF-beta(2) and TGF-beta(3) were expressed in alveolar macrophages, epithelial cells, and smooth muscle cells of vessels and bronchi of normal lungs and lungs with both inflammatory and fibrotic changes. Our findings suggest that while TGF-beta(2) and TGF-beta(3) are ubiquitously expressed in the lung, TGF-beta(1) is expressed in epithelial cells of fibrotic lungs where the presence of TGF-beta(1) is not disease-specific but an indication of the chronicity of the injury. C1 UNIV MANITOBA,MANITOBA INST CELL BIOL,MANITOBA CANC TREATMENT & RES FDN,DEPT PATHOL,WINNIPEG,MB R3E 0V9,CANADA. UNIV MANITOBA,MANITOBA INST CELL BIOL,MANITOBA CANC TREATMENT & RES FDN,DEPT SURG,WINNIPEG,MB R3E 0V9,CANADA. NIH,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP Khalil, N (reprint author), UNIV MANITOBA,MANITOBA INST CELL BIOL,MANITOBA CANC TREATMENT & RES FDN,DEPT INTERNAL MED,WINNIPEG,MB R3E 0V9,CANADA. NR 37 TC 207 Z9 215 U1 0 U2 5 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD FEB PY 1996 VL 14 IS 2 BP 131 EP 138 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA TU365 UT WOS:A1996TU36500004 PM 8630262 ER PT J AU Randell, SH Liu, JY Ferriola, PC Kaartinen, L Doherty, MM Davis, CW Nettesheim, P AF Randell, SH Liu, JY Ferriola, PC Kaartinen, L Doherty, MM Davis, CW Nettesheim, P TI Mucin production by SPOC1 cells - An immortalized rat tracheal epithelial cell line SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID EXPRESSION; MARKERS AB An airway epithelial mucous goblet cell line would be useful towards understanding mechanisms underlying the common problem of respiratory mucus hypersecretion. SPOC1 is a novel rat tracheal epithelial (RTE) cell line that developed cytologic features suggestive of mucous goblet cells when grown in tracheal grafts in vivo (Am. J. Respir. Cell Mel. Biol. 1995; 12:385-395). Our aims were to determine whether SPOC1 cells were capable of mucin synthesis and to directly compare mucin production by SPOC1 cells and RTE cells. Towards this end, we validated the use of monoclonal antibody (mAb) RTE11 (Exp. Lung Res. 1992; 18:323-342) as an immunologic probe for rat airway secretory mucin. Our results strongly suggest that mAb RTE11 detects a carbohydrate antigen that is a sensitive and specific marker for rat tracheobronchial secretory mucin. SPOC1 cells in tracheal grafts in vivo contained granules with ultrastructural features similar to mucous granules in normal rat airway goblet cells and they were strongly stained by mAb RTE11. Retinoic acid (RA) and culture on porous supports are known to profoundly modify airway epithelial cell phenotype in vitro. Expression of several retinoid-responsive proteins was similar in cultured SPOC1 and primary RTE cells, but major differences in mucin production were noted. Primary RTE cells in vitro only made mucin when grown on porous supports in the presence of RA, whereas SPOC1 cells produced mucin when grown on plastic or glass surfaces and even in the absence of RA. Interestingly, RA enhanced mucin secretion by SPOC1 cells during the early plateau stage of culture but there were no differences due to RA late in the culture period. SPOC1 cells are capable of mucin production and will be a useful tool for studying select aspects of airway secretory cell differentiation and function. C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. CHEM IND INST TOXICOL,DEPT CELL & MOLEC TOXICOL,RES TRIANGLE PK,NC 27709. RP Randell, SH (reprint author), UNIV N CAROLINA,CYST FIBROSIS PULM RES & TREATMENT CTR,CB 7248,7027 THURSTON BOWLES BLDG,CHAPEL HILL,NC 27599, USA. NR 14 TC 26 Z9 26 U1 0 U2 3 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD FEB PY 1996 VL 14 IS 2 BP 146 EP 154 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA TU365 UT WOS:A1996TU36500006 PM 8630264 ER PT J AU Dewsnup, DH Galgiani, JN Graybill, JR Diaz, M Rendon, A Cloud, GA Stevens, DA AF Dewsnup, DH Galgiani, JN Graybill, JR Diaz, M Rendon, A Cloud, GA Stevens, DA TI Is it ever safe to stop azole therapy for Coccidioides immitis meningitis? SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE coccidioidomycosis; meningitis, fungal; azoles; triazoles; recurrence ID ITRACONAZOLE THERAPY; FLUCONAZOLE THERAPY; KETOCONAZOLE; ANTIFUNGAL; MYCOSES AB Objective: To determine 1) whether patients with coccidioidal meningitis who had achieved remission with oral azole therapy were cured and 2) when oral atole therapy could be discontinued in these patients. Design: Data were gathered on patients with coccidioidal meningitis who had successfully responded to atole therapy in previous clinical trials. Setting: Referral centers, including university, county, and veterans' hospitals and clinics. Patients: 18 patients in whom atole therapy for meningitis had been discontinued, usually because of a presumption of cure. Main Outcome Measures: Clinical and cerebrospinal fluid relapse. Results: 14 of 18 patients (78% [95% CI, 52% to 94%]) had relapse with disseminated disease after discontinuation of therapy, for a total of 1 nonmeningeal and 15 meningeal relapses to date. Relapse occurred both soon and late (range, 0.5 to 30 months) after therapy was discontinued. The characteristics of patients who did not have relapse, including the particular atole used, the duration of therapy, the reason therapy was discontinued, and the cerebrospinal fluid indices before discontinuation, were similar to the characteristics of patients who had relapse. Relapse had serious consequences in some patients; 3 patients died. Conclusion: Our data suggest 1) that disease is only suppressed in patients with meningitis who achieve remission while receiving atole therapy and 2) that discontinuing atole therapy is unsafe. The alternative is lifelong treatment with azoles; this appears to be acceptable, because toxicity is uncommon with triazole therapy, even longterm triazole therapy. C1 SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,SAN JOSE,CA 95128. VET AFFAIRS MED CTR,DEPT MED,DIV INFECT DIS,TUCSON,AZ 85723. UNIV TEXAS,HLTH SCI CTR,DEPT INFECT DIS,AUDIE MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. UNIV ALABAMA,MED CTR,TUMOR INST,BIRMINGHAM,AL 35294. CALIF INST MED RES,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,STANFORD,CA 94305. NIAID,MYCOSES STUDY GRP,BETHESDA,MD. UNIV ARIZONA,TUCSON,AZ. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV AUTONOMA NUEVO LEON,MONTERREY,MEXICO. UNIV HOSP,MONTERREY,MEXICO. FU NIAID NIH HHS [N01-AI-15082] NR 23 TC 98 Z9 102 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD FEB 1 PY 1996 VL 124 IS 3 BP 305 EP & PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA TR596 UT WOS:A1996TR59600004 PM 8554225 ER PT J AU Liedtke, W Limmroth, V AF Liedtke, W Limmroth, V TI Validity of brain MRI as the primary outcome criterion in multiple sclerosis phase II clinical trials SO ANNALS OF NEUROLOGY LA English DT Letter C1 NIH,OFF DIRECTOR,LAB DIAGNOST RADIOL RES,BETHESDA,MD 20892. RP Liedtke, W (reprint author), NINCDS,NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892, USA. RI Liedtke, Wolfgang/G-4633-2011 NR 6 TC 0 Z9 0 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD FEB PY 1996 VL 39 IS 2 BP 276 EP 276 DI 10.1002/ana.410390221 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA TY533 UT WOS:A1996TY53300020 PM 8967762 ER PT J AU Georgopapadakou, NH Walsh, TJ AF Georgopapadakou, NH Walsh, TJ TI Antifungal agents: Chemotherapeutic targets and immunologic strategies SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; PNEUMOCYSTIS-CARINII PNEUMONIA; ELONGATION FACTOR-III; PROTEIN-KINASE-C; NOSOCOMIAL FUNGAL-INFECTIONS; COLONY-STIMULATING FACTOR; CEREVISIAE CELL-CYCLE; CANDIDA-ALBICANS; SACCHAROMYCES-CEREVISIAE; AMPHOTERICIN-B C1 ROCHE RES CTR, DEPT ONCOL, NUTLEY, NJ 07110 USA. NCI, INFECT DIS SECT, BETHESDA, MD 20892 USA. NR 300 TC 316 Z9 324 U1 0 U2 10 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0066-4804 EI 1098-6596 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD FEB PY 1996 VL 40 IS 2 BP 279 EP 291 PG 13 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA TT556 UT WOS:A1996TT55600001 PM 8834867 ER PT J AU Lewis, EN Gorbach, AM Marcott, C Levin, IW AF Lewis, EN Gorbach, AM Marcott, C Levin, IW TI High-fidelity Fourier transform infrared spectroscopic imaging of primate brain tissue SO APPLIED SPECTROSCOPY LA English DT Article DE vibrational spectroscopic imaging; chemical imaging; infrared microscopy; Fourier transform infrared spectroscopy; brain tissue ID RAMAN; MICROSCOPY AB We demonstrate a new mid-infrared and near-infrared imaging approach which is ideally suited to microscopic applications. The method employs an indium antimonide (InSb) focal-plane array detector and a commercially available step-scan Fourier transform infrared spectrometer (FTIR). With either a KBr or a CaF2 beamsplitter, images from 1 to 5.5 mu m (10,000-1818 cm(-1)) can be rapidly acquired with the use of all the available pixels on the detector. The spectral resolution for each image is easily varied by changing the number of acquired images during the interferometer scan. We apply this technique to noninvasively generate image contrast in sections of monkey brain tissue and to relate these data to specific lipid and protein fractions. In addition, we describe several computational methods to highlight the spatial distributions of components within a sample. C1 PROCTER & GAMBLE CO,MIAMI VALLEY LABS,CINCINNATI,OH 45253. RP Lewis, EN (reprint author), NIDDKD,NIH,PHYS CHEM LAB,BETHESDA,MD 20892, USA. NR 33 TC 90 Z9 90 U1 1 U2 8 PU SOC APPLIED SPECTROSCOPY PI FREDERICK PA PO BOX 1438, FREDERICK, MD 21701 SN 0003-7028 J9 APPL SPECTROSC JI Appl. Spectrosc. PD FEB PY 1996 VL 50 IS 2 BP 263 EP 269 DI 10.1366/0003702963906618 PG 7 WC Instruments & Instrumentation; Spectroscopy SC Instruments & Instrumentation; Spectroscopy GA TV879 UT WOS:A1996TV87900021 ER PT J AU Jeong, KS Lee, IJ Roberts, BJ Soh, Y Yoo, JK Lee, JW Song, BJ AF Jeong, KS Lee, IJ Roberts, BJ Soh, Y Yoo, JK Lee, JW Song, BJ TI Transcriptional inhibition of cytochrome P4502E1 by a synthetic compound, YH439 SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID RAT-LIVER; INDUCIBLE CYTOCHROME-P-450; DIISOPROPYL 1,3-DITHIOL-2-YLIDENEMALONATE; ACETAMINOPHEN HEPATOTOXICITY; HEPATIC P450IIE1; DIALLYL SULFIDE; ETHANOL; INDUCTION; ACTIVATION; ALCOHOL AB The molecular mechanism of cytochrome P4502E1 (CYP2E1) inhibition by a synthetic compound, YH439, was studied. In rats treated with YH439, N-nitrosodimethylamine demethylase activity and the amount of immunoreactive CYP2E1 were rapidly decreased in time- and dose-dependent manners. Within 2 h after a single dose of YH439 (150 mg/kg), the CYP2E1-catalyzed activity in uninduced rats was decreased by about 30% and by 43% at 24 h after YH439 injection. YH439 treatment also reduced the elevation of CYP2E1 enzyme activity in starved (induced) animals by 34%. More profound inhibition of CYP2E1 protein levels was observed by immunoblot analysis. The level of CYP2E1 catalytic activity and immunoreactive protein remained suppressed for at least 48 h and returned to normal level at 72 h after YH439 treatment. The levels of immunoreactive CYP2B1/2 protein and catalytic activity were moderately increased while little change was observed in the levels of NADPH-dependent P450 oxidoreductase activity and its protein after treatment with YH439. Unlike competitive inhibitors of CYP2E1, YH439 rapidly (within 2 h) decreased the level of CYP2E1 mRNA, while malotilate, a structural analog of YH439, slightly suppressed its level. Nuclear run-on transcription analyses at 2, 4, and 8 h post-YH439 administration revealed that the inhibition of CYP2E1 by YH439 is at the level of transcription, indicating that YH439 is a new class of CYP2E1 inhibitor. Our data demonstrate that YH439 is a powerful inhibitor of CYP2E1 expression and is thus potentially useful as a pharmacological tool to study CYP2E1 function as well as a potential therapeutic agent. C1 NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20852. NIAAA,CLIN STUDIES LAB,ROCKVILLE,MD 20852. YUHAN CORP,YUHAN RES CTR,KYONGGI DO,SOUTH KOREA. NR 45 TC 19 Z9 20 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD FEB 1 PY 1996 VL 326 IS 1 BP 137 EP 144 DI 10.1006/abbi.1996.0057 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TT885 UT WOS:A1996TT88500019 PM 8579361 ER PT J AU Merril, CR Zullo, S Ghanbari, H Herman, MM Kleinman, JE Bigelow, LB Bartko, JJ Sabourin, DJ AF Merril, CR Zullo, S Ghanbari, H Herman, MM Kleinman, JE Bigelow, LB Bartko, JJ Sabourin, DJ TI Possible relationship between conditions associated with chronic hypoxia and brain mitochondrial DNA deletions SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE mitochondria; DNA deletion mutations; chronic hypoxia; putamen; superior frontal gyrus; polymerase chain reaction; cardiovascular disease; pulmonary disease; brain; schizophrenia; alcoholism; suicide ID EXTERNAL OPHTHALMOPLEGIA; INCREASE; DISEASE; AGE; TISSUES; DAMAGE; ADULT AB The brain relies heavily on aerobic metabolism which requires functional mitochondria. Mitochondria are subcellular organelles with their own genome which codes for 13 essential protein subunits. By employing PCR assays to examine brain tissue from 43 age-comparable individuals (between ages 34 and 73), we found a correlation between mitochondrial DNA deletion mutations, mtDNA(4977) deletions, and conditions associated with chronic hypoxia. In prior studies, utilizing only 6 to 12 clinical samples, mtDNA(4977) deletions were reported to increase in specific regions of the brain with aging. However, we found 12-fold and 5-fold higher levels of mtDNA(4977) deletions in the putamen and the superior frontal gyrus of the cortex, respectively, from individuals who had conditions associated with chronic hypoxia when compared with individuals without evidence of such conditions. These findings suggest that chronic hypoxia should be more closely examined in the pathophysiology of central nervous system diseases. C1 NIMH,NIH,NIMH NEUROSCI CTR ST ELIZABETHS,BIOCHEM GENET LAB,WASHINGTON,DC 20032. MOLEC GERIATR CORP,LAKE BLUFF,IL 60044. NIMH,NIH,DIV EPIDEMIOL & SERV RES,BETHESDA,MD 20892. NIMH,NIH,NIMH NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NR 31 TC 25 Z9 26 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD FEB 1 PY 1996 VL 326 IS 1 BP 172 EP 177 DI 10.1006/abbi.1996.0062 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TT885 UT WOS:A1996TT88500024 PM 8579367 ER PT J AU Yancey, KB Hintner, H AF Yancey, KB Hintner, H TI Advances in the diagnosis of subepidermal bullous diseases SO ARCHIVES OF DERMATOLOGY LA English DT Editorial Material ID CHLORIDE-SEPARATED SKIN; EPIDERMOLYSIS-BULLOSA; IMMUNOFLUORESCENCE MICROSCOPY; PEMPHIGOID ANTIGEN; PROTEIN; ACQUISITA; AUTOANTIBODIES; HEMIDESMOSOME; MEMBRANES; KALININ RP Yancey, KB (reprint author), NCI,NIH,DERMATOL BRANCH,BLDG 10 ROOM 12N238,10 CTR DR MSC 1908,BETHESDA,MD 20892, USA. NR 30 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD FEB PY 1996 VL 132 IS 2 BP 220 EP 222 PG 3 WC Dermatology SC Dermatology GA TV312 UT WOS:A1996TV31200016 PM 8629832 ER PT J AU Sharp, DS Abbott, RD Burchfiel, CM Rodriguez, BL Tracy, RP Yano, K Curb, JD AF Sharp, DS Abbott, RD Burchfiel, CM Rodriguez, BL Tracy, RP Yano, K Curb, JD TI Plasma fibrinogen and coronary heart disease in elderly Japanese-American men SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE coronary heart disease; fibrinogen; non-insulin-dependent diabetes mellitus; smoking; erythrocyte indices ID RISK-FACTORS; MYOCARDIAL-INFARCTION; CARDIOVASCULAR HEALTH; HEMOSTATIC FUNCTION; ARTERY DISEASE; ASCERTAINMENT; PATHOGENESIS; DETERMINANTS; MECHANISMS; SMOKING AB Clinical and epidemiological studies consistently indicate that elevations in plasma fibrinogen concentration are associated with the presence and development of coronary heart disease (CHD). These elevations are strongly correlated with smoking behavior and may play a significant role in mediating a relation of smoking to CHD. This cross-sectional survey of 3571 elderly Japanese-American men, aged 71 through 93 years, represents survivors of the Honolulu Heart Program cohort. Active smokers are almost twice as likely to be represented in the highest quintile of the fibrinogen distribution compared with the lowest quintile (9.8% versus 5.3%, respectively). The highest prevalence of CHD (34%) was noted in past and current smokers who were in the highest quintile of fibrinogen. The age-adjusted relative odds of prevalent CHD comparing the average fibrinogen levels in the first and fifth quintiles were 1.36 (95% confidence interval, 1.13 to 1.64). After adjustment for smoking status, blood pressure, total and HDL cholesterol, diabetes status, hematocrit, and white cell count, the association between fibrinogen and CHD was changed slightly and remained statistically significant (P<.05). These findings in an elderly cohort of Japanese-American men are consistent with previous studies among middle-aged adults demonstrating fibrinogen to be associated with indicators of clinical CHD and CHD risk factors. Because of the cross-sectional nature of this study, it is not possible to distinguish whether the observed relation of fibrinogen to prevalent CHD is causal or whether it represents a marker of active and progressive disease. C1 NHLBI,EPIDEMIOL & BIOMETRY PROGRAM,HONOLULU EPIDEMIOL RES SECT,HONOLULU,HI. KUAKINI MED CTR,HONOLULU HEART PROGRAM,HONOLULU,HI. UNIV HAWAII MANOA,JOHN A BURNS SCH MED,DEPT MED,HONOLULU,HI 96822. UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405. UNIV VERMONT,DEPT BIOCHEM,BURLINGTON,VT 05405. UNIV VIRGINIA,SCH MED,DIV BIOSTAT,CHARLOTTESVILLE,VA 22908. FU NHLBI NIH HHS [N01-HC-05102] NR 38 TC 21 Z9 23 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1079-5642 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD FEB PY 1996 VL 16 IS 2 BP 262 EP 268 PG 7 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA TV417 UT WOS:A1996TV41700011 PM 8620341 ER PT J AU Nash, TE Yee, J AF Nash, TE Yee, J TI Earlier Giardia transfection SO ASM NEWS LA English DT Letter C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0044-7897 J9 ASM NEWS JI ASM News PD FEB PY 1996 VL 62 IS 2 BP 62 EP 62 PG 1 WC Microbiology SC Microbiology GA TV796 UT WOS:A1996TV79600002 ER PT J AU Dixon, DM Cox, R Cutler, J Deepe, G AF Dixon, DM Cox, R Cutler, J Deepe, G TI Researchers use molecular immunology and technology to combat fungal pathogens SO ASM NEWS LA English DT Article C1 NIAID,BETHESDA,MD 20892. TEXAS CTR INFECT DIS,DEPT IMMUNOL RES,SAN ANTONIO,TX. MONTANA STATE UNIV,BOZEMAN,MT 59717. UNIV CINCINNATI,COLL MED,DIV INFECT DIS,CINCINNATI,OH. NR 0 TC 6 Z9 6 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0044-7897 J9 ASM NEWS JI ASM News PD FEB PY 1996 VL 62 IS 2 BP 81 EP 84 PG 4 WC Microbiology SC Microbiology GA TV796 UT WOS:A1996TV79600016 ER PT J AU Murray, EA Gaffan, EA Flint, RW AF Murray, EA Gaffan, EA Flint, RW TI Anterior rhinal cortex and amygdala: Dissociation of their contributions to memory and food preference in rhesus monkeys SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID LESIONS; REWARD; HIPPOCAMPUS; IMPAIRMENT; DEFICITS; REMOVAL AB Rhesus monkeys were trained on 2 versions of delayed nonmatching-to-sample, one with multiple pairs of objects and the other with a single pair, to evaluate their ability to remember objects. They then received either bilateral aspiration lesions of the anterior rhinal cortex or bilateral excitotoxic lesions of the amygdala, or were retained as unoperated controls. On re-presentation of the multiple-pair task, monkeys with anterior rhinal cortex lesions failed to show the improvement observed in both other groups in remembering the objects over delay intervals ranging from 10 to 60 s. Also, monkeys with anterior rhinal cortex lesions were impaired relative to the controls in relearning the single-pair version of the task. Conversely, on a formal test of food preference, monkeys with amygdala lesions showed abnormal patterns of food choice, whereas monkeys with anterior rhinal cortex lesions did not. Visual memory impairments formerly attributed to amygdala damage are probably due to the rhinal cortex damage associated with aspiration lesions of the amygdala. C1 UNIV READING,DEPT PSYCHOL,READING,BERKS,ENGLAND. RP Murray, EA (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 49,ROOM 1B80,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI Murray, Elisabeth/0000-0003-1450-1642 NR 33 TC 65 Z9 66 U1 0 U2 3 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7044 J9 BEHAV NEUROSCI JI Behav. Neurosci. PD FEB PY 1996 VL 110 IS 1 BP 30 EP 42 DI 10.1037/0735-7044.110.1.30 PG 13 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA TW737 UT WOS:A1996TW73700005 PM 8652070 ER PT J AU Rosen, JB Hamerman, E Sitcoske, M Glowa, JR Schulkin, J AF Rosen, JB Hamerman, E Sitcoske, M Glowa, JR Schulkin, J TI Hyperexcitability: Exaggerated fear-potentiated startle produced by partial amygdala kindling SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID FOS MESSENGER-RNA; C-FOS; ELECTRICAL-STIMULATION; ACOUSTIC STARTLE; CENTRAL NUCLEUS; CONDITIONED FEAR; SEIZURE ACTIVITY; DENTATE GYRUS; WATER MAZE; LESIONS AB The present study asked whether partial amygdala kindling would affect the expression of conditioned fear-potentiated startle. Rats were conditioned to be fearful of a light. They were then stimulated bilaterally in the amygdala or hippocampus on 2 consecutive days (partial kindling). Rats were tested 24 hr later for fear-potentiated startle. Amygdala-kindled rats had exaggerated fear-potentiated startle compared to sham-kindled rats. Hippocampus-kindled rats also displayed fear-potentiated startle, but no greater than that of sham-kindled rats. Partial amygdala kindling induced c-fos messenger RNA (mRNA) expression, a marker for neuronal activation, throughout the limbic and neocortices. In contrast, partial hippocampus kindling induced c-fos mRNA in the hippocampus only. The data suggest that kindled-induced hyperexcitability of the amygdala and limbic cortices produced exaggerated conditioned fear-potentiated startle. C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD. NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD. NIDDK,MED CHEM LAB,BETHESDA,MD 20892. NR 58 TC 68 Z9 68 U1 7 U2 8 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7044 J9 BEHAV NEUROSCI JI Behav. Neurosci. PD FEB PY 1996 VL 110 IS 1 BP 43 EP 50 PG 8 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA TW737 UT WOS:A1996TW73700006 PM 8652071 ER PT J AU Kaler, SG Das, S Levinson, B Goldstein, DS Holmes, CS Patronas, NJ Packman, S Gahl, WA AF Kaler, SG Das, S Levinson, B Goldstein, DS Holmes, CS Patronas, NJ Packman, S Gahl, WA TI Successful early copper therapy in Menkes disease associated with a mutant transcript containing a small in-frame deletion SO BIOCHEMICAL AND MOLECULAR MEDICINE LA English DT Article ID BETA-HYDROXYLASE DEFICIENCY; KINKY-HAIR SYNDROME; NONSENSE MUTATIONS; EXPRESSION; PLASMA; MOUSE; GENE AB Classical Menkes disease is a fatal X-linked neurodegenerative disorder caused by defects in a gene (MNK) that encodes a copper-transporting ATPase. Treatment with parenteral copper has been proposed for patients identified before symptoms develop, We recently described suboptimal outcomes despite early copper replacement in two classical Menkes patients whose mutation predicts little if any functional copper transporter, Here, we describe successful copper replacement therapy in a patient with Menkes disease with a splice acceptor site mutation (IVS8,AS,dup5) that causes exon-skipping and generates a mutant transcript with a small in-frame deletion in a noncritical region. The patient was diagnosed by analysis of neurochemical levels in cord blood, and parenteral copper replacement was begun at 8 days of life, Throughout infancy, he showed normal head growth, brain myelination, and age-appropriate neurodevelopment, including independent walking at 14 months of age. In contrast, his affected half-brother and first cousin with the same mutation, but who were not diagnosed and treated from an early age, showed arrested head growth, cerebral atrophy, delayed myelination, and abnormal neurodevelopment. We propose that the successful neurological outcome in this patient was related to early repletion of circulating copper levels, in combination with residual copper transport by a partially functional MNK ATPase containing the small deletion. We hypothesize that raising plasma copper concentrations in patients with Menkes disease with some residual functional gene product can increase the ligand: transporter ratio and thus alter favorably the kinetics of copper transport into and within the brain. (C) 1996 Academic Press, Inc. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT RADIOL,NEURORADIOL SECT,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. CHILDRENS NATL MED CTR,DEPT MED GENET,WASHINGTON,DC 20052. CHILDRENS NATL MED CTR,DEPT PEDIAT,WASHINGTON,DC 20052. UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,SAN FRANCISCO,CA 94143. RP Kaler, SG (reprint author), NINCDS,NIH,CLIN NEUROSCI BRANCH,BLDG 10,ROOM 5N214,10 CTR DR MSC 1424,BETHESDA,MD 20892, USA. NR 42 TC 48 Z9 48 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1077-3150 J9 BIOCHEM MOL MED JI Biochem. Mol. Med. PD FEB PY 1996 VL 57 IS 1 BP 37 EP 46 DI 10.1006/bmme.1996.0007 PG 10 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA UE424 UT WOS:A1996UE42400007 PM 8812725 ER PT J AU Burke, LP Jones, T Mortin, MA AF Burke, LP Jones, T Mortin, MA TI Transcriptional competition and homeosis in Drosophila SO BIOCHEMICAL GENETICS LA English DT Article DE RNA polymerase II; ultrabithorax; transcription; alpha-amanitin; Drosophila melanogaster ID RNA-POLYMERASE-II; ALPHA-AMANITIN; LARGEST SUBUNIT; CAENORHABDITIS-ELEGANS; ULTRABITHORAX; MELANOGASTER; MUTATIONS; COMPLEX; GENE; EXPRESSION AB Interference between different classes of RNA polymerase II alleles causes a mutant phenotype called the ''Ubx effect'' that resembles one seen in flies haploinsufficient for the transcription factor Ultrabithorax (Ubx). Flies carrying the mutation in the largest subunit of Drosophila RNA polymerase II, RpII215(4), display the Ubx effect when heterozygous as in RpII215(4)/(+) but not when homozygous mutant or wild type, In this report we demonstrate that the interaction between alleles in different classes of polymerase occurs even in the absence of transcription by the wild-type polymerase. We utilized the resistance to the transcriptional inhibitor alpha-amanitin conferred by RpII215(4) to show that RpII215(4)/+ flies raised on alpha-amanitin-containing food still show the Ubx effect and are indistinguishable from flies raised on normal food. We demonstrate using HPLC that the intracellular concentration of alpha-amanitin in the developing larvae is sufficient to inhibit a transcription by alpha-amanirin-sensitive polymerase. Furthermore, fluorescein-labeled alpha-amanitin accumulates in imaginal discs which are the precursor cells for the tissue showing the homeotic a transformation in adults. We conclude that the interaction between different classes of RNA polymerase II alleles resulting in the Ubx effect occurs prior to the block in transcription caused by alpha-amanitin. C1 NCI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. RI Burke, Lillian/A-7334-2008; Mortin, Mark/B-4251-2008 NR 36 TC 2 Z9 2 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0006-2928 J9 BIOCHEM GENET JI Biochem. Genet. PD FEB PY 1996 VL 34 IS 1-2 BP 45 EP 59 DI 10.1007/BF02396239 PG 15 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA UF900 UT WOS:A1996UF90000004 PM 8935992 ER PT J AU Levavasseur, F Lietard, J Ogawa, K Theret, N Burbelo, PD Yamada, Y Guillouzo, A Clement, B AF Levavasseur, F Lietard, J Ogawa, K Theret, N Burbelo, PD Yamada, Y Guillouzo, A Clement, B TI Expression of laminin gamma 1 in cultured hepatocytes involves repeated CTC and GC elements in the LAMC1 promoter SO BIOCHEMICAL JOURNAL LA English DT Article ID DNA-BINDING PROTEINS; BASEMENT-MEMBRANE COMPONENTS; ADULT-RAT HEPATOCYTES; ZINC-FINGER PROTEIN; COLLAGEN TYPE-IV; C-MYC; CHLORAMPHENICOL ACETYLTRANSFERASE; DIFFERENTIAL EXPRESSION; BIDIRECTIONAL PROMOTER; NUCLEOTIDE-SEQUENCE AB Laminin gamma 1 chain is present in all basement membranes and is expressed at high levels in various diseases, such as hepatic fibrosis. We have identified cis- and trans-acting elements involved in the regulation of this gene in normal rat liver, as well as in hepatocyte primary cultures and hepatoma cell lines. Northern-blot analyses showed that laminin gamma 1 mRNA was barely detectable in freshly isolated hepatocytes and expressed at high levels in hepatocyte primary cultures, as early as 4 h after liver dissociation. Actinomycin D and cycloheximide treatment in vivo and in vitro indicated that laminin gamma 1 overexpression in cultured hepatocytes was under the control of transcriptional mechanisms. Transfection of deletion mutants of the 5' flanking region of murine LAMC1 gene in hepatoma cells that constitutively express laminin gamma 1 indicated that regulatory elements were located between -594 bp and -94 bp. This segment included GC- and CTC-containing motifs. Gel-shift analyses showed that two complexes were resolved with different affinity for the CTC sequence depending on the location of the GC box. The pattern of complex formation with nuclear factors from freshly isolated and cultured hepatocytes was different from that obtained with total liver and similar to that with hepatoma cells. Southwestern analysis indicated that several polypeptides bound the CTC-rich sequence. Affinity chromatography demonstrated that a M(r) 60 000 polypeptide was a major protein binding to the CTC motif. This polypeptide is probably involved in the transcriptional activation of various proto-oncogenes and extracellular matrix genes that are expressed at high levels in both hepatoma cells and early hepatocyte cultures. C1 CHRU PONTCHAILLOU,INSERM,U49,UNITE RECH HEPATOL,F-35033 RENNES,FRANCE. NIDR,NIH,DEV BIOL LAB,BETHESDA,MD 20892. RI Burbelo, Peter/B-1027-2009; Theret, Nathalie/I-2871-2015; Clement, Bruno/E-5546-2016 NR 62 TC 8 Z9 8 U1 1 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD FEB 1 PY 1996 VL 313 BP 745 EP 752 PN 3 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TU585 UT WOS:A1996TU58500007 PM 8611150 ER PT J AU Becerril, B Corona, M Coronas, FIV Zamudio, F CAlderonAranda, ES Fletcher, PL Martin, BM Possani, LD AF Becerril, B Corona, M Coronas, FIV Zamudio, F CAlderonAranda, ES Fletcher, PL Martin, BM Possani, LD TI Toxic peptides and genes encoding toxin gamma of the Brazilian scorpions Tityus bahiensis and Tityus stigmurus SO BIOCHEMICAL JOURNAL LA English DT Article ID AMINO-ACID-SEQUENCE; CENTRUROIDES-NOXIUS HOFFMANN; NUCLEOTIDE-SEQUENCE; VENOM; SERRULATUS; CHANNEL; PURIFICATION; NEUROTOXINS; CLONING; PROTEINS AB Seven toxic peptides from the venom of Tityus bahiensis and Tityus stigmurus were isolated and sequenced, five of them to completion. The most abundant peptide from each of these two species of scorpion was 95% identical with that of toxin gamma from the venom of Tityus serrulatus. They were consequently named yb and gamma-st respectively. The genes encoding these new gamma-like peptides were cloned and sequenced by utilizing oligonucleotides synthesized according to known cDNA sequences of toxin gamma, and amplified by PCR on templates of DNA purified from both T. bahiensis and T. stigmurus. They contain an intron of approx. 470 bp. Possible mechanisms of processing and expressing these peptides are discussed, in view of the fact that glycine is the first residue of the N-terminal sequence of T. stigmurus, whereas lysine is the residue at position 1 of toxin gamma from T. serrulatus and T. bahiensis. In addition, chemical characterization of the less abundant toxic peptides showed the presence of at least four distinct families of peptides in all three species of the genus Tityus studied. There is a large degree of similarity among peptides from different venoms of the same family. By using specific horse and rabbit antisera, the venoms of T. bahiensis, T. serrulatus and T. stigmurus were compared. They showed an extended degree of cross-reactivity. Thus these three species of scorpion have similar toxic components, the genes of which are similarly organized, processed and expressed. C1 UNIV NACL AUTONOMA MEXICO,INST BIOTECNOL,DEPT MOLEC RECOGNIT & STRUCT BIOL,CUERNAVACA 62271,MORELOS,MEXICO. UNIV AUTONOMA ESTADO MORELOS,CTR INVEST BIOTECHNOL,CUERNAVACA 62210,MORELOS,MEXICO. E CAROLINA UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,GREENVILLE,NC 27858. NIMH,CLIN NEUROSCI BRANCH,UNIT MOLEC STRUCT,BETHESDA,MD 20892. RI Possani, Lourival/J-2397-2013 NR 36 TC 54 Z9 64 U1 0 U2 2 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD FEB 1 PY 1996 VL 313 BP 753 EP 760 PN 3 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TU585 UT WOS:A1996TU58500008 PM 8611151 ER PT J AU Han, KH Park, KH Yoo, HJ Cha, H Suh, SW Thomas, F Moon, TS Kim, SM AF Han, KH Park, KH Yoo, HJ Cha, H Suh, SW Thomas, F Moon, TS Kim, SM TI Determination of the three-dimensional structure of hordothionin-alpha by nuclear magnetic resonance SO BIOCHEMICAL JOURNAL LA English DT Article ID RESTRAINED MOLECULAR-DYNAMICS; PANCREATIC TRYPSIN-INHIBITOR; WALL-BOUND THIONINS; 3-DIMENSIONAL STRUCTURE; DISTANCE GEOMETRY; CRYSTAL-STRUCTURE; PROTEIN CRAMBIN; BARLEY; ALPHA-1-PUROTHIONIN; RESOLUTION AB The high-resolution three-dimensional solution structure of the plant toxin hordothionin-alpha obtained from Korean barley was determined by using two-dimensional NMR techniques combined with distance geometry and restrained molecular dynamics. Experimentally derived restraints including 292 interproton distances from nuclear Overhauser effect measurements, 16 hydrogen bond restraints together with four disulphide bridge restraints were used as input to calculations of distance geometry and restrained molecular dynamics. Also included in the calculations were 36 phi and 17 chi(1) torsion angles obtained from (3)J(HK alpha)and (3)J(alpha beta) coupling constants in double quantum filtered COSY and primitive exclusive COSY experiments, respectively. The overall protein fold is similar to crambin and purothionin-alpha 1. Two alpha-helices running in opposite directions are found on the basis of (3)J(HN alpha), and (3)J(alpha beta) and deuterium exchange rates for backbone NH protons, and encompass residues 7-18 and 22-28. These two helices are connected by a turn and form a 'helix-turn-helix' motif. A short stretch of an anti-parallel beta-sheet exists between residues 1-4 and 31-34. The two protein termini of hordothionin-alpha are 'well-anchored': the N-terminus of the protein is immobilized by this short beta-sheet whereas the C-terminus is 'pasted' to the carbonyl group of Cys-4 by a very stable hydrogen bond. The average root-mean-square differences for the backbone and heavy atoms after the restrained molecular dynamics calculations are 0.62 and 1.16 Angstrom respectively. These numbers represent a significant improvement over the corresponding values for the previous NMR structures of other thionins. The distance violation from the experimental interproton distances for the final structures is 0.14 Angstrom for all atoms. C1 SEOUL NATL UNIV,DEPT CHEM,SEOUL 151742,SOUTH KOREA. NHLBI,MOLEC DIS BRANCH,NIH,BETHESDA,MD 20892. RP Han, KH (reprint author), KIST,KOREA RES INST BIOSCI & BIOTECHNOL,YUSONG POB 115,TAEJON 305600,SOUTH KOREA. RI Suh, Se Won/H-8306-2013 OI Suh, Se Won/0000-0002-1768-4635 NR 47 TC 9 Z9 9 U1 0 U2 5 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD FEB 1 PY 1996 VL 313 BP 885 EP 892 PN 3 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TU585 UT WOS:A1996TU58500028 PM 8611171 ER PT J AU Diamond, AM Jaffe, D Murray, JL Safa, AR Samuels, BL Hatfield, DL AF Diamond, AM Jaffe, D Murray, JL Safa, AR Samuels, BL Hatfield, DL TI Lovastatin effects on human breast carcinoma cells. Differential toxicity of an adriamycin-resistant derivative and influence on selenocysteine tRNAs SO BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL LA English DT Article ID SERINE TRANSFER-RNA; MAMMALIAN-CELLS; TRANSFER RNASEC; ESCHERICHIA-COLI; CANCER-CELLS; RAS FUNCTION; CODON; LIVER; UGA; INHIBITION AB Selenocysteine tRNA([Ser]Sec) isoacceptors contain the modified nucleotide i(6)A immediately 3' to the anticodon. Because synthesis of i(6)A is expected to be inhibited by lovastatin, the status of tRNA([Ser]Sec) isoacceptors was examined in human breast carcinoma cells. As part of the initial characterization of these cells, it was determined that an adriamycin resistant derivative of the MCF-7 cell line exhibited a dramatic increase in the sensitivity to the killing effects of lovastatin relative to the parental MCF-7 cells. When MCF-7(Adr) cells were incubated with high levels of lovastatin, there was a dramatic perturbation in the distribution of isoacceptors within the selenocysteine tRNA population. Lovastatin may therefore be a useful reagent for both the study of differential killing of drug-resistant tumor cells and selenoprotein biosynthesis. C1 UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. ONCOR INC,GAITHERSBURG,MD 20877. NCI,EXPT CARCINOGENESIS LAB,NIH,BETHESDA,MD 20892. RP Diamond, AM (reprint author), UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637, USA. FU NCI NIH HHS [R01 CA56078] NR 23 TC 12 Z9 12 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 1039-9712 J9 BIOCHEM MOL BIOL INT JI Biochem. Mol. Biol. Int. PD FEB PY 1996 VL 38 IS 2 BP 345 EP 355 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA VG880 UT WOS:A1996VG88000015 PM 8850530 ER PT J AU Oren, DA Levendosky, AA Kasper, S Duncan, CC Rosenthal, NE AF Oren, DA Levendosky, AA Kasper, S Duncan, CC Rosenthal, NE TI Circadian profiles of cortisol, prolactin, and thyrotropin in seasonal affective disorder SO BIOLOGICAL PSYCHIATRY LA English DT Article DE seasonal affective disorder; cortisol; prolactin; thyrotropin; circadian rhythms ID CORE BODY-TEMPERATURE; PELAGE COLOR CYCLE; DEPRESSED-PATIENTS; LIGHT THERAPY; ENDOGENOUS-DEPRESSION; HORMONAL-REGULATION; DJUNGARIAN HAMSTER; PHODOPUS-SUNGORUS; MAJOR DEPRESSION; PLASMA PROLACTIN AB To determine whether circadian profiles of various plasma hormones are abnormal in patients with winter seasonal affective disorder (SAD), we obtained 24-hour profiles of plasma cortisol, prolactin, and thyrotropin in subsets of a sample of 22 depressed patients with SAD on and off light therapy and in subsets of a sample of 24 normal controls. Cortisol levels did not differ between patients and controls, and levels in patients were not affected by light therapy. Prolactin levels were lower in patients than in controls throughout the day (p < 0.03) bmt were unaffected by light therapy. Independent of patient vs. control status, prolactin levels were higher in women than in men throughout the day (p < 0.003). Thyrotropin levels were no different in patients and controls, but levels in patients were lower following light therapy (p < 0.05). C1 NIMH,PSYCHOL & PSYCHOPATHOL LAB,BETHESDA,MD 20892. UNIV MICHIGAN,ANN ARBOR,MI 48109. UNIV VIENNA,DEPT PSYCHIAT,A-1010 VIENNA,AUSTRIA. RP Oren, DA (reprint author), NIMH,SECT ENVIRONM PSYCHIAT,CLIN PSYCHOBIOL BRANCH,BLDG 10,RM 4S-239,10 CTR DR MSC 1390,BETHESDA,MD 20892, USA. NR 81 TC 29 Z9 31 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD FEB 1 PY 1996 VL 39 IS 3 BP 157 EP 170 DI 10.1016/0006-3223(95)00079-8 PG 14 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA TV300 UT WOS:A1996TV30000002 PM 8837977 ER PT J AU Kaneda, K Sayers, TJ Wiltrout, TA Pilaro, AM Kojima, A Nagashima, K Gonda, MA Ward, JM Reynolds, CW Ortaldo, JR Wiltrout, RH AF Kaneda, K Sayers, TJ Wiltrout, TA Pilaro, AM Kojima, A Nagashima, K Gonda, MA Ward, JM Reynolds, CW Ortaldo, JR Wiltrout, RH TI Rod-cored vesicles in large granular lymphocyte (LGL) leukemia cells of rats: Alterations induced following metastasis to the liver SO BIOMEDICAL RESEARCH-TOKYO LA English DT Article ID NATURAL-KILLER ACTIVITY; PIT CELLS; CYTOPLASMIC GRANULES; AUGMENTATION; PURIFICATION; SINUSOIDS; TUMORS AB Rat transplantable large granular lymphocyte (LGL) tumor lines, termed RNK cells, have been used for the analysis of dense granules. It also has been reported that LGL from normal rats have rod-cored vesicles (RCV), which are considered to be a marker of NK cell maturation. There have been, however, no reports on the presence of RCV in RNK cells. All RNK cell lines examined here possessed RCV, although RNK-11 cells contained more empty 0.2 mu m vesicles and RCV than did RNK-16 and -7 cells. The high expression of vesicles of RNK-11 cells was maintained during several in vivo passages. RNK-16 and RNK-0 cells after rapid or delayed metastasis, respectively, exhibited more empty 0.2 mu m vesicles and RCV than those that metastasized to the spleen. There was, however, no significant difference in the number of dense granules between RNK cells in these two organs. The present study has revealed that RCV are maintained after the transformation of NK cells to tumorigenic RNK cells and that the expression of RCV in RNK cells is augmented by the Liver microenvironment. Therefore, RNK cells will serve as a useful model for the analysis of biochemical and functional properties of RCV. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,VET & TUMOR PATHOL SECT,OFF LAB ANIM SCI,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,LAB CELL & MOL STRUCT,FREDERICK,MD 21702. OSAKA CITY UNIV,SCH MED,DEPT ANAT,OSAKA 545,JAPAN. RI Sayers, Thomas/G-4859-2015 NR 16 TC 2 Z9 2 U1 0 U2 2 PU BIOMED RES FOUND PI TOKYO PA KANDA PO BOX 182 CHIYODAKU, TOKYO 101-91, JAPAN SN 0388-6107 J9 BIOMED RES-TOKYO JI Biomed. Res. PD FEB PY 1996 VL 17 IS 1 BP 53 EP 65 PG 13 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA UB438 UT WOS:A1996UB43800007 ER PT J AU Hasegawa, K Ohtsuka, K Shimizu, F Kawachi, Y Nakayama, M Sato, K Yamagiwa, S Tomiyama, K Asakura, H Abo, T AF Hasegawa, K Ohtsuka, K Shimizu, F Kawachi, Y Nakayama, M Sato, K Yamagiwa, S Tomiyama, K Asakura, H Abo, T TI Induction of NK cells and intermediate TCR cells with protective ability from viral infectious death, at the early phase of herpes virus infection SO BIOMEDICAL RESEARCH-TOKYO LA English DT Article ID EXTRATHYMIC T-CELLS; SIMPLEX VIRUS; LPR MICE; LIVER; LYMPHOCYTES; RECEPTOR; GAMMA AB Extrathymic T cells can be easily distinguished from thymus-derived T cells, in terms of their expression levels of TCR (or CD3) and IL-2 receptor beta-chain (IL-2R beta). In this study, we examined how extrathymic T cells and thymus-derived T cells were activated in various organs during viral infection. When C3H/He mice were intraperitoneally inoculated with herpes simplex virus (HSV) of type 1-GC(+) strain at a sublethal dose, 3 x 10(4) PFU/mouse, the number of mononuclear cells (MNC) in the liver and spleen was stable but that of thymocytes decreased gradually up to 7 days after infection. However; a striking change of lymphocyte subsets was seen in the liver, namely, an increase in the proportion of NK cells (CD3-IL-2R beta(+)) and extrathymic T cells (CD3-intermediate(+) IL-2R beta(+)) on day 3 and 7. Reflecting this change, gamma delta T cells and double-negative CD4(-)8(-) T cells, which are components of extrathymic T cells, became elevated on day 3. Pre-elimination of NK cells and intermediate CD3 cells by an in vivo injection of anti-IL-2R beta mAb made mice susceptible to death by infection. All irradiated (6Gy) mice also became susceptible to death, but 1 X 10(7) adoptive transfer of Liver MNC, but not of splenic MNC, obtained from HSV-immunized mice was effective in preventing death (50%). The experiment in which mice were treated with anti-asialoGM, antibody showed that NK cells were much more important for early phase protection than were intermediate CD3 cells. MNC were also isolated from the lung, the major target organ, in HSV-infected mice. Intermediate CD3 cells and granulocytes increased in this organ. These results suggest that a serial induction of primitive lymphocytes such as NK cells and extrathymic T cells may be crucial for early protection from viral infection. C1 NIIGATA UNIV,SCH MED,DEPT IMMUNOL,NIIGATA 951,JAPAN. NIIGATA UNIV,SCH MED,DEPT INTERNAL MED 3,NIIGATA 951,JAPAN. NIDR,ORAL MED LAB,BETHESDA,MD 20892. NR 28 TC 2 Z9 2 U1 0 U2 0 PU BIOMED RES FOUND PI TOKYO PA KANDA PO BOX 182 CHIYODAKU, TOKYO 101-91, JAPAN SN 0388-6107 J9 BIOMED RES-TOKYO JI Biomed. Res. PD FEB PY 1996 VL 17 IS 1 BP 67 EP 79 PG 13 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA UB438 UT WOS:A1996UB43800008 ER PT J AU Mienville, JM Clay, JR AF Mienville, JM Clay, JR TI Effects of intracellular K+ and Rb+ on gating of embryonic rat telencephalon Ca2+-activated K+ channels SO BIOPHYSICAL JOURNAL LA English DT Article ID POTASSIUM CHANNELS; SKELETAL-MUSCLE; SINGLE; CURRENTS; CONDUCTANCE; SELECTIVITY; RECORDINGS; RUBIDIUM; NERVE AB We have investigated the effects of intracellular K+ and Rb+ on single-channel currents recorded from the large-conductance Ca+2-activated K+ (BK) channel of the embryonic rat telencephalon using the inside-out patch-clamp technique, Our novel observation concerns the effects of these ions on rapid flickering of channel openings, Specifically, flicker gating was voltage dependent, i.e., it was reduced by depolarization in the -60 to -10 mV range with equimolar concentrations of K+ ions (150 K-0(+)/150K(i)(+)). Removal of K-i(+) resulted in significant flickering at all potentials in this voltage range, In other words, the voltage dependence of flicker gating was effectively eliminated by the removal of K-i(+). This suggests that a K+ ion entering the channel from the intracellular medium binds, in a voltage-dependent manner, at a site that locks the flicker gate in its open position, No effects of changes in K-i(+) were observed on the primary, voltage-dependent gate of the channel, The change in flickering did not cause a change in the mean burst duration, which indicates that the primary gate is stochastically independent of the flicker gate. Intracellular Rb+ can substitute for-and is even more effective than-K-i(+) with regard to suppression of flickering. Substitution of Rb-i(+) for K-i(+) also increased the mean burst duration for V greater than or equal to -30 mV. Both effects of Rb-i(+) were removed by membrane hyperpolarization. RP Mienville, JM (reprint author), NINCDS,NEUROPHYSIOL LAB,NIH,BLDG 36,ROOM 2C02,36 CONVENT DR MSC 4066,BETHESDA,MD 20892, USA. NR 27 TC 9 Z9 9 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP 778 EP 785 PG 8 WC Biophysics SC Biophysics GA TY684 UT WOS:A1996TY68400018 PM 8789094 ER PT J AU Alayash, AI Ryan, BAB Osawa, Y Cashon, RE Eich, R Olson, JS AF Alayash, AI Ryan, BAB Osawa, Y Cashon, RE Eich, R Olson, JS TI Oxidative reactions of sperm whale myoglobin and its distal pocket mutants with hydrogen peroxide SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD 20892. NHLBI,NIH,BETHESDA,MD 20892. UNIV MAINE,ORONO,ME 04469. RICE UNIV,HOUSTON,TX 77251. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP371 EP MP371 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201253 ER PT J AU Bertram, R Sherman, A AF Bertram, R Sherman, A TI Population dynamics of synaptic release sites. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP250 EP MP250 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201132 ER PT J AU Bettati, S Mozzarelli, A Rossi, GL Tsuneshige, A Yonetani, T Eaton, WA Henry, ER AF Bettati, S Mozzarelli, A Rossi, GL Tsuneshige, A Yonetani, T Eaton, WA Henry, ER TI The problem of cooperativity and the inequivalence of alpha and beta subunits in T state hemoglobin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV PARMA,I-43100 PARMA,ITALY. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. NIDDK,NIH,BETHESDA,MD 20892. RI Mozzarelli, Andrea/C-3615-2014 OI Mozzarelli, Andrea/0000-0003-3762-0062 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP373 EP MP373 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201254 ER PT J AU BhatiaDey, N Conti, MA Adelstein, RS AF BhatiaDey, N Conti, MA Adelstein, RS TI Comparative study of nonmuscle myosin heavy chains A and B during embryonic development in Xenopus laevis. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MPO42 EP MPO42 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200927 ER PT J AU Chang, CK Hu, Y Takahashi, S Rousseau, DL Eaton, WA Hofrichter, J AF Chang, CK Hu, Y Takahashi, S Rousseau, DL Eaton, WA Hofrichter, J TI Protein folding kinetics studied by ultrafast mixing. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,CHEM PHYS LAB,BETHESDA,MD. AT&T BELL LABS,MURRAY HILL,NJ 07974. NR 1 TC 0 Z9 0 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP140 EP MP140 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201021 ER PT J AU Chanturiya, AN Zimmerberg, J Chernomordik, LV AF Chanturiya, AN Zimmerberg, J Chernomordik, LV TI Transient pores in fusion of lipid vesicles with planar lipid membrane. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,NIH,LTPB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MPME8 EP MPME8 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200868 ER PT J AU Chen, YD Tsong, TY AF Chen, YD Tsong, TY TI Analyses of enzymic transduction of fluctuating electric signals SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. HONG KONG UNIV SCI & TECHNOL,DEPT BIOCHEM,HONG KONG,HONG KONG. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP426 EP MP426 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201308 ER PT J AU Driscoll, S Hawkins, M Balis, FM Pfeiderer, W Laws, WR AF Driscoll, S Hawkins, M Balis, FM Pfeiderer, W Laws, WR TI Studies on the fluorescent nucleotide 3-methyl-isoxanthopterine incorporated into oligonucleotides. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 MT SINAI SCH MED,DEPT BIOCHEM,NEW YORK,NY 10029. NCI,NIH,BETHESDA,MD 20892. UNIV KONSTANZ,FAK CHEM,W-7750 CONSTANCE,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP132 EP MP132 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201014 ER PT J AU Durell, SR Wallqvist, A AF Durell, SR Wallqvist, A TI Comparison of solvent-induced interactions between hydrophilic and hydrophobic groups in a simple model compound. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,MATH BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP440 EP MP440 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201326 ER PT J AU Fisher, G Ballou, B Srivastava, M Farkas, DL AF Fisher, G Ballou, B Srivastava, M Farkas, DL TI Far-red fluorescence-based high specificity tumor imaging in vivo SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 CARNEGIE MELLON UNIV,CTR LIGHT MICROSCOPE IMAGING & BIOTECHNOL,PITTSBURGH,PA 15213. NIDDK,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP343 EP MP343 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201227 ER PT J AU Guy, HR Durell, SR AF Guy, HR Durell, SR TI Structural models of the S5-P-S6 portion of the Shaker K+ channel. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,DCBDC,MATH BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MAMA9 EP MAMA9 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200706 ER PT J AU Hagen, SJ Eaton, WA AF Hagen, SJ Eaton, WA TI Explaining non-exponential structural relaxation in proteins. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,CHEM PHYS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP372 EP MP372 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201256 ER PT J AU Hagen, SJ Hofrichter, J Eaton, WA AF Hagen, SJ Hofrichter, J Eaton, WA TI Diffusional dynamics of an unfolded protein. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,CHEM PHYS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP142 EP MP142 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201025 ER PT J AU Henry, ER AF Henry, ER TI Techniques for large-scale kinetic modeling of spectroscopic data sets. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP436 EP MP436 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201321 ER PT J AU Horsky, J Rifkind, J AF Horsky, J Rifkind, J TI Allosteric effect in autooxidation of hemoglobin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,NIH,BALTIMORE,MD 21224. RI Horsky, Jiri/G-3442-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP374 EP MP374 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201257 ER PT J AU Lustig, B Jernigan, RL AF Lustig, B Jernigan, RL TI Calculation of DNA base-amino acid interaction energies for structures and sequences SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 SAN JOSE STATE UNIV,DEPT CHEM,SAN JOSE,CA 95112. NCI,NIH,MATH BIOL LAB,BETHESDA,MD 20892. RI Jernigan, Robert/A-5421-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MAMJ3 EP MAMJ3 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200776 ER PT J AU Malinchik, S Xu, S Yu, L AF Malinchik, S Xu, S Yu, L TI Structural transitions in relaxed skinned muscle fiber while changing temperature and ionic strength SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MPO46 EP MPO46 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200929 ER PT J AU Rajendran, B Brennan, JD Cyr, S Duforc, D Hogue, CWV Szabo, AG AF Rajendran, B Brennan, JD Cyr, S Duforc, D Hogue, CWV Szabo, AG TI Fluorescence monitoring of the reversible unfolding of F102W and F102(7AW) rat parvalbumin in aqueous solution. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV WINDSOR,DEPT CHEM & BIOCHEM,WINDSOR,ON N9B 3P4,CANADA. BROCK UNIV,DEPT CHEM,ST CATHARINES,ON L2S 3A1,CANADA. NCBI,NIH,BETHESDA,MD 20894. RI Hogue, Christopher/B-6726-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP325 EP MP325 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201209 ER PT J AU Redowicz, MJ Rau, DC Korn, ED Hammer, JA AF Redowicz, MJ Rau, DC Korn, ED Hammer, JA TI Sequence determinants for a myosin hinge. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,LCB,BETHESDA,MD 20892. NIDDK,LBM,BETHESDA,MD 20892. RI Redowicz, Maria Jolanta/R-4083-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MPO39 EP MPO39 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200920 ER PT J AU Schuck, P AF Schuck, P TI Mass transport and kinetic analysis of ligand-receptor interactions as detected with an evanescent wave biosensor. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,LBP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP341 EP MP341 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201226 ER PT J AU Steinbach, PJ AF Steinbach, PJ TI 2-D distributions of activation enthalpy and entropy from kinetics by the maximum entropy method SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract ID DYNAMICS C1 NIH,DCRT,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP375 EP MP375 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201258 ER PT J AU Sweeney, HL Faust, L Smith, JE Brown, F Milligan, RA Sellers, JR Stein, LA AF Sweeney, HL Faust, L Smith, JE Brown, F Milligan, RA Sellers, JR Stein, LA TI Function of the 25/50 KDa loop of the myosin II motor. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV PENN, SCH MED, PHILADELPHIA, PA 19104 USA. SCRIPPS RES INST, LA JOLLA, CA 92037 USA. NHLBI, BETHESDA, MD 20892 USA. SUNY STONY BROOK, STONY BROOK, NY 11794 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MPMD2 EP MPMD2 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200855 ER PT J AU Szabo, AG Brennan, JD Hogue, CWV Rajendran, B AF Szabo, AG Brennan, JD Hogue, CWV Rajendran, B TI Probing protein unfolding reactions using non-natural amino acids: An examination of wild type and W92(7AW) tryptophanyl tRNA synthetase using fluorescence techniques. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV WINDSOR,DEPT CHEM & BIOCHEM,WINDSOR,ON N9B 3P4,CANADA. BROCK UNIV,DEPT CHEM,ST CATHARINES,ON L2S 3A1,CANADA. NCBI,NIH,BETHESDA,MD 20894. RI Hogue, Christopher/B-6726-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP329 EP MP329 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201214 ER PT J AU Thompson, PA Eaton, WA Hofrichter, J AF Thompson, PA Eaton, WA Hofrichter, J TI Protein folding initiated by laser T-jump. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,CHEM PHYS LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MP141 EP MP141 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201024 ER PT J AU Urbaneja, FA Fisher, RJ Fivash, M Bladen, S Rein, A Arthur, LO Henderson, LE CasasFinet, JR AF Urbaneja, FA Fisher, RJ Fivash, M Bladen, S Rein, A Arthur, LO Henderson, LE CasasFinet, JR TI Interactions of HIV-1 nucleocapsid protein with single-stranded nucleic acids SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,DATA MANAGEMENT SERV,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. SAIC,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. SAIC,LAB CELLULAR BIOCHEM,FREDERICK,MD 21702. RI Fisher, Robert/B-1431-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MAMJ7 EP MAMJ7 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200781 ER PT J AU Wang, F Conti, MA Jiang, H Harvey, EV Sellers, JR AF Wang, F Conti, MA Jiang, H Harvey, EV Sellers, JR TI Molecular genetic expression and characterization of chicken brush border myosin I. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MPO44 EP MPO44 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200928 ER PT J AU Wang, L Voloshin, ON Kinal, H CameriniOtero, RD AF Wang, L Voloshin, ON Kinal, H CameriniOtero, RD TI The structure and activities of the mobile loop L2 of RecA, the homologous pairing domain SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP MAMJ8 EP MAMJ8 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200784 ER PT J AU Barnett, SM Dracheva, S Hendler, RW Levin, JW AF Barnett, SM Dracheva, S Hendler, RW Levin, JW TI Protein and lipid structural characteristics associated with the recovery of normal bacteriorhodopsin photocycle behavior in Triton-treated purple membrane SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. NHLBI,NIH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU445 EP SU445 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200631 ER PT J AU Beuron, F Kocsis, E Kessel, M Maurizi, M Steven, AC Booy, FP AF Beuron, F Kocsis, E Kessel, M Maurizi, M Steven, AC Booy, FP TI Cryo-electron microscopy of the energy-dependent CLP-AP protease SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS,NIH,LSBR,BETHESDA,MD 20892. NCI,NIH,LCB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU157 EP SU157 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200344 ER PT J AU Bezrukov, SM Vodyanoy, I Parsegian, VA AF Bezrukov, SM Vodyanoy, I Parsegian, VA TI Lipid bilayer surface charge effects on alamethicin channel conductance and noise SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 ONR,LONDON NW1 5TH,ENGLAND. NIH,DCRT,BETHESDA,MD 20892. NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 3 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU279 EP SU279 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200464 ER PT J AU Blumenthal, R Sarkar, DP Durell, S Howard, DE Morris, SJ AF Blumenthal, R Sarkar, DP Durell, S Howard, DE Morris, SJ TI Individual influenza hemagglutinin-mediated membrane fusion events from fusion pore opening to dilation SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. UMKC,KANSAS CITY,KS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU292 EP SU292 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200479 ER PT J AU Cuda, G Pate, E Cooke, R Sellers, J AF Cuda, G Pate, E Cooke, R Sellers, J TI In vitro actin filament sliding velocities produced by mixtures of different myosin types. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,BETHESDA,MD 20892. RI Cuda, Giovanni/F-5359-2012 OI Cuda, Giovanni/0000-0001-6313-1866 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SUP53 EP SUP53 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200239 ER PT J AU Dai, R Robinson, RC Friedman, FK AF Dai, R Robinson, RC Friedman, FK TI Cytochrome p450 recognition sites for NADPH cytochrome p450 reductase SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RI Friedman, Fred/D-4208-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU162 EP SU162 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200347 ER PT J AU Dracheva, S Mukhopadhyay, A Bose, S Hendler, RW AF Dracheva, S Mukhopadhyay, A Bose, S Hendler, RW TI Specific lipid requirements for normal function of bacteriorhodopsin (BR) photocycle SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU442 EP SU442 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200627 ER PT J AU Edith, ST Ward, GE Zimmerberg, J AF Edith, ST Ward, GE Zimmerberg, J TI New insights into parasite-host cell interactions, as revealed by simultaneous electrical and optical measurements SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU312 EP SU312 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200495 ER PT J AU Frolov, VA DuninaBarkovskaya, AY Zimmerberg, J Chizmadzhev, YA AF Frolov, VA DuninaBarkovskaya, AY Zimmerberg, J Chizmadzhev, YA TI Double whole cell recordings of HA-mediated fusion between HAb2 and PLC cells. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 AN FRUMKIN ELECTROCHEM INST,MOSCOW 117071,RUSSIA. MSU,BELOZERSKY INST PHYSICOCHEM BIOL,MOSCOW 119899,RUSSIA. NICHHD,NIH,LTPB,BETHESDA,MD 20892. RI Chizmadzhev, Yuri/L-1984-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU297 EP SU297 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200482 ER PT J AU Hendler, RW Mukhopadhyay, A Smith, PD Cascio, H AF Hendler, RW Mukhopadhyay, A Smith, PD Cascio, H TI Monitoring system for energy transduction by bacteriorhodopsin (BR) liposomes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,CELL BIOL LAB,BETHESDA,MD 20892. NCRR,NIH,BEIP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU443 EP SU443 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200630 ER PT J AU Ho, MWY Shears, SB Bruzik, K Duszyk, M French, AS AF Ho, MWY Shears, SB Bruzik, K Duszyk, M French, AS TI Direct evidence of down-regulation of calcium-dependent chloride current by inositol(3,4,5,6) tetrakisphosphate in CFPAC-1 cells. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV ALBERTA,DEPT PHYSIOL,EDMONTON,AB,CANADA. UNIV ALBERTA,DEPT MED,EDMONTON,AB,CANADA. NIEHS,INOSITOL LIPID SECT,RES TRIANGLE PK,NC 27709. UNIV CHICAGO,DEPT MED CHEM,CHICAGO,IL 60637. DALHOUSIE UNIV,DEPT PHYSIOL & BIOPHYS,HALIFAX,NS,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU220 EP SU220 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200405 ER PT J AU Hogue, CWV Bryant, SH AF Hogue, CWV Bryant, SH TI Sequence-structure threading of tyrosyl- and tryptophanyl-tRNA synthetase sequences: The evolution of several similar enzymes. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NATL CTR BIOTECHNOL INFORMAT,NIH,BETHESDA,MD 20894. RI Hogue, Christopher/B-6726-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU499 EP SU499 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200684 ER PT J AU Iwasa, KH AF Iwasa, KH TI Mechanisms for the fast motility of the outer hair cell SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDCD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SUAM1 EP SUAM1 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200030 ER PT J AU Jiang, H Chang, A Poetter, K Epstein, ND Fananapazir, L Sellers, JR AF Jiang, H Chang, A Poetter, K Epstein, ND Fananapazir, L Sellers, JR TI Increased speed of actin movement by mutant cardiac myosin from patients with familial hypertrophic cardiomyopathy in an in vitro motility assay SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NHLBI,NIH,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SUAM2 EP SUAM2 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200016 ER PT J AU Jin, A Mudd, CP Gershfeld, NL AF Jin, A Mudd, CP Gershfeld, NL TI High sensitivity measurement of thermal conductivity and specific heat in phase transitions by a temperature excitation relaxation method SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 DCRT,NIH,BETHESDA,MD 20892. NCRR,NIH,BETHESDA,MD 20892. NIAMS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU460 EP SU460 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200645 ER PT J AU Kasianowicz, JJ Bezrukov, SM AF Kasianowicz, JJ Bezrukov, SM TI Solvent isotope substitution effects on the kinetics of amino acid residue ionization in the alpha-toxin channel SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIST,DIV BIOTECHNOL,GAITHERSBURG,MD 20899. NIH,DORT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU278 EP SU278 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200461 ER PT J AU Kelley, CA Sellers, JR Bui, D Adelstein, RS Baines, IC AF Kelley, CA Sellers, JR Bui, D Adelstein, RS Baines, IC TI The nonmuscle myosin heavy chain II isoforms, MHC-A and MHC-B, have different enzymatic activities and subcellular localizations SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SUAM3 EP SUAM3 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200014 ER PT J AU Kidder, LH Herne, TM Huang, C Levin, IW AF Kidder, LH Herne, TM Huang, C Levin, IW TI A Raman spectroscopic study of monounsaturated phosphatidylcholines effect of double bond position SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV VIRGINIA,SCH MED,DEPT BIOCHEM,CHARLOTTESVILLE,VA 22908. NIDDKD,CHEM PHYS LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU349 EP SU349 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200534 ER PT J AU Kliger, Y Aharoni, A Rapaport, D Jones, P Blumenthal, R Shai, Y AF Kliger, Y Aharoni, A Rapaport, D Jones, P Blumenthal, R Shai, Y TI HIV derived fusion peptides: Organization within membranes and capacity to inhibit cell-cell fusion SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 WEIZMANN INST SCI,DEPT MEMBRANE RES & BIOPHYS,IL-76100 REHOVOT,ISRAEL. NCI,MATH BIOL LAB,NIH,SECT MEMBRANE STRUCT & FUNCT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU290 EP SU290 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200475 ER PT J AU Kocsis, E Kessel, M Maurizi, M Trus, BL Steven, AC AF Kocsis, E Kessel, M Maurizi, M Trus, BL Steven, AC TI 3-D reconstruction of the CLP-AP protease from E-coli. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS,NIH,LSBR,BETHESDA,MD 20892. NCI,NIH,LCB,BETHESDA,MD 20892. DCRT,NIH,CBEL,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU156 EP SU156 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200341 ER PT J AU Kozlov, MM Leikin, S Fuller, N Rand, RP AF Kozlov, MM Leikin, S Fuller, N Rand, RP TI Structural and elastic properties of DOPE/DOG mixtures SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 FREE UNIV BERLIN,FACHBEREICH PHYS,W-1000 BERLIN,GERMANY. NIH,DCRT,BETHESDA,MD 20892. BROCK UNIV,ST CATHARINES,ON,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU294 EP SU294 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200480 ER PT J AU Kuznetsova, N Rau, DC Parsegian, VA Leikin, S AF Kuznetsova, N Rau, DC Parsegian, VA Leikin, S TI Solvation forces between collagen triple helices in nonaqueous solvents. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 RUSSIAN ACAD SCI,ENGELHARDT INST MOLEC BIOL,MOSCOW,RUSSIA. NIH,DCRT,LSB,BETHESDA,MD 20892. NIDDK,NIH,ODIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU198 EP SU198 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200383 ER PT J AU Luo, G Zhang, JQ Herrera, AH Horowits, R AF Luo, G Zhang, JQ Herrera, AH Horowits, R TI Nebulin-related proteins in mouse muscle: Sequence analysis and localization. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SUA17 EP SUA17 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200081 ER PT J AU Meuse, CW Levin, IW AF Meuse, CW Levin, IW TI Microdomains in membrane architecture. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU339 EP SU339 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200526 ER PT J AU Miller, JH Fedoronko, DA Hass, BD Myint, M Kempner, ES AF Miller, JH Fedoronko, DA Hass, BD Myint, M Kempner, ES TI Radiation effects on the native structure of proteins; Fragmentation without dissociation. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU194 EP SU194 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200378 ER PT J AU Mukhopadhyay, A Dracheva, S Bose, S Hendler, RW AF Mukhopadhyay, A Dracheva, S Bose, S Hendler, RW TI Native purple membrane (PM) lipids control both normal and cooperative heterogeneous behavior of the bacteriorhodopsin (BR) photocycle SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU444 EP SU444 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200628 ER PT J AU Pemrick, SM Abarzua, P Kratzeisen, C Sturzenbecker, LJ Levin, AA Hunziker, W Marks, MS Medin, JA Ozato, K Grippo, JF AF Pemrick, SM Abarzua, P Kratzeisen, C Sturzenbecker, LJ Levin, AA Hunziker, W Marks, MS Medin, JA Ozato, K Grippo, JF TI Functional comparison of retinoic acid receptors with heterologous ligand binding domains SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 HOFFMANN LA ROCHE INC,DEPT METAB DIS,NUTLEY,NJ 07110. HOFFMANN LA ROCHE INC,DEPT ONCOL,NUTLEY,NJ 07110. NCI,NIH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU483 EP SU483 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200670 ER PT J AU Plonsky, I Zimmerberg, J AF Plonsky, I Zimmerberg, J TI Cooperative model for baculovirus-induced membrane fusion kinetics. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU298 EP SU298 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200485 ER PT J AU Remeta, DP Krumbiegel, M Blumenthal, R Ginsburg, A AF Remeta, DP Krumbiegel, M Blumenthal, R Ginsburg, A TI Unfolding pathways of influenza hemagglutinin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU291 EP SU291 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200476 ER PT J AU Sen, A Chen, YD Chalovich, JM AF Sen, A Chen, YD Chalovich, JM TI Reciprocal effects of caldesmon and myosin Sl on the rate of binding to actin. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 E CAROLINA UNIV,SCH MED,GREENVILLE,NC 27858. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SUP95 EP SUP95 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200278 ER PT J AU Silver, DL Vorotnikov, AV Watterson, DM Shirinsky, VP Sellers, JR AF Silver, DL Vorotnikov, AV Watterson, DM Shirinsky, VP Sellers, JR TI Binding of kinase-related protein to unphosphorylated smooth muscle myosin. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 CARDIOL RES CTR,INST EXPTL CARDIOL,MOLEC ENDOCRINOL LAB,MOSCOW 121552,RUSSIA. NORTHWESTERN UNIV,DEPT MOLEC PHARMACOL,CHICAGO,IL. NHLBI,NIH,BETHESDA,MD 20892. RI Vorotnikov, Alexander/A-8392-2014 OI Vorotnikov, Alexander/0000-0002-1460-971X NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU113 EP SU113 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200296 ER PT J AU Singerman, RW Denison, TJ Balaban, RS Wen, H AF Singerman, RW Denison, TJ Balaban, RS Wen, H TI Simulations of radio frequency fields in cardiac MRI SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,CARDIAC ENERGET LAB,BETHESDA,MD 20892. RI Wen, Han/G-3081-2010 OI Wen, Han/0000-0001-6844-2997 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU410 EP SU410 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200594 ER PT J AU Yoo, SH Lewis, MS AF Yoo, SH Lewis, MS TI Effects of pH and Ca2+ on hetero-dimer and heterotetramer formation by chromogranin A and chromogranin B. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDCD,NIH,BETHESDA,MD 20892. NCRR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU148 EP SU148 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200331 ER PT J AU Zhang, FL Lucke, C Baier, LJ Sacchettini, JC Hamilton, JA AF Zhang, FL Lucke, C Baier, LJ Sacchettini, JC Hamilton, JA TI Multidimensional NMR studies of the structure of human intestinal fatty acid binding protein (I-FABP) SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,DEPT BIOPHYS,BOSTON,MA 02118. NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,NIH,PHOENIX,AZ 85016. ALBERT EINSTEIN COLL MED,DEPT BIOCHEM,NEW YORK,NY 10461. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SU388 EP SU388 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200572 ER PT J AU Zhang, JQ Luo, G Horowits, R AF Zhang, JQ Luo, G Horowits, R TI Characterization and expression of nebulin clones from mouse skeletal muscle. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SUP12 EP SUP12 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200198 ER PT J AU Zhou, HX Chen, YD AF Zhou, HX Chen, YD TI Chemically driven motility of Brownian particles SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. HONG KONG UNIV SCI & TECHNOL,DEPT BIOCHEM,HONG KONG,HONG KONG. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP SUP66 EP SUP66 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68200249 ER PT J AU Bogdanov, K Vinogradova, T Lakatta, E Spurgeon, H AF Bogdanov, K Vinogradova, T Lakatta, E Spurgeon, H TI Polyunsaturated fatty acid (PUFA) inhibition of ionic currents in rat ventricular myocytes. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. CARDIOL RES CTR,MOSCOW 121552,RUSSIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TUP89 EP TUP89 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201611 ER PT J AU Brasier, AR CasasFinet, JR Wolfe, WA AF Brasier, AR CasasFinet, JR Wolfe, WA TI Thermodynamic characterization of the association of NF-IL6 bZIP tryptic core domain with its specific DNA sequence SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,MED BRANCH,SEALY CTR MOLEC SCI,GALVESTON,TX 77555. NCI,FREDERICK CANC RES & DEV CTR,SAIC,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TU454 EP TU454 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201974 ER PT J AU CasasPinet, JR Urbaneja, MA Lam, WC Maki, AH Henderson, LE AF CasasPinet, JR Urbaneja, MA Lam, WC Maki, AH Henderson, LE TI Fluorescence, phosphorescence and ODMR (optically detected magnetic resonance) investigation of the nucleic acid binding of nucleocapsid (NC) proteins SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. UNIV CALIF DAVIS,DEPT CHEM,DAVIS,CA 95616. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TU455 EP TU455 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201975 ER PT J AU Chatelier, RC Minton, AP AF Chatelier, RC Minton, AP TI Effect of excluded surface area upon the adsorption of proteins to surfaces. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 CSIRO,DIV CHEM & POLYMERS,CLAYTON,VIC 3168,AUSTRALIA. NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 3 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TU196 EP TU196 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201717 ER PT J AU Dantzig, JA Leonard, ME Fananapazir, L Epstein, N Goldman, YE Levine, RJC Sweeney, HL AF Dantzig, JA Leonard, ME Fananapazir, L Epstein, N Goldman, YE Levine, RJC Sweeney, HL TI A-band length, slack length and tension in skinned soleus fibers from patients with hypertrophic cardiomyopathy caused by a mutation in the beta-myosin heavy chain. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 MED COLL PENN,PHILADELPHIA,PA 19129. HAHNEMANN UNIV,PHILADELPHIA,PA 19129. NHLBI,BETHESDA,MD 20892. UNIV PENN,PA MUSCLE INST,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TU154 EP TU154 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201680 ER PT J AU Davenport, L Knutson, JR Ahmed, SA Miles, EW AF Davenport, L Knutson, JR Ahmed, SA Miles, EW TI Decay associated spectra of tryptophan synthase as a function of applied hydrostatic pressure. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 CUNY BROOKLYN COLL,DEPT CHEM,BROOKLYN,NY 11210. NHLBI,LCB,BETHESDA,MD 20892. NIDDK,NIH,LPB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TU251 EP TU251 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201770 ER PT J AU Ehrenstein, D Iwasa, KH AF Ehrenstein, D Iwasa, KH TI Viscoelastic relaxation in the membrane of the auditory outer hair cell SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDCD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TU421 EP TU421 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201940 ER PT J AU Flucher, BE Andrews, SB Shainberg, A AF Flucher, BE Andrews, SB Shainberg, A TI Amiodarone attenuates excitation-contraction coupling in skeletal muscle. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV INNSBRUCK, INST BIOCHEM PHARMACOL, INNSBRUCK, AUSTRIA. NIH, NEUROBIOL LAB, BETHESDA, MD USA. BAR ILAN UNIV, DEPT LIFE SCI, RAMAT GAN, ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TUAM7 EP TUAM7 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201357 ER PT J AU Froehlich, JP Albers, RW Yokoyama, T Taniguchi, K AF Froehlich, JP Albers, RW Yokoyama, T Taniguchi, K TI Kinetics of the phosphoenzyme interconversion reaction in BIBP-labeled pig kidney Na,K-ATPase. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,NIH,BALTIMORE,MD 21224. NINCDS,NIH,BETHESDA,MD 20892. HOKKAIDO UNIV,DEPT CHEM,SAPPORO,HOKKAIDO 060,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TU377 EP TU377 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201895 ER PT J AU Galdzicki, Z Ehrenstein, G Balbo, A Rapoport, SI Castellino, FJ Chibber, BAK AF Galdzicki, Z Ehrenstein, G Balbo, A Rapoport, SI Castellino, FJ Chibber, BAK TI New evidence that Alzheimer's beta-amyloid peptide enters cell membranes. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,NIH,NEUROSCI LAB,BETHESDA,MD 20892. NINCDS,NIH,BIOPHYS SECT,BETHESDA,MD 20892. UNIV NOTRE DAME,DEPT CHEM & BIOCHEM,NOTRE DAME,IN 46556. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TUAM3 EP TUAM3 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201386 ER PT J AU Gorin, AA Olson, WK Zhurkin, VB AF Gorin, AA Olson, WK Zhurkin, VB TI DNA folding in complexes with proteins: Local anisotropic bending and global non-planar looping. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 RUTGERS STATE UNIV,DEPT CHEM,NEW BRUNSWICK,NJ 08903. NCI,NIH,MATH BIOL LAB,BETHESDA,MD 20892. RI Gorin, Andrey/B-1545-2014 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TUAM3 EP TUAM3 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201421 ER PT J AU Gronenborn, AM AF Gronenborn, AM TI Complexes of human thioredoxin and its target peptides SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TUAM1 EP TUAM1 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201340 ER PT J AU Hawkins, ME Pfleiderer, W Knutson, JR Porter, D Balis, F AF Hawkins, ME Pfleiderer, W Knutson, JR Porter, D Balis, F TI Fluorescent pteridine nucleoside analogs as probes for monitoring protein DNA interactions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. UNIV KONSTANZ,FAK CHEM,W-7750 CONSTANCE,GERMANY. NHLBI,NIH,LCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TU466 EP TU466 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201986 ER PT J AU Kawahara, M Kuroda, Y Arispe, N Rojas, E AF Kawahara, M Kuroda, Y Arispe, N Rojas, E TI Direct incorporation of amyloid beta-protein cation channels into excised membrane patches from GnRH neurons SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV CHILE,FAC MED,DEPT PHYSIOL BIOPHYS,SANTIAGO,CHILE. NIDDK,NIH,LCBG,BETHESDA,MD. TOKYO METROPOLITAN INST NEUROSCI,TOKYO,JAPAN. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1996 VL 70 IS 2 BP TUAM5 EP TUAM5 PN 2 PG 1 WC Biophysics SC Biophysics GA TZ682 UT WOS:A1996TZ68201389 ER EF