FN Thomson Reuters Web of Science™ VR 1.0 PT J AU MARTIN, JF MIANO, JM HUSTAD, CM COPELAND, NG JENKINS, NA OLSON, EN AF MARTIN, JF MIANO, JM HUSTAD, CM COPELAND, NG JENKINS, NA OLSON, EN TI A MEF2 GENE THAT GENERATES A MUSCLE-SPECIFIC ISOFORM VIA ALTERNATIVE MESSENGER-RNA SPLICING SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ENHANCER-BINDING-FACTOR; SERUM RESPONSE ELEMENT; MYOCARDIAL-CELLS; FACTOR-II; PROTEIN; TRANSCRIPTION; PROMOTER; EXPRESSION; SEQUENCE; SKELETAL AB Members of the myocyte-specific enhancer-binding factor 2 (MEF2) family of transcription factors bind a conserved A/T-rich sequence in the control regions of numerous muscle-specific genes. Mammalian MEF2 proteins have been shown previously to be encoded by three genes, Mef2, xMef2, and Mef2c, each of which gives rise to multiple alternatively spliced transcripts. We describe the cloning of a new member of the MEF2 family from mice, termed MEF2D, which shares extensive homology with other MEF2 proteins but is the product of a separate gene. MEF2D binds to and activates transcription through the MEF2 site and forms heterodimers with other members of the MEF2 family. Deletion mutations show that the carboxyl terminus of MEF2D is required for efficient transactivation. MEF2D transcripts are widely expressed, but alternative splicing of MEF2D transcripts gives rise to a muscle-specific isoform which is induced during myoblast differentiation. The mouse Mef2, Mef2c, and Mef2d genes map to chromosomes 7, 13, and 3, respectively. The complexity of the MEF2 family of regulatory proteins provides the potential for fine-tuning of transcriptional responses as a consequence of combinatorial interactions among multiple MEF2 isoforms encoded by the four Mef2 genes. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT BIOCHEM & MOLEC BIOL,HOUSTON,TX 77030. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 54 TC 185 Z9 185 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 1994 VL 14 IS 3 BP 1647 EP 1656 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MX640 UT WOS:A1994MX64000012 PM 8114702 ER PT J AU ARCANGIOLI, B COPELAND, TD KLAR, AJS AF ARCANGIOLI, B COPELAND, TD KLAR, AJS TI SAP1, A PROTEIN THAT BINDS TO SEQUENCES-REQUIRED FOR MATING-TYPE SWITCHING, IS ESSENTIAL FOR VIABILITY IN SCHIZOSACCHAROMYCES-POMBE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HOMOTHALLIC FISSION YEAST; MEIOTIC RECOMBINATION; DNA STRANDS; GENES; FREQUENCY; CELLS; INTERCONVERSION; TRANSPOSITION; TRANSCRIPTION; PURIFICATION AB The pattern of mating-type switching in cell pedigrees of the fission yeast Schizosaccharomyces pombe is dictated by the inheritance of specific DNA chains at the mating-type locus (mat1). The recombination event essential for switching is initiated by a site-specific double-strand break at mat1. The switch-activating protein, Sap1, binds in vitro to a mat1 cis-acting site that was shown earlier to be essential for efficient mating-type switching. We isolated the sap1 gene by using oligonucleotides corresponding to the amino acid sequence of purified Sap1 protein. The sequence of that gene predicted a 30-kDa protein with no significant homology to other canonical DNA-binding protein motifs. To facilitate its biochemical characterization, Sap1 was expressed in Escherichia coli. The protein expressed in bacteria displayed the same DNA-binding specificities as the protein purified from S. pombe. Interestingly, analysis of a sap1 null mutation showed that the gene is essential for growth even in a strain in which mating-type snitching is prohibited because of a defect in generation of the double-strand break. Thus, the sap1 gene product implicated in mating-type switching is shown to be essential for cell viability. C1 NCI, FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM, EUKARYOT GENE EXPRESS LAB,DEV G, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LA, FREDERICK, MD 21702 USA. FU PHS HHS [N01-C0-74101] NR 48 TC 22 Z9 23 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 EI 1098-5549 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1994 VL 14 IS 3 BP 2058 EP 2065 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MX640 UT WOS:A1994MX64000055 PM 8114737 ER PT J AU FINBLOOM, DS PETRICOIN, EF HACKETT, RH DAVID, M FELDMAN, GM IGARASHI, K FIBACH, E WEBER, MJ THORNER, MO SILVA, CM LARNER, AC AF FINBLOOM, DS PETRICOIN, EF HACKETT, RH DAVID, M FELDMAN, GM IGARASHI, K FIBACH, E WEBER, MJ THORNER, MO SILVA, CM LARNER, AC TI GROWTH-HORMONE AND ERYTHROPOIETIN DIFFERENTIALLY ACTIVATE DNA-BINDING PROTEINS BY TYROSINE PHOSPHORYLATION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID INTERFERON-ALPHA; TRANSCRIPTION FACTOR; STIMULATED TRANSCRIPTION; CYTOPLASMIC ACTIVATION; IFN-GAMMA; RECEPTOR; PROMOTER; DESIGN; ISGF3 AB Binding of growth hormone (GH) and erythropoietin (EPO) to their respective receptors results in receptor clustering and activation of tyrosine kinases that initiate a cascade of events resulting not only in the rapid tyrosine phosphorylation of several proteins but also in the induction of early-response genes. In this report, we show that GH and EPO induce the tyrosine phosphorylation of cellular proteins with molecular masses of 93 kDa and of 91 and 84 kDa, respectively, and that these proteins form DNA-binding complexes which recognize an enhancer that has features in common with several rapidly induced genes such as c-fos. Assembly of the protein complexes required tyrosine phosphorylation, which occurred within minutes after addition of ligand. The activated complexes translocated from the cytoplasm to the nucleus. The protein activated by GH is antigenically similar to p91, a protein common to several transcription complexes that are activated by interferons and other cytokines. In contrast, the proteins activated by EPO are distinct from p91. These findings establish the outlines for a cytokine-induced intracellular signaling pathway, which begins with ligand-induced receptor clustering that activates one or more tyrosine kinases. These data are the first to demonstrate that GH- and EPO-activated tyrosine-phosphorylated proteins can specifically recognize a well-defined enhancer and therefore provide a mechanism for rapidly transducing signals from the membrane to the nucleus. C1 NIDDKD,CHEM BIOL LAB,BETHESDA,MD 20892. UNIV VIRGINIA,HLTH SCI CTR,DEPT MED,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,HLTH SCI CTR,DEPT MICROBIOL,CHARLOTTESVILLE,VA 22908. RP FINBLOOM, DS (reprint author), CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,8800 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU NIDDK NIH HHS [DK08942] NR 35 TC 87 Z9 87 U1 0 U2 0 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 1994 VL 14 IS 3 BP 2113 EP 2118 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MX640 UT WOS:A1994MX64000060 PM 7509451 ER PT J AU MARAIA, RJ KENAN, DJ KEENE, JD AF MARAIA, RJ KENAN, DJ KEENE, JD TI EUKARYOTIC TRANSCRIPTION TERMINATION FACTOR LA MEDIATES TRANSCRIPT RELEASE AND FACILITATES REINITIATION BY RNA-POLYMERASE-III SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ALPHA-FETOPROTEIN GENE; LUPUS ANTIGEN-LA; XENOPUS-LAEVIS; SIGNAL RECOGNITION; PROTEIN-BINDING; RIBOSOMAL-RNA; ALU INSERTION; 7SL RNA; 3' END; COMPLEXES AB Ample evidence indicates that Alu family interspersed elements retrotranspose via primary transcripts synthesized by RNA polymerase III (pol III) and that this transposition sometimes results in genetic disorders in humans. However, Alu primary transcripts can be processed posttranscriptionally, diverting them away from the transposition pathway. The pol III termination signal of a web-characterized murine B1 (Alu-equivalent) element inhibits RNA 3' processing, thereby stabilizing the putative transposition intermediary. We used an immobilized template-based assay to examine transcription termination by VA1, 7SL, and Alu class III templates and the role of transcript release in the pol III terminator-dependent inhibition of processing of B1-Alu transcripts. We found that the RNA-binding protein La confers this terminator-dependent 3' processing inhibition on transcripts released from the B1-Alu template. Using pure recombinant La protein and affinity-purified transcription complexes, we also demonstrate that La facilitates multiple rounds of transcription reinitiation by pot III. These results illustrate an important role for La in RNA production by demonstrating its ability to clear the termination sites of class III templates, thereby promoting efficient use of transcription complexes by pol III. The role of La as a potential regulatory factor in transcript maturation and how this might apply to Alu interspersed elements is discussed. C1 DUKE UNIV,MED CTR,DEPT MICROBIOL,DURHAM,NC 27710. RP MARAIA, RJ (reprint author), NICHHD,MOLEC GROWTH REGULAT LAB,BLDG 6,ROOM 416,BETHESDA,MD 20892, USA. NR 75 TC 128 Z9 128 U1 0 U2 0 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 1994 VL 14 IS 3 BP 2147 EP 2158 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MX640 UT WOS:A1994MX64000064 PM 8114745 ER PT J AU BLISKOVSKII, VV AF BLISKOVSKII, VV TI HUMAN GENES WITH VARIABLE NUMBER OF ABSOLUTE TANDEM REPEATS IN THE CODING REGION - POSSIBLE ROLE IN PATHOGENESIS (A REVIEW) SO MOLECULAR BIOLOGY LA English DT Review DE TANDEM REPEATS; HYPERVARIABLE GENES; VNTR LOCI; MINISATELLITES; TRANSCRIPT POLYDISPERSITY; APOLIPOPROTEIN (A); MUCINS; ATHEROSCLEROSIS; MAMMARY ADENOCARCINOMA ID EPITHELIAL TUMOR-ANTIGEN; CORONARY HEART-DISEASE; MUCIN GENE; APOLIPOPROTEIN(A) PHENOTYPES; RISK FACTOR; EXPRESSION; LIPOPROTEIN(A); HETEROGENEITY; SEQUENCES; CLONING AB The review covers such aspects as the transcription of genes with variable-number absolute tandem repeats (hypervariable minisatellites) in the coding regions and the possible role of these genes in pathogenesis; association of the apo(a) gene short alleles with atherosclerosis; the possible role of the MUC1 gene product (episialin) in carcinogenesis; the probable causes of the polydispersity of apo(a) and mucin gene transcripts. The latter is supposed to result from transcription of repeats. The possible association between repeat transcription and recombination is discussed. Both the apo(a) and the MUC1 genes display an inverse relationship between allele length (repeat number) and extent of full-gene transcription. The VNTR gene length is assessed as a risk factor in human pathologies. C1 VA ENGELHARDT MOLEC BIOL INST,MOSCOW 117984,RUSSIA. RP BLISKOVSKII, VV (reprint author), NCI,9000 ROCKVILLE PIKE,BG 37,RM 5B16,BETHESDA,MD 20892, USA. NR 25 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA CONSULTANTS BUREAU 233 SPRING ST, NEW YORK, NY 10013 SN 0026-8933 J9 MOL BIOL+ JI Mol. Biol. PD MAR-APR PY 1994 VL 28 IS 2 BP 185 EP 189 PN 1 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PM242 UT WOS:A1994PM24200003 ER PT J AU GONZALEZ, P HERNANDEZCALZADILLA, C RAO, PV RODRIGUEZ, IR ZIGLER, JS BORRAS, T AF GONZALEZ, P HERNANDEZCALZADILLA, C RAO, PV RODRIGUEZ, IR ZIGLER, JS BORRAS, T TI COMPARATIVE-ANALYSIS OF THE ZETA-CRYSTALLIN QUINONE REDUCTASE GENE IN GUINEA-PIG AND MOUSE SO MOLECULAR BIOLOGY AND EVOLUTION LA English DT Article DE GUINEA PIG; MOUSE; ALTERNATIVE PROMOTER; OCULAR LENS; MOLECULAR EVOLUTION ID ALPHA-B-CRYSTALLIN; HEREDITARY CATARACT; ENZYME CRYSTALLINS; MESSENGER-RNAS; LENS PROTEIN; EYE LENS; EXPRESSION; EVOLUTION; ELEMENT; IDENTIFICATION AB zeta-Crystallin is a novel nicotinamide adenine dinucleotide phosphate:quinone reductase, present at enzymatic levels in various tissues of different species, which is highly expressed in the lens of some hystricomorph rodents and camelids. We report here the complementary DNA (cDNA) cloning of zeta-crystallin from liver libraries in guinea pig (Cavia porcellus), where zeta-crystallin is highly expressed in the lens, and in the laboratory mouse (Mus musculus), where expression in the lens occurs only at enzymatic levels. A 5' untranslated sequence different from the one previously reported for the guinea pig lens cDNA was found in these clones. We also report the isolation of genomic clones including the complete guinea pig zeta-crystallin gene and the 5' region of this gene in mouse. These results show the presence of two promoters in the guinea pig zeta-crystallin gene, one responsible for expression at enzymatic levels and the other responsible for the high expression in the lens. The guinea pig lens promoter is not present in the mouse gene. This is the first example in which the recruitment of an enzyme as a lens crystallin can be explained by the acquisition of an alternative lens-specific promoter. C1 NEI,MECHANISMS OCULAR DIS LAB,BETHESDA,MD 20892. UNIV LA LAGUNA,DEPT BIOQUIM & BIOL MOLEC,LA LAGUNA,SPAIN. NR 37 TC 21 Z9 22 U1 0 U2 0 PU SOC MOLECULAR BIOLOGY EVOLUTION PI LAWRENCE PA PO BOX 1897, LAWRENCE, KS 66044-8897 SN 0737-4038 J9 MOL BIOL EVOL JI Mol. Biol. Evol. PD MAR PY 1994 VL 11 IS 2 BP 305 EP 315 PG 11 WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity GA MZ888 UT WOS:A1994MZ88800013 PM 8170370 ER PT J AU VARMUS, H AF VARMUS, H TI BASIC SCIENCE AND THE NIH SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article RP VARMUS, H (reprint author), NIH,BETHESDA,MD 20892, USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD MAR PY 1994 VL 5 IS 3 BP 267 EP 272 PG 6 WC Cell Biology SC Cell Biology GA NG464 UT WOS:A1994NG46400002 PM 8049519 ER PT J AU CERRUTI, C PILOTTE, NS UHL, G KUHAR, MJ AF CERRUTI, C PILOTTE, NS UHL, G KUHAR, MJ TI REDUCTION IN DOPAMINE TRANSPORTER MESSENGER-RNA AFTER CESSATION OF REPEATED COCAINE ADMINISTRATION SO MOLECULAR BRAIN RESEARCH LA English DT Article DE DOPAMINE TRANSPORTER; DOPAMINE UPTAKE; GENE EXPRESSION; TRANSPORTER REGULATION; COCAINE ID VENTRAL TEGMENTAL AREA; RAT NUCLEUS-ACCUMBENS; EXTRACELLULAR DOPAMINE; MESENCEPHALIC TEGMENTUM; MESSENGER-RNA; H-3 DOPAMINE; STRIATUM; WITHDRAWAL; EXPRESSION; CLONING AB Male, Lewis rats were treated intravenously for 2 weeks with saline or cocaine using a dose and injection schedule that is similar to the doses and patterns of cocaine intake in self-administration studies. Ten days after cessation of treatment, dopamine transporter binding levels were decreased in the nucleus accumbens but not in the striatum. In situ hybridization studies revealed decreases in dopamine transporter mRNA that were restricted to cells of the interfascicular and caudal linear nuclei; these dopaminergic cell groups, found in the ventral tegmentum, project to the nucleus accumbens and other limbic areas. Other dopaminergic cell groups in midbrain which project mainly to other areas did not show a decrease in mRNA. These results indicate that gene expression can be altered many days after withdrawal from cocaine, and provide an example of transporter regulation by a change in gene expression. C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224. NIDA,ADDICT RES CTR,MOLEC NEUROBIOL BRANCE,BALTIMORE,MD 21224. NR 57 TC 72 Z9 72 U1 2 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 1994 VL 22 IS 1-4 BP 132 EP 138 DI 10.1016/0169-328X(94)90040-X PG 7 WC Neurosciences SC Neurosciences & Neurology GA MZ438 UT WOS:A1994MZ43800015 ER PT J AU GONZALEZ, AM WALTHER, D PAZOS, A UHL, GR AF GONZALEZ, AM WALTHER, D PAZOS, A UHL, GR TI SYNAPTIC VESICULAR MONOAMINE TRANSPORTER EXPRESSION - DISTRIBUTION AND PHARMACOLOGICAL PROFILE SO MOLECULAR BRAIN RESEARCH LA English DT Article DE SYNAPTIC VESICLE; MONOAMINE TRANSPORTER; DIHYDROTETRAHYDROBENAZINE; RESERPINE; SEROTONIN; DOPAMINE; NOREPINEPHRINE; EPINEPHRINE ID RAT-BRAIN; HISTIDINE-DECARBOXYLASE; DOPAMINE TRANSPORTER; CHROMAFFIN GRANULES; NERVOUS-SYSTEM; CLONING; SEROTONIN; VESICLES; MEMBRANE; BINDING AB The human vesicular monoamine transporter (hSVMT) cDNA predicts a protein of 515 amino acids that shares 92% amino acid identity with the rat cDNA. Northern analyses reveal expression of 4.3 kb SVMT mRNAs in rat hypothalamus, midbrain and brainstem, a 3 kb hSVMT mRNA in human brainstem and a 4.8 kb hSVMT mRNA in human hypothalamus. In situ hybridization documents significant SVMT expression in human nigra compacta neurons and in rat hypothalamic neurons whose distribution patterns are identical to those previously reported to display histaminergic markers. COS cell hSVMT expression yielded nanomolar affinities for tetrabenazine and reserpine, micromolar affinities for haloperidol, GBR12909, serotonin, mazindol, nomifensin and d-amphetamine, while dopamine, epinephrine, norepinephrine and histamine each displayed millimolar affinities. These observations extend the pharmacological characterization of hSVMT and studies of its distribution, and indicate likely physiological roles for SVMT in packaging monoamine transmitters including histamine. C1 JOHNS HOPKINS UNIV,SCH MED,NATL INST DRUG ABUSE,ADDICT RES CTR,MOLEC NEUROBIOL BRANCH,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. UNIV CANTABRIA,SCH MED,DEPT PHYSIOL & PHARMACOL,PHARMACOL UNIT,E-39005 SANTANDER,SPAIN. NR 47 TC 50 Z9 51 U1 1 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 1994 VL 22 IS 1-4 BP 219 EP 226 DI 10.1016/0169-328X(94)90050-7 PG 8 WC Neurosciences SC Neurosciences & Neurology GA MZ438 UT WOS:A1994MZ43800025 ER PT J AU WELLER, M MONTPIED, P PAUL, SM AF WELLER, M MONTPIED, P PAUL, SM TI NMDA RECEPTOR-MEDIATED EXCITOPROTECTION OF CULTURED CEREBELLAR GRANULE NEURONS FAILS TO ALTER GLUTAMATE-INDUCED EXPRESSION OF C-FOS AND C-JUN MESSENGER-RNAS SO MOLECULAR BRAIN RESEARCH LA English DT Article DE GLUTAMATE; NMDA; MK-801; C-FOS; C-JUN; ONCOGENE; NEUROPROTECTION; EXCITOPROTECTION; NEUROTOXICITY; EXCITOTOXICITY; CEREBELLUM NEURON ID PROTEIN-KINASE-C; D-ASPARTATE PROMOTES; ONCOGENE EXPRESSION; BINDING ACTIVITIES; CELLS-INVITRO; STIMULATION; ACTIVATION; SURVIVAL; RNA; TOXICITY AB Exposure of cultured cerebellar granule neurons to subtoxic concentrations of N-methyl-D-aspartate (NMDA) induces a state of excitoprotection when measured by subsequent exposure to toxic concentrations of glutamate. This NMDA-induced excitoprotective state is prevented by inhibitors of new RNA and protein synthesis. Since the neurotrophic and excitoprotective effects of NMDA in cerebellar granule neurons may involve changes in the expression of the immediate early genes c-fos and c-jun, we measured c-fos and c-jun mRNAs in cerebellar;granule neurons after exposure to either toxic concentrations of glutamate or excitoprotective (subtoxic) concentrations of NMDA. Exposure of cerebellar granule neurons to toxic concentrations of glutamate induced a dramatic increase in c-fos and c-jun mRNAs which was not associated with a corresponding increase in c-fos and c-jun proteins as measured immunocytochemically. However, the increase in c-fos and c-jun mRNAs induced by toxic concentrations of glutamate was not altered by preexposing cerebellar granule neurons to NMDA, suggesting that increased expression of c-fos and c-jun mRNAs is not sufficient for glutamate toxicity of these neurons. Preexposure of cerebellar granule neurons to NMDA for 24 h, which induced a maximal excitoprotective state, resulted in a transient increase in c-fos, and to a lesser degree c-jun, mRNAs similar to that induced by toxic concentrations of glutamate. The induction of c-fos, but not that of c-jun, mRNA both by excitoprotective concentrations of NMDA and by neurotoxic concentrations of glutamate was blocked by the non-competitive NMDA receptor antagonist, MK-801. These data show that c-fos and c-jun may play a role in NMDA receptor-mediated excitoprotection as well as in NMDA receptor-mediated neurotoxicity. NMDA receptor-mediated excitoprotection is likely to interfere with the intracellular cascade of glutamate toxicity by acting on an element downstream of c-fos and c-jun-dependent transcriptional regulation. C1 NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BETHESDA,MD 20892. NR 28 TC 19 Z9 19 U1 0 U2 0 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 1994 VL 22 IS 1-4 BP 227 EP 235 DI 10.1016/0169-328X(94)90051-5 PG 9 WC Neurosciences SC Neurosciences & Neurology GA MZ438 UT WOS:A1994MZ43800026 ER PT J AU STACHOWIAK, MK GOC, A HONG, JS POISNER, A JIANG, HK STACHOWIAK, EK AF STACHOWIAK, MK GOC, A HONG, JS POISNER, A JIANG, HK STACHOWIAK, EK TI REGULATION OF TYROSINE-HYDROXYLASE GENE-EXPRESSION IN DEPOLARIZED NONTRANSFORMED BOVINE ADRENAL-MEDULLARY CELLS - 2ND MESSENGER SYSTEMS AND PROMOTER MECHANISMS SO MOLECULAR BRAIN RESEARCH LA English DT Note DE TYROSINE HYDROXYLASE; GENE REGULATION; DEPOLARIZATION; ADRENAL MEDULLA ID PHENYLETHANOLAMINE N-METHYLTRANSFERASE; FOS PROTO-ONCOGENE; CHROMAFFIN CELLS; C-FOS; CYCLIC-AMP; MEMBRANE DEPOLARIZATION; NUCLEOTIDE-SEQUENCE; COLD STRESS; CDNA CLONE; RAT AB Activation of the tyrosine hydroxylase (TH) gene in the adrenal medulla during stress is mediated by trans-synaptic mechanisms and may involve cholinergic receptors. Stimulation of nicotinic receptors in adrenal medullary cells induces cell depolarization, influx of Ca2+ ions and increases levels of cAMP. We have shown that both cAMP and membrane depolarization produce an increase in the expression of the TH gene in cultured bovine adrenal medullary cells (BAMC). Others have proposed that transcriptional activation of the TH gene by cAMP is mediated through the sequence homologous to a cAMP responsive element (CRE) located in the proximal region of the TH gene promoter. In the present study we have examined the mechanisms by which membrane depolarization increases the TH gene activity. Treatment of serum-free BAMC cultures with the depolarizing agent, veratridine, increased the extracellular concentration of catecholamines, Met(5)-enkephalin, and the relative abundance of TH mRNA. Veratridine treatment also increased the levels of mRNAs for the catecholamine biosynthetic enzyme phenylethanolamine N-methyltransferase (PNMT), and proenkephalin A (PEK). Treatment for longer than 3 h was required to increase TH mRNA levels. By contrast, our previous studies indicated that cAMP stimulation for 2 h produces a maximal increase in TH mRNA levels in BAMC. The effects of veratridine and forskolin on TH mRNA levels were additive, further indicating that depolarization and cAMP activate TH gene expression via different pathways. Calmidazolium, an antagonist of calmodulin, had no effect on the veratridine-induced increase in TH mRNA levels. Similarly sphingosine treatment or preincubation with PMA, which reduce protein kinase C (PKC) activity and attenuate the induction of TH mRNA by PMA or the hormone, angiotensin II, did not affect the induction by veratridine. To identify promoter mechanisms of TH gene activation in depolarized cells we transfected BAMC with a plasmid pTHgoodLuc and treated with veratridine for 24 h. pTHgoodLUC contains a luciferase reporter gene linked to a -428/+21 bp fragment of the bovine TH gene promoter (relative to the transcription start site). Veratridine increased the expression of luciferase from the TH promoter 2.5-fold. Deletion of the -194/-54 bp promoter region containing SP-1 and POU/Oct sites reduced veratridine stimulation by 40%. Additional deletion of the -269 to -190 bp promoter segment, including an AP-1 element, further reduced veratridine stimulation to a statistically non-significant level. In conclusion, activation of TH gene expression upon depolarization is not mediated by calmodulin and PKC. Promoter sequences involved in this activation are located upstream from the CRE. Depolarization may activate TH gene transcription by acting on more than one regulatory region. C1 NIEHS, INTEGRAT BIOL LAB, NEUROPHARMACOL SECT, RES TRIANGLE PK, NC 27709 USA. UNIV KANSAS, MED CTR, DEPT PHARMACOL, KANSAS CITY, KS 66103 USA. RP STACHOWIAK, MK (reprint author), ST JOSEPHS HOSP, MED CTR,BARROW NEUROL INST,DIV NEUROBIOL, MOLEC NEUROBIOL LAB, 350 W THOMAS RD, PHOENIX, AZ 85013 USA. RI Goc, Anna/F-3423-2013 NR 42 TC 38 Z9 38 U1 0 U2 0 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 1994 VL 22 IS 1-4 BP 309 EP 319 DI 10.1016/0169-328X(94)90059-0 PG 11 WC Neurosciences SC Neurosciences & Neurology GA MZ438 UT WOS:A1994MZ43800034 ER PT J AU HANSEN, LA TENNANT, R AF HANSEN, LA TENNANT, R TI FOCAL TRANSGENE EXPRESSION ASSOCIATED WITH PAPILLOMA DEVELOPMENT IN V-HA-RAS-TRANSGENIC TG.AC MICE SO MOLECULAR CARCINOGENESIS LA English DT Article DE MOUSE SKIN TUMORIGENESIS; 12-O-TETRADECANOYLPHORBOL-13-ACETATE; TRANSGENIC MICE ID PROTEIN-KINASE-C; CELL NUCLEAR ANTIGEN; ORNITHINE DECARBOXYLASE ACTIVITY; DNA POLYMERASE-DELTA; MURINE SARCOMA-VIRUS; MOUSE SKIN; TUMOR PROMOTION; PHORBOL ESTERS; AUXILIARY PROTEIN; MAMMARY-GLAND AB The homozygous transgenic mouse line TG.AC contains a v-Ha-ras transgene and rapidly develops epidermal papillomas in response to either wounding or treatment with tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). The transgenic v-Ha-ras protein product was detected in all papillomas removed from TPA-treated TG.AC mice but not in vehicle- or TPA-treated TG.AC skin without tumors. In situ hybridization demonstrated that focal expression of the transgene was limited to regions of papilloma development and further localized the expression of the transgene message to the epidermal component of the papillomas, with the strongest signal in the basal epidermoid cells. Cellular proliferation, as indicated by immunohistochemical staining for proliferating-cell nuclear antigen (PCNA), was similarly localized primarily to basal epidermoid cells and, to a lesser extent, stratum spinosum cells in all papillomas analyzed. Cells that stained positively for PCNA were much more common in the papillomas than in the surrounding, normal-appearing skin. The focal nature of papilloma development was also evidenced by protein kinase C activity and hyperplasia after TPA treatment. As early as 18 d after the start of TPA treatment, focal hyperplasias associated with the follicular epidermis were observed in TG.AC but not nontransgenic FVB/N skin; these hyperplasias were assumed to be the precursors of the epidermal papillomas. To explain the development of transgene-expressing tumors from apparently transgene-negative, normal-appearing skin, we hypothesize that the papillomas arise from the clonal expansion of focal areas of epidermal cells that overexpress the transgene. We also propose that the TG.AC line is an excellent model for studying very early events in papillomagenesis. (C) 1994 Wiley-Liss, Inc. C1 NIEHS,ENVIRONM CARCINOGENESIS & MUTAGENESIS LAB,POB 12233,RES TRIANGLE PK,NC 27709. NR 53 TC 58 Z9 58 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD MAR PY 1994 VL 9 IS 3 BP 143 EP 154 DI 10.1002/mc.2940090306 PG 12 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA NB964 UT WOS:A1994NB96400005 PM 7908201 ER PT J AU JERRY, DJ BUTEL, JS DONEHOWER, LA PAULSON, EJ COCHRAN, C WISEMAN, RW MEDINA, D AF JERRY, DJ BUTEL, JS DONEHOWER, LA PAULSON, EJ COCHRAN, C WISEMAN, RW MEDINA, D TI INFREQUENT P53 MUTATIONS IN 7,12-DIMETHYLBENZ[A]ANTHRACENE INDUCED MAMMARY-TUMORS IN BALB/C AND P53 HEMIZYGOTIC MICE SO MOLECULAR CARCINOGENESIS LA English DT Article DE MOUSE; 7,12-DIMETHYLBENZ[A]ANTHRACENE; BREAST CANCER; P53; CHEMICAL CARCINOGENESIS ID HUMAN BREAST-CANCER; ATAXIA-TELANGIECTASIA; GENE-MUTATIONS; RAS ONCOGENE; WILD-TYPE; EXPRESSION; PROTEIN; CELLS; TRANSFORMATION; INVITRO AB We conducted experiments to determine if p53 alterations, which are frequent in human breast cancers, were also common in murine mammary tumors. In 13 mammary tumors from 7,12-dimethylbenz[a]anthracene (DMBA)-treated BALB/c mice were immunohistochemically analyzed for overexpression of p53; p53 protein was not detectable. Three of the tumors were established as cell lines in vitro. p53 protein was rarely detected at passage 4 in these lines but was overexpressed by passage 8 in two of them. The p53 nucleotide sequence was shown to be wild type in one primary mammary tumor and in the two p53-overexpressing cell lines. One cell line that overexpressed p53 in vitro was implanted into BALB/c mice. The resulting tumors retained the wild-type p53 nucleotide sequence but no longer expressed detectable levels of p53 protein, suggesting that the overexpression of wild-type p53 was related to in vitro culture conditions. The effect of DMBA on mammary-tumor development was also tested in mice rendered hemizygous for p53. These mice and wild-type littermate controls had no differences in susceptibility to induction of mammary tumors by oral administration of DMBA. Furthermore, Southern blot hybridizations detected no gross alterations in the wild-type p53 allele in mammary tumors from the p53-deficient mice. Point mutation of the wild-type p53 allele was also infrequent in the DMBA-induced mammary tumors from hemizygous p53 mice; it occurred in only one of seven tumors. Thus, the p53 gene is apparently not a primary target for genetic alterations in DMBA-induced mammary tumors. Next, we examined mammary tumors derived from D1 and D2 transplantable hyperplastic alveolar nodule (HAN) outgrowths, which rapidly form tumors containing Ha-ras mutations after DMBA treatment. As ras and p53 mutants can cooperate in transformation, we examined whether D1 and D2 HAN outgrowths have p53 mutations. Unlike in the DMBA-induced primary mammary tumors, nuclear p53 accumulation was observed frequently (10 of 14) in tumors that arose from D1 and D2 HAN outgrowths. Direct sequencing of the entire coding region of the p53 cDNA from six D1 and D2 tumors confirmed that the sequence was wild type. Although wild-type p53 was retained in both DMBA-induced mammary tumors and mammary tumors derived from D1 and D2 preneoplastic outgrowths, wild-type p53 overexpression was detected only in D1 and D2 tumors. Therefore, D1 and D2 tumors appear to arise by a pathway in which p53 expression is altered, whereas DMBA induction affects a different pathway that does not require such alteration. (C) 1994 Wiley-Liss, Inc. C1 BAYLOR COLL MED,DEPT CELL BIOL,1 BAYLOR PLAZA,HOUSTON,TX 77030. BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. FU NCI NIH HHS [CA25215, CA33369, CA54897] NR 57 TC 59 Z9 59 U1 0 U2 2 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 1994 VL 9 IS 3 BP 175 EP 183 DI 10.1002/mc.2940090309 PG 9 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA NB964 UT WOS:A1994NB96400008 PM 8142019 ER PT J AU PETERSON, KM DAVIS, PS JUDD, BH AF PETERSON, KM DAVIS, PS JUDD, BH TI THE DETERMINED STATE OF WHITE EXPRESSION IN THE DROSOPHILA EYE IS MODIFIED BY ZESTE1 IN THE WZM FAMILY OF MUTANTS SO MOLECULAR & GENERAL GENETICS LA English DT Article DE DROSOPHILA-MELANOGASTER; TRANSVECTION; CHROMATIN CONFIGURATION; TRANSPOSONS; POSITION-EFFECT VARIEGATION ID GENE-REGULATION; MOLECULAR ANALYSIS; MELANOGASTER; TRANSVECTION; DNA; MUTATIONS; LOCUS; CHROMOSOME; SEQUENCES; ENHANCER AB Analysis of the white(zeste mottled) (w(zm)) mutant family suggests that the zeste gene product functions in establishing and stabilizing a transcriptionally active chromatin domain for white locus expression. The z1 mutation reduces expression of paired or proximate copies of white, while single or unpaired copies maintain wild-type levels of expression. The w(zm) mutation, caused by the insertion of the retrotransposon BEL into the 5' intron of white, alters the zeste-white interaction to produce a mottled eye phenotype in hemizygous z1 w(zm) males. We have determined the molecular structure of four w(zm) derivatives. w(zl) results from the insertion of an additional transposable element into the 5' regulatory region of white. w(zvl) is a deletion of sequences upstream of the white locus. Two others, w(halo) and w(cres), result from the transposition of w(zm) plus the entire verticals-roughest region into heterochromatin near the tip of chromosome 3L. They variegate for roughest but not for white; rather, the z1 effect on w(zm) now causes white expression to become non-autonomous and non-clonal. The analysis of these five mutations shows that the neomorphic zeste1 product, in combination with structural changes imposed by transposons and intercalary heterochromatin, modifies the determination and stability of white expression. We propose that the normal zeste product functions as part of a complex that stimulates transcription by changing chromatin conformation to establish and maintain transcriptionally active domains. The unpairing of homologs is proposed to be one of the initial results of conformational change, providing an explanation for the role of zeste in transvection. C1 NIEHS,GENET LAB,RES TRIANGLE PK,NC 27709. NR 40 TC 16 Z9 16 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD MAR PY 1994 VL 242 IS 6 BP 717 EP 726 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA NC621 UT WOS:A1994NC62100012 PM 8152422 ER PT J AU LABUTTA, RJ MILES, RB SANES, JN HALLETT, M AF LABUTTA, RJ MILES, RB SANES, JN HALLETT, M TI MOTOR PROGRAM MEMORY STORAGE IN PARKINSONS-DISEASE PATIENTS TESTED WITH A DELAYED-RESPONSE TASK SO MOVEMENT DISORDERS LA English DT Article DE REACTION TIME; DELAYED RESPONSE TASK; PARKINSONS DISEASE; MEMORY STORAGE; MOTOR PROGRAM ID REACTION-TIME PERFORMANCE; TARGETED FORCE IMPULSES; MOVEMENT DIRECTION; TRAJECTORY CONTROL; EYE-MOVEMENTS; EXECUTION; AMPLITUDE; MONKEY; ALZHEIMERS AB We used a delayed response paradigm to test the hypothesis that the prolonged reaction time in patients with Parkinson's disease (PD) is related to a deficiency in their ability to store a motor program in memory while waiting to move. PD patients, both on and off medication, were compared with age-matched normal subjects during arm movements directed toward a target light. The target light was displayed either during a 3- to 9-s delay or for only 1 s followed by a 2- to 8-s delay before the go signal. At the end of the delay, subjects were required to begin movement rapidly. The reaction time of PD patients was longer than normal and increased slightly when the patients were off medication. The patients had no excessive increase in reaction time with delay in either task compared with the control subjects. We conclude that patients with PD can hold a motor program in memory storage for at least 8 s. C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. BROWN UNIV,DEPT NEUROSCI,PROVIDENCE,RI. NR 41 TC 7 Z9 7 U1 1 U2 1 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 1994 VL 9 IS 2 BP 218 EP 222 DI 10.1002/mds.870090217 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA NA179 UT WOS:A1994NA17900016 PM 8196687 ER PT J AU LOU, JS VALLSSOLE, J TORO, C HALLETT, M AF LOU, JS VALLSSOLE, J TORO, C HALLETT, M TI FACIAL ACTION MYOCLONUS IN PATIENTS WITH OLIVOPONTOCEREBELLAR ATROPHY SO MOVEMENT DISORDERS LA English DT Note DE ACTION MYOCLONUS; ATROPHY, OLIVOPONTOCEREBELLAR (OPCA); ELECTROMYOGRAPHY (EMG); MYOKYMIA, FACIAL ID MYOKYMIA; TREMOR AB We studied four patients with familial olivopontocerebellar atrophy (OPCA) who had abnormal twitching of the cheeks and perioral muscles induced by facial movements. With the muscles at rest, electromyographic (EMG) recordings of the orbicularis oris and risorius muscles revealed myokymic discharges in the absence of visible movements. With voluntary contraction, the EMG showed synchronous discharges in the orbicularis oris and risorius muscles ipsilaterally associated with visible twitching. The duration of the EMG bursts was 10 to 75 ms with a frequency of 8 to 25 Hz, which suggested that the abnormal twitching was most consistent with a myoclonic disorder. Because it was induced by activation of the facial muscles, this movement disorder represents a form of action myoclonus. C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NR 18 TC 12 Z9 12 U1 0 U2 0 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 1994 VL 9 IS 2 BP 223 EP 226 DI 10.1002/mds.870090218 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA NA179 UT WOS:A1994NA17900017 PM 8196688 ER PT J AU WILLIAMS, WM CHANG, MCJ RAPOPORT, SI AF WILLIAMS, WM CHANG, MCJ RAPOPORT, SI TI CEREBRAL MICROVESSEL PHOSPHOLIPASE A(2) ACTIVITY IN SENESCENT MOUSE SO NEUROCHEMICAL RESEARCH LA English DT Article DE PHOSPHOLIPASE A(2); FATTY ACIDS; AGING; BRAIN; MOUSE; MICROVESSELS ID ARACHIDONIC-ACID; BRAIN; CELLS; METABOLISM; VESICLES AB Phospholipase A(2) activity was measured in cerebral microvessels isolated from 5 to 6 month (young adult) and 21 to 24 month (aged adult) old mice. Radiolabeled 1-stearoyl-2-[1-C-14]arachidonyl choline phosphoglyceride was used as the enzyme substrate, and enzyme activity determined at pH 8 and pH 9. Activity in older animals was significantly less than in younger animals at both pH's. With choline phosphoglyceride as a substrate, phospholipase A(2) activity was predominantly Ca2+-dependent, although a small, but measurable Ca2+-independent component was present. Negligible production of diacylglycerol indicated little or no phospholipase C activity. These findings indicate that activity of a phospholipase A(2), which utilizes choline phosphoglyceride as a substrate, is affected by the aging process. Moreover, a change in PLA(2) activity would result in altered metabolism of specific phosphoglycerides and turnover of fatty acids at the sn-2 position in cerebral microvessels. RP NIA, NEUROSCI LAB, BLDG 10, ROOM 6C-103, BETHESDA, MD 20892 USA. NR 26 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0364-3190 EI 1573-6903 J9 NEUROCHEM RES JI Neurochem. Res. PD MAR PY 1994 VL 19 IS 3 BP 317 EP 320 DI 10.1007/BF00971580 PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MV307 UT WOS:A1994MV30700012 PM 8177371 ER PT J AU ARNETT, PA RAO, SM BERNARDIN, L GRAFMAN, J YETKIN, FZ LOBECK, L AF ARNETT, PA RAO, SM BERNARDIN, L GRAFMAN, J YETKIN, FZ LOBECK, L TI RELATIONSHIP BETWEEN FRONTAL-LOBE LESIONS AND WISCONSIN CARD SORTING TEST-PERFORMANCE IN PATIENTS WITH MULTIPLE-SCLEROSIS SO NEUROLOGY LA English DT Article ID NEUROPSYCHOLOGICAL ASSESSMENT; MRI; IMPAIRMENT; MEMORY; DYSFUNCTION AB Conceptual reasoning deficits are common in patients with multiple sclerosis (MS) and are typically associated with focal lesions involving the frontal lobes' - In this study, we predicted that MS patients with frontal white matter lesions (MS-F) would be more impaired on a standard conceptual reasoning task (Wisconsin Card Sorting Test; WCST) than patients with minimal frontal lesions (MS-NF), even if the total cerebral-lesion area (TLA), measured from MRI, was equivalent across groups. We subdivided 43 definite MS patients into three groups based on MRI findings: seven in the MS-F group (mean TLA = 41.4 cm2) and seven in the MS-NF group (mean TLA = 50.0 cm2); 29 MS patients served as a low lesion burden control group (MS-C; mean TLA = 6.4 cm2). The groups did not differ with regard to demographic and illness characteristics. Although the three subgroups obtained comparable scores on a measure of global cognitive functioning (verbal intelligence), the MS-F group achieved significantly fewer categories and made more total errors on the WCST than did the MS-NF and MS-C groups. The MS-F group made significantly more perseverative responses than the MS-C group and nonsignificantly more than the MS-NF group. These results suggest that the pattern of cognitive decline in MS is a function of the location of demyelinating lesions within the cerebral hemispheric white matter. Finally, we supplement the group study results with a case report of an MS patient who was studied serially with MRI and cognitive testing. C1 MED COLL WISCONSIN,DEPT RADIOL,MILWAUKEE,WI 53226. NINCDS,COGNIT NEUROSCI SECT,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892. RP ARNETT, PA (reprint author), MED COLL WISCONSIN,DEPT NEUROL,NEUROPSYCHOL SECT,9200 W WISCONSIN AVE,MILWAUKEE,WI 53226, USA. RI Rao, Stephen/A-2460-2010; OI Rao, Stephen/0000-0002-6463-7460; Grafman, Jordan H./0000-0001-8645-4457 FU NINDS NIH HHS [K04 NS01055, NINDS R01 NS22128] NR 42 TC 220 Z9 222 U1 4 U2 6 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR PY 1994 VL 44 IS 3 BP 420 EP 425 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA NB934 UT WOS:A1994NB93400009 PM 8145908 ER PT J AU PASCUALLEONE, A GOMEZTORTOSA, E GRAFMAN, J ALWAY, D NICHELLI, P HALLETT, M AF PASCUALLEONE, A GOMEZTORTOSA, E GRAFMAN, J ALWAY, D NICHELLI, P HALLETT, M TI INDUCTION OF VISUAL EXTINCTION BY RAPID-RATE TRANSCRANIAL MAGNETIC STIMULATION OF PARIETAL LOBE SO NEUROLOGY LA English DT Article; Proceedings Paper CT 45th Annual Meeting of the American-Academy-of-Neurology CY APR, 1993 CL NEW YORK, NY SP AMER ACAD NEUROL ID UNILATERAL NEGLECT; CORTEX AB We used repetitive, rapid-rate transcranial magnetic stimulation (rTMS) for the noninvasive study of visual attention in humans. Six right-handed volunteers completed eight blocks of 20 single- and 10 double-visual-stimulus trials. The visual stimulus was a single asterisk on the right or left side of a computer screen or two asterisks presented simultaneously. The subject had to respond to the stimulus by pressing the right or left response key or both keys simultaneously. During six of the blocks, we applied focal rTMS in trains of five pulses at 25 Hz and 115% of the subject's motor threshold intensity to scalp positions O1, O2, P3, P4, T5, or T6. Occipital rTMS led to a large number of misses of the contralateral asterisk regardless of whether a single or double stimulus was presented. Parietal rTMS did not induce misses of single stimuli but led to a large number of misses of the contralateral asterisk in the double-stimulus condition. The effects of temporal rTMS were inconsistent. We conclude that rTMS to the occipital lobe causes a sensory detection block, whereas rTMS to the parietal lobe can induce selective extinction of contralateral visual stimuli during a simultaneous double stimulus. C1 NINCDS,MED NEUROL BRANCH,BLDG 10,ROOM 55209,BETHESDA,MD 20892. NINCDS,HUMAN MOTOR CONTROL SECT,HUMAN CRITICAL PHYSIOL UNIT,BETHESDA,MD 20892. RI Pascual-Leone, Alvaro/G-6566-2011; Nichelli, Paolo/F-7336-2015; OI Nichelli, Paolo/0000-0001-9756-6796; Grafman, Jordan H./0000-0001-8645-4457 NR 21 TC 151 Z9 152 U1 1 U2 3 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR PY 1994 VL 44 IS 3 BP 494 EP 498 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA NB934 UT WOS:A1994NB93400022 PM 8145921 ER PT J AU BHARUCHA, VA PEDEN, KWC TENNEKOON, GI AF BHARUCHA, VA PEDEN, KWC TENNEKOON, GI TI SV40 LARGE T-ANTIGEN WITH C-JUN DOWN-REGULATES MYELIN P-0 GENE-EXPRESSION - A MECHANISM FOR PAPOVAVIRAL T-ANTIGEN-MEDIATED DEMYELINATION SO NEURON LA English DT Article ID RAT SCHWANN-CELLS; TRANSCRIPTION FACTOR AP-1; PROTEIN-DNA COMPLEXES; TRANSGENIC MICE; MESSENGER-RNA; SV40-TRANSFORMED CELLS; PERIPHERAL-NERVE; MAJOR MYELIN; BINDING-SITE; ONCOGENE AB Expression of myelin proteins has been shown to be altered in transgenic mice that express papovaviral large tumor (T) antigens. This paper analyzes the effect on P-0 gene expression in secondary Schwann cells transfected with the SV40 T antigen gene and in Schwann cells immortalized by T antigen. In secondary Schwann cells, both T antigen and c-jun are required for significant inhibition of the P-0 promoter; expression of only one of the proteins is insufficient for repression of the P-0 gene. T antigen, c-jun (p39), and c-jun-related protein (p47) form an immunoprecipitable complex in SV40 immortalized Schwann cell lines, and T antigen and c-jun bind independently and as a complex to the P-0 promoter. Our data suggest that the probable molecular mechanism underlying the hypomyelination observed in transgenic animals expressing T antigen may be due to the repression of the P-0 gene by T antigen and c-jun. C1 NIH,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP BHARUCHA, VA (reprint author), UNIV MICHIGAN,DEPT PEDIAT,DIV PEDIAT NEUROL,ANN ARBOR,MI 48109, USA. FU NINDS NIH HHS [NS 29710, NS 21700] NR 65 TC 25 Z9 25 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD MAR PY 1994 VL 12 IS 3 BP 627 EP 637 DI 10.1016/0896-6273(94)90218-6 PG 11 WC Neurosciences SC Neurosciences & Neurology GA NC769 UT WOS:A1994NC76900014 PM 7512351 ER PT J AU STEPHENS, RM LOEB, DM COPELAND, TD PAWSON, T GREENE, LA KAPLAN, DR AF STEPHENS, RM LOEB, DM COPELAND, TD PAWSON, T GREENE, LA KAPLAN, DR TI TRK RECEPTORS USE REDUNDANT SIGNAL-TRANSDUCTION PATHWAYS INVOLVING SHC AND PLC-GAMMA-1 TO MEDIATE NGF RESPONSES SO NEURON LA English DT Article ID NERVE GROWTH-FACTOR; PROTEIN-TYROSINE PHOSPHORYLATION; SERINE THREONINE KINASE; PDGF BETA-RECEPTOR; PHOSPHATIDYLINOSITOL 3-KINASE; NEURONAL DIFFERENTIATION; PHEOCHROMOCYTOMA CELLS; PHOSPHOLIPASE-C; PC12 CELLS; NEUROTROPHIN RECEPTORS AB In response to NCF, the Trk receptor tyrosine kinase forms a complex with SHC, a protein that couples receptor tyrosine kinases to p21(ras). Complex formation between Trk and SHC, SHC tyrosine phosphorylation, and association of SHC with Grb2 were mediated by autophosphorylation at Y490 in Trk (NPQYFSD). To determine the role of SHC and other Trk substrates in NGF signaling, Trk receptors with mutations in Y490 and Y785 (the PLC-gamma 1 association site) were introduced into PC12nnr5 cells. NGF treatment of PC12nnr5 cells expressing Trk with mutations in either substrate-binding site resulted in normal neurite outgrowth and Erk1 activity and tyrosine phosphorylation. However, PC12nnr5 cells expressing Trk with mutations at both sites failed to stably extend neurites and efficiently induce Erk1 activity and tyrosine phosphorylation in response to NGF. We postulate that Trk receptors can activate Erk1 by either SHC- or PLC-gamma 1-dependent signaling pathways. These results suggest a model whereby Trk receptors utilize at least partially redundant signal transduction pathways to mediate NGF responses. C1 COLUMBIA UNIV,DEPT PATHOL,NEW YORK,NY 10032. COLUMBIA UNIV,CTR NEUROBIOL & BEHAV,NEW YORK,NY 10032. UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO,ON,CANADA. RP STEPHENS, RM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702, USA. RI Pawson, Tony/E-4578-2013 FU NCI NIH HHS [N01-CO-74101] NR 83 TC 441 Z9 446 U1 1 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD MAR PY 1994 VL 12 IS 3 BP 691 EP 705 DI 10.1016/0896-6273(94)90223-2 PG 15 WC Neurosciences SC Neurosciences & Neurology GA NC769 UT WOS:A1994NC76900019 PM 8155326 ER PT J AU TSUBOKAWA, H OGURO, K ROBINSON, HPC MASUZAWA, T RHEE, TSG TAKENAWA, T KAWAI, N AF TSUBOKAWA, H OGURO, K ROBINSON, HPC MASUZAWA, T RHEE, TSG TAKENAWA, T KAWAI, N TI INOSITOL 1,3,4,5-TETRAKISPHOSPHATE AS A MEDIATOR OF NEURONAL DEATH IN ISCHEMIC HIPPOCAMPUS SO NEUROSCIENCE LA English DT Article ID GLUTAMATE RECEPTOR ACTIVATION; LONG-TERM POTENTIATION; SEA-URCHIN EGGS; RAT-BRAIN; CELL-DEATH; CALCIUM; TRISPHOSPHATE; TETRAKISPHOSPHATE; ACCUMULATION; PHOSPHATES AB Selective death of CA1 pyramidal neurons after transient forebrain ischemia has attracted interest for its possible relation to the pathogenesis of memory deficits and dementia. Using whole cell patch-clamp recording from CA1 pyramidal neurons in hippocampal slices of gerbils after ischemia we studied the intracellular signaling mechanisms related to the phosphoinositide cycle. Intracellular application of an antibody against phosphatidylinositol 4,5-bisphosphate rescued ischemic neurons from stimulus-induced irreversible depolarization. Furthermore, application of inositol 1,3,4,5-tetrakisphosphate in normal cells caused an irreversible depolarization in response to synaptic input, which mimicked the deterioration of ischemic neurons. Depolarization of both ischemic and normal neurons in the presence of inositol 1,3,4,5-tetrakisphosphate was prevented by the addition of the Ca2+ chelator, 1,2-bis(o-aminophenoxy) ethane-N,N,N',N'-tetra-acetate. Application of antibody against inositol 1,4,5-triphosphate 3-kinase, which blocks formation of inositol 1,3,4,5-tetrakisphosphate, also protected against cell deterioration. Our results suggest that the vulnerability of hippocampal pyramidal neurons following ischemia is caused by a disturbed phosphoinositide cascade, with one metabolite, inositol 1,3,4,5-tetrakisphosphate, playing a key role in the induction of Ca2+ accumulation, which leads to neuronal death. C1 JICHI MED SCH,DEPT NEUROSURG,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. UNIV CAMBRIDGE,PHYSIOL LAB,CAMBRIDGE CB2 3EG,ENGLAND. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV TOKYO,INST MED SCI,DEPT MOLEC ONCOL,MINATO KU,TOKYO 108,JAPAN. RP TSUBOKAWA, H (reprint author), JICHI MED SCH,DEPT PHYSIOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. NR 35 TC 39 Z9 39 U1 0 U2 0 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 1994 VL 59 IS 2 BP 291 EP 297 DI 10.1016/0306-4522(94)90597-5 PG 7 WC Neurosciences SC Neurosciences & Neurology GA NC414 UT WOS:A1994NC41400006 PM 8008193 ER PT J AU BARRETT, JE ZHANG, L GLEESON, S GAMBLE, EH AF BARRETT, JE ZHANG, L GLEESON, S GAMBLE, EH TI ANXIOLYTIC AND ANTIDEPRESSANT MECHANISMS OF 5-HT1A DRUGS IN THE PIGEON - CONTRIBUTIONS FROM BEHAVIORAL-STUDIES SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Article DE ANXIOLYTIC; 5-HT1A; BUSPIRONE; SEROTONIN; 5-HT; ANXIETY; DEPRESSION; CONFLICT; DRUG DISCRIMINATION; 8-OH-DPAT; PIGEON; ANTIDEPRESSANT; PUNISHMENT ID DISCRIMINATIVE STIMULUS PROPERTIES; 8-HYDROXY-2-(DI-NORMAL-PROPYLAMINO) TETRALIN 8-OH-DPAT; GENERALIZED ANXIETY DISORDER; PUNISHED BEHAVIOR; 8-OH-DPAT LABELS; SEROTONIN ANTAGONIST; MAJOR DEPRESSION; SQUIRREL-MONKEYS; RAT STRIATUM; ANIMAL-MODEL AB The discovery that compounds acting through 5-hydroxytryptamine (5-HT) receptor subtypes can produce anxiolytic and/or antidepressant therapeutic effects in humans has resulted in considerable interest in the role of the 5-HT receptor system in both anxiety and depressive disorders. Because many of the clinically efficacious 5-HT1A anxiolytic drugs are either ineffective or produce inconsistent results in traditional or standard types of preclinical punishment or conflict procedures with rodents and other nonhuman mammals, there is considerable need for alternative behavioral assays sensitive to and selective for these compounds. In contrast to data with nonhuman mammals, 5-HT1A drugs are quite effective in pigeons studied under a punishment procedure. This paper reviews the use of the pigeon conflict procedure as a method for the detection and analysis of potential anxiolytic drugs acting through 5-HT1A receptors. Additionally, recent studies, also with the pigeon, have indicated that, in contrast to the rat, it is possible to establish an antidepressant such as imipramine as a discriminative stimulus, and then to use this procedure to evaluate the neuropharmacological bases for the behavioral and, presumably, therapeutic actions of these drugs. Using the drug discrimination procedure, it has been possible to examine a number of selective compounds that substitute for imipramine, thereby clarifying specific substrates for the antidepressant activity of this and related drugs. The pigeon promises to be a useful species in the pharmacological analyses of novel anxiolytic drugs and provides new approaches to the analysis and understanding of traditional as well as the more recently introduced antidepressant drugs. C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PHYSIOL & PHARMACOL,WINSTON SALEM,NC 27103. UNIFORMED SERV UNIV HLTH SCI,DEPT PSYCHIAT,BETHESDA,MD 20814. RP BARRETT, JE (reprint author), AMER CYANAMID CO,DIV MED RES,LEDERLE RES LABS,CENT NERVOUS SYST RES,PEARL RIVER,NY 10965, USA. NR 92 TC 24 Z9 24 U1 2 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0149-7634 J9 NEUROSCI BIOBEHAV R JI Neurosci. Biobehav. Rev. PD SPR PY 1994 VL 18 IS 1 BP 73 EP 83 DI 10.1016/0149-7634(94)90038-8 PG 11 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA MW879 UT WOS:A1994MW87900005 PM 7909594 ER PT J AU FREED, WJ AF FREED, WJ TI GLUTAMATERGIC MECHANISMS MEDIATING STIMULANT AND ANTIPSYCHOTIC DRUG EFFECTS SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Article DE EXCITATORY AMINO ACIDS; GLUTAMATE; QUISQUALIC ACID; DOPAMINE; STIMULANTS; AMPHETAMINE; NEUROLEPTICS; SCHIZOPHRENIA; PSYCHOSIS; CEREBRAL CORTEX ID METHYL-D-ASPARTATE; MONOAMINE-DEPLETED MICE; EXCITATORY AMINO-ACIDS; IDENTIFIED STRIATONIGRAL NEURONS; CAT CAUDATE NEURONS; NUCLEUS-ACCUMBENS; SUBSTANTIA NIGRA; DOPAMINE RELEASE; RAT NEOSTRIATUM; NMDA RECEPTOR AB This paper presents an hypothesis regarding the functions of striatal dopaminergic and glutamatergic neurotransmission. It is suggested that the principal functional role of dopaminergic neurotransmission is to regulate the efficacy of cortico-striatal and cortico-accumbens neurotransmission. Increased activity at dopamine-mediated synapses is suggested to interact with neurotransmission at adjacent cortically derived glutamate-mediated synapses, facilitating communication from the cerebral cortex, and thereby causing behavioral stimulation. Decreased activity at dopaminergic synapses, as produced by neuroleptic drugs, causes changes in the activation of cortically derived synapses in the corpus striatum and nucleus accumbens which result in behavioral sedation and decreased activity. This hypothesis suggests that activity at dopaminergic synapses produces behavioral effects only insofar as these changes modulate cortico-striatal (or corticoaccumbens) activity, and further, that the manifestations of activity in cortico-striatal systems are modulated by activity at dopaminergic synapses. It is further suggested that when neuroleptics are administered chronically, adjustments in the efficacy of cortico-striatal neurotransmission are responsible for the antipsychotic effect of neuroleptic drugs. RP FREED, WJ (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,2700 MARTIN LUTHER KING AVE,WASHINGTON,DC 20032, USA. NR 112 TC 38 Z9 38 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0149-7634 J9 NEUROSCI BIOBEHAV R JI Neurosci. Biobehav. Rev. PD SPR PY 1994 VL 18 IS 1 BP 111 EP 120 DI 10.1016/0149-7634(94)90041-8 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA MW879 UT WOS:A1994MW87900008 PM 7909593 ER PT J AU WITKIN, JM AF WITKIN, JM TI PHARMACOTHERAPY OF COCAINE ABUSE - PRECLINICAL DEVELOPMENT SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Article DE COCAINE; DRUG ABUSE; PHARMACOTHERAPY; BEHAVIOR; TOXICITY ID DISCRIMINATIVE STIMULUS PROPERTIES; D1 DOPAMINE RECEPTOR; INDUCED LOCOMOTOR HYPERACTIVITY; SCHEDULE-CONTROLLED BEHAVIOR; MEDIAL PREFRONTAL CORTEX; RHESUS-MONKEYS; D-AMPHETAMINE; SQUIRREL-MONKEYS; INTRAVENOUS COCAINE; ANTAGONIST SCH-23390 AB Preclinical models of behavioral and toxic effects of cocaine are reviewed and their potential for predicting compounds with efficacy and safety in the medical management of cocaine abuse and toxicity is assessed. Many of the existing models appear to be good predictors of the effects of compounds against specific behavioral or toxicological actions of cocaine. However, the utility of the models for prediction of the efficacy of new therapeutic entities must await clinical validation as no accepted or standard pharmacotherapy currently exists. Preclinical data generated by these models with drugs currently under clinical investigation for cocaine abuse treatment as well as with other compounds are reviewed. These compounds include buprenorphine, bromocriptine, desmethylimipramine, carbamazepine, dopaminergic agonists, antagonists and partial agonists, dopamine reuptake inhibitors, sigma ligands, serotonin antagonists, and excitatory amino acid antagonists. Preclinical information on several drug classes appears sufficiently promising to warrant further evaluation. These include dopamine agonists and partial agonists, D-1 receptor antagonists, selective sigma ligands, and modulators of the N-methyl-D-aspartate subtype glutamate receptor. RP NIDA, ADDICT RES CTR, DRUG DEV GRP, POB 5180, BALTIMORE, MD 21224 USA. NR 216 TC 88 Z9 89 U1 5 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0149-7634 EI 1873-7528 J9 NEUROSCI BIOBEHAV R JI Neurosci. Biobehav. Rev. PD SPR PY 1994 VL 18 IS 1 BP 121 EP 142 DI 10.1016/0149-7634(94)90042-6 PG 22 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA MW879 UT WOS:A1994MW87900009 PM 8170620 ER PT J AU JEZZARD, P HEINEMAN, F TAYLOR, J DESPRES, D WEN, H BALABAN, RS TURNER, R AF JEZZARD, P HEINEMAN, F TAYLOR, J DESPRES, D WEN, H BALABAN, RS TURNER, R TI COMPARISON OF EPI GRADIENT-ECHO CONTRAST CHANGES IN CAT BRAIN CAUSED BY RESPIRATORY CHALLENGES WITH DIRECT SIMULTANEOUS EVALUATION OF CEREBRAL OXYGENATION VIA A CRANIAL WINDOW SO NMR IN BIOMEDICINE LA English DT Article ID FUNCTIONAL ARCHITECTURE; SENSORY STIMULATION; INTRINSIC SIGNALS; BLOOD; TIME; ACTIVATION; RESOLUTION; ISCHEMIA; FIELDS; INVIVO AB A gradient-echo echo planar imaging (EPI) sequence has been used to generate images of cat brain during respiratory challenges. Direct spectrophotometric measurements have been made simultaneously in order to correlate the changes in oxygen saturation as measured by spectrophotometry with the image intensity changes seen in the gradient-echo images. When blood volume remains approximately constant, as derived from the spectrophotometry data, good correlation is seen between calculated plots made of changes in the transverse relaxation rate, Delta R(2)*, and the oxygen saturation as measured by spectrophotometry for much of the time course of the respiratory challenges of anoxia, apnea and hypercapnia. In some cases, the correlation is poorer during the recovery periods of the apnea and anoxia challenges. Those lower correlations can often be accounted for by changes in blood volume, which also effects the NMR relaxation rate. These results contribute to the understanding of the image intensity changes seen during functional brain imaging studies in humans. C1 NIH,CTR INVIVO NMR,BETHESDA,MD 20892. RP JEZZARD, P (reprint author), NHLBI,CARDIAC ENERGET LAB,BLDG 10,RM B1D161,BETHESDA,MD 20892, USA. RI Turner, Robert/C-1820-2008; Balaban, Robert/A-7459-2009; Wen, Han/G-3081-2010; OI Balaban, Robert/0000-0003-4086-0948; Wen, Han/0000-0001-6844-2997; Jezzard, Peter/0000-0001-7912-2251 NR 20 TC 74 Z9 75 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0952-3480 J9 NMR BIOMED JI NMR Biomed. PD MAR PY 1994 VL 7 IS 1-2 BP 35 EP 44 DI 10.1002/nbm.1940070107 PG 10 WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA NL280 UT WOS:A1994NL28000006 PM 8068524 ER PT J AU DUYN, JH MOONEN, CTW VANYPEREN, GH DEBOER, RW LUYTEN, PR AF DUYN, JH MOONEN, CTW VANYPEREN, GH DEBOER, RW LUYTEN, PR TI INFLOW VERSUS DEOXYHEMOGLOBIN EFFECTS IN BOLD FUNCTIONAL MRI USING GRADIENT ECHOES AT 1.5 T SO NMR IN BIOMEDICINE LA English DT Article ID HUMAN VISUAL-CORTEX; HUMAN BRAIN; SENSORY STIMULATION; OXYGENATION; CONTRAST; ACTIVATION; EPI AB Modified gradient-echo MR techniques were applied to study the effects of inflow on functional brain imaging studies using visual and motor cortex stimulation. The results demonstrate that the large signal changes, seen in previously reported gradient-echo studies at 1.5-2.0 T, are dominated by direct inflow effects, in particular when using a large hip angle and a thin slice. The findings suggest that inflow-based functional imaging, along with Blood Oxygenation Level Dependent (BOLD) functional MRI, may play an important role in future research towards the functional organization of the human brain. C1 NIH,DIAGNOST RADIOL RES LAB,BETHESDA,MD 20892. NIH,INVIVO NMR RES CTR,BETHESDA,MD 20892. PHILIPS MED SYST,5680 DA BEST,NETHERLANDS. RI Duyn, Jozef/F-2483-2010 NR 22 TC 166 Z9 167 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0952-3480 J9 NMR BIOMED JI NMR Biomed. PD MAR PY 1994 VL 7 IS 1-2 BP 83 EP 88 DI 10.1002/nbm.1940070113 PG 6 WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA NL280 UT WOS:A1994NL28000012 PM 8068530 ER PT J AU BALABAN, RS TAYLOR, JF TURNER, R AF BALABAN, RS TAYLOR, JF TURNER, R TI EFFECT OF CARDIAC FLOW ON GRADIENT RECALLED ECHO IMAGES OF THE CANINE HEART SO NMR IN BIOMEDICINE LA English DT Article ID SENSORY STIMULATION; PERFUSION; CONTRAST; MRI AB The effect of coronary flow on the signal intensity of gradient recalled echo (GRE) MR images of the canine heart was evaluated at 4 T. Using a fully instrumented canine model, hyperperfusion (local adenosine infusion) and ischemia (local occlusion) were evaluated while coronary blood flow and venous oxygen tension were monitored. These studies demonstrated an increase in GRE signal intensity with increases in coronary blood flow and venous oxygenation. A local occlusion resulted in a small decrease in signal intensity in the affected area of the heart. The dependence of the signal changes on TE and TR indicated that the effects of high Bow were associated with changes in the apparent T-2 and T-1. Both relaxation effects could reflect changes in tissue blood volume associated with the conditions studied. In addition, the apparent T-2 changes were consistent with alterations in total tissue deoxyhemoglobin concentration and the changes in apparent T-1 were consistent with inflow effects. RP BALABAN, RS (reprint author), NHLBI,CARDIAC ENERGET LAB,BLDG 10,RM B1D161,BETHESDA,MD 20817, USA. RI Turner, Robert/C-1820-2008; Balaban, Robert/A-7459-2009 OI Balaban, Robert/0000-0003-4086-0948 NR 12 TC 26 Z9 26 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0952-3480 J9 NMR BIOMED JI NMR Biomed. PD MAR PY 1994 VL 7 IS 1-2 BP 89 EP 95 DI 10.1002/nbm.1940070114 PG 7 WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA NL280 UT WOS:A1994NL28000013 PM 8068531 ER PT J AU SPARKS, SM AF SPARKS, SM TI THE EDUCATIONAL-TECHNOLOGY NETWORK (ETNET(TM)) SO NURSING & HEALTH CARE LA English DT Article RP SPARKS, SM (reprint author), NATL LIB MED,BETHESDA,MD 20209, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL LEAGUE FOR NURSING PI NEW YORK PA 350 HUDSON ST #3FL, NEW YORK, NY 10014-4504 SN 0276-5284 J9 NURS HEALTH CARE PD MAR PY 1994 VL 15 IS 3 BP 134 EP 141 PG 8 WC Nursing SC Nursing GA NK492 UT WOS:A1994NK49200007 PM 8152638 ER PT J AU BROWN, PH CHEN, TK BIRRER, MJ AF BROWN, PH CHEN, TK BIRRER, MJ TI MECHANISM OF ACTION OF A DOMINANT-NEGATIVE MUTANT OF C-JUN SO ONCOGENE LA English DT Article ID TRANSCRIPTIONAL ACTIVATION; MAMMALIAN-CELLS; PROTO-ONCOGENE; LEUCINE ZIPPER; FOS; PROTEINS; AP-1; TRANSFORMATION; DOMAIN; ONCOPROTEIN AB The AP-1 transcriptional activating complex, made up of Jun and Fos proteins, is involved in controlling many cellular processes such as cell proliferation, differentiation and transformation. We have previously characterized a dominant-negative mutant of c-Jun called TAM-67 which forms dimers with c-Jun and c-Fos, and binds DNA as a homodimer or heterodimer with c-Jun or c-Fos. This dominant-negative mutant is a potent inhibitor of AP-1 mediated transactivation, as well as c-jun/ras and TPA/ras-induced transformation. The present report describes experiments designed to elucidate the exact molecular mechanism of this dominant-negative inhibitor. The DNA binding kinetics of both TAM-67:TAM-67 homodimers as well as TAM-67:Fos heterodimers were studied and compared to those of c-Jun and other transactivation-deficient mutants of c-Jun. These studies demonstrated that the TAM-67 proteins have similar DNA binding kinetics to c-Jun and other Jun mutant proteins. Thus, the deletion of the amino-terminal end of the Jun protein does not significantly alter the protein's affinity for DNA. In addition, to determine whether TAM-67 functions through the formation of homodimers, or through interactions with endogenous c-Jun or c-Fos, we constructed a pair of chimeric proteins made by replacing the leucine zipper of TAM-67 with the leucine zippers of GCN4 and c-Fos. These chimeric proteins, termed TAM/GCN4 and TAM/Fos, were then tested for their ability to bind DNA, inhibit c-Jun-induced transactivation, and inhibit TPA/ras-mediated transformation. The results of these studies show that while both chimeric proteins bind equally well to DNA, only the TAM/Fos protein, and not the TAM/GCN4 protein, inhibits AP-1-induced transactivation and TPA/ras-induced transformation. When compared to the TAM-67 protein, the TAM/Fos protein is an equally potent inhibitor of transactivation and transformation. These results suggest that TAM-67 inhibits AP-1-mediated processes through a 'quenching' mechanism by inhibiting the function of endogenous Jun and/or Fos proteins. The implications of these mechanistic findings on the development of potent inhibitors of signal transduction pathways are discussed. C1 NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD 20850. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NR 30 TC 203 Z9 203 U1 1 U2 4 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR PY 1994 VL 9 IS 3 BP 791 EP 799 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA MW551 UT WOS:A1994MW55100014 PM 8108121 ER PT J AU VALENTINIS, B PORCU, P QUINN, K BASERGA, R AF VALENTINIS, B PORCU, P QUINN, K BASERGA, R TI THE ROLE OF THE INSULIN-LIKE GROWTH-FACTOR-I RECEPTOR IN THE TRANSFORMATION BY SIMIAN-VIRUS-40 T-ANTIGEN SO ONCOGENE LA English DT Article ID RETINOBLASTOMA SUSCEPTIBILITY GENE; CELLULAR DNA-SYNTHESIS; MESSENGER-RNA LEVELS; SV40-TRANSFORMED CELLS; PERMISSIVE CELLS; SOMATOMEDIN-C; A REGULATION; PROTEIN; BINDING; PHOSPHORYLATION AB Balb/c 3T3 cells transformed by the tsA58 temperature-sensitive (ts) mutant of SV40 large T antigen, BalbA58 cells, grow in 1% serum at the permissive temperature of 34 degrees C but fail to grow at the restrictive temperature of 39.6 degrees C. Although incapable of growing, BalbA58 cells, in low serum at 39.6 degrees C, stilt synthesize DNA and tend to accumulate in the G(2) phase of the cell cycle. Growth in 1% serum at 39.6 degrees C resumes if BalbA58 cells are treated with insulin-like growth factor I (IGF-I). By using cells overexpressing the IGF-I receptor, and cells with a targeted disruption of the IGF-I receptor genes, we show that: 1) the activation of the IGP-I receptor by its ligand(s) plays a major role in the ability of the SV40 large T antigen to promote growth in low serum; and 2) the IGF-I receptor plays a role in the progression of cells not only through G(1), but also through the S and G(2) phases of the cell cycle. These findings, together with other recent findings from the literature, suggest that one of the mechanisms by which oncogenes and tumor suppresser genes regulate cell growth is through the modulation of growth factors and their receptors. C1 THOMAS JEFFERSON UNIV,JEFFERSON CANC CTR,PHILADELPHIA,PA 19107. NCI,DCPC,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD. FU NCI NIH HHS [CA56309] NR 49 TC 53 Z9 54 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR PY 1994 VL 9 IS 3 BP 825 EP 831 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA MW551 UT WOS:A1994MW55100018 PM 8108125 ER PT J AU LANOIX, J LACOSTE, J PEPIN, N RICE, N HISCOTT, J AF LANOIX, J LACOSTE, J PEPIN, N RICE, N HISCOTT, J TI OVERPRODUCTION OF NFKB2(LYT-1O) AND C-REL - A MECHANISM FOR HTLV-I TAX-MEDIATED TRANSACTIVATION VIA THE NF-KAPPA-B SIGNALING PATHWAY SO ONCOGENE LA English DT Article ID CELL LEUKEMIA-VIRUS; CANDIDATE PROTOONCOGENE BCL-3; ENHANCER-BINDING PROTEINS; LONG TERMINAL REPEAT; HUMAN T-CELLS; DNA-BINDING; TRANSCRIPTIONAL ACTIVATION; ONCOGENIC TRANSFORMATION; GENE-EXPRESSION; PROTO-ONCOGENE AB Molecular, biochemical and epidemiological evidence implicate HTLV-I as an etiologic agent of adult T cell leukemia (ATL). The Tax protein of HTLV-I, a positive transcriptional activator of HTLV-I gene expression, is a viral oncogene that also increases transcription of cellular genes including GM-CSF, IL-2R alpha and IL-2. One of the cellular targets of the trans-activating effects of Tax is the NF-kappa B/Rel family of transcription factors, pleiotropic regulators of immunoregulatory, cytokine and viral gene expression. In this report, we demonstrate that NFKB2, (lyt-10) and c-Rel are overexpressed in HTLV-I infected and Tax-expressing cells and, together, account for the majority of the constitutive NF-kappa-B binding activity in these cells before and after PMA stimulation. Most importantly, we show a Tax-dependent correlation between expression of NFKB2(p100) and processing to the DNA binding NFKB2(p52) form, induction of c-Rel, and trans-activation of NF-kappa B-mediated gene expression. Furthermore, the NFKB2 precursor is physically associated with c-Rel and with Tax in HTLV-I infected cells. We propose that NFKB2 synthesis and processing allows continuous nuclear expression of an otherwise cytoplasmic protein and, in conjunction with overexpression of c-Rel, NFKB2 alters the NF-kappa B signalling pathway and contributes to leukemic transformation of T cells by HTLV-I. C1 SIR MORTIMER B DAVIS JEWISH HOSP,LADY DAVIS INST MED RES,ABE STERN CANC RES LAB,MONTREAL H3T 1E2,PQ,CANADA. MCGILL UNIV,DEPT MICROBIOL & IMMUNOL,MONTREAL,PQ,CANADA. FREDERICK CANC RES & DEV CTR,BASIC RES PROGRAM,ABL,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD. FU NCI NIH HHS [N01-CO-74101] NR 73 TC 73 Z9 73 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR PY 1994 VL 9 IS 3 BP 841 EP 852 PG 12 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA MW551 UT WOS:A1994MW55100020 PM 8108127 ER PT J AU LI, HS HULTCRANTZ, M AF LI, HS HULTCRANTZ, M TI AGE-RELATED DEGENERATION OF THE ORGAN OF CORTI IN 2 GENOTYPES OF MICE SO ORL-JOURNAL FOR OTO-RHINO-LARYNGOLOGY AND ITS RELATED SPECIALTIES LA English DT Article DE ORGAN OF CORTI; DEGENERATION; MORPHOLOGY; ELECTRON MICROSCOPY; MICE; GENOTYPE AB Degenerative changes in the organ of Corti were investigated in two genotypes of mice, CBA/Ca (moderate age-related late-onset hearing loss) and 7BL/6J (spontaneous early-onset auditory deterioration), ranging in age from 1 to 21 months (C57BL) and from 1 to 33 months (CBA). Light, transmission and scanning electron microscopes were used for qualitative and quantitative analyses. Alterations of deterioration in the CBA-mouse cochlea showed a late-onset loss of hair cells, lipofuscin in the outer hair cells (OHCs), giant stereocilia on the inner hair cells and elevated pillar heads. In C57BL mice, the primary lesions of the organ of Corti include early damage of stereocilia on OHCs, missing OHCs, and a ruptured reticular lamina. Giant cilia and elevated pillar heads were not evident in C57BL mice. In the aged C57BL mouse cochlea, the whole organ of Corti was collapsed and replaced by the supporting cells, whilst in the oldest CBA mice, completely normal-looking OHCs still remained even in severely deteriorated areas of the organ of Corti. The results indicate that the patterns of degeneration of the organ of Corti are different between CBA/Ca and C57BL/6J mice, probably under the control of different genes. RP LI, HS (reprint author), NIDOCD,NEUROCHEM LAB,BETHESDA,MD 20892, USA. NR 0 TC 33 Z9 33 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-1569 J9 ORL J OTO-RHINO-LARY JI ORL-J. Oto-Rhino-Laryngol. Relat. Spec. PD MAR-APR PY 1994 VL 56 IS 2 BP 61 EP 67 PG 7 WC Otorhinolaryngology SC Otorhinolaryngology GA MY052 UT WOS:A1994MY05200001 PM 8177586 ER PT J AU OBRIEN, T GLEASON, CA JONES, MD CONE, EJ LONDON, ED TRAYSTMAN, RJ AF OBRIEN, T GLEASON, CA JONES, MD CONE, EJ LONDON, ED TRAYSTMAN, RJ TI CEREBRAL RESPONSES TO SINGLE AND MULTIPLE COCAINE INJECTIONS IN NEWBORN SHEEP SO PEDIATRIC RESEARCH LA English DT Article ID BLOOD-FLOW; GLUCOSE-UTILIZATION; METABOLITES; FETAL; ABUSE; BRAIN; RAT AB Newborn infants exposed to cocaine near birth display a wide range of neurologic abnormalities, but the mechanism or mechanisms for these injuries remain unknown. We studied the cerebral effects of a single acute dose (4 mg/kg; n = 7) and multiple binge doses (4 mg/kg hourly for 5 h; n = 7) of i.v. cocaine in unanesthetized newborn (5 +/- 1 d old) sheep. We measured cerebral blood flow, mean arterial blood pressure, arterial blood gases, and cerebral Oz metabolism. Measurements were made at baseline; 30 s; and 5, 15, and 60 min after a single injection of cocaine in the acute group and at the same time intervals after the 5th dose of cocaine in the binge group. CBF increased by 98 +/- 68% (mean +/- SD) at 30 s after a single acute dose and by 97 +/- 94% at 30 s after the 5th of five hourly binge doses. Although it returned to baseline by 5 min in the acute group, cerebral blood flow remained elevated 5, 15, and 60 min after the 5th cocaine dose in the binge group. At 30 s, mean arterial blood pressure increased by 57 +/- 21% in the acute group and 46 +/- 15% in the binge group. In both groups, mean arterial blood pressure remained elevated at 5 min. Although no change occurred in cerebral O-2 metabolism in the acute group, an increase in cerebral O-2 consumption (7.4 +/- 1.3 mL/100 g/ min versus 5.5 +/- 1.1 at baseline) was observed at 5 min in the binge group. Thus, injection of cocaine as a single acute dose or after multiple binge doses results in acute cerebral vasodilation and hypertension in newborn sheep. Acute cerebral vasodilation, when combined within hypertension, may partially explain the pathogenesis of cocaine-associated neonatal neurologic abnormalities. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,EUDOWOOD NEONATAL PULM DIV,BALTIMORE,MD 21287. JOHNS HOPKINS UNIV,SCH MED,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21287. JOHNS HOPKINS UNIV,SCH MED,DEPT GYNECOL & OBSTET,BALTIMORE,MD 21287. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201. FU NIDA NIH HHS [NIDA 06658] NR 25 TC 13 Z9 13 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD MAR PY 1994 VL 35 IS 3 BP 339 EP 343 DI 10.1203/00006450-199403000-00013 PG 5 WC Pediatrics SC Pediatrics GA MY397 UT WOS:A1994MY39700012 PM 8190523 ER PT J AU SZEKELY, JI SHARPE, LG KATZ, JL AF SZEKELY, JI SHARPE, LG KATZ, JL TI EFFECTS OF CARAMIPHEN AND PHENCYCLIDINE ALONE AND IN COMBINATION ON BEHAVIOR IN THE RAT SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE LOCOMOTOR ACTIVITY; STEREOTYPY; ATAXIA; DEXTROMETHORPHAN; PHENCYCLIDINE; CARAMIPHEN ID HIGH-AFFINITY DEXTROMETHORPHAN; INDUCED STEREOTYPED BEHAVIOR; LOCOMOTOR-ACTIVITY; BINDING-SITES; RECEPTOR; BRAIN; NEUROLEPTICS; ANTAGONISTS; ASPARTATE; NMDA AB Because dextromethorphan (DM) has been shown to inhibit the locomotor stimulant effects of phencyclidine (PCP), this study explored further the possible interaction between drugs acting on DM and PCP receptor sites. Caramiphen, an antitussive that binds with high affinity to the DM site, was injected (IF) alone (15-120 mg/kg) or at two doses (15 or 60 mg/kg) 15 min before a challenge dose of PCP (1.25-20 mg/kg). Caramiphen alone dose-dependently increased ataxia, increased stereotypy, and had no effect on locomotor activity. PCP alone dose-dependently increased ataxia, stereotypy, and locomotor activity, the latter showing an inverted U-shaped function. At both pretreatment doses, caramiphen enhanced locomotor activity and stereotypy when combined with low PCP doses but decreased these behaviors at high PCP doses. Caramiphen produced a dose-dependent additive effect on ataxia when combined with all PCP doses. It was concluded that, although caramiphen, like DM, inhibited the locomotor stimulant effects of selected doses of PCP, that interaction appeared to be due to other behaviors (e.g., ataxia/stereotypy) elicited by caramiphen combined with high doses of PCP. This study underscored the importance of using full dose ranges of PCP when attempting to antagonize its behavioral effects with other drugs. C1 NATL INST DRUG ABUSE,ADDICT RES CTR,PSYCHOBIOL SECT,BALTIMORE,MD 21224. INST DRUG RES,H-1325 BUDAPEST,HUNGARY. OI Katz, Jonathan/0000-0002-1068-1159 NR 25 TC 3 Z9 3 U1 0 U2 0 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 1994 VL 47 IS 3 BP 709 EP 713 DI 10.1016/0091-3057(94)90177-5 PG 5 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA MZ396 UT WOS:A1994MZ39600045 PM 8208792 ER PT J AU SMOTHERMAN, WP ROBINSON, SR VARLINSKAYA, EI PETROV, ES ORLOWSKI, M DECOSTA, BR RICE, KC AF SMOTHERMAN, WP ROBINSON, SR VARLINSKAYA, EI PETROV, ES ORLOWSKI, M DECOSTA, BR RICE, KC TI CENTRAL ADMINISTRATION OF THE ENDOPEPTIDASE-24.15 INHIBITOR CFP-AAF-PAB SUGGESTS DYNORPHIN AS THE ENDOGENOUS LIGAND UNDERLYING BEHAVIORAL-EFFECTS OF MILK IN THE FETAL-RAT SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE CFP-AAF-PAB; ENDOPEPTIDASE 24.15; KAPPA; MU; DELTA; OPIOID; RAT FETUS; NOR-BINALTORPHIMINE; CTOP; NALTRINDOLE ID OPIOID RECEPTORS; ANTAGONIST; SUBTYPES; ONTOGENY; PEPTIDES; BRAIN AB Intraoral infusion of milk to the rat fetus promotes opioid activity that results in reduced responsiveness in a behavioral bioassay involving perioral cutaneous stimulation. Intracisternal administration of cFP-AAF-pAB, an inhibitor of endopeptidase 24.15, prolonged the opioid activity induced by milk infusion. Treatment with the selective kappa opioid antagonist nor-binaltorphimine blocked the effect of cFP-AAF-pAB on milk-induced opioid activity, but treatment with the mu antagonist CTOP or the delta antagonist naltrindole did not. These findings imply that milk may exert its effect on fetal behavior by increasing levels of dynorphin in the fetal central nervous system. C1 SUNY BINGHAMTON,DEPT PSYCHOL,CTR DEV PSYCHOBIOL,PERINATAL NEUROETHOL LAB,BINGHAMTON,NY 13902. RUSSIAN ACAD MED SCI,INST EXPTL MED,PAVLOVIAN PHYSIOL DEPT,ST PETERSBURG P-22,RUSSIA. MT SINAI SCH MED,DEPT PHARMACOL,NEW YORK,NY 10029. NIDDKD,MED CHEM LAB,BETHESDA,MD 20892. RI Robinson, Scott/J-6024-2012 FU NICHD NIH HHS [NICH HD 16102, NICH HD 28231] NR 28 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 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD MAR PY 1994 VL 47 IS 3 BP 715 EP 719 DI 10.1016/0091-3057(94)90178-3 PG 5 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA MZ396 UT WOS:A1994MZ39600046 PM 7911578 ER PT J AU FORBES, JA BATES, JA EDQUIST, IA BURCHFIELD, WH SMITH, FG SCHWARTZ, MK KIT, V HYATT, J BELL, WE BEAVER, WT AF FORBES, JA BATES, JA EDQUIST, IA BURCHFIELD, WH SMITH, FG SCHWARTZ, MK KIT, V HYATT, J BELL, WE BEAVER, WT TI EVALUATION OF 2 OPIOID-ACETAMINOPHEN COMBINATIONS AND PLACEBO IN POSTOPERATIVE ORAL-SURGERY PAIN SO PHARMACOTHERAPY LA English DT Article ID ANALGESICS AB Study Objective. To determine the relative analgesic potency and adverse effect liability of hydrocodone bitartrate 7.5 mg with acetaminophen 500 mg, codeine phosphate 30 mg with acetaminophen 300 mg, and placebo in the treatment of pain following oral surgery. Design. Randomized, double-blind, single-dose, placebo-controlled, parallel-group study with self-ratings at 30 minutes and then at hourly intervals from hour 1 to hour 6. Setting. Private, oral surgery practice sites. Patients. Three hundred twenty-four outpatients with moderate or severe pain after the surgical removal of impacted third molars were selected. One was lost to follow-up and 32 did not need an analgesic; 232 patients had valid efficacy data. Interventions. Patients were treated with a single oral dose of hydrocodone bitartrate 7.5 mg with acetaminophen 500 mg, codeine phosphate 30 mg with acetaminophen 300 mg, or placebo when they experienced steady, moderate or severe pain that, in their opinion, required an analgesic. Using a self-rating record, subjects rated their pain and its relief for 6 hours after medicating; estimates of peak and total analgesia were derived from these subjective reports. Measurements and Main Results. This study was a valid analgesic assay. Both active treatments were significantly superior to placebo for all measures of analgesic efficacy. The hydrocodone-acetaminophen combination was significantly superior to the codeine-acetaminophen combination for total pain relief and the number of evaluations with 50% relief. Both active treatments manifested an analgesic effect within 30 minutes; the effect persisted for 5 hours for the codeine combination and 6 hours for the hydrocodone combination. Adverse effects were transient, consistent with the pharmacologic profiles of opioids, and none required treatment. Conclusions. A slight advantage in analgesic efficacy was demonstrated in this single-dose study for the hydrocodone-acetaminophen combination. Repeat-dose studies, however, should be conducted to determine the clinical significance of the difference in analgesic effect of these opioid combinations. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21205. HUNT VALLEY MED CTR,COCKEYSVILLE,MD. NIH,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20057. GEORGETOWN UNIV,SCH MED,DEPT ANESTHESIA,WASHINGTON,DC 20057. NR 14 TC 16 Z9 16 U1 0 U2 3 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER BOX 806 171 HARRISON AVE, BOSTON, MA 02111 SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD MAR-APR PY 1994 VL 14 IS 2 BP 139 EP 146 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA ND068 UT WOS:A1994ND06800002 PM 8197031 ER PT J AU DAHL, TA BILSKI, P RESZKA, KJ CHIGNELL, CF AF DAHL, TA BILSKI, P RESZKA, KJ CHIGNELL, CF TI PHOTOCYTOTOXICITY OF CURCUMIN SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID OXYGEN; BACTERIA AB Curcumin, bis(4-hydroxy-3-methoxyphenyl)-1,6-diene-3,5-dione, is a yellow-orange dye derived from the rhizome of the plant Curcuma longa. Curcumin has demonstrated phototoxicity to several species of bacteria under aerobic conditions (Dahl, T. A., et al., 1989, Arch. Microbiol. 151 183), denoting photodynamic inactivation. We have now found that curcumin is also phototoxic to mammalian cells, using a rat basophilic leukemia cell model, and that this phototoxicity again requires the presence of oxygen. The spectral and photochemical properties of curcumin vary with environment, resulting in the potential for multiple or alternate pathways for the exertion of photodynamic effects. For example, curcumin photogenerates singlet oxygen and reduced forms of molecular oxygen under several conditions relevant to cellular environments. In addition, we detected carbon-centered radicals, which may lead to oxidation products (see accompanying paper). Such products may be important reactants in curcumin's phototoxicity since singlet oxygen and reduced oxygen species alone could not explain the biological results, such as the relatively long lifetime (t(1/2) = 27 s) of the toxicant responsible for decreased cell viability. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. TUFTS UNIV,SCH VET MED,DEPT PHARMACOL & EXPTL THERAPEUT,BOSTON,MA 02111. NR 20 TC 96 Z9 97 U1 0 U2 12 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD MAR PY 1994 VL 59 IS 3 BP 290 EP 294 DI 10.1111/j.1751-1097.1994.tb05036.x PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NF318 UT WOS:A1994NF31800005 PM 8016207 ER PT J AU CHIGNELL, CF BILSKI, P RESZKA, KJ MOTTEN, AG SIK, RH DAHL, TA AF CHIGNELL, CF BILSKI, P RESZKA, KJ MOTTEN, AG SIK, RH DAHL, TA TI SPECTRAL AND PHOTOCHEMICAL PROPERTIES OF CURCUMIN SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID SINGLET MOLECULAR-OXYGEN; ROSE-BENGAL; AQUEOUS-SOLUTION; STATE; PHOSPHORESCENCE; LIFETIMES; KINETICS; SOLVENTS; DYE AB Curcumin, bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione, is a natural yellow-orange dye derived from the rhizome of Curcuma longa, an East Indian plant. In order to understand the photobiology of curcumin better we have studied the spectral and photochemical properties of both curcumin and 4-(4-hydroxy-3-methoxyphenyl)-3-buten-2-one (hC, half curcumin) in different solvents. In toluene, the absorption spectrum of curcumin contains some structure, which disappears in more polar solvents, e.g. ethanol, acetonitrile. Curcumin fluorescence is a broad band in acetonitrile (lambda(max) = 524 nm), ethanol (lambda(max) = 549 nm) or micellar solution (lambda(max) = 557 nm) but has some structure in toluene (lambda(max) = 460, 488 nm). The fluorescence quantum yield of curcumin is low in sodium dodecyl sulfate (SDS) solution (phi = 0.011) but higher in acetonitrile (phi = 0.104). Curcumin produced singlet oxygen upon irradiation (lambda > 400 nm) in toluene or acetonitrile (phi = 0.11 for 50 mu M curcumin); in acetonitrile curcumin also quenched O-1(2) (k(q) = 7 x 10(6) M(-1) s(-1)). Singlet oxygen production was about 10 times lower in alcohols and was hardly detectable when curcumin was solubilized in a D2O micellar solution of Triton X-100. In SDS micelles containing curcumin no singlet oxygen phosphorescence could be observed. Curcumin photogenerates superoxide in toluene and ethanol, which was detected using the electron paramagnetic resonance/spin-trapping technique with 5,5-dimethyl-pyrroline-N-oxide as a trapping agent. Unidentified carbon-centered radicals were also detected. These findings indicate that the spectral and photochemical properties of curcumin are strongly influenced by solvent. In biological systems, singlet oxygen, superoxide and products of photodegradation may all participate in curcumin phototoxicity depending on the environment of the dye. C1 TUFTS UNIV,SCH VET MED,DEPT PHARMACOL,BOSTON,MA 02111. RP CHIGNELL, CF (reprint author), NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 26 TC 186 Z9 188 U1 9 U2 71 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD MAR PY 1994 VL 59 IS 3 BP 295 EP 302 DI 10.1111/j.1751-1097.1994.tb05037.x PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NF318 UT WOS:A1994NF31800006 PM 8016208 ER PT J AU ROSENTHAL, NE BROWN, C OREN, DA GALETTO, G SCHWARTZ, PJ MALLEY, JD AF ROSENTHAL, NE BROWN, C OREN, DA GALETTO, G SCHWARTZ, PJ MALLEY, JD TI EFFECTS OF LIGHT ON T-CELLS IN HIV-INFECTED SUBJECTS ARE NOT DEPENDENT ON HISTORY OF SEASONAL AFFECTIVE-DISORDER SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; LYMPHOCYTE SUBSETS; HOMOSEXUAL MEN; DEPRESSION; RADIATION; MELATONIN; EFFICACY; SYMPTOMS; THERAPY AB In order to evaluate the effect of light on helper- and suppressor-T-cell counts in HIV-infected individuals, with and without a history of seasonal affective disorder (SAD), we treated 35 subjects with 45 min of light therapy in the morning, in a crossover design involving two 2 week treatment conditions: visible white light (half-peak band width, 530-620 nm; 10 000 lux) and visible red light (half-peak band width, 615-685 nm; 175 lux). We found small but significant differences between the two treatment conditions, with higher CD4 and CD8 levels during the white, as compared with the red, condition. There were no differences between baseline and treatment conditions. Both light treatment conditions were associated with significant mood improvements in the SAD, but not the non-SAD, subjects. There was no evidence that the higher cell counts seen under the bright light conditions were mediated by the effects of light on mood or on plasma cortisol levels. While the size of the light effect on T-cells renders questionable the potential therapeutic value of this treatment modality for HIV, the finding is of theoretical interest and is reassuring for those HIV-infected individuals who require light treatment for other reasons. C1 NCI,MED BRANCH,BETHESDA,MD 20892. DIV COMP RES & TECHNOL,STAT & MATH METHODOL LAB,BETHESDA,MD 20892. RP ROSENTHAL, NE (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,BLDG 10,ROOM 4S-239,BETHESDA,MD 20892, USA. NR 37 TC 7 Z9 8 U1 0 U2 1 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD MAR PY 1994 VL 59 IS 3 BP 314 EP 319 DI 10.1111/j.1751-1097.1994.tb05040.x PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NF318 UT WOS:A1994NF31800009 PM 7912442 ER PT J AU MUSIAL, F CROWELL, MD AF MUSIAL, F CROWELL, MD TI EFFECT OF RECTAL DISTENSION AND FEEDING ON CECAL TONE IN PIGS SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE PIGS; BAROSTAT; CECAL TONE; VISCERO-VISCERAL REFLEXES ID MOTOR-ACTIVITY; DISTENSION; TRANSIT AB Effect of rectal distention and feeding on cecal tone in pigs. PHYSIOL BEHAV 55(3) 537-539, 1994.-The effects of eating and rectal distention on cecal tone were evaluated. Cecal tone was measured using a computer-controlled barostat in four female 30 to 40 kg Yucatan Micropigs fitted with cecal fistulas. Each pig underwent two separate trials of pre and postprandial measurements of cecal tone, either with or without continuous rectal distention with a 30 mi water-filled balloon. Cecal tone was measured 10 min prior to, during, and 10 min following a high-fat (60%) liquid meal (473 mi). Cecal tone significantly increased (intrabag volume decreased) after feeding (119.6+/-9.1 ml vs. 81.2+/-7.9 ml; p=0.008). Rectal distention tended to reduce the postprandial change in cecal tone (142.8+/-11.5 vs. 130.9+/-12.6 ml; p=0.196). There was also a strong tendency for cecal volumes to be higher (decreased tone) with rectal distention preprandially (142.8+/-11.5 ml vs. 119.6+/-9.1 ml; p=0.024). Nutrient ingestion significantly increased cecal tone and rectal distention abolished this effect. These findings may indicate a regulatory pathway that allows additional storage of fecal material in the event that the output of the system is disturbed. C1 BAPTIST MED CTR,CTR PHYSIOL STUDIES,DEPT RES,OKLAHOMA CITY,OK 73112. JOHNS HOPKINS UNIV,SCH MED,DIV DIGEST DIS,BALTIMORE,MD 21224. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. HEINRICH HEINE UNIV,DEPT PSYCHOL,BIOL CYBERNET & PSYCHOBIOL SECT,DUSSELDORF,GERMANY. UNIV OKLAHOMA,HLTH SCI CTR,OKLAHOMA CITY,OK 73112. NR 11 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 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD MAR PY 1994 VL 55 IS 3 BP 537 EP 539 DI 10.1016/0031-9384(94)90114-7 PG 3 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA MY684 UT WOS:A1994MY68400024 PM 8190775 ER PT J AU DECOSTERD, L GUSTAFSON, KR CARDELLINA, JH CRAGG, GM BOYD, MR AF DECOSTERD, L GUSTAFSON, KR CARDELLINA, JH CRAGG, GM BOYD, MR TI THE DIFFERENTIAL CYTOTOXICITY OF CARDENOLIDES FROM THEVETIA-AHOUIA SO PHYTOTHERAPY RESEARCH LA English DT Article DE CARDENOLIDES; DIFFERENTIAL CYTOTOXICITY; THEVETIA-AHOUIA ID AGENTS AB Bioassay-guided fractionation of the cytotoxic organic extracts of the wood of Thevetia ahouia (Apocyanaceae) led to the isolation of three cardenolide glycosides, neriifolin, 3'-O-methylevomonoside and 2'-acetyl-neriifolin [1-3]. These agents exhibited a distinctive pattern of differential cytotoxicity in the National Cancer Institute's human disease-oriented 60-cell line tumour screening panel, which suggests that follow-up in vivo xenograft evaluations may be warranted. These patterns may be useful in future dereplication studies of extracts potentially containing this class of compound. C1 NCI,DRUG DISCOVERY RES & DEV LAB,BLDG 1052,ROOM 121,FREDERICK,MD 21702. NCI,NAT PROD BRANCH,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702. NR 18 TC 10 Z9 10 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0951-418X J9 PHYTOTHER RES JI Phytother. Res. PD MAR PY 1994 VL 8 IS 2 BP 74 EP 77 DI 10.1002/ptr.2650080204 PG 4 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA ND078 UT WOS:A1994ND07800003 ER PT J AU WELLER, B AF WELLER, B TI UNMET NEEDS FOR DEVELOPMENTAL-DISABILITIES SERVICES SO POPULATION AND ENVIRONMENT LA English DT Article AB Data collected from a representative sample of persons who are developmentally disabled living in three counties in Florida in 1989 were analyzed to determine the number of services these persons receive, the extent to which they do not receive services they need, the reasons these services are not received, and the factors which are related to satisfaction with services. A battery of 90 services which can be grouped into 8 general categories was used, and the data were collected in face-to-face interviews with 312 persons. RP WELLER, B (reprint author), NIH,DIV RES GRANTS,BETHESDA,MD 20892, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU HUMAN SCI PRESS INC PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 SN 0199-0039 J9 POPUL ENVIRON JI Popul. Env. PD MAR PY 1994 VL 15 IS 4 BP 279 EP 302 DI 10.1007/BF02208461 PG 24 WC Demography; Environmental Studies SC Demography; Environmental Sciences & Ecology GA MW356 UT WOS:A1994MW35600004 ER PT J AU LEE, IJ DRIGGERS, PH MEDIN, JA NIKODEM, VM OZATO, K AF LEE, IJ DRIGGERS, PH MEDIN, JA NIKODEM, VM OZATO, K TI RECOMBINANT THYROID-HORMONE RECEPTOR AND RETINOID-X RECEPTOR STIMULATE LIGAND-DEPENDENT TRANSCRIPTION IN-VITRO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CELL-FREE TRANSCRIPTION; RNA POLYMERASE-II; INVITRO TRANSCRIPTION; RESPONSE ELEMENTS; RXR-BETA; FUNCTIONAL-CHARACTERIZATION; GLUCOCORTICOID RECEPTOR; VITELLOGENIN PROMOTER; GENE-TRANSCRIPTION; NUCLEAR RECEPTOR AB The thyroid hormone and retinoid X receptors form a heterodimer with each other and mediate thyroid hormone (T3)-dependent transcription. Retinoid X receptor, in addition, forms a homodimer and mediates 9-cis-retinoic acid-dependent transcription. Here, recombinant thyroid hormone receptor and recombinant retinoid X receptor beta expressed from baculovirus vectors have been studied for ligand-mediated activation of transcription in vitro. We show that the two recombinant receptors, most likely as a heterodimer, cooperatively enhance transcription in vitro from a template containing functional T3 responsive elements. The enhancement was specific for the T3 responsive element and was greatest when T3 was added to the reaction (approximate to 14-fold increase). Albeit to a lesser degree, the two receptors also directed transcription in the absence of T3. Template competition experiments suggest that the two receptors enhance formation of the preinitiation complex and that activation by T3 occurs when the ligand binds the receptor prior to (or during), but not after, the formation of the preinitiation complex. Although 9-cis-retinoic acid had no effect on the T3-dependent transcription, this ligand activated transcription in vitro directed by recombinant retinoic X receptor beta, most likely as a homodimer. This activation was observed when using nuclear extracts from embryonal carcinoma cells as a source of basal transcription factors, but not those from B lymphocytes. These results demonstrate that transcriptional activation mediated by T3 and 9-cis-retinoic acid can be reconstituted in vitro with the respective recombinant receptors. C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 45 TC 30 Z9 30 U1 0 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 MAR 1 PY 1994 VL 91 IS 5 BP 1647 EP 1651 DI 10.1073/pnas.91.5.1647 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MZ094 UT WOS:A1994MZ09400012 PM 8127860 ER PT J AU MOORE, SP GARFINKEL, DJ AF MOORE, SP GARFINKEL, DJ TI EXPRESSION AND PARTIAL-PURIFICATION OF ENZYMATICALLY ACTIVE RECOMBINANT TY1 INTEGRASE IN SACCHAROMYCES-CEREVISIAE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID VIRUS-LIKE PARTICLES; VIRAL-DNA; ELEMENT TRANSPOSITION; REVERSE-TRANSCRIPTASE; BINDING PROPERTIES; ESCHERICHIA-COLI; PROTEIN INVITRO; HIV DNA; YEAST; SEQUENCE AB Integration of the Saccharomyces cerevisiae retrotransposon Ty1 into the genome requires Ty1 integrase (LN). Apparent functions of Ty1 IN are target-site determination, cleavage, and joining of donor strands. To further study the mechanism of Ty1 integration, an IN expression plasmid has been constructed for use in yeast. The recombinant IN coding sequence differs from mature Ty1 IN associated with Ty1 virus-like particles only in that it has several additional N-terminal amino acid codons. Inclusion of a polyhistidine tag facilitates purification of recombinant IN by metal chelate chromatography. Recombinant Ty1 IN is active in an in vitro assay with short double-stranded oligonucleotide substrates and has biochemical properties similar to those observed with Ty1 virus-like particles. The full-length Ty1 LN produced in yeast should be useful for further biochemical, genetic, and structural analyses of Ty1 integration and for comparative analyses with retroviral IN proteins. RP MOORE, SP (reprint author), NCI,FREDERICK CANC RES & DEV CTR,EUKARYOT GENE EXPRESS LAB,ADV BIOSCI LABS,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 38 TC 31 Z9 32 U1 1 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 MAR 1 PY 1994 VL 91 IS 5 BP 1843 EP 1847 DI 10.1073/pnas.91.5.1843 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MZ094 UT WOS:A1994MZ09400052 PM 8127892 ER PT J AU TALKAD, VD FORTUNE, KP POLLO, DA SHAH, GN WANK, SA GARDNER, JD AF TALKAD, VD FORTUNE, KP POLLO, DA SHAH, GN WANK, SA GARDNER, JD TI DIRECT DEMONSTRATION OF 3 DIFFERENT STATES OF THE PANCREATIC CHOLECYSTOKININ RECEPTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ANTAGONIST RADIOLIGAND; FUNCTIONAL EXPRESSION; CALCIUM MOBILIZATION; MOLECULAR-CLONING; ENZYME-SECRETION; ACINAR-CELLS; CCK RECEPTOR; BINDING; RAT; POTENT AB We used rat pancreatic acini as well as COS-7 cells transfected with the cloned pancreatic cholecystokinin (CCK) receptor and measured the abilities of CCK octapeptide (CCK-8) and L-364,718 (a CCK receptor antagonist) to inhibit binding of I-125-labeled CCK-8 (I-125-CCK-8) and [H-3]L-364,718. With pancreatic acini I-125-CCK-8 bound to two different states of the CCK receptor. The high-affinity state (1% of the receptors) had a K-d for CCK-8 of 985 pM and the low-affinity state (19% of the receptors) had a K-d for CCK-8 of 30 nM. [H-3]L-364,718 bound to low-affinity receptors and to a previously unrecognized very-low-affinity state (80% of the receptors) having a K-d for CCK-8 of 13 mu M. L-364,718 had the same affinity (K-d 3 nM) for each of the three different states of the CCK receptor. Similar measurements using transfected COS cells also identified three different states of the CCK receptor, with the very-low-affinity state being the most abundant. Thus, the ability of the CCK receptor to exist in three different states is an intrinsic property of the CCK receptor molecule itself. C1 ST LOUIS UNIV,HLTH SCI CTR,SCH MED,DEPT INTERNAL MED,ST LOUIS,MO 63104. NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. ST LOUIS UNIV,MED CTR,DEPT INTERNAL MED,ST LOUIS,MO 63104. NR 31 TC 48 Z9 49 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 MAR 1 PY 1994 VL 91 IS 5 BP 1868 EP 1872 DI 10.1073/pnas.91.5.1868 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MZ094 UT WOS:A1994MZ09400057 PM 8127897 ER PT J AU GUSTCHINA, A SANSOM, C PREVOST, M RICHELLE, J WODAK, SY WLODAWER, A WEBER, IT AF GUSTCHINA, A SANSOM, C PREVOST, M RICHELLE, J WODAK, SY WLODAWER, A WEBER, IT TI ENERGY CALCULATIONS AND ANALYSIS OF HIV-1 PROTEASE INHIBITOR CRYSTAL-STRUCTURES SO PROTEIN ENGINEERING LA English DT Article DE AIDS DRUGS; HYDROGEN BONDS; INHIBITION; MOLECULAR MECHANICS ID HUMAN IMMUNODEFICIENCY VIRUS-1; TYPE-1 PROTEASE; RETROVIRAL PROTEASES; ACTIVE-SITE; RESOLUTION; COMPLEX; SIMULATIONS; PROTEINASES; PEPTIDE; BINDING AB The interactions between HIV-1 protease and its bound inhibitors have been investigated by molecular mechanics calculations and by analysis of crystal structures of the complexes in order to determine general rules for inhibitor and substrate binding to the protease. Fifteen crystal structures of HIV-1 protease with different peptidomimetic inhibitors showed conservation of hydrogen bond interactions between the main chain C=O and NH groups of the inhibitors and the C=O and NH groups of the protease extending from P3 C=O to P3' NH. The mean length of the hydrogen bonds between the inhibitor and the flexible flaps and the conserved water molecule (2.9 Angstrom) is slightly shorter than the mean length of hydrogen bonds between the inhibitor and the more rigid active site region (3.1 Angstrom) of the protease. The two hydrogen bonds between the conserved water and P2 and P1' carbonyl oxygen atoms of the inhibitor are the shortest and are predicted to be important for the tight binding of inhibitors. Molecular mechanics analysis of three crystal structures of HIV-1 protease with different inhibitors with independent calculations using the programs Discover and Brugel gave an estimate of 56-68% for the contribution of all the inhibitor main chain atoms to the total calculated protease-inhibitor interaction energy. The contribution of individual inhibitor residues to the interaction energy was calculated using Brugel. The main chain atoms of residue P2 had a consistently large favorable contribution to the total interaction energy, probably due to the presence of the two short hydrogen bonds to the flexible flap. The contribution of individual inhibitor side chains depended on the size of the side chain and the presence of specific hydrogen bond interactions with the protease. C1 UNIV LIBRE BRUXELLES, UNITE CONFORMAT MACROMOLEC BIOL, B-1050 BRUSSELS, BELGIUM. THOMAS JEFFERSON UNIV, JEFFERSON CANC INST, DEPT PHARMACOL, PHILADELPHIA, PA 19107 USA. RP GUSTCHINA, A (reprint author), NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MACROMOLECT STRUCT LAB, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74101] NR 37 TC 66 Z9 67 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PD MAR PY 1994 VL 7 IS 3 BP 309 EP 317 DI 10.1093/protein/7.3.309 PG 9 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA MX920 UT WOS:A1994MX92000003 PM 8177879 ER PT J AU HOPE, JN CHEN, HC HEJTMANCIK, JF AF HOPE, JN CHEN, HC HEJTMANCIK, JF TI BETA-A3/A1-CRYSTALLIN ASSOCIATION - ROLE OF THE N-TERMINAL ARM SO PROTEIN ENGINEERING LA English DT Article DE BACULOVIRUS EXPRESSION SYSTEM; LENS PROTEIN REASSOCIATION; IN VITRO MUTAGENESIS ID BOVINE BETA-CRYSTALLIN; X-RAY-ANALYSIS; MONOMERIC GAMMA-CRYSTALLIN; EYE-LENS; ALPHA-CRYSTALLIN; GENE FAMILY; PROTEINS; EVOLUTION; AGGREGATION; REASSOCIATION AB The beta- and gamma-crystallins of the lens form a protein superfamily, the beta gamma-crystallins and have highly conserved two-domain core structures. Whereas gamma-crystallins exist as monomers, the beta-crystallins associate into large aggregates. The N-terminal extensions to the core domains of beta-crystallins are postulated to be essential for their aggregation characteristics. To test this hypothesis, we compared the aggregation properties of a recombinant mouse beta A3/A1-crystallin without its N-terminal extension (r beta A3tr) to a normal recombinant mouse beta A3/A1-crystallin (r beta A3). The identity of the baculovirus system-expressed recombinant crystallins was confirmed by gel electrophoresis, immunoblots and N-terminal sequence analysis. Circular dichroism measurements indicate that the recombinant crystallins have mostly beta-sheet conformation, similar to normal beta-crystallins. The normal r beta A3 migrates on gel filtration chromatography as a homodimer, whereas the r beta A3trmigrates mostly as a monomer. After relocating the recombinant crystallins with mouse lens soluble extract, r beta A3 migrated with the dimeric beta L2 fractions and to a lesser extent with tetrameric beta L1 fractions. The reassociated r beta A3tr migrated with the trailing edge of the beta L2 fractions (40 kDa). These results suggest that the N-terminal arm of beta A3/A1-crystallin facilitates dimer formation and is necessary for higher-order associations. C1 NEI,MECHANISMS OCULAR LAB,BETHESDA,MD 20892. NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. NR 36 TC 37 Z9 39 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PD MAR PY 1994 VL 7 IS 3 BP 445 EP 451 DI 10.1093/protein/7.3.445 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA MX920 UT WOS:A1994MX92000019 PM 8177894 ER PT J AU CLORE, GM GRONENBORN, AM AF CLORE, GM GRONENBORN, AM TI STRUCTURES OF LARGER PROTEINS, PROTEIN LIGAND AND PROTEIN-DNA COMPLEXES BY MULTIDIMENSIONAL HETERONUCLEAR NMR SO PROTEIN SCIENCE LA English DT Article DE CALMODULIN; GATA-1; HETERONUCLEAR NMR; INTERLEUKIN-1-BETA; MULTIDIMENSIONAL NMR; PROTEIN DNA COMPLEXES; PROTEIN PEPTIDE COMPLEXES; PROTEINS; SOLUTION STRUCTURE ID NUCLEAR-MAGNETIC-RESONANCE; LIGHT-CHAIN KINASE; CALMODULIN-BINDING DOMAIN; RESOLUTION 3-DIMENSIONAL STRUCTURE; X-RAY-SCATTERING; DISTANCE GEOMETRY; CENTRAL HELIX; STEREOSPECIFIC ASSIGNMENTS; PHOSPHORYLASE-KINASE; HUMAN INTERLEUKIN-4 AB The recent development of a whole panoply of multidimensional heteronuclear-edited and -filtered NMR experiments has revolutionized the field of protein structure determination by NMR, making it possible to extend the methodology from the 10-kDa limit of conventional 2-dimensional NMR to systems up to potentially 35-40 kDa. The basic strategy for solving 3-dimensional structures of larger proteins and protein-ligand complexes in solution using 3- and 4-dimensional NMR spectroscopy is summarized, and the power of these methods is illustrated using 3 examples: interleukin-1beta, the complex of calmodulin with a target peptide, and the specific complex of the transcription factor GATA-1 with its cognate DNA target site. RP CLORE, GM (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 5,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 91 TC 77 Z9 78 U1 0 U2 1 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 1994 VL 3 IS 3 BP 372 EP 390 PG 19 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NC411 UT WOS:A1994NC41100002 PM 8019409 ER PT J AU GOLDBERG, TE TORREY, EF BERMAN, KF WEINBERGER, DR AF GOLDBERG, TE TORREY, EF BERMAN, KF WEINBERGER, DR TI RELATIONS BETWEEN NEUROPSYCHOLOGICAL PERFORMANCE AND BRAIN MORPHOLOGICAL AND PHYSIOLOGICAL MEASURES IN MONOZYGOTIC TWINS DISCORDANT FOR SCHIZOPHRENIA SO PSYCHIATRY RESEARCH-NEUROIMAGING LA English DT Article DE MAGNETIC RESONANCE IMAGING; CEREBRAL BLOOD FLOW; FRONTAL LOBE; HIPPOCAMPUS; WISCONSIN CARD SORTING TEST ID CEREBRAL BLOOD-FLOW; LATERAL VENTRICULAR SIZE; DORSOLATERAL PREFRONTAL CORTEX; POSITRON EMISSION TOMOGRAPHY; COGNITIVE IMPAIRMENT; NEGATIVE SYMPTOMS; MEMORY SYSTEM; ABNORMALITIES; ENLARGEMENT; DYSFUNCTION AB Correlational approaches that examine the relation between neuropsychological measures and brain morphology or physiology in schizophrenia have yielded inconsistent results. This may be due in part to difficulties in ascertaining precisely to what degree each measure deviates from its genetically and enviromentally determined potential level. We attempted to surmount this problem in a paradigm involving monozygotic twin pairs discordant for schizophrenia. In this paradigm, the difference score between the unaffected member and affected member of a twin pair should represent the degree of pathologic involvement irrespective of actual level. In correlating intrapair difference scores of anatomic structures measured from magnetic resonance imaging (n = 15) and prefrontal regional cerebral blood flow (rCBF) (n = 10) with cognitive abilities (after partialing IQ), we found strong associations between (1) the left hippocampus and a parameter of verbal memory, and (2) prefrontal rCBF with symptom scores and perseveration on the Wisconsin Card Sorting Test. These results support other research implicating medial temporal and prefrontal regions as important in the symptomatic expression and cognitive failures of schizophrenia. Overall, however, there was a relative paucity of significant associations between neuroanatomic and neurocognitive variables. This may have been due to the relatively restricted ranges of hippocampal size or cognitive ability found in this sample. C1 NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032. NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032. RP GOLDBERG, TE (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. NR 55 TC 103 Z9 104 U1 0 U2 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0925-4927 J9 PSYCHIAT RES-NEUROIM JI Psychiatry Res. Neuroimaging PD MAR PY 1994 VL 55 IS 1 BP 51 EP 61 DI 10.1016/0925-4927(94)90011-6 PG 11 WC Clinical Neurology; Neuroimaging; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ157 UT WOS:A1994NJ15700004 PM 8047629 ER PT J AU GLOWA, JR SHAW, AE RILEY, AL AF GLOWA, JR SHAW, AE RILEY, AL TI COCAINE-INDUCED CONDITIONED TASTE-AVERSIONS - COMPARISONS BETWEEN EFFECTS IN LEW/N AND F344/N RAT STRAINS SO PSYCHOPHARMACOLOGY LA English DT Article DE CONDITIONED TASTE AVERSION; COCAINE; RAT STRAIN; LEWIS, F344; BEHAVIORAL GENETICS ID CORTICOTROPIN RELEASING HORMONE; INDIVIDUAL VULNERABILITY; MOLECULAR MECHANISMS; FISCHER RATS; LEWIS; ADDICTION; MORPHINE AB Recent studies have found the LEW/N rat self-administers drugs of abuse at higher rates than the F344/N rat, suggesting a genetic predisposition toward the abuse potential of drugs. The current study compared the acquisition of a conditioned taste aversion (CTA) to cocaine in these strains. During an initial 20-min daily session a 0.1% saccharin solution was available and a dose (0-50 mg/kg, SC) of cocaine was given immediately after that session. Water was available during sessions on the following 3 days. Fluid consumption was assessed over three saccharin/water cycles, and a final saccharin session. Vehicle injections (0 mg/kg) that followed exposure to saccharin had no effect on subsequent saccharin consumption. In contrast, when cocaine followed exposure to saccharin, rates of saccharin consumption decreased over successive saccharin sessions in a dose-related manner in both strains. The lowest dose(18 mg/kg) decreased consumption in LEW/N rats but not in F344/N rats. An intermediate dose (32mg/kg) decreased consumption maximally in LEW/N rats and only marginally in F344/N rats. The highest dose (50 mg/kg) decreased consumption completely in LEW/N rats and almost completely in F344/N rats. These findings demonstrate that significant differences in sensitivity to stimuli paired with cocaine occur between these strains. These differences are consistent with previous reports that the LEW/N rat is uniquely sensitive to both behavioral and biochemical effects of drugs of abuse. The current report extends this sensitivity to the noxious effects of these drugs. To the extent that noxious and reinforcing effects of cocaine are unrelated, these results suggest that the LEW/N rat does not exhibit a genetic predisposition to factors related only to the abuse potential of drugs. C1 AMERICAN UNIV,DEPT PSYCHOL,PSYCHOPHARMACOL LAB,WASHINGTON,DC 20016. RP GLOWA, JR (reprint author), NIDDK,LMC,BEHAV PHARMACOL UNIT,BLDG 14D RM 311,BETHESDA,MD 20892, USA. NR 18 TC 65 Z9 65 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD MAR PY 1994 VL 114 IS 2 BP 229 EP 232 DI 10.1007/BF02244841 PG 4 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA NA384 UT WOS:A1994NA38400006 PM 7838912 ER PT J AU KAUFMANN, PG PARKER, SR LENFANT, C AF KAUFMANN, PG PARKER, SR LENFANT, C TI BEHAVIORAL AND BIOMEDICAL-RESEARCH - A PARTNERSHIP FOR BETTER HEALTH SO PSYCHOSOMATIC MEDICINE LA English DT Editorial Material ID MYOCARDIAL-INFARCTION; HYPERTENSION; DISEASE; SUPPORT RP KAUFMANN, PG (reprint author), NHLBI,BLDG 31,ROOM 5A52,BETHESDA,MD 20892, USA. NR 22 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD MAR-APR PY 1994 VL 56 IS 2 BP 87 EP 89 PG 3 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA NE119 UT WOS:A1994NE11900001 PM 8008801 ER PT J AU HAYTHORNTHWAITE, JA LIPP, MN HURWITZ, BE ANDERSON, DE AF HAYTHORNTHWAITE, JA LIPP, MN HURWITZ, BE ANDERSON, DE TI CARDIOVASCULAR-RESPONSES PREPARING FOR AN RESPONDING TO SOCIAL CHALLENGES SO PSYCHOSOMATIC MEDICINE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. CATHOLIC UNIV CAMPINAS,CAMPINAS,BRAZIL. UNIV MIAMI,CORAL GABLES,FL 33124. NIA,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD MAR-APR PY 1994 VL 56 IS 2 BP 159 EP 159 PG 1 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA NE119 UT WOS:A1994NE11900062 ER PT J AU BROWN, LJ BEAZOGLOU, T HEFFLEY, D AF BROWN, LJ BEAZOGLOU, T HEFFLEY, D TI ESTIMATED SAVINGS IN UNITED-STATES DENTAL EXPENDITURES, 1979-89 SO PUBLIC HEALTH REPORTS LA English DT Article AB The American public saved more than $39 billion (1990 dollars) in dental expenditures from 1979 through 1989 in contrast to the substantial increases in expenditures in other sectors of the U.S. health care system that have pushed the system to the brink of major reform. The dental savings were estimated after controlling for the influence of economic factors, such as changes in prices, insurance, and income, as well as noneconomic factors that could influence the extent of dental disease in the U. S. population. Results of the analysis confirm the importance of both economic and noneconomic factors in the determination of the savings in dental expenditures. C1 UNIV CONNECTICUT,CTR HLTH,DEPT PEDIAT DENT,FARMINGTON,CT 06032. UNIV CONNECTICUT,DEPT PAEDIAT,STORRS,CT 06268. RP BROWN, LJ (reprint author), NIDR,EODPP,ROOM 528 WESTWOOD BLDG,5333 WESTBARD AVE,BETHESDA,MD 20892, USA. NR 24 TC 11 Z9 11 U1 1 U2 1 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 1994 VL 109 IS 2 BP 195 EP 203 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NG261 UT WOS:A1994NG26100022 PM 8153270 ER PT J AU GONZALES, JJ MAGRUDER, KM KEITH, SJ AF GONZALES, JJ MAGRUDER, KM KEITH, SJ TI MENTAL-DISORDERS IN PRIMARY-CARE SERVICES - AN UPDATE SO PUBLIC HEALTH REPORTS LA English DT Article; Proceedings Paper CT 1992 United-States/Israel Binational Symposium CY MAR 25-27, 1992 CL BETHESDA, MD ID AMBULATORY MEDICAL-CARE; PSYCHIATRIC-DISORDERS; HEALTH-SERVICES; DEPRESSION; RECOGNITION; MANAGEMENT; INTERVENTION; PERSPECTIVE; INTERNISTS; PHYSICIANS AB Frank mental disorders, such as depression and panic disorder, are prevalent in primary care; they cause people substantial suffering and interfere with daily functioning. Even subthreshold or ''subsyndromal'' conditions, with fewer symptoms than necessary for making a diagnosis, cause substantial morbidity. Recent literature on mental disorders in primary care, where many, if not most, people with mental health problems are seen, is reviewed with focus on recognition and diagnosis issues, management of these problems in primary care, obstacles to accurate diagnosis and appropriate treatment, and prevention issues. In addition to a review of recent research, there is an effort to place these topics in the context Of various directives, including research and Federal documents, that have direct implications for better treatment in primary care of people with mental disorders (for example, practice guidelines). Mental health problems and disorders seen in primary care are a public health problem meriting immediate attention and substantial work at many levels-clinical, educational, organizational, and budgetary. C1 GEORGETOWN UNIV,MED CTR,DEPT MED,CLIN ECON RES UNIT,WASHINGTON,DC 20007. NIMH,DIV EPIDEMIOL & SERV RES,SERV RES BRANCH,BETHESDA,MD 20892. UNIV NEW MEXICO,SCH MED,DEPT PSYCHIAT,MENTAL HLTH PROGRAM,ALBUQUERQUE,NM 87131. RP GONZALES, JJ (reprint author), GEORGETOWN UNIV,MED CTR,DEPT PSYCHIAT,3800 RESERVOIR RD NW,WASHINGTON,DC 20007, USA. NR 56 TC 26 Z9 26 U1 3 U2 3 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 1994 VL 109 IS 2 BP 251 EP 258 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NG261 UT WOS:A1994NG26100029 PM 8153277 ER PT J AU BRAUN, MM WIESNER, PJ AF BRAUN, MM WIESNER, PJ TI TUBERCULOSIS PREVENTION PRACTICES AND PERSPECTIVES OF PHYSICIANS IN DEKALB COUNTY, GA SO PUBLIC HEALTH REPORTS LA English DT Article ID DECISION-ANALYSIS; REACTORS; LEAVE AB Knowing the reasons some physicians do not adhere to the disease prevention and treatment recommendations of expert committees can assist in the development of future recommendations more likely to be adopted by physicians. The authors describe the attitudes and practices of physicians relative to tuberculosis prevention in DeKalb County, GA. Tuberculosis is an important problem in the county, which includes part of the City of Atlanta, as well as suburban areas. Questionnaires for anonymous reply were mailed to 1,621 physicians in the county in 1991, and 848 (53 percent) were completed and returned. The final sample was 793 physicians, who were grouped into 5 specialty areas. Primary care physicians were the group most commonly involved in specific tuberculosis screening and prevention activities. Medical and pediatric specialists, surgeons, obstetricians-gynecologists, and other physicians were significantly less likely to be involved in such activities. Given that primary care physicians constitute a decreasing proportion of physicians in the United States, the findings suggest the importance of ensuring that future strategies for tuberculosis prevention take into account the increasingly specialized nature of the medical practice environment. RP BRAUN, MM (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,EPN 443,BETHESDA,MD 20892, USA. NR 14 TC 4 Z9 4 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 1994 VL 109 IS 2 BP 259 EP 265 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NG261 UT WOS:A1994NG26100030 PM 8153278 ER PT J AU GINSBURG, A ZOLKIEWSKI, M AF GINSBURG, A ZOLKIEWSKI, M TI TEMPERATURE AND GUANIDINE INDUCED UNFOLDING OF DODECAMERIC GLUTAMINE-SYNTHETASE FROM ESCHERICHIA-COLI SO PURE AND APPLIED CHEMISTRY LA English DT Article; Proceedings Paper CT International Conference on Thermodynamics of Solutions and Biological Systems CY JAN 03-06, 1993 CL NEW DELHI, INDIA SP INT UNION PURE & APPL CHEM, PHYS CHEM DIV, INDIAN NATL SCI ACAD, INDIAN INST TECHNOL, NEW DELHI & PANJAB UNIV ID STATISTICAL MECHANICAL DECONVOLUTION; ESCHERICHIA-COLI; THERMAL TRANSITIONS; SITE; MACROMOLECULES; BINDING AB Glutamine synthetase (GS) of 622000 M(r) from E. coli is composed of 12 identical subunits which are structurally arranged in two superimposed hexagonal rings with active sites at subunit interfaces. The enzyme undergoes reversible, thermally induced, partial unfolding without dissociation of subunits at pH 7 in the presence of 100 mM KCl and 1.0 mM MnCl2. Cooperative interactions link partial unfolding reactions of all subunits within the Mn.GS dodecamer (DELTAH(cal) = 750 kJ/mol) and only two, two-state transitions with similar T(m) values (324+/-2 K) are observed. Enthalpies at 310 K for subunit dissociation and subsequent unfolding were estimated to be approximately 61 and approximately 55 J/g, respectively, or approximately 100-fold the value of DELTAH for thermal unfolding. RP GINSBURG, A (reprint author), NHLBI,BIOCHEM LAB,PROT CHEM SECT,BETHESDA,MD 20892, USA. NR 17 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0033-4545 J9 PURE APPL CHEM JI Pure Appl. Chem. PD MAR PY 1994 VL 66 IS 3 BP 469 EP 472 DI 10.1351/pac199466030469 PG 4 WC Chemistry, Multidisciplinary SC Chemistry GA NL198 UT WOS:A1994NL19800017 ER PT J AU LIEBMANN, J DELUCA, AM EPSTEIN, A STEINBERG, SM MORSTYN, G MITCHELL, JB AF LIEBMANN, J DELUCA, AM EPSTEIN, A STEINBERG, SM MORSTYN, G MITCHELL, JB TI PROTECTION FROM LETHAL IRRADIATION BY THE COMBINATION OF STEM-CELL FACTOR AND TEMPOL SO RADIATION RESEARCH LA English DT Article ID COLONY-STIMULATING FACTOR; RADIOPROTECTION; MICE AB Cytokines that stimulate growth and differentiation of hematopoietic precursor cells have been used as protectors in vivo against ionizing radiation. Recently, we have shown that the nitroxide tempol is also an effective radiation protector in vivo. The purpose of the present study was to determine if the combination of tempol with stem cell factor (SCF, c-kit ligand) would provide enhanced radiation protection in C57 mice compared with the protection afforded by either agent alone. Mice were exposed to whole-body irradiation and assessed for survival at 30 days after irradiation. No control mice survived doses of more than 9 Gy. Treatment of mice before and after radiation with SCF alone (100 mu g/kg at -20 h, -4 h and +4 h) protected mice from radiation at doses of as high as 10 Gy (76% survival). Tempol (350 mg/kg) given 10 min prior to radiation was a radioprotector at 9 Gy (55% survival). The combination of SCF and tempol increased the survival of mice exposed to radiation doses up to 11 Gy (32% survival for the combination vs 4% for SCF alone and 0% for tempol alone; P < 0.001 for the combination vs either agent alone). Lower doses of SCF alone (1 mu g/kg) or tempol alone (275 mg/kg) did not protect mice from radiation. However, the combination of these reduced doses of SCF and tempol protected mice from lethal irradiation at 10 Gy. Stem cell factor and tempol given either singly or together were well tolerated by the animals. These data show that SCF and tempol are radiation protectors and that their radioprotective effects are more than additive when the agents are given together. C1 NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. AMGEN CORP,THOUSAND OAKS,CA 91320. RP LIEBMANN, J (reprint author), NCI,CLIN ONCOL PROGRAM,RADIAT ONCOL BRANCH,RADIOBIOL SECT,BETHESDA,MD 20892, USA. NR 16 TC 16 Z9 17 U1 0 U2 1 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD MAR PY 1994 VL 137 IS 3 BP 400 EP 404 DI 10.2307/3578716 PG 5 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA MY441 UT WOS:A1994MY44100017 PM 7511822 ER PT J AU SIMONSMORTON, BG TAYLOR, WC HUANG, IW AF SIMONSMORTON, BG TAYLOR, WC HUANG, IW TI VALIDITY OF THE PHYSICAL-ACTIVITY INTERVIEW AND CALTRAC WITH PREADOLESCENT CHILDREN SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT LA English DT Note DE CHILDREN; PHYSICAL ACTIVITY; MEASUREMENT ID MONITOR C1 UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,CTR HLTH PROMOT RES & DEV,HOUSTON,TX 77225. RP SIMONSMORTON, BG (reprint author), NICHHD,DESPR,6100 EXECUT BLVD,7B05,ROCKVILLE,MD 20892, USA. RI Schmoelz, Camilie/D-1707-2012; OI Schmoelz, Camilie/0000-0003-2221-9954; Simons-Morton, Bruce/0000-0003-1099-6617 NR 9 TC 36 Z9 37 U1 0 U2 0 PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE PI RESTON PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 SN 0270-1367 J9 RES Q EXERCISE SPORT JI Res. Q. Exerc. Sport PD MAR PY 1994 VL 65 IS 1 BP 84 EP 88 PG 5 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA MY552 UT WOS:A1994MY55200012 PM 8184216 ER PT J AU ISONO, M BRAUN, D POLTORAK, M FREED, WJ AF ISONO, M BRAUN, D POLTORAK, M FREED, WJ TI IMMUNOLOGICAL REACTIONS FOLLOWING INTRACEREBROVENTRICULAR TRANSPLANTATION OF ADRENAL-MEDULLA SO RESTORATIVE NEUROLOGY AND NEUROSCIENCE LA English DT Article DE ADRENAL MEDULLA GRAFT; IMMUNOLOGICAL REACTION; GRAFT REJECTION; XENOGRAFT ID BOVINE CHROMAFFIN CELLS; RAT PERIAQUEDUCTAL GRAY; PARKINSONS-DISEASE; ROTATIONAL BEHAVIOR; SUBSTANTIA NIGRA; BASAL GANGLIA; CEBUS MONKEYS; GRAFTS; SURVIVAL; BRAIN AB Immunological reactions after intracerebroventricular syn-, allo- and xenogenic transplantation of adrenal medulla were investigated histologically. In xenografts only, T cell infiltration and graft rejection were observed. Syngrafts and allografts were not rejected and were not infiltrated by T cells, although expression of MHC class II antigen was observed at all survival times. Major histocompatibility complex (MHC) class I immunoreactivity was strongly expressed in adrenal cortex syngrafts, which could play a role in the rejection of grafts containing mixed cell populations. The survival of chromaffin cells in allografts was decreased as compared to syngrafts, and there were fewer allograft animals with large numbers of surviving chromaffin cells. There was some increased cellularity (microglia and macrophages) in allografts even though no T cell infiltration was found. Therefore, it appears that this limited survival of intracerebral adrenal medulla allografts is not due to T cell-mediated graft rejection. C1 NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,PRECLIN NEUROSCI SECT,WASHINGTON,DC 20032. NR 36 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0922-6028 J9 RESTOR NEUROL NEUROS JI Restor. Neurol. Neurosci. PD MAR PY 1994 VL 6 IS 2 BP 89 EP 95 PG 7 WC Neurosciences SC Neurosciences & Neurology GA NF005 UT WOS:A1994NF00500002 PM 21551735 ER PT J AU UNSER, M EDEN, M AF UNSER, M EDEN, M TI FIR APPROXIMATIONS OF INVERSE FILTERS AND PERFECT RECONSTRUCTION FILTER BANKS SO SIGNAL PROCESSING LA English DT Article DE LEAST-SQUARES DESIGN; INVERSE FILTER; PERFECT RECONSTRUCTION FILLER BANK; WAVELET TRANSFORM; SPLINE FUNCTIONS; CUBIC SPLINES; B-SPLINES; GABOR TRANSFORM; INTERPOLATION AB This paper first describes an algorithm that finds the approximate finite impulse response (FIR) inverse of an FIR filter by minimizing the inversion (or reconstruction) error constrained to zero-bias. The generalization of the inverse filtering problem in the two channel case is the design of perfect reconstruction filter banks that use critical sampling. These considerations lead to the derivation of an algorithm that provides a minimum error and unbiased FIR/FIR approximation of a perfect reconstruction IIR/FIR (or FIR/IIR) filter bank. The one-channel algorithm is illustrated with the design of an FIR filter to compute the B-spline coefficients for cubic spline signal interpolation. The two-channel algorithm is applied to the design of a FIR/FIR filter bank that implements the cubic B-spline wavelet transform. Finally, we consider a modification of this technique for the design of modulated-filter banks, which are better suited for subband coding. RP UNSER, M (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13,BETHESDA,MD 20892, USA. RI Unser, Michael/A-1550-2008 NR 0 TC 18 Z9 18 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-1684 J9 SIGNAL PROCESS JI Signal Process. PD MAR PY 1994 VL 36 IS 2 BP 163 EP 174 DI 10.1016/0165-1684(94)90205-4 PG 12 WC Engineering, Electrical & Electronic SC Engineering GA NE152 UT WOS:A1994NE15200003 ER PT J AU MENTIS, MJ SALERNO, J HORWITZ, B GRADY, C SCHAPIRO, MB MURPHY, DGM RAPOPORT, SI AF MENTIS, MJ SALERNO, J HORWITZ, B GRADY, C SCHAPIRO, MB MURPHY, DGM RAPOPORT, SI TI REDUCTION OF FUNCTIONAL NEURONAL CONNECTIVITY IN LONG-TERM TREATED HYPERTENSION SO STROKE LA English DT Article DE CAROTID ARTERIES; CEREBRAL BLOOD FLOW; GLUCOSE; HYPERTENSION; TOMOGRAPHY, EMISSION-COMPUTED ID CEREBRAL BLOOD-FLOW; GLUCOSE-UTILIZATION; METABOLIC RATES; ALZHEIMERS-DISEASE; RISK-FACTORS; AGE; BRAIN; INTERCORRELATIONS; HYPOTENSION; DISORDER AB Background and Purpose Anatomic imaging of patients with chronic well-treated hypertension has demonstrated dilatation of the lateral cerebral ventricles and left brain atrophy, whereas positron emission tomography has shown only subtle reductions in regional cerebral metabolic rates for glucose in some subcortical nuclei. To further explore the implications of the imaging changes, an analytic technique designed to determine functional neuronal connectivity between regions of interest (ROIs) was applied to the data on regional cerebral metabolic rates for glucose to determine if and where in the brain reduction of functional neuronal connectivity occurred. Methods Glucose metabolism was measured by positron emission tomography in 17 older men (age, 68+/-8 years) with well-controlled, noncomplicated hypertension of at least 10 years' duration and in 25 age- and sex-matched healthy control subjects. A significant correlation difference analysis was performed to determine which ROI pairs had reduced correlation coefficients (reduced functional neuronal connectivity). The vascular pattern of the reduction was determined after allocating the ROIs to their appropriate vascular territories. Results Compared with the control subjects, hypertensive patients had reduced correlation coefficients in cortical territories of the internal carotid arteries but not of the vertebrobasilar arteries. The border zone supplied by the middle and anterior cerebral arteries was most affected. Conclusions The border zone between the anterior and middle cerebral arteries is vulnerable to ischemia from carotid pathology, systemic hypotension, or both. We hypothesize that although these hypertensive patients were ''well controlled'' and had normal neuropsychological tests, they may have experienced ischemia severe enough to cause border zone reduction of functional neuronal connectivity as a result of carotid pathology, antihypertensive medications, hypotensive episodes with a right-shifted autoregulation curve, or other factors in isolation or combination. RP MENTIS, MJ (reprint author), NIA,NEUROSCI LAB,BLDG 10,RM 6C414,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 45 TC 43 Z9 45 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD MAR PY 1994 VL 25 IS 3 BP 601 EP 607 PG 7 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA MZ807 UT WOS:A1994MZ80700010 PM 8128513 ER PT J AU LEE, J MARQUEZ, VE LEWIN, NE BLUMBERG, PM AF LEE, J MARQUEZ, VE LEWIN, NE BLUMBERG, PM TI SYNTHESIS OF 2 RIGID DIACYLGLYCEROL ANALOGS HAVING A 1,7-DIOXASPIRO[4.4]NONANE BIS-GAMMA-BUTYROLACTONE SKELETON .4. SO SYNLETT LA English DT Note AB The stereoselective synthesis of two new bis-gamma-butyrolactones, constructed on a dioxaspiro[4.4]nonane template, was efficiently completed in 11 steps from L-xylose. One of two isomers (2a) showed good binding affinity towards protein kinase C. C1 NCI,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NR 9 TC 17 Z9 17 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0936-5214 J9 SYNLETT JI Synlett PD MAR PY 1994 IS 3 BP 206 EP 208 PG 3 WC Chemistry, Organic SC Chemistry GA NA597 UT WOS:A1994NA59700022 ER PT J AU BLOMBACK, M ABILDGAARD, U VANDENBESSELAAR, AMHP CLEMENTSON, KJ DAHLBACK, B EXNER, T FRANCIS, CW GAFFNEY, P GRALNICK, H HOYER, LW JOHNSON, GJ KASPER, C LANE, D LIJNEN, HR LUSHER, JM MANNUCCI, PM POLLER, L RAPAPORT, SI SAITO, H STOCKER, K THOMAS, D BARROWCLIFFE, TW HEMKER, C THORSEN, S ARONSON, D MANN, KG MEYER, D ROBERTS, HR DYBKAER, R JORGENSEN, K OLESEN, H AF BLOMBACK, M ABILDGAARD, U VANDENBESSELAAR, AMHP CLEMENTSON, KJ DAHLBACK, B EXNER, T FRANCIS, CW GAFFNEY, P GRALNICK, H HOYER, LW JOHNSON, GJ KASPER, C LANE, D LIJNEN, HR LUSHER, JM MANNUCCI, PM POLLER, L RAPAPORT, SI SAITO, H STOCKER, K THOMAS, D BARROWCLIFFE, TW HEMKER, C THORSEN, S ARONSON, D MANN, KG MEYER, D ROBERTS, HR DYBKAER, R JORGENSEN, K OLESEN, H TI NOMENCLATURE OF QUANTITIES AND UNITS IN THROMBOSIS AND HEMOSTASIS (RECOMMENDATION 1993) - A COLLABORATIVE PROJECT OF THE SCIENTIFIC AND STANDARDIZATION COMMITTEE OF THE INTERNATIONAL-SOCIETY-ON-THROMBOSIS-AND-HEMOSTASIS (ISTH SSC) AND THE COMMISSION COMMITTEE ON QUANTITIES AND UNITS (IN CLINICAL-CHEMISTRY) OF THE INTERNATIONAL-UNION-OF-PURE-AND-APPLIED-CHEMISTRY INTERNATIONAL-FEDERATION-OF-CLINICAL-CHEMISTRY (IUPAC-IFCC CQU(CC)) SO THROMBOSIS AND HAEMOSTASIS LA English DT Article C1 AKER HOSP,MED DEPT A,OSLO 5,NORWAY. LEIDEN UNIV HOSP,THROMBOSIS RES CTR,2333 AA LEIDEN,NETHERLANDS. UNIV BERN,THEODOR KOCHER INST,CH-3001 BERN,SWITZERLAND. LUND UNIV,DEPT COAGULAT VISORDERS,S-22101 LUND,SWEDEN. WESTMEAD HOSP,DEPT HAEMATOL,SYDNEY,AUSTRALIA. UNIV ROCHESTER,DEPT MED,ROCHESTER,NY 14627. NIH,HEMATOL SERV,BETHESDA,MD 20892. AMER RED CROSS,HOLLAND LAB,BETHESDA,MD 20814. UNIV MINNESOTA,SCH VET ADM HOSP,MINNEAPOLIS,MN 55455. ORTHOPED HOSP,LOS ANGELES,CA 90007. CHARING CROSS & WESTMINSTER HOSP,SCH MED,DEPT HAEMATOL,LONDON,ENGLAND. CTR MOLEC & VASC BIOL,LOUVAIN,BELGIUM. CHILDRENS HOSP MICHIGAN,DETROIT,MI 48201. HEMOPHILIA THROMBOSIS CTR,MILAN,ITALY. WITHINGTON HOSP,UNITED KINGDOM REFERENCE LAB ANTICOAGULANTS & CONTROL,MANCHESTER M20 8LR,LANCS,ENGLAND. UNIV CALIF SAN DIEGO,MED CTR,LA JOLLA,CA 92093. NAGOYA UNIV,DEPT INTERNAL MED 1,NAGOYA,AICHI 464,JAPAN. PENTAPHARM AG,BASEL,SWITZERLAND. UNIV COPENHAGEN HOSP,DEPT CLIN BIOCHEM,DK-2100 COPENHAGEN,DENMARK. GEORGE WASHINGTON UNIV,SCH MED,WASHINGTON,DC 20052. HOP BICETRE,F-94270 LE KREMLIN BICETR,FRANCE. UNC,SCH MED,ISTH,INT HEADQUARTERS,CHAPEL HILL,NC. FREDERIKSBERG UNIV HOSP,DEPT CLIN CHEM,DK-2000 COPENHAGEN,DENMARK. RI Mannucci, Pier/C-3102-2014 NR 4 TC 26 Z9 26 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD MAR PY 1994 VL 71 IS 3 BP 375 EP 394 PG 20 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA NB800 UT WOS:A1994NB80000021 PM 8029803 ER PT J AU HIDAKA, A KASAGI, K TAKEUCHI, R IIDA, Y MISAKI, T GROLLMAN, EF KONISHI, J AF HIDAKA, A KASAGI, K TAKEUCHI, R IIDA, Y MISAKI, T GROLLMAN, EF KONISHI, J TI STIMULATED IODIDE UPTAKE IN FRTL-5 CELLS PREINCUBATED WITH GRAVES IMMUNOGLOBULINS IN NACL-FREE MEDIUM - A SENSITIVE ASSAY FOR THYROID-STIMULATING ANTIBODIES SO THYROID LA English DT Article ID ADENOSINE-3',5'-MONOPHOSPHATE SIGNAL ACTION; THYROTROPIN-BINDING; PRACTICAL ASSAY; CLINICAL ASSAY; TSH; HYDROCORTISONE; MECHANISMS; FRACTIONS; TRANSPORT; INCREASE AB The present study was designed to increase the sensitivity of iodide uptake assay for detecting thyroid-stimulating antibodies (TSAb). Based on the previous observations that TSAb are more active to increase cAMP levels in the NaCl-free condition, we improved the assay procedure and defined the optimum conditions: FRTL-5 cells were incubated with immunoglobulin (IgG) in NaCl-free medium for 3 days, and then I-125 uptake in the cells was determined after 60 min. The sensitivity of iodide uptake assay for TSAb increased 3-fold by the modification, when assessed by the IgG concentration required to elicit the same response. The described assay is as sensitive as that using cAMP measurement in NaCl-free buffer. Thus, it could detect TSAb in all 21 patients with active Graves' disease and in 7 of 8 with ophthalmic Graves' disease but not in 29 of 30 control subjects. Thyroid stimulating activities assessed by these two assays correlated with each other (it = 29, r = 0.707, p < 0.001). False positive results obtained in 4 hypothyroid patients with Hashimoto's thyroiditis (serum TSH concentrations, 11-171 mU/L) could be prevented using anti-TSH antibodies. In summary, the described assay allows evaluation of stimulated thyroid function directly without affecting the detection of TSAb. C1 KYOTO UNIV,SCH MED,DEPT NUCL MED,KYOTO 606,JAPAN. NIDDKD,BIOCHEM & METAB LAB,CELL REGULAT SECT,BETHESDA,MD 20892. NR 28 TC 1 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD SPR PY 1994 VL 4 IS 1 BP 31 EP 36 DI 10.1089/thy.1994.4.31 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NJ425 UT WOS:A1994NJ42500010 PM 7914446 ER PT J AU AKAMIZU, T INOUE, D KOSUGI, S KOHN, LD MORI, T AF AKAMIZU, T INOUE, D KOSUGI, S KOHN, LD MORI, T TI FURTHER-STUDIES OF AMINO-ACIDS (268-304) IN THYROTROPIN (TSH) LUTROPIN/CHORIONIC GONADOTROPIN (LH/CG) RECEPTOR CHIMERAS - CYSTEINE-301 IS IMPORTANT IN TSH BINDING AND RECEPTOR TERTIARY STRUCTURE SO THYROID LA English DT Article ID THYROID-STIMULATING ANTIBODIES; EXTRACELLULAR DOMAIN; FUNCTIONAL EXPRESSION; BLOCKING ANTIBODIES; IDIOPATHIC MYXEDEMA; MOLECULAR-CLONING; RABBIT ANTIBODIES; IMMUNOGLOBULIN; SEQUENCE; HORMONE AB Our previous study of chimeric TSH-LH/CG receptors showed that substituting amino acid residues 268-304 of the TSH receptor with homologous residues from the LJ/CG receptor markedly decreased high affinity TSH binding as evidenced by ligand displacement assays [Akamizu ct al. Endocr J 40:363-372, 1993]. Despite this change in TSH binding, there was a minimal change in TSH-stimulated activity in cAMP assays. To explain this dissociation of TSH binding and function, further characterization of individual residues within the 268-304 segment was performed. Five additional chimeric TSH-LH/CG receptors within this region were constructed by substituting corresponding residues of rat LH/CG receptor. After transfection in Cos-7 cells, TSH receptor activities of these chimeras were evaluated. A single point mutation of cysteine-301 to glutamate resulted in a mutant receptor that exhibited the same receptor bioactivity as the chimeric receptor with amino acids 268-304 substituted by LH/CG receptor residues: apparent low affinity TSH binding in ligand displacement assays but significant retention of the cAMP response to TSH. The four other chimeric substitutions yielded cDNAs coding for receptors that behaved like wild-type receptors. Western blot analyses using a TSH receptor-specific antibody showed that all five of the new mutants were synthesized and integrated in the membrane. These results suggest that cysteine-301 is the critical residue whose mutation accounts for the original chimeric results and the dissociation of binding and functional activity. The possibility must be considered that cysteine-301 is involved in disulfide bond formation and is important in tertiary structure and that conformational changes in the receptor result from its mutation. C1 NIDDKD,BIOCHEM & METAB LAB,CELL REGULAT SECT,BETHESDA,MD 20892. RP AKAMIZU, T (reprint author), KYOTO UNIV,SCH MED,DEPT LAB MED,SAKYO KU,54 SHOGOIN KAWAHARACHO,KYOTO 606,JAPAN. NR 35 TC 20 Z9 20 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD SPR PY 1994 VL 4 IS 1 BP 43 EP 48 DI 10.1089/thy.1994.4.43 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NJ425 UT WOS:A1994NJ42500012 PM 8054860 ER PT J AU BOORMAN, GA MARONPOT, RR EUSTIS, SL AF BOORMAN, GA MARONPOT, RR EUSTIS, SL TI RODENT CARCINOGENICITY BIOASSAY - PAST, PRESENT, AND FUTURE SO TOXICOLOGIC PATHOLOGY LA English DT Article DE HAZARD IDENTIFICATION; CHEMICAL CARCINOGENESIS; RISK ASSESSMENT; RAT; MOUSE; 2-YR STUDIES AB Toxicity/carcinogenicity studies in rodents have played a pivotal role in identifying chemicals that are potentially hazardous to humans. In fact, nearly all of the known human carcinogens are also carcinogenic in 1 or more rodent species. During the past 20 yr the quality and consistency of rodent studies has improved considerably, and much has been learned about mechanisms whereby chemicals initiate or promote the carcinogenic process in rats and mice. The process of identifying chemicals that cause toxicity or carcinogenicity in rodents is quite well established, but the procedures for extrapolating this data for risk management decisions in the protection of human health have lagged far behind. While many would accept the assumptions that genotoxic chemicals that cause cancer in animals pose a cancer risk to humans and that genotoxic chemicals causing cancer at high doses pose a risk at lower doses, there is much less certainty with respect to nongenotoxic chemicals. The confusion about risk extrapolation for nongenotoxic chemicals has often lead to criticism of the hazard identification process for chemicals in general. There is increasing awareness of the complexity of the carcinogenic process that has made species extrapolation and dose extrapolation from rodent studies to humans more complex. Although newer molecular biological techniques and cell kinetic measurements offer exciting possibilities for better risk assessment, it is the combination of well-designed rodent studies with appropriate mechanistic studies that offers the best hope for regulatory decisions based on sound scientific principles. RP BOORMAN, GA (reprint author), NIEHS,ENVIRONM TOXICOL PROGRAM,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 22 Z9 23 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 1994 VL 22 IS 2 BP 105 EP 111 PG 7 WC Pathology; Toxicology SC Pathology; Toxicology GA NY189 UT WOS:A1994NY18900004 PM 7973358 ER PT J AU MCCONNELL, EE EUSTIS, SL AF MCCONNELL, EE EUSTIS, SL TI PEER-REVIEW IN CARCINOGENICITY BIOASSAYS - USES ABUSES SO TOXICOLOGIC PATHOLOGY LA English DT Article DE PATHOLOGY WORKING GROUP AB ''Truth is the essence of science,'' and ''peer review'' is a key element in assuring the ''truth.'' Peer review is particularly important with regard to diagnostic pathology in bioassays used for regulatory purposes and approval of drugs and medical devices for at least 2 reasons: (a) If a study is designed correctly and conducted properly, the bottom-line results rely almost entirely on pathological interpretations, and (b) diagnostic pathology is a subjective science that relies on the training and experience of the pathologist and therefore is subject to individual bias. ''Bias'' can be introduced during the collection and preparation of pathological materials, use of inconsistent terminology during the pathology evaluation and interpretation of the results. Peer review can help in reducing this bias. However, peer review is also subject to bias by knowledge of treatment groups, selection of inappropriate slides for review, in the type of question asked of the reviewers, and in the selection of the reviewers. When done correctly, pathology peer review can be an effective and important part of a process to assure the results of a study, but when done improperly it can cloud the issue and have a negative impact on the credibility of the study. C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 1 Z9 1 U1 0 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 1994 VL 22 IS 2 BP 141 EP 144 PG 4 WC Pathology; Toxicology SC Pathology; Toxicology GA NY189 UT WOS:A1994NY18900007 PM 7973361 ER PT J AU HINES, RN CASHMAN, JR PHILPOT, RM WILLIAMS, DE ZIEGLER, DM AF HINES, RN CASHMAN, JR PHILPOT, RM WILLIAMS, DE ZIEGLER, DM TI THE MAMMALIAN FLAVIN-CONTAINING MONOOXYGENASES - MOLECULAR CHARACTERIZATION AND REGULATION OF EXPRESSION SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID PRIMARY SEQUENCE; COVALENT STRUCTURE; LIVER-MICROSOMES; PIG-LIVER; METABOLISM; NICOTINE; CLONING; LUNG; OXYGENASE; SMOKING AB The flavin-containing monooxygenase (FMO) has been characterized in several mammalian species, including human. The FMO forms a stable NADP(H)- and oxygen-dependent 4 alpha-hydroperoxy flavin enzyme intermediate in the absence of an oxygenatable substrate. As such, substrate specificity appears to be controlled by access to this stabilized intermediate, resulting in this enzyme's ability to metabolize a wide variety of xenobiotics. These include tertiary and secondary alkyl- and arylamines, many hydrazines, thiocarbamides, thioamides, sulfides, disulfides, thiols, and other soft nucleophiles. Although some of these compounds are oxidized to less active derivatives, several examples of metabolic activation to potentially toxic intermediates also exist. Mercaptopyrimidines and thiocarbamides, for example, appear to be activated predominately by FMO. Thus, this enzyme system may play an important role in the early steps of chemical toxicity. Often, the contribution of FMO to the metabolism of a given compound can be assessed by its unique stereoselectivity relative to other oxygenases. For example, the cytochromes P450 oxidize (S)-nicotine to a mixture of cis- and trans-N-1'-oxides. In contrast, (S)-nicotine is oxidized by human FMO3 exclusively to the trans-N-1'-oxide. With the purification and cloning of FMO from multiple tissues and species it became apparent that more than one FMO exists. Further, there are considerable tissue- and species-specific differences in FMO expression that likely contribute to observed differences in detoxication competency and toxicant susceptibility. (C) 1994 Academic Press, Inc. C1 IGEN RES INST,SEATTLE,WA 98109. NIEHS,RES TRIANGLE PK,NC 27709. OREGON STATE UNIV,DEPT FOOD SCI & TECHNOL,CORVALLIS,OR 97331. UNIV TEXAS,CLAYTON FDN BIOCHEM INST,DEPT CHEM & BIOCHEM,AUSTIN,TX 78712. RP HINES, RN (reprint author), WAYNE STATE UNIV,SCH MED,DEPT PHARMACOL,540 E CANFIELD AVE,DETROIT,MI 48201, USA. OI Hines, Ronald/0000-0002-3094-4200 FU NCI NIH HHS [CA53105]; NHLBI NIH HHS [HL38650]; NIGMS NIH HHS [GM36426] NR 36 TC 93 Z9 96 U1 0 U2 7 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 1994 VL 125 IS 1 BP 1 EP 6 DI 10.1006/taap.1994.1042 PG 6 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA NA188 UT WOS:A1994NA18800001 PM 8128486 ER PT J AU SHIRAISHI, N WAALKES, MP AF SHIRAISHI, N WAALKES, MP TI ENHANCEMENT OF METALLOTHIONEIN GENE-EXPRESSION IN MALE WISTAR (WF/NCR) RATS BY TREATMENT WITH CALMODULIN INHIBITORS - POTENTIAL ROLE OF CALCIUM REGULATORY PATHWAYS IN METALLOTHIONEIN INDUCTION SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID CADMIUM-BINDING PROTEINS; HEPATIC METALLOTHIONEIN; TUMOR PROMOTERS; METAL TOXICITY; CD-113 NMR; TESTES; MICE; PHOSPHODIESTERASE; INVITRO; INVIVO AB Recent reports indicate that calmodulin inhibitors (CIs) can modify cadmium toxicity in rodents. For instance, pretreatment with CIs prevents cadmium-induced testicular damage in mice and substantially reduces such damage in rats, the latter effect coinciding with significant alterations in cadmium distribution. Although the basis of these effects is unclear, it is frequently observed that metal-binding proteins such as metallothionein (MT) are involved in acquired tolerance to cadmium and this could be true of tolerance induced by CIs. Thus, we examined the effects of various CIs on MT gene expression. Treatment of WF/NCr rats with known CIs, including trifluoperazine (TPZ), N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide (W7), calmidazolium (CMZ), chlorpromazine (CPZ), and the calcium ionophore, A23187, increased hepatic MT gene expression, as assessed by mRNA levels, in all cases. Furthermore, hepatic MT protein levels were 40 to 180 mu g MT/g wet wt (g ww) in rats treated with CIs or A23187 compared to control levels of 10 mu g MT/g ww. Treatment with CPZ and CMZ did not increase renal MT protein after exposure, although increases in renal MT mRNA were observed. However, the CIs TPZ and W7 and the calcium ionophore increased both renal MT protein and MT mRNA levels. In contrast, no increases in testicular MT mRNA or the testicular cadmium binding protein (TCBP) levels were seen with any of the treatments. Treatment with CIs or A23187 produced increases in zinc levels in the liver, but not in the kidneys or testes. These results indicate that CIs, such as TPZ, W7, CMZ, and CPZ, as well as the calcium ionophore A23187, have a marked stimulatory effect on hepatic and renal MT gene expression and that calcium regulatory pathways may play an important role in this induction of MT. (C) 1994 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,CARCINOGENESIS SECT,FREDERICK,MD 21702. NR 45 TC 21 Z9 22 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 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD MAR PY 1994 VL 125 IS 1 BP 97 EP 103 DI 10.1006/taap.1994.1053 PG 7 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA NA188 UT WOS:A1994NA18800012 PM 8128501 ER PT J AU DRAGNEV, KH BEEBE, LE JONES, CR FOX, SD THOMAS, PE NIMS, RW LUBET, RA AF DRAGNEV, KH BEEBE, LE JONES, CR FOX, SD THOMAS, PE NIMS, RW LUBET, RA TI SUBCHRONIC DIETARY EXPOSURE TO AROCLOR-1254 IN RATS - ACCUMULATION OF PCBS IN LIVER, BLOOD, AND ADIPOSE-TISSUE AND ITS RELATIONSHIP TO INDUCTION OF VARIOUS HEPATIC DRUG-METABOLIZING-ENZYMES SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID POLYCHLORINATED-BIPHENYLS PCBS; EATING SEA BIRDS; SYNTHETIC OLIGODEOXYRIBONUCLEOTIDE PROBES; IRISH COASTAL WATERS; MOLECULAR-FEATURES; IMMUNOCHEMICAL QUANTITATION; AROMATIC-HYDROCARBONS; FLUOROMETRIC ASSAY; CONGENERS; CYTOCHROME-P-450 AB Female F344/NCr rats were exposed continuously (7-84 days) or discontinuously (7 days exposure/21 days control diet or 28 days exposure/56 days control diet) to various dietary concentrations (1-100 ppm) of Aroclor 1254. There were dose- and time-dependent increases in PCB levels in liver, blood, and adipose tissue. Following removal of the rats from diet containing Aroclor 1254, there was a relatively rapid decrease in PCB levels, particularly in rats exposed to higher concentrations of Aroclor 1254. In parallel with the alterations in PCB levels observed, the rats showed striking dose- and time-dependent increases in hepatic levels of CYP1A1 and CYP1A2, as determined by various methods [RNA analysis, immunochemical detection, or measurement of the O-dealkylation of methoxyresorufin (CYP1A2) or ethoxyresorufin (CYP1A1)]. In rats removed from the Aroclor 1254 diet, catalytic activity for CYP1A1 as well as RNA levels for both CYP1A1 and CYP1A2 rapidly diminished. In contrast to the high levels of induction of CYP1A1 and CYP1A2 observed, limited induction (<5-fold) of epoxide hydrolase, quinone oxidoreductase, and aldehyde dehydrogenase was detected, even in rats exposed to the highest concentration of Aroclor (100 ppm) for up to 84 days. Furthermore, induction of these non-CYP hepatic drug-metabolizing genes exhibited distinctly different concentration-response curves. The ratios of hepatic CYP1A1 activity to hepatic PCB burden were similar for rats exposed continuously to Aroclor in the diet for 7, 28, or 84 days, and for rats exposed discontinuously (7 days Aroclor/21 days control diet or 28 days Aroclor/56 days control diet). Thus, hepatic PCB levels alone appeared to be reasonably predictive of CYP1A1 levels under a variety of modes of exposure. When the ratio of CYP1A1 activity to adipose or blood PCB concentration was determined, similar ratios were observed for rats exposed continuously for 7, 28, or 84 days. However, lower ratios were observed for rats discontinuously exposed to Aroclor in the diet. These results have important implications with respect to: (a) employing PCB levels in various tissues to predict biological effects, and (b) determining different concentration-response curves for the various biological effects induced by PCBs. C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BCDP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,CSAL,PRI DYNCORP,FREDERICK,MD 21702. RUTGERS STATE UNIV,COLL PHARM,PISCATAWAY,NJ 08855. FU NCI NIH HHS [N01-CO-74102] NR 56 TC 20 Z9 20 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 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD MAR PY 1994 VL 125 IS 1 BP 111 EP 122 DI 10.1006/taap.1994.1055 PG 12 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA NA188 UT WOS:A1994NA18800014 PM 7510429 ER PT J AU DALY, JW GUSOVSKY, F MYERS, CW YOTSUYAMASHITA, M YASUMOTO, T AF DALY, JW GUSOVSKY, F MYERS, CW YOTSUYAMASHITA, M YASUMOTO, T TI 1ST OCCURRENCE OF TETRODOTOXIN IN A DENDROBATID FROG (COLOSTETHUS-INGUINALIS), WITH FURTHER REPORTS FOR THE BUFONID GENUS ATELOPUS SO TOXICON LA English DT Article ID TARICHA; ANALOGS; CYNOPS; SKIN AB The water-soluble toxin present in skin of Colostethus inguinalis (Dendrobatidae) was identified as tetrodotoxin by fluorometric HPLC analysis. The amount of tetrodotoxin per frog skin was estimated by HPLC, mouse toxicity, and inhibition of [H-3]saxitoxin binding to brain membranes as 0.1 to 1.2 mug. Small amounts of anhydrotetrodotoxin and 4-epietrodotoxin also were present. Tetrodotoxin-like activity was not detected by inhibition of [H-3]saxitoxin binding in other species of Colostethus nor in other dendrobatids (Aromobates, Dendrobates, Phyllobates). Tetrodotoxin-like activity was present in extracts of skin of five species of Atelopus (Bufonidae). HPLC analysis identified tetrodotoxin as the major toxic component in Atelopus spumarius and A. varius, as a minor component in A. spurrelli, and as a trace component in A. ignescens and A. zeteki. The major tetrodotoxin-like compounds in the last three species were not identified. Tetrodotoxin-like activity was not detected by inhibition of [H-3]saxitoxin binding in skin extracts from three other genera of bufonids. C1 AMER MUSEUM NAT HIST,DEPT HERPETOL & ICHTHYOL,NEW YORK,NY 10024. TOHOKU UNIV,FAC AGR,AOBA KU,SENDAI 981,JAPAN. RP DALY, JW (reprint author), NIH,BIOORGAN CHEM LAB,BETHESDA,MD 20892, USA. NR 17 TC 52 Z9 55 U1 0 U2 10 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0041-0101 J9 TOXICON JI Toxicon PD MAR PY 1994 VL 32 IS 3 BP 279 EP 285 DI 10.1016/0041-0101(94)90081-7 PG 7 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA ND561 UT WOS:A1994ND56100005 PM 8016850 ER PT J AU BUSCH, MP VALINSKY, JE PAGLIERONI, T PRINCE, HE CRUTCHER, GJ GJERSET, GF OPERSKALSKI, EA CHARLEBOIS, E BIANCO, C HOLLAND, PV PETERSEN, LR HOLLINGSWORTH, CG MOSLEY, JW AF BUSCH, MP VALINSKY, JE PAGLIERONI, T PRINCE, HE CRUTCHER, GJ GJERSET, GF OPERSKALSKI, EA CHARLEBOIS, E BIANCO, C HOLLAND, PV PETERSEN, LR HOLLINGSWORTH, CG MOSLEY, JW TI SCREENING OF BLOOD-DONORS FOR IDIOPATHIC CD4+ T-LYMPHOCYTOPENIA SO TRANSFUSION LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; PNEUMOCYSTIS-CARINII PNEUMONIA; FLOW-CYTOMETRY; TRANSFUSION SAFETY; CELL DEFICIENCY; INFECTION; SUBSETS; AIDS; HIV; IMMUNOPHENOTYPES AB Background: The recent recognition of idiopathic CD4+ T-lymphocytopenia (ICL) has led to concern that an unknown immunodeficiency virus may be transmissible by transfusion. Study Design and Methods: To evaluate the prevalence and significance of low CD4+ values among blood donors, CD4, data on 2030 blood donors who were negative for antibody to human immunodeficiency virus type 1 (HIV-1) were compiled. Those with CD4+ values below ICL cutoffs (<300 CD4+ T cells/muL, or <20% CD4+ T cells) were recalled for follow-up investigations. Serial CD4+ data on 55 homosexual men who seroconverted during prospective follow-up and data on 139 anti-HIV-1-positive blood donors initially evaluated in 1986 were reviewed as well. Results: Five seronegative donors (0.25%) had absolute CD4+ counts <300 cells per muL and/or <20 percent. On follow-up, all five donors had immunologic findings within normal ranges, lacked HIV risk factors, and tested negative for HIV types 1 and 2 and human T-lymphotropic virus type I and II infections by antibody and polymerase chain reaction assays. Four of five donors reported transient illnesses shortly after their low CD4+ count donations. The median interval from HIV-1 seroconversion to an initial CD4+ value below ICL CD4+ cutoffs was 63 months for infected homosexual men. Of 139 HIV-1-infected blood donors studied 1 to 2 years after seropositive donations, 34 (24%) had CD4+ counts <300 cells per muL and/or <20 percent. Conclusion: Low CD4+ counts are rare among anti-HIV-1 -negative volunteer blood donors and are generally associated with transient illnesses. If any unknown virus progresses similarly to HIV-1, CD4+ count donor screening would be a poor surrogate for its detection. C1 NEW YORK BLOOD CTR,SPECIAL DIAGNOST LAB,NEW YORK,NY 10021. SACRAMENTO MED FDN CTR BLOOD RES,SACRAMENTO,CA. AMER RED CROSS,TISSUE SERV,LOS ANGELES,CA. CTR DIS CONTROL,NATL CTR INFECT DIS,DIV HIV AIDS,HIV SEROEPIDEMIOL BRANCH,ATLANTA,GA 30333. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. AMER RED CROSS,BLOOD SERV,LOS ANGELES,CA. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. PUGET SOUND BLOOD CTR,SEATTLE,WA 98104. NHLBI,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,SCH MED,DEPT EPIDEMIOL & BIOSTAT,SAN FRANCISCO,CA 94110. RP BUSCH, MP (reprint author), IRWIN MEM BLOOD CTR,270 MASON AVE,SAN FRANCISCO,CA 94118, USA. FU NHLBI NIH HHS [N01-HB-97074, N01-HB-7-7003, N01-HB-4-7002] NR 32 TC 30 Z9 30 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 1994 VL 34 IS 3 BP 192 EP 197 DI 10.1046/j.1537-2995.1994.34394196614.x PG 6 WC Hematology SC Hematology GA ND081 UT WOS:A1994ND08100002 PM 7908469 ER PT J AU KOONIN, EV RUDD, KE AF KOONIN, EV RUDD, KE TI A CONSERVED DOMAIN IN PUTATIVE BACTERIAL AND BACTERIOPHAGE TRANSGLYCOSYLASES SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Article ID ESCHERICHIA-COLI; MUREIN TRANSGLYCOSYLASE; SEQUENCE; GENE RP KOONIN, EV (reprint author), NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 12 TC 46 Z9 51 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 1994 VL 19 IS 3 BP 106 EP 107 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA888 UT WOS:A1994NA88800005 PM 8203016 ER PT J AU HENGEN, PN AF HENGEN, PN TI METHODS AND REAGENTS - GHOST PLASMID OF PBLUESCRIPT SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Note RP HENGEN, PN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702, USA. NR 3 TC 5 Z9 5 U1 0 U2 1 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 1994 VL 19 IS 3 BP 139 EP 140 DI 10.1016/0968-0004(94)90208-9 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA888 UT WOS:A1994NA88800013 PM 8203022 ER PT J AU UHL, GR CHILDERS, S PASTERNAK, G AF UHL, GR CHILDERS, S PASTERNAK, G TI AN OPIATE-RECEPTOR GENE FAMILY REUNION SO TRENDS IN NEUROSCIENCES LA English DT Editorial Material ID DELTA-OPIOID RECEPTOR; EXPRESSION; CLONING C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21224. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PHYSIOL & PHARMACOL,WINSTON SALEM,NC 27103. MEM SLOAN KETTERING CANC CTR,DEPT NEUROL,NEW YORK,NY 10021. CORNELL UNIV,SCH MED,NEW YORK,NY 10021. RP UHL, GR (reprint author), NIDA,ADDICT RES CTR,BALTIMORE,MD 21224, USA. NR 17 TC 212 Z9 213 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD MAR PY 1994 VL 17 IS 3 BP 89 EP 93 DI 10.1016/0166-2236(94)90110-4 PG 5 WC Neurosciences SC Neurosciences & Neurology GA NA301 UT WOS:A1994NA30100001 PM 7515530 ER PT J AU KEITEL, WA BOND, NL ZAHRADNIK, JM CRAMTON, TA ROBBINS, JB AF KEITEL, WA BOND, NL ZAHRADNIK, JM CRAMTON, TA ROBBINS, JB TI CLINICAL AND SEROLOGICAL RESPONSES FOLLOWING PRIMARY AND BOOSTER IMMUNIZATION WITH SALMONELLA-TYPHI-VI CAPSULAR POLYSACCHARIDE VACCINES SO VACCINE LA English DT Article DE SALMONELLA TYPHI; VI CAPSULAR POLYSACCHARIDE; TYPHOID VACCINE ID INFLUENZAE TYPE-B; FIELD TRIAL; FEVER; VACCINATION; PERSISTENCE; PREVENTION AB Clinical and serum antibody responses following intramuscular injection of two formulations of Salmonella typhi Vi capsular polysaccharide (Vi) were assessed in a double-blind evaluation. Healthy adults were randomly assigned to receive a 25 mu g dose of liquid (Vi-Liq, n = 182) or freeze-dried Vi vaccine (Vi-Lyoph; n = 55), or placebo (n = 86). Erythema and/or induration greater than or equal to 1 cm in diameter at the injection site developed in 13/182 (7%) of Vi-Liq and 3/55 (5%) of Vi-Lyoph recipients (not significant, n.s.). Fever (oral temperature greater than or equal to 100 degrees F(37.8 degrees C)) occurred in <2% of vaccinees. The frequencies of rises of fourfold or greater and of maximal Vi antibody levels were similar in the two vaccine groups. Fourfold or greater rises in ser um Vi antibody levels (RIA) developed in 53% of Vi-Lyoph and 60% of Vi-Liq recipients by I week (n.s.), and 98 and 93%, respectively, by I month (n.s.). The frequencies of adverse reactions and mean Vi antibody levels following booster immunization with Vi-Liq 27 to 34 months after primary immunization (n = 55) were similar to those observed following primary immunization, although subjects given a booster dose were more likely to develop local reactions greater than or equal to 1 cm in diameter than those given a first dose (10/55 versus 13/182, p = 0.013 by the chi(2) test). Primary and booster immunizations with the Vi vaccines are well tolerated in healthy adults, mean Vi antibody levels remain significantly elevated for up to 34 months after primary immunization. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. MERIEUX INST INC,MIAMI,FL. NICHHD,DEV & MOLEC IMMUN LAB,BETHESDA,MD 20892. RP KEITEL, WA (reprint author), BAYLOR COLL MED,DEPT MICROBIOL & IMMUNOL,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. RI Zahradnik, Jiri/P-9682-2016 OI Zahradnik, Jiri/0000-0002-1307-2957 NR 25 TC 71 Z9 71 U1 0 U2 1 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 1994 VL 12 IS 3 BP 195 EP 199 DI 10.1016/0264-410X(94)90194-5 PG 5 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MU369 UT WOS:A1994MU36900001 PM 8165850 ER PT J AU DIXON, D YOSHITOMI, K BOORMAN, GA MARONPOT, RR AF DIXON, D YOSHITOMI, K BOORMAN, GA MARONPOT, RR TI LIPOMATOUS LESIONS OF UNKNOWN CELLULAR-ORIGIN IN THE LIVER OF B6C3F1 MICE SO VETERINARY PATHOLOGY LA English DT Article DE LIVER; LIPOMATOUS; PERISINUSOIDAL STELLATE (ITO) CELL; HISTOMORPHOLOGY; ULTRASTRUCTURE; B6C3F1 MICE ID FAT-STORING CELLS; PERISINUSOIDAL STELLATE CELLS; ITO-CELLS; RAT-LIVER; VITAMIN-A; DESMIN; PROLIFERATION; SINUSOIDS; FIBROSIS; INJURY AB The gross, microscopic, and ultrastructural features of lipomatous lesions in the liver of B6C3F1 mice are described. The cases were selected from a database of 45,406 male and 45,674 female mice used as treated, control, or vehicle-control animals in the National Cancer Institute's Bioassays or the National Toxicology Program's 2-year carcinogenicity studies. Thirteen hepatic lesions identified from cases within the database were re-evaluated microscopically and selected for further study. These lesions were present in ten males and three females that were between 85 and 113 weeks of age at the time of death. Grossly, the liver lesions were described as white to yellow or red to brown nodules/masses or foci that ranged from 2.0 to 25 mm in diameter. The lesions commonly involved the median and left lateral hepatic lobes. Microscopically, many of the lesions closely resembled lipomas described in the liver of human beings, and they consisted of nonencapsulated mature adipose-like tissue with irregular margins. The majority of the cells that comprised the lipomatous lesions were signet-ring shaped. These cells were positive for lipid as evidenced with oil red-O. The lipid droplets were also present within the hepatocytes that comprised the hepatic plates trapped within or surrounding many of the lipomatous lesions. At the margins of many of the lesions there were spindle-shaped cells that contained small intracytoplasmic lipid vacuoles. These cells were often within a stromal matrix that had focal areas of collagen and mucopolysaccharides, as evidenced by weak staining with Masson's trichrome and periodic acid-Schiffs stains, respectively. There was also disruption of the reticulum fibers in many of the lesions, as noted with a Gomori's reticulum stain. Ultrastructurally, cytoplasmic organelles, such as rough endoplasmic reticulum, free ribosomes and small lipid vacuoles, were present in the spindle-shaped cells, whereas signet-ring-shaped cells had few discernible organelles due to peripheral compression of the cytoplasm by single large vacuoles occupying the cytoplasmic space. The spindle-shaped cells were free of lysosomes. Thin collagen fibers were seen in contact with some of the spindle-shaped cells and were located between these cells and adjacent hepatocytes, or endothelial cells lining sinusoidal capillaries. A distinct basal lamina was not associated with spindle- or signet-ring-shaped cells. Similar lipomatous lesions were not found in other visceral organs. The exact cellular origin of the hepatic lesions described here is not known. C1 NIEHS,NATL TOXICOL PROGRAM,PATHOL BRANCH,RES TRIANGLE PK,NC. EXPTL PATHOL LABS INC,RES TRIANGLE PK,NC. RP DIXON, D (reprint author), NIEHS,EXPTL PATHOL LAB,POB 12233,MD C2-09,RES TRIANGLE PK,NC 27709, USA. NR 41 TC 6 Z9 6 U1 0 U2 0 PU AMER COLL VET PATHOLOGIST PI LAWRENCE PA 810 EAST 10TH STREET, LAWRENCE, KS 66044 SN 0300-9858 J9 VET PATHOL JI Vet. Pathol. PD MAR PY 1994 VL 31 IS 2 BP 173 EP 182 PG 10 WC Pathology; Veterinary Sciences SC Pathology; Veterinary Sciences GA MZ295 UT WOS:A1994MZ29500003 PM 8203079 ER PT J AU ALEXANDERSEN, S LARSEN, S AASTED, B UTTENTHAL, A BLOOM, ME HANSEN, M AF ALEXANDERSEN, S LARSEN, S AASTED, B UTTENTHAL, A BLOOM, ME HANSEN, M TI ACUTE INTERSTITIAL PNEUMONIA IN MINK KITS INOCULATED WITH DEFINED ISOLATES OF ALEUTIAN MINK DISEASE PARVOVIRUS SO VETERINARY PATHOLOGY LA English DT Article DE ALEUTIAN MINK DISEASE PARVOVIRUS; INTERSTITIAL PNEUMONIA; ISOLATES; LUNG; MINK; MORTALITY; PARVOVIRUS; PATHOLOGY; PNEUMONIA; VIRUS ID INFECTED MINK; PULMONARY SURFACTANT; NUCLEOTIDE-SEQUENCE; VIRAL REPLICATION; VIRUS; LUNG; ANTIBODIES; ADV; IMMUNOELECTROPHORESIS; HYBRIDIZATION AB The present study addressed the causal role of Aleutian mink disease parvovirus (ADV) in acute interstitial pneumonia in mink kits. All the examined isolates of ADV caused interstitial pneumonia in newborn kits, although the severity of disease and the mortality varied. These findings indicate that ADV is the direct causal agent of this disease in mink kits and that cofactors, which could have been present in the original ADV-K isolate, do not play a role. Acute interstitial pneumonia characterized by hypertrophy and hyperplasia of alveolar type II cells, intranuclear viral inclusions, interstitial edema, and hyaline membrane formation was experimentally reproduced in mink kits infected as newborns with live different isolates of ADV. Four hundred forty-nine newborn mink kits were included in the study, of which 247 were necropsied. The lesions caused by the different isolates were indistinguishable by histopathologic examination, but the incidence (50-100%) and severity (mortality of 30-100%, n = 218) of disease among the mink kits varied. Also, the content of ADV antigens in the lungs of infected kits varied among the groups. According to these features, the examined isolates could be placed in groups of high and low virulence. ADV-K, ADV-Utah I, and ADV-DK were in a highly virulent group producing a mortality of 90-100% (n = 110) in mink inoculated as newborns. ADV-GL and ADV-Pullman belonged to a group of low virulence, with an incidence of clinical disease of 50-70% and a mortality of approximately 30-50% (n = 118) in kits inoculated as newborns. The mortality in the control group receiving a mock inoculum was around 12% (n = 34). The period from infection to development of fatal disease varied from approximately 12 days for the highly virulent isolates up to around 20 days for the isolates of low virulence. The 107 mink kits that survived inoculation with ADV as newborns developed lesions typical of classical Aleutian disease irrespective of the ADV isolate used. The lesions consisted of chronic immune complex-mediated glomerulonephritis and infiltrations with mononuclear cells, including plasma cells in lung, liver, spleen, kidney, mesenteric lymph node, and intestine. Surviving kits also had hypertrophy of the bronchus-associated lymphoid tissue and focal subpleural, intraalveolar accumulations of large cells with foamy cytoplasm, so-called lipid pneumonia. C1 ROYAL VET & AGR UNIV,DEPT PHARMACOL & PATHOBIOL,VET PATHOL LAB,DK-1870 FREDERIKSBERG C,DENMARK. ROYAL VET & AGR UNIV,DEPT VET MICROBIOL,VIROL & IMMUNOL LAB,DK-1870 FREDERIKSBERG C,DENMARK. DANISH FUR BREEDERS ASSOC,GLOSTRUP,DENMARK. NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. RP ALEXANDERSEN, S (reprint author), ROYAL VET & AGR UNIV,DEPT PHARMACOL & PATHOBIOL,MOLEC PATHOBIOL LAB,DK-1870 FREDERIKSBERG C,DENMARK. OI Alexandersen, Soren/0000-0002-5039-3178 NR 48 TC 38 Z9 42 U1 1 U2 8 PU AMER COLL VET PATHOLOGIST PI LAWRENCE PA 810 EAST 10TH STREET, LAWRENCE, KS 66044 SN 0300-9858 J9 VET PATHOL JI Vet. Pathol. PD MAR PY 1994 VL 31 IS 2 BP 216 EP 228 PG 13 WC Pathology; Veterinary Sciences SC Pathology; Veterinary Sciences GA MZ295 UT WOS:A1994MZ29500009 PM 8203085 ER PT J AU SERENO, MM GORZIGLIA, MI AF SERENO, MM GORZIGLIA, MI TI THE OUTER CAPSID PROTEIN VP4 OF MURINE ROTAVIRUS STRAIN EB REPRESENTS A TENTATIVE NEW P-TYPE SO VIROLOGY LA English DT Note ID AMINO-ACID-SEQUENCE; COMPLETE NUCLEOTIDE-SEQUENCE; PORCINE ROTAVIRUS; NEUTRALIZATION EPITOPES; ANTIGENIC RELATIONSHIPS; RHESUS ROTAVIRUS; UNIQUE VP4; G-SEROTYPE; GENE; IDENTIFICATION AB The nucleotide and deduced amino acid sequence of the gene 4 of murine rotavirus strain Eb were determined. The gene is 2359 nucleotides in length and encodes for a protein of 775 amino acids. Comparison of the VP4 amino acid sequence of the Eb strain with several human and animal rotavirus strains which represent all of the currently recognized distinct VP4 genotypes revealed amino acid identities of from 55.7-75.1% for VP4, 37.1-63.3% for VP8, and 23.9-52.1% for the B region (amino acids 84-180). In addition, antisera to recombinant VP4s of five distinct rotavirus serotypes and two subtypes failed to react significantly by neutralization assay with the Eb strain. Thus, it appears that the Eb strain should be considered a new VP4 genotype and/or serotype. (C) 1994 Academic Press, Inc. C1 NIAID,INFECT DIS LAB,EPIDEMIOL SECT,BETHESDA,MD 20892. NR 45 TC 53 Z9 57 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 PY 1994 VL 199 IS 2 BP 500 EP 504 DI 10.1006/viro.1994.1153 PG 5 WC Virology SC Virology GA MY848 UT WOS:A1994MY84800031 PM 8122380 ER PT J AU SONNTAG, KC SCHNITZLER, P KOONIN, EV DARAI, G AF SONNTAG, KC SCHNITZLER, P KOONIN, EV DARAI, G TI CHILE IRIDESCENT VIRUS ENCODES A PUTATIVE HELICASE BELONGING TO A DISTINCT FAMILY WITHIN THE DEAD/H SUPERFAMILY - IMPLICATIONS FOR THE EVOLUTION OF LARGE DNA VIRUSES SO VIRUS GENES LA English DT Article DE IRIDOVIRIDAE; INSECT IRIDESCENT VIRUS TYPE 6; DNA NUCLEOTIDE SEQUENCING; COMPUTER ANALYSIS; PROTEIN ALIGNMENT ID YEAST SACCHAROMYCES-CEREVISIAE; CIRCULAR PERMUTATION; GENOME; TYPE-6; PROTEIN; IDENTIFICATION; REPLICATION; REPAIR; RECOMBINATION; EXPRESSION AB The complete nucleotide sequence of the EceRI DNA fragment M (7099 bp; 0.310-0.345 map units) of the genome of insect iridescent virus type 6-Chilo iridescent virus (CIV)-was determined. A 606 codon open reading frame located in this region encoded a protein (p69) related to a distinct family of putative DNA and/or RNA helicases belonging to the ''DEAD/H'' superfamily. Unique sequence signatures were derived that allowed selective retrieval of the putative helicases of the new family from amino acid sequence databases. The family includes yeast, Drosophila, mammalian, and bacterial proteins involved in transcription regulation and in repair of damaged DNA. It is hypothesized that p69 of CIV may be a DNA or RNA helicase possibly involved in viral transcription. A distant relationship was observed to exist between this family of helicases and another group of proteins that consists of putative helicases of poxviruses, African swine fever virus, and yeast mitochondrial plasmids. It is shown that p69 of CIV is much more closely related to cellular helicases than any of the other known viral helicases. Phylogenetic analysis suggested an independent origin for the p69 gene and the genes encoding other viral helicases. C1 UNIV HEIDELBERG, INST MED VIROL, D-69120 HEIDELBERG, GERMANY. NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA. NR 43 TC 15 Z9 16 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0920-8569 EI 1572-994X J9 VIRUS GENES JI Virus Genes PD MAR PY 1994 VL 8 IS 2 BP 151 EP 158 DI 10.1007/BF01703072 PG 8 WC Genetics & Heredity; Virology SC Genetics & Heredity; Virology GA NL202 UT WOS:A1994NL20200008 PM 8073636 ER PT J AU DEAN, M ALLIKMETS, R GERRARD, B STEWART, C KISTLER, A SHAFER, B MICHAELIS, S STRATHERN, J AF DEAN, M ALLIKMETS, R GERRARD, B STEWART, C KISTLER, A SHAFER, B MICHAELIS, S STRATHERN, J TI MAPPING AND SEQUENCING OF 2 YEAST GENES BELONGING TO THE ATP-BINDING CASSETTE SUPERFAMILY SO YEAST LA English DT Article DE MULTIDRUG RESISTANCE; ABC GENE; CHROMOSOME XII; CHROMOSOME XVI ID RESISTANCE P-GLYCOPROTEIN; CLASS-II REGION; MULTIDRUG-RESISTANCE; SACCHAROMYCES-CEREVISIAE; TRANSPORT; DNA; PROTEINS; PRODUCT; PATHWAY; CLONING AB ATP-binding cassette (ABC) transporters share significant sequence identity within their ATP-binding domains. Degenerate oligonucleotides based on highly conserved portions of the ATP-binding domain genes were used to clone portions of two members of the ABC gene superfamily from Saccharomyces cerevisiae DNA. These genes were designated MDL1 and MDL2 (for multidrug resistance-like). Each MDL gene is predicted to encode a single set of transmembrane domains and a single ATP-binding domain, thus the MDL gene products are 'half-molecule' ABC proteins. The two genes were mapped to precise regions on chromosomes XII and XVI and show a considerable similarity to the mammalian P-glycoprotein/multidrug resistance (MDR) and peptide transporter (TAP) genes. Preliminary analysis of null mutants constructed by gene replacement has indicated that the MDL genes are not essential for viability of yeast. The sequences have been deposited in the GenBank data library under Accession Numbers L16958 (Locus YSCBCSA) and L16959 (Locus YSCBCSB). C1 NCI, FREDERICK CANC RES & DEV CTR, PROGRAM RESOURCES INC DYNCORP, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, EUKARYOT GENE EXPRESS LAB, FREDERICK, MD 21702 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT CELL BIOL & ANAT, BALTIMORE, MD 21205 USA. RP NCI, FREDERICK CANC RES & DEV CTR, BIOL CARCINOGENESIS & DEV PROGRAM, VIRAL CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 FU NCI NIH HHS [N0-CO-74101] NR 31 TC 51 Z9 55 U1 0 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0749-503X EI 1097-0061 J9 YEAST JI Yeast PD MAR PY 1994 VL 10 IS 3 BP 377 EP 383 DI 10.1002/yea.320100310 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology GA NC497 UT WOS:A1994NC49700009 PM 7912468 ER PT J AU BABILA, T KLEIN, DC AF BABILA, T KLEIN, DC TI CHOLERA TOXIN-INDUCED G(S)ALPHA DOWN-REGULATION IN NEURAL TISSUE - STUDIES ON THE PINEAL-GLAND SO BRAIN RESEARCH LA English DT Article DE CHOLERA TOXIN; PINEAL; CYCLIC AMP; G(S)ALPHA; N-ACETYLTRANSFERASE ID BINDING-PROTEIN GS; SEROTONIN N-ACETYLTRANSFERASE; ALPHA-SUBUNIT; CELLS; BETA; DEGRADATION; STIMULATION; ANTIBODIES; ACTIVATION; ABUNDANCE AB Cholera toxin (CT) treatment (50 mu g/ml) was used to down regulate the alpha subunit of the stimulatory guanine nucleotide binding protein (Gs alpha) in pineal glands in organ culture, as has been seen in non-neural tissue. A 15 h treatment reduces G(s) alpha by similar to 75% as measured using semi-quantitative Western blot technology. In contrast, this treatment does not alter the abundance of G beta, G(i) alpha or G(0) alpha. This effect on G(5) alpha was still apparent following a 36-h washout period. The 48-h CT treatment increased cyclic AMP accumulation 10- to 17-fold but blocked the norepinephrine (NE)-induced increase in cyclic AMP accumulation, presumably reflecting the loss of G(s) alpha. This treatment did not, however, inhibit protein synthesis or stimulation of arylalkylamine N-acetyltransferase (NAT) activity produced by treatment with either DB-cyclic AMP (N-6,2'-O-dibutyryl adenosine 3',5'-monophosphate) or 8 Br-cyclic AMP, stable cyclic AMP derivatives. This indicates that a 48-h CT treatment was not generally toxic. In contrast, this treatment blocked subsequent CT stimulation of NAT. The effects of CT treatment on the adrenergic stimulation of NAT was examined using treatments which selectively produced alpha- or beta-adrenergic stimulation. alpha(1)-Adrenergic activation of the pineal gland elevates [Ca2+](i), which potentiates effects of cyclic AMP; in these studies the response to alpha-adrenergic activation was markedly increased in 48-h CT-treated glands, reflecting Ca2+ potentiation of the effects of elevated levels of cyclic AMP. In contrast, the effects of the selective beta-adrenergic agonist isoproterenol was reduced by similar to 75%. These studies not only establish CT-induced G(s) alpha down-regulation as a new tool for the study of adrenergic signal transduction in the pineal gland, but indicate that this paradigm is probably useful in all neural tissue. C1 NICHHD,DEV NEUROBIOL LAB,NEUROENDOCRINOL SECT,BETHESDA,MD 20892. NR 25 TC 4 Z9 4 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD FEB 28 PY 1994 VL 638 IS 1-2 BP 151 EP 156 DI 10.1016/0006-8993(94)90644-0 PG 6 WC Neurosciences SC Neurosciences & Neurology GA MZ355 UT WOS:A1994MZ35500019 PM 8199855 ER PT J AU BURNET, PWJ MICHELSON, D SMITH, MA GOLD, PW STERNBERG, EM AF BURNET, PWJ MICHELSON, D SMITH, MA GOLD, PW STERNBERG, EM TI THE EFFECT OF CHRONIC IMIPRAMINE ADMINISTRATION ON THE DENSITIES OF 5-HT1A AND 5-HT2 RECEPTORS AND THE ABUNDANCIES OF 5-HT RECEPTOR AND TRANSPORTER MESSENGER-RNA IN THE CORTEX, HIPPOCAMPUS AND DORSAL RAPHE OF 3 STRAINS OF RAT SO BRAIN RESEARCH LA English DT Article ID FRONTAL-CORTEX; MESSENGER-RNA; BINDING-SITES; AUTORADIOGRAPHIC ANALYSIS; ELECTROCONVULSIVE SHOCK; SEROTONIN-2 RECEPTORS; SEROTONERGIC MEASURES; SUICIDE VICTIMS; BRAIN; ANTIDEPRESSANTS AB We have recently demonstrated that the LEW/N rat contains lower concentrations of cortical and hippocampal 5-HT1A receptors compared with the F344/N and out-bred HSD rats. To further characterize these strains, we investigated the effect of chronic (8 wk) imipramine administration (5 mg/kg/day) on 5-HT1A and 5-HT2 receptor densities and mRNA in the cortex and hippocampus and 5-HT transporter mRNA in the dorsal raphe of LEW/N, HSD and F344/N rats, using quantitative autoradiography and in situ hybridization histochemistry. After imipramine treatment, a significant increase in the levels of hippocampal 5-HT1A receptors, but not mRNA, was observed in LEW/N rats while the abundance of hippocampal 5-HT1A receptor mRNA, but not 5-HT1A receptor densities, decreased in F344/N rats. Cortical and hippocampal 5-HT2receptor densities, but not mRNA, significantly decreased after imipramine administration in all three strains. Finally, 5-HT1A receptor densities and the abundance of mRNAs encoding the 5-HT1A receptor and 5-HT transporter in the dorsal raphe remained unaltered after imipramine administration in all three strains. The effects of imipramine on the levels of cortical and hippocampal 5-HT1A and 5-HT2 receptors and their transcripts, therefore, appear to be strain-dependent. The implications of these findings are discussed. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,NEUROENDOCRINE IMMUNOL & BEHAV UNIT,BETHESDA,MD 20892. NR 30 TC 86 Z9 87 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD FEB 28 PY 1994 VL 638 IS 1-2 BP 311 EP 324 DI 10.1016/0006-8993(94)90664-5 PG 14 WC Neurosciences SC Neurosciences & Neurology GA MZ355 UT WOS:A1994MZ35500039 PM 8199869 ER PT J AU BERGER, P FARREL, D SHARP, F SKOLNICK, P AF BERGER, P FARREL, D SHARP, F SKOLNICK, P TI DRUGS ACTING AT THE STRYCHNINE-INSENSITIVE GLYCINE RECEPTOR DO NOT INDUCE HSP-70 PROTEIN IN THE CINGULATE CORTEX SO NEUROSCIENCE LETTERS LA English DT Article DE GLYCINE; NMDA; ACPC; HA-966; 7-CHLOROKYNURENIC ACID; D-CYCLOSERINE ID D-ASPARTATE RECEPTOR; PHENCYCLIDINE; NEURONS; SCHIZOPHRENIA; ANTAGONIST; MECHANISM; KETAMINE; HSP70; RAT AB The potential for compounds acting at the strychnine-insensitive glycine receptor to injure neurons was examined using induction of a 70 kDa heat shock protein (HSP-70) as a marker. HSP-70 was consistently detected in retrosplenial and cingulate cortices after MK-801 but not glycine drug treatment. Elsewhere in the cortex, mild diffuse HSP-70 immunoreactivity was detected following 7-chlorokynurenic acid. Following HA-966, intense hippocampal HSP-70 immunoreactivity was observed. These findings indicate that even after very high doses, drugs acting at the strychnine-insensitive glycine receptor are less likely to injure cingulate cortical neurons than other classes of NMDA antagonists. C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. RP BERGER, P (reprint author), UCSF,SFVAMC,PSYCHIAT & NEUROL LAB,PSYCHIAT 116M,4150 CLEMENT ST,SAN FRANCISCO,CA 94121, USA. NR 20 TC 35 Z9 35 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 28 PY 1994 VL 168 IS 1-2 BP 147 EP 150 DI 10.1016/0304-3940(94)90437-5 PG 4 WC Neurosciences SC Neurosciences & Neurology GA MZ905 UT WOS:A1994MZ90500037 PM 8028768 ER PT J AU NOMIZU, M OTAKA, A BURKE, TR ROLLER, PP AF NOMIZU, M OTAKA, A BURKE, TR ROLLER, PP TI SYNTHESIS OF PHOSPHONOMETHYL-PHENYLALANINE AND PHOSPHOTYROSINE-CONTAINING CYCLIC-PEPTIDES AS INHIBITORS OF PROTEIN-TYROSINE KINASE/SH2 INTERACTIONS SO TETRAHEDRON LA English DT Article ID SOLID-PHASE SYNTHESIS; RECEPTOR; HEXAPEPTIDES; SEQUENCES; ANALOG AB Linear and cyclic hexameric peptides were synthesized with the amino acid sequence Gly-Tyr-Val-Pro-Met-Leu, which corresponds to the autophosphorylation segment around Y751 of PDGF receptor B subunit. The natural L-tyrosine (position 2) was also substituted in peptide analogs with P-Tyr, L-tyrosine phosphate, and L- and D4-phosphonomerhyl-phenylalanine (Pmp). Fmoc chemistry-based SPPS methodology, and Rink resin support were used with diphenylphosphoryl azide as the cyclizing agent. The linear and cyclic peptides were characterized by circulardichroism spectroscopy. The peptides described were designed as inhibitors of receptor tyrosine kinase/src homology region 2 interactions that mediate mitogenic signal transduction pathways. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. RI Burke, Terrence/N-2601-2014 NR 29 TC 27 Z9 27 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4020 J9 TETRAHEDRON JI Tetrahedron PD FEB 28 PY 1994 VL 50 IS 9 BP 2691 EP 2702 DI 10.1016/S0040-4020(01)86985-4 PG 12 WC Chemistry, Organic SC Chemistry GA MY730 UT WOS:A1994MY73000006 ER PT J AU BURBELO, PD GABRIEL, GC KIBBEY, MC YAMADA, Y KLEINMAN, HK WEEKS, BS AF BURBELO, PD GABRIEL, GC KIBBEY, MC YAMADA, Y KLEINMAN, HK WEEKS, BS TI LZIP-1 AND LZIP-2 - 2 NOVEL MEMBERS OF THE BZIP FAMILY SO GENE LA English DT Note DE TRANSCRIPTION FACTOR; MOUSE MELANOMA; LEUCINE ZIPPER; DIMERIZATION ID CAMP-RESPONSIVE-ELEMENT; LEUCINE ZIPPER PROTEINS; DNA-BINDING PROTEIN; FOS-JUN INTERACTION; CYCLIC-AMP; CELLS; GENE; RECOGNITION; SEQUENCE; PROMOTER AB A large family of bZIP proteins, containing a basic DNA-binding domain and a leucine zipper, have been described that recognize the CRE and AP-1 elements. Here, we have identified two new members, designated LZIP-1 and LZIP-2. The murine cDNA for LZIP-1 coded for a 379-amino-acid (aa) residue protein containing several distinct domains, including a Ser-rich region, a basic DNA-binding region, and an unusually long leucine zipper. A second form, LZIP-2, contained an additional 25 aa in the N-terminal region. Western immunoblotting revealed that antibody raised against part of recombinant LZIP-1 detected both forms in a variety of tissues. Gel mobility shift assays demonstrated that the recombinant protein possessed specific DNA-binding activity for both the CRE and AP-1 sites. The present identification of two more ubiquitous members of the bZIP family emphasizes the complex nature of transcription factor interactions at the CRE and AP-1 sites. RP BURBELO, PD (reprint author), NIDR,DEV BIOL LAB,BLDG 30,ROOM 410,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Burbelo, Peter/B-1027-2009 NR 30 TC 28 Z9 30 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD FEB 25 PY 1994 VL 139 IS 2 BP 241 EP 245 DI 10.1016/0378-1119(94)90763-3 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA NA749 UT WOS:A1994NA74900017 PM 8112612 ER PT J AU TAKAHASHI, N BREITMAN, TR AF TAKAHASHI, N BREITMAN, TR TI RETINOYLATION OF VIMENTIN IN THE HUMAN MYELOID-LEUKEMIA CELL-LINE HL-60 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ACUTE PROMYELOCYTIC LEUKEMIA; RETINOIC ACID RECEPTOR; INTERMEDIATE FILAMENT PROTEINS; MAMMARY EPITHELIAL-CELLS; AVIAN MYOGENIC CELLS; GRANULOCYTIC DIFFERENTIATION; EPIDERMAL-KERATINOCYTES; NUCLEAR-ENVELOPE; GENE-EXPRESSION; HL-60 CELLS AB Retinoylation (retinoic acid acylation) is a posttranslational modification of proteins occurring in many eukaryotic cell lines. The widespread occurrence of retinoylation suggests that it may play a role in many effects of retinoic acid (RA) on cells. The regulatory subunits of cyclic AMP dependent protein kinase are retinoylated in the human myeloid leukemia cell line HL60 (Takahashi, N., Liapi, C., Anderson, W. B., and Breitman, T R. (1991) Arch. Biochem. Biophys. 290, 293-302), and cytokeratins are retinoylated in normal human keratinocytes (Takahashi, N., Jetten, A. M., and Breitman, T R. (1991) Biochem. Biophys. Res. Commun. 180, 393-400), We show, in this study, that the intermediate filament protein vimentin is retinoylated in HL60 cells during a 24-h exposure to 100 nM [H-3]RA. We found that a retinoylated protein of M(r) 55,000 coeluted on anion exchange chromatography and comigrated on either one- or two-dimensional polyacrylamide gel electrophoresis with a protein that also was stained on immunoblots by an anti-vimentin antibody. About 50% of the [H-3]RA was released from this M(r) 55,000 retinoylated protein after hydrolysis with either NH2OH (1 M, pH 10) or CH3OH, 0.1 m KOH. These results indicated that a large fraction of the RA was bound to vimentin by an ester bond. Both the M(r) 55,000 retinoylated protein and immunoreactive vimentin were associated with cell nuclei isolated by two procedures. They were detached during exposure to a nonionic detergent buffer, suggesting that they are bound to the nuclear envelope. These results indicate that retinoylation is a new modification of vimentin that may be an early event in RA-induced differentiation of HL60 cells. RP TAKAHASHI, N (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BIOL CHEM LAB,BLDG 37,RM 5D-02,BETHESDA,MD 20892, USA. NR 84 TC 34 Z9 34 U1 0 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 25 PY 1994 VL 269 IS 8 BP 5913 EP 5917 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MY840 UT WOS:A1994MY84000067 PM 7509793 ER PT J AU JOUVIN, MHE ADAMCZEWSKI, M NUMEROF, R LETOURNEUR, O VALLE, A KINET, JP AF JOUVIN, MHE ADAMCZEWSKI, M NUMEROF, R LETOURNEUR, O VALLE, A KINET, JP TI DIFFERENTIAL CONTROL OF THE TYROSINE KINASES LYN AND SYK BY THE 2 SIGNALING CHAINS OF THE HIGH-AFFINITY IMMUNOGLOBULIN-E RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BASOPHILIC LEUKEMIA-CELLS; T-CELL; ANTIGEN RECEPTOR; IGE RECEPTOR; ZETA-CHAIN; PHOSPHOLIPASE C-GAMMA-1; CYTOPLASMIC DOMAINS; MONOCLONAL-ANTIBODY; TRANSFECTED CELLS; MOLECULAR-CLONING AB Nonreceptor tyrosine kinases such as the newly described 70-kDa (ZAP-70/Syk) and Src-related tyrosine kinases are coupled to a variety of receptors, including the antigen receptors on B- and T-cells and the Fc receptors for IgE (Fc epsilon RI) and IgG (Fc gamma RI, Fc gamma RIII/CD16). Various subunits of these receptors contain homologous activation motifs which appear capable of autonomously triggering cell activation. Two forms of this motif are present in the Fc epsilon RI multimeric complex: one in the beta chain and one in the gamma chain. Here we show that each of the two tyrosine kinases known to be involved in Fc epsilon RI signaling is controlled by a distinct motif-containing chain. Lyn associates with the nonactivated beta chain, whereas gamma promotes the activation of Syk. We also show that neither the beta nor the gamma motif alone can account for the full signaling capacity of the entire receptor. We propose that, upon triggering of the tetrameric receptor, Lyn already bound to beta becomes activated and phosphorylates beta and gamma; the phosphorylation of gamma induces the association of Syk with gamma and also the activation of Syk, resulting in the phosphorylation and activation of phospholipase C gamma(1). Cooperative recruitment of specific kinases by the various signaling chains found in this family of antigen receptors could represent a way to achieve the full signaling capacity of the multimeric complexes. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. NR 49 TC 330 Z9 331 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 25 PY 1994 VL 269 IS 8 BP 5918 EP 5925 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MY840 UT WOS:A1994MY84000068 PM 8119935 ER PT J AU PARK, K CHOE, J OSIFCHIN, NE TEMPLETON, DJ ROBBINS, PD KIM, SJ AF PARK, K CHOE, J OSIFCHIN, NE TEMPLETON, DJ ROBBINS, PD KIM, SJ TI HUMAN RETINOBLASTOMA SUSCEPTIBILITY GENE PROMOTER IS POSITIVELY AUTOREGULATED BY ITS OWN PRODUCT SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSFORMING GROWTH FACTOR-BETA-1; CELL-CYCLE; BINDING PROTEIN; C-MYC; TRANSCRIPTION; EXPRESSION; IDENTIFICATION; CLONING; PHOSPHORYLATION; INACTIVATION AB The product of the retinoblastoma susceptibility gene is a 1O5-kDa protein that has properties of a cell cycle regulatory factor. Previous reports indicated that two distinct DNA-binding factors, RBF-1 and ATF, play an important part in the transcription of the human retinoblastoma gene (Rb). Recently, we demonstrated that pRb activates expression of the human transforming growth factor-beta 2 gene through ATF-B Since the human Rb gene promoter also contains an ATF-a-like binding site, we examined whether pRb can regulate its own expression through ATF-2. Here we report that overexpression of Rb stimulates Rb promoter activity through the ATF binding site in a variety of different cell types. Mutation of the ATF binding site of the Rb promoter abolishes the Rb autoinduction. We have also determined that the carboxyl-terminal domain of pRb is responsible for the Rb autoinduction through ATF-2. Rb autoinduction may be important for maintaining the action of pRb during cell growth, and loss of autoinducibility may contribute to retinoblastoma. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. CASE WESTERN RESERVE UNIV,SCH MED,INST PATHOL,CLEVELAND,OH 44106. RI Templeton, Dennis/F-7695-2011 FU NCI NIH HHS [CA-55227] NR 40 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 25 PY 1994 VL 269 IS 8 BP 6083 EP 6088 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MY840 UT WOS:A1994MY84000091 PM 8119953 ER PT J AU LEE, DC GONZALEZ, P WISTOW, G AF LEE, DC GONZALEZ, P WISTOW, G TI ZETA-CRYSTALLIN - A LENS-SPECIFIC PROMOTER AND THE GENE RECRUITMENT OF AN ENZYME AS A CRYSTALLIN SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Note DE GENE RECRUITMENT; CRYSTALLIN; LENS; PROMOTER; ENZYME ID GUINEA-PIG LENS; DNA-BINDING; REGULATORY ELEMENTS; STRUCTURAL PROTEIN; EPITHELIAL-CELLS; TRANSGENIC MICE; ALPHA-ENOLASE; SINGLE-COPY; MOUSE LENS; EXPRESSION C1 NEI,MOLEC & DEV BIOL LAB,MOLEC STRUCT & FUNCT SECT,BETHESDA,MD 20892. NEI,MECHANISMS OCULAR DIS LAB,BETHESDA,MD 20892. NR 47 TC 25 Z9 25 U1 1 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 25 PY 1994 VL 236 IS 3 BP 669 EP 678 DI 10.1006/jmbi.1994.1178 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MY715 UT WOS:A1994MY71500001 PM 8114084 ER PT J AU BAUER, WR HAYES, JJ WHITE, JH WOLFFE, AP AF BAUER, WR HAYES, JJ WHITE, JH WOLFFE, AP TI NUCLEOSOME STRUCTURAL-CHANGES DUE TO ACETYLATION SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Note DE NUCLEOSOME; HISTONE ACETYLATION; DNA HELICAL REPEAT; SURFACE LINKING NUMBER; CLOSED CIRCULAR DNA ID LINKING DEFICIENCY; CORE HISTONES; DNA; CHROMATIN; HYPERACETYLATION; MINICHROMOSOMES; ORGANIZATION; DISTORTION; PARTICLE; NUMBER C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,DEPT MATH,LOS ANGELES,CA 90024. RP BAUER, WR (reprint author), SUNY STONY BROOK,HLTH SCI CTR,DEPT MICROBIOL,STONY BROOK,NY 11794, USA. NR 32 TC 111 Z9 113 U1 0 U2 0 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 25 PY 1994 VL 236 IS 3 BP 685 EP 690 DI 10.1006/jmbi.1994.1180 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MY715 UT WOS:A1994MY71500003 PM 8114086 ER PT J AU MORRISON, AR AF MORRISON, AR TI ANIMAL RIGHTS AND RADICAL POLITICS SO SCIENCE LA English DT Letter RP MORRISON, AR (reprint author), NIMH,PROGRAM ANIM RES ISSUES,PARKLAWN BLDG,ROOM 17C-26,BETHESDA,MD 20892, USA. NR 7 TC 1 Z9 1 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 25 PY 1994 VL 263 IS 5150 BP 1073 EP 1074 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX759 UT WOS:A1994MX75900002 ER PT J AU CRITCHFIELD, JM RACKE, MK ZUNIGAPFLUCKER, JC CANNELLA, B RAINE, CS GOVERMAN, J LENARDO, MJ AF CRITCHFIELD, JM RACKE, MK ZUNIGAPFLUCKER, JC CANNELLA, B RAINE, CS GOVERMAN, J LENARDO, MJ TI T-CELL DELETION IN HIGH ANTIGEN DOSE THERAPY OF AUTOIMMUNE ENCEPHALOMYELITIS SO SCIENCE LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; LYMPHOCYTES-T; CLONAL ANERGY; INVITRO; INTERLEUKIN-2; TOLERANCE; SUPPRESSION; ACTIVATION; RECEPTOR AB Encounters with antigen can stimulate T cells to become activated and proliferate, become nonresponsive to antigen, or to die. T cell death was shown to be a physiological response to interleukin-2-stimulated cell cycling and T cell receptor reengagement at high antigen doses. This feedback regulatory mechanism attenuates the immune response by deleting a portion of newly dividing, antigen-reactive T cells. This mechanism deleted autoreactive T cells and abrogated the clinical and pathological signs of autoimmune encephalomyelitis in mice after repetitive administration of myelin basic protein. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT PATHOL,DIV NEUROPATHOL,BRONX,NY 10461. UNIV WASHINGTON,SCH MED,DEPT MOLEC BIOTECHNOL,SEATTLE,WA 98195. RI Zuniga-Pflucker, Juan/H-1295-2012; Ain, Kenneth/A-5179-2012; OI Ain, Kenneth/0000-0002-2668-934X; Zuniga-Pflucker, Juan Carlos/0000-0003-2538-3178 NR 62 TC 476 Z9 479 U1 0 U2 6 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 25 PY 1994 VL 263 IS 5150 BP 1139 EP 1143 DI 10.1126/science.7509084 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX759 UT WOS:A1994MX75900033 PM 7509084 ER PT J AU LEE, JW MARQUEZ, VE LEWIN, NE BLUMBERG, PM AF LEE, JW MARQUEZ, VE LEWIN, NE BLUMBERG, PM TI CONFORMATIONALLY CONSTRAINED ANALOGS OF DAG .7. INTERACTION OF A MEDIUM-SIZE EPSILON-LACTONE WITH PROTEIN-KINASE-C (PK-C) SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID ACTIVATION; RECEPTOR; ESTERS; GAMMA AB Synthesis of (5R,6S)-5-O-tetradecanoyl-6-hydroxymethyl-6-heptanolide (3), designed as a rigid diacylglycerol (DAG) analogue, was achieved in 17 steps from L-xylose. Protein kinase (PK-C) binding affinity for this epsilon-lactone template was less than that observed for the stereochemically equivalent gamma- and delta-lactones. A critical ring-size for PK-C binding affinity in larger lactones is proposed based on our data and results from the published literature. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,MOLEC MECHANISMS TUMOR PROMOT SECT,BETHESDA,MD 20892. NR 21 TC 5 Z9 5 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD FEB 24 PY 1994 VL 4 IS 4 BP 543 EP 548 DI 10.1016/S0960-894X(01)80151-7 PG 6 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA NB233 UT WOS:A1994NB23300002 ER PT J AU KOZIKOWSKI, AP MA, DW DU, L LEWIN, NE BLUMBERG, PM AF KOZIKOWSKI, AP MA, DW DU, L LEWIN, NE BLUMBERG, PM TI SYNTHESIS OF THE BENZOFURAN ANALOG OF ILV, A NEW-PROTEIN KINASE-C (PKC) ACTIVATOR SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID LYNGBYATOXIN-A; (-)-INDOLACTAM-V AB In order to probe the effect of small structural changes on the PKC activity of the natural product indolactam V (ILV), a synthesis of its benzofuran analogue was developed. This compound was found to be similar in its activity to ILV, exhibiting a Ki of 17.3 +/- 3.7 nM in the displacement of [H-3]PDBU from PKC alpha. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,MOLEC MECHANISMS TUMOR PROMOT SECT,BETHESDA,MD 20892. RP KOZIKOWSKI, AP (reprint author), MAYO FDN MED EDUC & RES,4500 SAN PABLO RD,JACKSONVILLE,FL 32224, USA. NR 21 TC 6 Z9 6 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD FEB 24 PY 1994 VL 4 IS 4 BP 637 EP 640 DI 10.1016/S0960-894X(01)80169-4 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA NB233 UT WOS:A1994NB23300020 ER PT J AU DURELL, SR BROOKS, BR BENNAIM, A AF DURELL, SR BROOKS, BR BENNAIM, A TI SOLVENT-INDUCED FORCES BETWEEN 2 HYDROPHILIC GROUPS SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID HYDROPHOBIC INTERACTION; MOLECULAR-DYNAMICS; LIQUID WATER AB Molecular dynamics simulations were used to calculate the force between two simple hydrophilic solutes in dilute aqueous solution. The ''solutes'' were two water molecules in the same relative orientation as the next-nearest neighbors in hexagonal ice I. Both the direct and solvent-induced contributions to the force were calculated as a function of separation distance. The total force between the solutes was found to be most attractive at 5.0 Angstrom (-1.6 kcal/mol/Angstrom). The potential of mean force had a minimum at 4.3 Angstrom, which is 0.2 Angstrom closer than the next-nearest-neighbor distance in ice. A parallel set of simulations were conducted with the partial charges on the ''solutes'' removed to examine hydrophobic analogs. In this case, the total force was most attractive at 3.5 Angstrom (-0.9 kcal/mol/Angstrom), and the minimum of the potential was at the contact distance of 3.2 Angstrom. In agreement with earlier predictions, the maximum solvent-induced contribution to the potential was ca. 4 times more negative for the hydrophilic ''solutes'' than for the hydrophobic ones, These differences are shown to be due predominantly to a solvent water molecule which simultaneously hydrogen bonds to both hydrophilic ''solutes''. The results support earlier assertions that solvent-induced interactions between polar amino acid residues are more important in protein folding and stability than generally considered. C1 NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,DEPT PHYS CHEM,IL-91904 JERUSALEM,ISRAEL. RP DURELL, SR (reprint author), NCI,MATH BIOL LAB,ROOM 217,6010 EXECUT BLVD,ROCKVILLE,MD 20852, USA. NR 24 TC 234 Z9 236 U1 2 U2 14 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 24 PY 1994 VL 98 IS 8 BP 2198 EP 2202 DI 10.1021/j100059a038 PG 5 WC Chemistry, Physical SC Chemistry GA MY355 UT WOS:A1994MY35500038 ER PT J AU FIORE, MC EPPS, RP MANLEY, MW ALDEN, ER BECKETT, WS BERGEISEN, L BLUM, AM DOWNING, JW HAFLER, JP LOBECK, CC MATORY, WE POMREHN, PR WILKES, MS AF FIORE, MC EPPS, RP MANLEY, MW ALDEN, ER BECKETT, WS BERGEISEN, L BLUM, AM DOWNING, JW HAFLER, JP LOBECK, CC MATORY, WE POMREHN, PR WILKES, MS TI A MISSED OPPORTUNITY - TEACHING MEDICAL-STUDENTS TO HELP THEIR PATIENTS SUCCESSFULLY QUIT SMOKING SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID UNITED-STATES; TOBACCO USE; PHYSICIANS; CESSATION; PREVENTION; ATTITUDES; PROGRAM; SCHOOLS C1 UNIV WISCONSIN, SCH MED, DEPT MED, GEN INTERNAL MED SECT, MADISON, WI USA. NCI, DIV CANC PREVENT & CONTROL, CANC CONTROL SCI PROGRAM, BETHESDA, MD 20892 USA. NCI, SMOKING TOBACCO & CANC PROGRAM, BETHESDA, MD USA. AMER ACAD PEDIAT, DEPT EDUC, WASHINGTON, DC USA. YALE UNIV, SCH MED, DEPT MED, NEW HAVEN, CT 06510 USA. YALE UNIV, SCH MED, DEPT EPIDEMIOL, NEW HAVEN, CT USA. YALE UNIV, SCH MED, DEPT PUBL HLTH, NEW HAVEN, CT 06510 USA. ASSOC AMER MED COLL, WASHINGTON, DC USA. DOCTORS OUGHT CARE, HOUSTON, TX USA. HOWARD UNIV, COLL MED, ASSOC MED SCH PEDIAT, WASHINGTON, DC USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. UNIV WISCONSIN, SCH MED, DEPT PEDIAT, MADISON, WI USA. UNIV WISCONSIN, SCH MED, DEPT PREVENT MED, MADISON, WI USA. NCI, APPLICAT PREVENT & EARLY DETECT SECT, BETHESDA, MD USA. UNIV IOWA, COLL MED, IOWA CITY, IA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. RP FIORE, MC (reprint author), UNIV WISCONSIN, CTR TOBACCO RES & INTERVENT, SCH MED, ROOM 7575 MSC, 1300 UNIV AVE, MADISON, WI 53606 USA. NR 35 TC 67 Z9 68 U1 2 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 23 PY 1994 VL 271 IS 8 BP 624 EP 626 DI 10.1001/jama.271.8.624 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA MW477 UT WOS:A1994MW47700028 PM 8301797 ER PT J AU GRZESIEK, S BAX, A NICHOLSON, LK YAMAZAKI, T WINGFIELD, P STAHL, SJ EYERMANN, CJ TORCHIA, DA HODGE, CN LAM, PYS JADHAV, PK CHANG, CH AF GRZESIEK, S BAX, A NICHOLSON, LK YAMAZAKI, T WINGFIELD, P STAHL, SJ EYERMANN, CJ TORCHIA, DA HODGE, CN LAM, PYS JADHAV, PK CHANG, CH TI NMR EVIDENCE FOR THE DISPLACEMENT OF A CONSERVED INTERIOR WATER MOLECULE IN HIV PROTEASE BY A NONPEPTIDE CYCLIC UREA-BASED INHIBITOR SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Note ID AQUEOUS-SOLUTION; BOUND WATER; PROTEINS; HYDRATION C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NIDR,BONE RES BRANCH,BETHESDA,MD 20892. NIH,PROT EXPRESS LAB,BETHESDA,MD 20892. DUPONT MERCK PHARMACEUT CO,DEPT VIROL,WILMINGTON,DE 19880. DUPONT MERCK PHARMACEUT CO,DEPT CHEM & PHYS SCI,WILMINGTON,DE 19880. NR 18 TC 44 Z9 44 U1 0 U2 1 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 23 PY 1994 VL 116 IS 4 BP 1581 EP 1582 DI 10.1021/ja00083a058 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA MZ287 UT WOS:A1994MZ28700058 ER PT J AU GOLDSTEIN, JA FALETTO, MB ROMKESSPARKS, M SULLIVAN, T KITAREEWAN, S RAUCY, JL LASKER, JM GHANAYEM, BI AF GOLDSTEIN, JA FALETTO, MB ROMKESSPARKS, M SULLIVAN, T KITAREEWAN, S RAUCY, JL LASKER, JM GHANAYEM, BI TI EVIDENCE THAT CYP2C19 IS THE MAJOR (S)-MEPHENYTOIN 4'-HYDROXYLASE IN HUMANS SO BIOCHEMISTRY LA English DT Article ID POLYMERASE CHAIN-REACTION; OXIDATIVE DRUG-METABOLISM; MEPHENYTOIN HYDROXYLATION; SACCHAROMYCES-CEREVISIAE; GENETIC-POLYMORPHISM; MESSENGER-RNAS; RAT-LIVER; EXPRESSION; PROTEIN; 4-HYDROXYLASE AB The present study assesses the role of members of the human CYP2C subfamily in the 4'-hydroxylation of(S)-mephenytoin, When recombinant CYP2C proteins were expressed using a yeast cDNA expression system, 2C19 stereospecifically 4'-hydroxylated (S)-mephenytoin with a turnover number at least 10 times higher than that of human liver microsomes. 2C9 (both Ile(359) and Leu(359) alleles) and 2C18 (Thr(385) and Met(385) alleles) metabolized this substrate at a rate 100-fold lower than 2C19, and metabolism by these 2C proteins was not stereospecific for the S-enantiomer. 2C8 exhibited very little mephenytoin 4'-hydroxylase activity. In contrast, the Ile(359) allele of 2C9 had a high turnover number for the hydroxylation of tolbutamide, while the Leu(359) allele was less active toward this substrate. Immunoblot analysis of 16 human liver donor samples indicated that (S)-mephenytoin 4'-hydroxylase activity correlated with the hepatic CYP2C19 content, but it did not correlate with the hepatic content of CYP2C9. Moreover, direct sequencing of the polymerase chain reaction (PCR) products of 2C9 mRNA from six of these human livers through areas of known allelic variations indicated that the identity of the allele of 2C9 (Cys(144) vs Arg, Tyr(358) vs Cys, Ile(359) vs Leu, or Gly(417) VS Asp) did not appear to influence (S)-mephenytoin 4'-hydroxylase activity in these samples. These data indicate that 2C19 is the principal determinant of (S)-mephenytoin 4'-hydroxylase activity in human liver. C1 UNIV NEW MEXICO,COLL PHARM,TOXICOL PROGRAM,ALBUQUERQUE,NM 87131. VET ADM MED CTR,CTR ALCOHOL RES & TREATMENT,NEW YORK,NY 10468. MT SINAI SCH MED,NEW YORK,NY 10468. RP GOLDSTEIN, JA (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. FU NIAAA NIH HHS [ADAMHA AA-07842, ADAMHA AA-08139] NR 48 TC 339 Z9 346 U1 1 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 22 PY 1994 VL 33 IS 7 BP 1743 EP 1752 DI 10.1021/bi00173a017 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MY842 UT WOS:A1994MY84200017 PM 8110777 ER PT J AU PENTCHEV, PG BRADY, RO BLANCHETTEMACKIE, EJ VANIER, MT CARSTEA, ED PARKER, CC GOLDIN, E ROFF, CF AF PENTCHEV, PG BRADY, RO BLANCHETTEMACKIE, EJ VANIER, MT CARSTEA, ED PARKER, CC GOLDIN, E ROFF, CF TI THE NIEMANN-PICK C-LESION AND ITS RELATIONSHIP TO THE INTRACELLULAR-DISTRIBUTION AND UTILIZATION OF LDL CHOLESTEROL SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE LA English DT Review DE NIEMANN-PICK C DISEASE; INTRACELLULAR CHOLESTEROL TRANSPORT; CELLULAR CHOLESTEROL PROCESSING; CHOLESTEROL ID LOW-DENSITY LIPOPROTEIN; DISEASE TYPE-C; HAMSTER OVARY CELLS; STEROL CARRIER PROTEIN-2; STORAGE DISORDER; PLASMA-MEMBRANE; FAMILIAL HYPERCHOLESTEROLEMIA; ATHEROSCLEROTIC LESIONS; CULTURED FIBROBLASTS; SPHINGOMYELINASE DEFICIENCY C1 NIDDKD, CELLULAR & DEV BIOL LAB, ENDOCRINOL SECT, BETHESDA, MD 20892 USA. FAC MED LYON SUD, INSERM, U189, BIOCHIM LAB, F-69921 OULLINS, FRANCE. RP PENTCHEV, PG (reprint author), NINCDS, DEV & METAB NEUROL BRANCH, MOLEC & CELLULAR PATHOPHYSIOL SECT, BETHESDA, MD 20892 USA. NR 85 TC 100 Z9 102 U1 0 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4439 J9 BBA-MOL BASIS DIS JI Biochim. Biophys. Acta-Mol. Basis Dis. PD FEB 22 PY 1994 VL 1225 IS 3 BP 235 EP 243 DI 10.1016/0925-4439(94)90001-9 PG 9 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA NA555 UT WOS:A1994NA55500001 PM 8312368 ER PT J AU OHUOHA, DC KNABLE, MB WOLF, SS KLEINMAN, JE HYDE, TM AF OHUOHA, DC KNABLE, MB WOLF, SS KLEINMAN, JE HYDE, TM TI THE SUBNUCLEAR DISTRIBUTION OF 5-HT3 RECEPTORS IN THE HUMAN NUCLEUS OF THE SOLITARY TRACT AND OTHER STRUCTURES OF THE CAUDAL MEDULLA SO BRAIN RESEARCH LA English DT Article DE SEROTONIN RECEPTOR; NUCLEUS TRACTUS SOLITARIUS; AREA POSTREMA; EMESIS; HUMAN BRAIN-STEM ID BRAIN-STEM PROJECTIONS; DORSAL MOTOR NUCLEUS; RAT CEREBRAL-CORTEX; RECOGNITION SITES; AREA POSTREMA; VAGUS COMPLEX; CONNECTIONS; COMPONENTS; BINDING; NERVE AB The distribution of 5-HT3, receptors was examined in the human medulla using [H-3]LY278584, a highly selective 5-HT3 receptor antagonist. The highest density of 5-HT3, receptors was found in the substantia gelatinosus subnucleus of nucleus of the solitary tract (NTs) throughout its rostrocaudal extent, followed by the dorsal subnucleus, the area postrema (AP), the commissural subnucleus, the medial subnucleus, and in an arc corresponding to the pars gelatinosus of the spinal trigeminal nucleus (nSp5). The distribution of 5-HT3 receptors in the brain may help explain some of the reported CNS activities of 5-HT3-selective drugs. The anti-emetic and antinociceptive activities of 5-HT3 antagonists may be mediated by receptors in sensory areas of the brainstem. C1 ST ELIZABETH HOSP,CTR NEUROSCI,NIMH,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NR 48 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD FEB 21 PY 1994 VL 637 IS 1-2 BP 222 EP 226 DI 10.1016/0006-8993(94)91236-X PG 5 WC Neurosciences SC Neurosciences & Neurology GA MY436 UT WOS:A1994MY43600027 PM 8180799 ER PT J AU VONLUBITZ, DKJE PAUL, IA JI, XD CARTER, M JACOBSON, KA AF VONLUBITZ, DKJE PAUL, IA JI, XD CARTER, M JACOBSON, KA TI CHRONIC ADENOSINE A(1) RECEPTOR AGONIST AND ANTAGONIST - EFFECT ON RECEPTOR DENSITY AND N-METHYL-D-ASPARTATE INDUCED SEIZURES IN MICE SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE ADENOSINE ANALOG; SEIZURE; NMDA (N-METHYL-D-ASPARTATE); (MOUSE) ID RAT CEREBRAL-CORTEX; MODULATION AB The effect of chronic administration of the adenosine A(1) receptor agonist N-6-cyclopentyladenosine (CPA) and the adenosine A(1) antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX) on N-methyl-D-aspartate (NMDA)-evoked seizures was studied in C57BL/6 mice (20/ group). Animals were injected i.p. for 9 days with either 1.0 mg/kg CPA or 1.0 mg/kg CPX followed by 2 injection-free days (the washout period) and subsequent administration of a single dose of 60 mg/kg NMDA. As in our previous study, this dose of NMDA caused clonic/tonic seizures resulting in high (60%) mortality within 3 h after injection of the drug. Despite insignificant changes in seizure latency, chronic pretreatment with CPA increased the incidence of clonic tonic episodes and end-point mortality. Conversely, chronic exposure to CPX completely eliminated clonic/tonic episodes, significantly increased average survival time, and reduced end-point mortality (P < 0.05). The results indicate that chronic treatment with adenosine A(1) receptor antagonist may protect against NMDA-evoked seizures to the same degree as previously observed following a single, acute exposure to CPA. Since the density of adenosine receptor binding sites was unchanged after chronic treatment with either CPX or CPA, it is likely that the mechanism behind the observed protection may rest at the level of second messenger systems coupled to adenosine A(1) receptors. C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. RP VONLUBITZ, DKJE (reprint author), NIDDK,BIOORGAN CHEM LAB,MOLEC RECOGNIT SECT,BLDG 8,RM 111,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 31 TC 50 Z9 50 U1 0 U2 0 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 21 PY 1994 VL 253 IS 1-2 BP 95 EP 99 DI 10.1016/0014-2999(94)90762-5 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY562 UT WOS:A1994MY56200013 PM 8013554 ER PT J AU DUDEK, RW DOHM, GL HOLMAN, GD CUSHMAN, SW WILSON, CM AF DUDEK, RW DOHM, GL HOLMAN, GD CUSHMAN, SW WILSON, CM TI GLUCOSE-TRANSPORTER LOCALIZATION IN RAT SKELETAL-MUSCLE - AUTORADIOGRAPHIC STUDY USING ATB-[2-H-3]BMPA PHOTOLABEL SO FEBS LETTERS LA English DT Article DE GLUT4; GLUCOSE TRANSPORT; SKELETAL MUSCLE; BIS-MANNOSE; PHOTOAFFINITY LABEL ID TRANSVERSE TUBULES; GLUT4; TRANSLOCATION AB Surface glucose transporters of intact muscles were photolabeled with the membrane impermeant ATB-[2-H-3]BMPA reagent and localized by autoradiography. We found sparse labeling of the glucose transporters by ATB-[2-H-3]BMPA on the sarcolemmal membrane around the muscle fiber. The majority of label was on the interior of the muscle fiber, at a discrete site which matched the distribution of AI junctions and which was presumed to be on the exterior surface of T-tubules. The amount of photolabel on the T-tubule was increased in response to insulin and was blocked by cytochalasin B. These results support the concept that glucose transport may occur predominately across the T-tubule membrane under basal and insulin-stimulated conditions. C1 E CAROLINA UNIV,SCH MED,DEPT BIOCHEM,GREENVILLE,NC 27858. NIDDK,DB,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD. UNIV BATH,DEPT BIOCHEM,BATH BA2 7AY,AVON,ENGLAND. RP DUDEK, RW (reprint author), E CAROLINA UNIV,SCH MED,DEPT CELL BIOL,GREENVILLE,NC 27858, USA. FU NIDDK NIH HHS [R01-DK-46121, R01-DK-38416] NR 14 TC 41 Z9 41 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD FEB 21 PY 1994 VL 339 IS 3 BP 205 EP 208 DI 10.1016/0014-5793(94)80416-8 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA MZ659 UT WOS:A1994MZ65900001 PM 8112456 ER PT J AU LI, YX RINZEL, J AF LI, YX RINZEL, J TI EQUATIONS FOR INSP(3) RECEPTOR-MEDIATED [CA2+](I) OSCILLATIONS DERIVED FROM A DETAILED KINETIC-MODEL - A HODGKIN-HUXLEY LIKE FORMALISM SO JOURNAL OF THEORETICAL BIOLOGY LA English DT Article ID INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; PITUITARY GONADOTROPHS; CA2+ RELEASE; SARCOPLASMIC-RETICULUM; SYMPATHETIC NEURONS; LAEVIS OOCYTES; CALCIUM; CHANNELS; CA-2+; ACTIVATION RP LI, YX (reprint author), NIDDKD,MATH RES BRANCH,BETHESDA,MD 20892, USA. NR 44 TC 277 Z9 287 U1 2 U2 16 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 1994 VL 166 IS 4 BP 461 EP 473 DI 10.1006/jtbi.1994.1041 PG 13 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA NA058 UT WOS:A1994NA05800009 PM 8176949 ER PT J AU DUBNER, R MESSERSMITH, DJ IADAROLA, MJ AF DUBNER, R MESSERSMITH, DJ IADAROLA, MJ TI CHANGES IN GENE-EXPRESSION FOLLOWING TISSUE-INJURY SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT 24th International Narcotics Research Conference (INRC): Towards a Molecular Basis in Opioid Research CY JUL 10-15, 1993 CL SKOVDE, SWEDEN ID SPINAL-CORD; INFLAMMATION; NEURONS; HYPERALGESIA; DYNORPHIN; HYBRIDIZATION; FOS RP DUBNER, R (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892, USA. NR 8 TC 0 Z9 0 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 21 PY 1994 SU 1 BP S65 EP S66 PG 2 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA NA245 UT WOS:A1994NA24500034 ER PT J AU IZENWASSER, S WEEMS, HB COTE, TE AF IZENWASSER, S WEEMS, HB COTE, TE TI INCREASED OPIOID EFFICACY FOR INHIBITION OF ADENYLYL-CYCLASE IN RAT-BRAIN AND 7315C CELL-MEMBRANES INDUCED BY CHRONIC NALTREXONE TREATMENT SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT 24th International Narcotics Research Conference (INRC): Towards a Molecular Basis in Opioid Research CY JUL 10-15, 1993 CL SKOVDE, SWEDEN ID OPIATE RECEPTOR; SUPER-SENSITIVITY; BINDING C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PHARMACOL,BETHESDA,MD 20814. RP IZENWASSER, S (reprint author), NIDA,ADDICT RES CTR,PSYCHOBIOL SECT,BALTIMORE,MD 21224, USA. NR 6 TC 0 Z9 0 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 21 PY 1994 SU 1 BP S119 EP S120 PG 2 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA NA245 UT WOS:A1994NA24500061 ER PT J AU STEIN, C SCHAFER, M CARTER, L CZLONKOWSKI, A MOUSA, S EPPLEN, C AF STEIN, C SCHAFER, M CARTER, L CZLONKOWSKI, A MOUSA, S EPPLEN, C TI CYTOKINE-INDUCED ANTINOCICEPTION MEDIATED BY OPIOIDS RELEASED FROM IMMUNE CELLS SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT 24th International Narcotics Research Conference (INRC): Towards a Molecular Basis in Opioid Research CY JUL 10-15, 1993 CL SKOVDE, SWEDEN ID INFLAMED TISSUE; INFLAMMATION; RECEPTORS AB Immune cell-derived opioid peptides (1,2) apparently play an important role in the local inhibition of pain within inflamed tissue of animals and humans (3,4,5). Proopiomelanocortin- and proenkephalin-mRNA's, as well as beta-endorphin (END) and [Met]enkephalin (and small amounts of dynorphin) are detectable within inflamed subcutaneous tissue (3,6,7). These peptides are localized in T- and B-lymphocytes, monocytes and macrophages. Upon local administration of cytokines, inflammatory pain can be attenuated. This effect is reversible by immunosuppression with cyclosporine A (CsA), by passive immunization with antibodies against END, and by opioid antagonists. These findings are consistent with the notion that cytokines release END from resident immune cells, which subsequently activates opioid receptors on sensory nerves (3,8,9) to inhibit nociception. C1 NIDA,BALTIMORE,MD 21287. MAX PLANCK INST PSYCHIAT,DEPT NEUROPHARMACOL,W-8033 MARTINSRIED,GERMANY. MAX PLANCK INST PSYCHIAT,DEPT NEUROIMMUNOL,W-8033 MARTINSRIED,GERMANY. RP STEIN, C (reprint author), JOHNS HOPKINS UNIV,DEPT ANESTHESIOL,BALTIMORE,MD 21287, USA. NR 9 TC 0 Z9 0 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 21 PY 1994 SU 1 BP S191 EP S192 PG 2 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA NA245 UT WOS:A1994NA24500096 ER PT J AU GANDJBAKHCHE, AH MILLS, P SNABRE, P AF GANDJBAKHCHE, AH MILLS, P SNABRE, P TI LIGHT-SCATTERING TECHNIQUE FOR THE STUDY OF ORIENTATION AND DEFORMATION OF RED-BLOOD-CELLS IN A CONCENTRATED SUSPENSION SO APPLIED OPTICS LA English DT Article DE RED BLOOD CELLS; DEFORMATION-ORIENTATION; LIGHT SCATTERING; CONCENTRATED SUSPENSION ID MEMBRANE; ABSORPTION; BEHAVIOR; MODEL; FLOW AB The backscattered and transmitted diagrams of He-Ne laser light illuminating a concentrated suspension of red blood cells (RBC's) are investigated. The shapes of these diagrams are closely related to the state of the suspension (at rest or submitted to a simple shear flow) and to the parameters that govern the non-Newtonian behavior of the blood suspension (such as the viscosity of the suspending medium and the volume concentration of the cells). An asymmetry in the backscattering diagram, which is absent on transmitted diagrams, is observed when the suspension is in a simple shear flow. This asymmetry is related to the deformation and orientation of the RBC's. The propagation of light through the suspension is modeled and a set of Monte Carlo simulations is performed to substantiate the inference that the relative variation of the backscattered flux is proportional to the gradients of deformation of the RBC's, and that such gradients must be known in order to apply a rheological model describing the non-Newtonian behavior of RBC membranes. C1 UNIV PARIS 07, BIORHEOL & HYDRODYNAM PHYSICOCHIM LAB, CNRS, URA 343, F-75221 PARIS 05, FRANCE. RP GANDJBAKHCHE, AH (reprint author), NIH, DIV COMP RES & TECHNOL, PHYS SCI LAB, BLDG 12A, ROOM 2007, BETHESDA, MD 20892 USA. NR 29 TC 38 Z9 40 U1 1 U2 2 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA SN 0003-6935 J9 APPL OPTICS JI Appl. Optics PD FEB 20 PY 1994 VL 33 IS 6 BP 1070 EP 1078 PG 9 WC Optics SC Optics GA NA381 UT WOS:A1994NA38100029 PM 20862118 ER PT J AU LEHEL, C OLAH, Z MISCHAK, H MUSHINSKI, JF ANDERSON, WB AF LEHEL, C OLAH, Z MISCHAK, H MUSHINSKI, JF ANDERSON, WB TI OVEREXPRESSED PROTEIN-KINASE C-DELTA AND C-EPSILON SUBTYPES IN NIH 3T3 CELLS EXHIBIT DIFFERENTIAL SUBCELLULAR-LOCALIZATION AND DIFFERENTIAL REGULATION OF SODIUM-DEPENDENT PHOSPHATE-UPTAKE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LLC-PK1 CELLS; PKC-EPSILON; RAT-BRAIN; EXPRESSION; COTRANSPORT; ACTIVATION; CDNA; SPECIFICITY; STIMULATION; MECHANISMS AB To examine the biological properties of protein kinase C (PHC)-delta and -epsilon NIH 3T3 cells were stably transfected with metallothionein-based expression vectors that overexpressed these isoforms. In addition to their inducibility by Zn2+, the protein levels of these two PKC subtypes, but not that of endogenous PKC-alpha, increased with increasing cell density. An unexpected role for Mg2+ in the subcellular localization of PKC-delta was found. This isoenzyme was predominantly membrane-associated when cell fractionation was carried out in the absence of Mg2+ but cytosolic when the fractionation was performed in the presence of 10 mM Mg2+. In contrast, the predominant localization of cytosolic PKC-alpha and of membrane-associated PKC-epsilon was not influenced by Mg2+. In vivo and in vitro studies of [H-3]phorbol 12,13-dibutyrate binding in the overexpressing cell lines confirmed the cytosolic localization of PHC-alpha, the membrane-associated state of PHC-epsilon, and the presence of PKC-delta at both locations. Readdition of serum for 5 min to serum-starved, quiescent cell lines initiated the redistribution of PKC-alpha to the particulate fraction, while the location of PKC-delta and PKC-epsilon was not affected. Zn2+-induced overexpression of PKC-delta- and PKC-epsilon-stimulated sodium dependent phosphate uptake. Overexpression of PKC-delta caused an increase in the V-max of Na+/P-i uptake, while overexpression of PKC-epsilon resulted in a decrease in K-m, for orthophosphate. A further stimulation of Na+/P-i uptake in the overexpressing cells could be achieved by phorbol ester activation of endogenous PKC-alpha. These results suggest that each of the three PKC isotypes contribute to the regulation of sodium-dependent phosphate uptake, but through distinct mechanisms. C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NCI,GENET LAB,BETHESDA,MD 20892. RI Mischak, Harald/E-8685-2011 NR 36 TC 53 Z9 53 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 18 PY 1994 VL 269 IS 7 BP 4761 EP 4766 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX571 UT WOS:A1994MX57100013 PM 8106444 ER PT J AU RYU, S GARGES, S AF RYU, S GARGES, S TI PROMOTER SWITCH IN THE ESCHERICHIA-COLI PTS OPERON SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BACTERIAL PHOSPHOTRANSFERASE SYSTEM; CYCLIC-AMP; TRANSCRIPTION ACTIVATION; SALMONELLA-TYPHIMURIUM; POSITIVE REGULATION; RECEPTOR PROTEIN; MESSENGER-RNA; 2 PROMOTERS; CRR GENES; DNA AB The ptsH operon of Escherichia coli is controlled by two promoters P0 and P1, each of which is regulated by cyclic AMP receptor protein (CRP) complexed with cAMP (CRP.cAMP). We have studied the in vitro as well as in vivo transcriptional regulation of these two promoters. Each promoter exhibits a switching mechanism in vitro, where, depending upon the presence or absence of CRP.cAMP, transcription is initiated from different start sites termed a and b.P0 (P0a) is affected by supercoliing: when the template is linear, transcription initiation is switched to a site 3 base pairs upstream (P0b) and becomes more CRP.cAMP dependent. Transcription from the P1 promoter (P1a) switches initiation sites to 7 base pairs downstream (P1b) in the presence of CRP.cAMP. Most transcription in vivo was from P1a, and P0b could not be detected in vivo. Glucose has independent positive effects on pts expression in vivo. The results indicate that the two different regulatory mechanisms (one through CRP.cAMP, the other through glucose) are working together for fine control of pts expression. RP RYU, S (reprint author), NCI, MOLEC BIOL LAB, BLDG 37, RM 2E06, BETHESDA, MD 20892 USA. NR 32 TC 32 Z9 32 U1 0 U2 1 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 18 PY 1994 VL 269 IS 7 BP 4767 EP 4772 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX571 UT WOS:A1994MX57100014 PM 8106445 ER PT J AU MINTZ, KP FISHER, LW GRZESIK, WJ HASCALL, VC MIDURA, RJ AF MINTZ, KP FISHER, LW GRZESIK, WJ HASCALL, VC MIDURA, RJ TI CHLORATE-INDUCED INHIBITION OF TYROSINE SULFATION ON BONE SIALOPROTEIN SYNTHESIZED BY A RAT OSTEOBLAST-LIKE CELL-LINE (UMR 106-01 BSP) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYROSYLPROTEIN SULFOTRANSFERASE; BALANCE-SHEET; PROTEINS; PROTEOGLYCANS; INVITRO; SECRETION; RESIDUES; PURIFICATION; SUBSTRATE; CULTURES AB Bone sialoprotein (BSP) is a major noncollagenous, RGD-containing glycoprotein found in the extracellular matrix of bone. The RGD sequence is flanked by two tyrosine-rich regions, which fit the established consensus requirements for tyrosine sulfation. Tyrosine sulfation is suggested to be important in the regulation of protein secretion and function. The role of this posttranslational modification on the cell attachment activity and secretion of a highly sulfated form of BSP isolated from a rat osteoblast-like cell line (UMR 106-01 BSP) was investigated by inhibiting sulfation with chlorate. [S-35]Sulfate, [H-3]glucosamine, and [H-3]tyrosine were used as metabolic precursors to monitor biosynthetic products. Chlorate was effective in inhibiting to tal [S-35]sulfate incorporation by 90% without altering overall protein synthesis and secretion in cultures up to 72 h under serum-free conditions. Isolated proteoglycans and purified BSP were analyzed for sulfate incorporation. Proteoglycans isolated from the medium of cells treated with chlorate displayed a difference in the hydrodynamic properties of the molecules as compared with control cultures. An increase in the specific activity of proteoglycans labeled with [H-3]glucosamine isolated from chlorate-treated cells was also observed suggesting a change in hexosamine metabolism induced by chlorate. BSP purified from the medium of chlorate-treated cells contained similar to 7% of the S-35 incorporation as compared with nontreated control cultures. Quantification of sulfate incorporation into glycoconjugates versus tyrosine sulfate of BSP indicates that the amount of sulfate associated with N- and O-linked oligosaccharides was reduced by similar to 97%, while that on tyrosine residues was reduced by similar to 90%. Using normal human bone cells, the cell attachment activity of the reduced sulfate form of BSP was nearly equivalent to that of the fully sulfated product. C1 NIDR, BONE RES BRANCH, BETHESDA, MD 20892 USA. NR 41 TC 17 Z9 17 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 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 18 PY 1994 VL 269 IS 7 BP 4845 EP 4852 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX571 UT WOS:A1994MX57100025 PM 8106456 ER PT J AU KUKULJAN, M ROJAS, E CATT, KJ STOJILKOVIC, SS AF KUKULJAN, M ROJAS, E CATT, KJ STOJILKOVIC, SS TI MEMBRANE-POTENTIAL REGULATES INOSITOL 1,4,5-TRISPHOSPHATE-CONTROLLED CYTOPLASMIC CA2+ OSCILLATIONS IN PITUITARY GONADOTROPHS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PAROTID ACINAR-CELLS; CYTOSOLIC CALCIUM; XENOPUS OOCYTES; TRISPHOSPHATE; CHANNELS; RELEASE; ENTRY; MOBILIZATION; ACTIVATION; INFLUX AB The influence of membrane potential (V-m) on cytoplasmic calcium ([Ca2+](i)) oscillations during the sustained extracellular Ca2+-dependent phase of the Ca2+ signaling response to gonadotropin-releasing hormone (GnRH) was analyzed in cultured pituitary gonadotrophs. In agonist- and inositol (1,4,5)-trisphosphate (Ins(1,4,5)P-3)-stimulated cells, sustained [Ca2+](i) oscillations were extinguished by hyperpolarization after 3-15 min despite the availability of Ca2+ in the extracellular medium. Single depolarizing pulses transiently restored the amplitude of the sustained spiking in a dihydropyridine- and extracellular Ca2+-sensitive manner. The responses to depolarization showed a marked dependence on V-m that was correlated with the steady state inward Ca2+ current. In addition, repetitive application of brief depolarizing pulses modulated the frequency of agonist- and Ins(1,4,5)Ps-controlled spiking; depolarization pulses at frequencies lower than the intrinsic rate of episodic Ca2+ release triggered large transients between the autonomous spikes, whereas higher frequencies of depolarizing pulses overcame the original Ca2+ spiking frequency. These extrinsically driven and extracellular Ca2+-dependent oscillations were sensitive to the Ca2+-ATPase blocker, thapsigargin, but not to ryanodine. On the other hand, spontaneous firing and application of depolarizing pulses to nonstimulated cells failed to induce thapsigargin-sensitive oscillations. These findings demonstrate that the pattern of Ca2+ signaling in gonadotrophs does not depend exclusively on the Ins(1,4,5)P-3 concentration, but also on the excitable status of the cell. Such modulation of the Ins(1,4,5)P-3-controlled Ca2+ signaling system by changes in V-m could provide a mechanism for the integration of multiple inputs that utilize diverse signal transduction pathways. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892. NR 45 TC 46 Z9 46 U1 0 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 18 PY 1994 VL 269 IS 7 BP 4860 EP 4865 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX571 UT WOS:A1994MX57100027 PM 8106457 ER PT J AU MINOGUCHI, K SWAIM, WD BERENSTEIN, EH SIRAGANIAN, RP AF MINOGUCHI, K SWAIM, WD BERENSTEIN, EH SIRAGANIAN, RP TI SRC FAMILY TYROSINE KINASE P53/56(LYN), A SERINE KINASE AND FC-EPSILON-RI ASSOCIATE WITH ALPHA-GALACTOSYL DERIVATIVES OF GANGLIOSIDE GD(1B) IN RAT BASOPHILIC LEUKEMIA RBL-2H3 CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AFFINITY IGE RECEPTOR; GROWTH-FACTOR RECEPTOR; MONOCLONAL-ANTIBODIES; SIGNAL TRANSDUCTION; HISTAMINE-RELEASE; IMMUNOGLOBULIN-E; MAST-CELLS; PROTEIN; PHOSPHORYLATION; SURFACE AB The monoclonal antibody (mAb) AA4 recognizes two alpha-galactosyl derivatives of the GD(1b) ganglioside on rat mast cells and on the rat basophilic leukemia RBL-2H3 cultured cell line. Here we demonstrate that mAb AA4 coprecipitated both protein tyrosine and serine kinases. In contrast, a monoclonal antibody to the GD(3) ganglioside did not coprecipitate any kinase activity. In kinase assays of mAb AA4 immunoprecipitates there were phosphorylated proteins of 71-80, 53/56, and 41/42 kDa. All proteins were phosphorylated on tyrosine, whereas the 71-80- and 41/42-kDa proteins were also phosphorylated on serine residues. The precipitation of these proteins by mAb AA4 correlated with the presence of the alpha-galactosyl derivatives of GD(1b). The 53/56-kDa proteins were identified as the Src-related tyrosine kinase p53/56(lyn). The presence of p53/56(lyn) in the mAb AA4 immunoprecipitates was specific and was observed when several different detergents were used. The same 71-80-kDa tyrosine-phosphorylated proteins were immunoprecipitated by mAb AA4 and anti-Lyn antibodies and may play a role in the interaction of p53/56(lyn) with the gangliosides. Although there is a weak association of the high affinity IgE receptor with these gangliosides, the coprecipitation of p53/56(lyn) with mAb AA4 was not secondary to the association of this kinase with receptor. These complexes of gangliosides and several proteins that include p53/56(lyn), a serine kinase, and the high affinity IgE receptor could play an important role in receptor-mediated signal transduction. RP MINOGUCHI, K (reprint author), NIDR, IMMUNOL LAB, BLDG 10-1N-106, BETHESDA, MD 20892 USA. NR 47 TC 56 Z9 56 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 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 18 PY 1994 VL 269 IS 7 BP 5249 EP 5254 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX571 UT WOS:A1994MX57100085 PM 8106508 ER PT J AU RUI, H KIRKEN, RA FARRAR, WL AF RUI, H KIRKEN, RA FARRAR, WL TI ACTIVATION OF RECEPTOR-ASSOCIATED TYROSINE KINASE JAK2 BY PROLACTIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GROWTH SIGNAL TRANSDUCTION; PROTEIN-KINASE; CYTOKINE RECEPTORS; CYTOPLASMIC REGION; BETA-SUBUNIT; FAMILY; HORMONE; DOMAIN; FORM; PHOSPHORYLATION AB JAK family tyrosine kinases have recently been implicated in intracellular signal transduction by transmembrane cytokine receptors of the interferon (IFN) and hematopoietin receptor families. Using the prolactin (PRL) dependent rat pre-T cell line Nb2, a PRL receptor-associated, candidate tyrosine kinase of 120-130 kDa was recently characterized (1). In the present work this protein is identified as JAK2, based upon reciprocal anti-JAK2 and anti-phosphotyrosine immunoprecipitation and immunoblotting. JAK2 underwent rapid and transient tyrosine phosphorylation in response to receptor activation, reaching peak levels within 5 min of exposure to 100 nm PRL at 37 degrees C. In vitro tyrosine kinase assays using either [gamma-P-32]ATP and autoradiography or unlabeled ATP combined with anti-phosphotyrosine immunoblotting, demonstrated that the activity of JAK2 was stimulated by PRL. Phosphoamino acid analysis of JAK2 after in vitro tyrosine kinase assay revealed that the majority of phosphate was incorporated into tyrosine residues. Furthermore, JAK2 was associated with PRL receptors to a comparable extent before and after PRL binding, as demonstrated by anti-receptor immunoprecipitation and subsequent anti-JAK2 immunoblotting. We propose that binding of ligand to the PRL receptor activates preassociated JAK2, and that this enzyme generates the initial signal in the intracellular communication cascade. RP RUI, H (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,FREDERICK,MD 21702, USA. FU FIC NIH HHS [5FO5 TWO4300-02] NR 48 TC 300 Z9 301 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 18 PY 1994 VL 269 IS 7 BP 5364 EP 5368 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX571 UT WOS:A1994MX57100099 PM 7508935 ER PT J AU DELAHUNTY, MD WILSON, SH KARPEL, RL AF DELAHUNTY, MD WILSON, SH KARPEL, RL TI STUDIES ON PRIMER BINDING OF HIV-1 REVERSE-TRANSCRIPTASE USING A FLUORESCENT-PROBE SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE REVERSE TRANSCRIPTASE; NUCLEOTIDE ANALOG; PRIMER BINDING SITE; FLUORESCENCE ID HUMAN-IMMUNODEFICIENCY-VIRUS; STEADY-STATE KINETICS; DNA-POLYMERASE; RNASE-H; TRANSFER RNALYS; AIDS VIRUS; MECHANISM; IDENTIFICATION; SUBSTRATE; INHIBITOR C1 UNIV MARYLAND BALTIMORE CTY, DEPT CHEM & BIOCHEM, BALTIMORE, MD 21228 USA. NCI, BIOCHEM LAB, BETHESDA, MD 20892 USA. FU NIGMS NIH HHS [1R55GM46247] NR 36 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD FEB 18 PY 1994 VL 236 IS 2 BP 469 EP 479 DI 10.1006/jmbi.1994.1158 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX209 UT WOS:A1994MX20900008 PM 7508989 ER PT J AU PARRIS, CN LEVY, DD JESSEE, J SEIDMAN, MM AF PARRIS, CN LEVY, DD JESSEE, J SEIDMAN, MM TI PROXIMAL AND DISTAL EFFECTS OF SEQUENCE CONTEXT ON ULTRAVIOLET MUTATIONAL HOTSPOTS IN A SHUTTLE VECTOR REPLICATED IN XERODERMA CELLS SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE MUTAGENESIS; HUMAN CELLS ID ESCHERICHIA-COLI; POINT MUTATIONS; EXCISION REPAIR; DNA-POLYMERASE; HOT-SPOTS; LACI GENE; PLASMID; MUTAGENESIS; SPECIFICITY; PIGMENTOSUM C1 OTSUKA PHARMACEUT CO LTD, ROCKVILLE, MD 20850 USA. NCI, MOLEC CARCINOGENESIS LAB, BETHESDA, MD 20892 USA. LIFE TECHNOL INC, GAITHERSBURG, MD 20850 USA. NR 38 TC 28 Z9 28 U1 0 U2 2 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 EI 1089-8638 J9 J MOL BIOL JI J. Mol. Biol. PD FEB 18 PY 1994 VL 236 IS 2 BP 491 EP 502 DI 10.1006/jmbi.1994.1160 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX209 UT WOS:A1994MX20900010 PM 8107135 ER PT J AU LEVY, R DANA, R LETO, TL MALECH, HL AF LEVY, R DANA, R LETO, TL MALECH, HL TI THE REQUIREMENT OF P47 PHOSPHORYLATION FOR ACTIVATION OF NADPH OXIDASE BY OPSONIZED ZYMOSAN IN HUMAN NEUTROPHILS SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE PROTEIN KINASE C INHIBITOR; NADPH OXIDASE ACTIVITY; P47 PHOSPHORYLATION; SUPEROXIDE PRODUCTION; OPSONIZED ZYMOSAN; (NEUTROPHIL); (HUMAN) ID PROTEIN-KINASE-C; CHRONIC GRANULOMATOUS-DISEASE; RESPIRATORY BURST OXIDASE; SUPEROXIDE PRODUCTION; LIPOTEICHOIC ACID; 2 FORMS; STIMULATION; COMPONENTS; MEMBRANE; CALCIUM AB Protein kinase C (PKC) inhibitors, staurosporine or 1,5-isoquinolinesulfonyl)-2-methylpiperazine (H7), inhibited NADPH oxidase activity and phosphorylation of 47 kDa protein (p47) in PMA-stimulated neutrophils in a dose-dependent manner. These PKC inhibitors, at the same doses, did not affect oxidase activity and caused only partial inhibition of p47 phosphorylation in OZ-stimulated neutrophils. There was residual (20%) phosphorylated p47 in the membranes of OZ-stimulated cells in the presence of PKC inhibitors, at concentrations which caused total inhibition of oxidase activity and p47 phosphorylation in PMA-stimulated neutrophils. In the presence of ionomycin, which increased intracellular calcium ion concentrations, staurosporine was less effective in inhibiting both superoxide generation and p47 phosphorylation stimulated by PMA, similar to its effect in OZ-stimulated cells. The results indicate that some phosphorylation of p47 always accompanied oxidase activation induced by PMA or OZ, though the degree of phosphorylation of membrane-bound p47 does not directly correlate with rates of superoxide production. C1 BEN GURION UNIV NEGEV,IL-84105 BEER SHEVA,ISRAEL. NIAID,BETHESDA,MD. RP LEVY, R (reprint author), SOROKA MED CTR KUPAT HALIM,FAC HLTH SCI,INFECT DIS LAB,CLIN BIOCHEM UNIT,IL-84105 BEER SHEVA,ISRAEL. NR 55 TC 26 Z9 26 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 17 PY 1994 VL 1220 IS 3 BP 253 EP 260 DI 10.1016/0167-4889(94)90146-5 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY078 UT WOS:A1994MY07800004 PM 8305497 ER PT J AU LEVY, R NAGAUKER, O SIKULER, E LETO, TL SCHLAEFFER, F AF LEVY, R NAGAUKER, O SIKULER, E LETO, TL SCHLAEFFER, F TI ELEVATED NADPH-OXIDASE ACTIVITY IN NEUTROPHILS FROM BILE-DUCT-LIGATED RATS - CHANGES IN THE KINETIC-PARAMETERS AND IN THE OXIDASE CYTOSOLIC FACTOR P47 SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE NADPH OXIDASE ACTIVITY; SUPEROXIDE GENERATION; CELL-FREE SYSTEM; CYTOSOLIC FACTOR P47; (NEUTROPHIL); (RAT) ID CHRONIC GRANULOMATOUS-DISEASE; MOUSE PERITONEAL-MACROPHAGES; RESPIRATORY BURST; ACTIVATION; EXPRESSION; COMPONENT; LIPOPOLYSACCHARIDE; PHAGOCYTES; MEMBRANE; CELLS AB Stimulated superoxide generation was 2-fold higher in neutrophils from 20 rats with common bile-duct ligation (CBDL) compared to that of 20 sham-operated control rats. In order to study the mechanism of the higher NADPH oxidase activity in CBDL rats, the kinetic parameters of NADPH oxidase were analyzed. The V-max of the NADPH oxidase in CBDL rat neutrophils was significantly higher than that of control rat neutrophils (10.2 and 5.3 nmol/min, respectively). The membrane and cytosol fractions of the oxidase were studied in a cell-free system. Neutrophil cytosol from CBDL rats added to neutrophil membranes from either CBDL or control rats produced 22.4 +/- 1.6 and 21.0 +/- 1.4 nmol/10(6) cells per 10 min, respectively. When neutrophil cytosol from control rats was mixed with neutrophil membranes from control or CBDL rats the generation of superoxide was 10.6 +/- 1.4 and 10.0 +/- 1.5 nmol/10(6) cells per 10 min, respectively. These results suggest that the cytosol components of the oxidase regulate its activity. By immunoblot analysis it was shown that the amount of the cytosolic factor p47 in neutrophils of CBDL rats is higher than that present in an equal number of neutrophils from control rats. C1 SOROKA MED CTR KUPAT HOLIM,DEPT INTERNAL MED,IL-84105 BEER SHEVA,ISRAEL. BEN GURION UNIV NEGEV,FAC HLTH SCI,IL-84105 BEER SHEVA,ISRAEL. NIAID,BETHESDA,MD. RP LEVY, R (reprint author), SOROKA MED CTR KUPAT HOLIM,INFECT DIS LAB,CLIN BIOCHEM UNIT,IL-84105 BEER SHEVA,ISRAEL. NR 23 TC 8 Z9 8 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 17 PY 1994 VL 1220 IS 3 BP 261 EP 265 DI 10.1016/0167-4889(94)90147-3 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY078 UT WOS:A1994MY07800005 PM 8305498 ER PT J AU HU, ZZ BUCZKO, E ZHUANG, L DUFAU, ML AF HU, ZZ BUCZKO, E ZHUANG, L DUFAU, ML TI SEQUENCE OF THE 3'-NONCODING REGION OF THE LUTEINIZING-HORMONE RECEPTOR GENE AND IDENTIFICATION OF 2 POLYADENYLATION DOMAINS THAT GENERATE THE MAJOR MESSENGER-RNA FORMS SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Note DE LUTEINIZING HORMONE RECEPTOR; 3'-NONCODING REGION; POLYADENYLATION SITE; REPETITIVE DNA; MESSENGER-RNA HETEROGENEITY; (RAT) ID FOLLICLE-STIMULATING-HORMONE; STRUCTURAL ORGANIZATION; CLONING; CDNA; EXPRESSION; LACKING AB We present 6.2 kb of the 3'-noncoding region sequence of the rat luteinizing hormone receptor (LHR) gene and identification of two functional polyadenylation (pA) domains, H1 (nt 2368-2491) and H2 (nt 5579-5768) responsible for 3'-end processing of the 2.6/2.3 kb and the 5.8 kb LHR mRNA, respectively. Two identical copies of pA elements AAUAUA in H1 and of AAUAAA in H2 account for micro-heterogeneous poly(A) addition at each of the two pA regions. Both LH holoreceptor and major splice variant form B (lacking the first 266 bp of exon 11) are identified in Hi-terminated (2.6 kb and 2.3 kb) and H2-terminated (5.8 kb) mRNA transcripts. A rodent repetitive DNA LINE R domain 3' of H1 within the major 5.8 kb species and a B2 element downstream of H2 were identified. Alignment of the 3'-noncoding region of LHR with TSH, FSH and beta(2)-adrenergic receptors indicate that H1 pA signal is unique to the LHR and may represent an insertion domain. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,MOLEC ENDOCRINOL SECT,BETHESDA,MD 20892. NR 22 TC 19 Z9 19 U1 0 U2 1 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 17 PY 1994 VL 1220 IS 3 BP 333 EP 337 DI 10.1016/0167-4889(94)90158-9 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY078 UT WOS:A1994MY07800016 PM 8305508 ER PT J AU WARD, Y GUPTA, S JENSEN, P WARTMANN, M DAVIS, RJ KELLY, K AF WARD, Y GUPTA, S JENSEN, P WARTMANN, M DAVIS, RJ KELLY, K TI CONTROL OF MAP KINASE ACTIVATION BY THE MITOGEN-INDUCED THREONINE/TYROSINE PHOSPHATASE PAC1 SO NATURE LA English DT Article ID GROWTH-FACTOR RECEPTOR; PROTEIN-KINASE; ENCODED PROTEIN; PHOSPHORYLATION; SEQUENCE; GENE AB INTRACELLULAR Signalling following mitogenic stimulation of quiescent cells involves the initiation of a phosphorylation cascade that leads to the rapid and reversible activation of the mitogen-activated protein (MAP) kinases ERK1 and ERK2 (refs 1, 2). MAP kinase activation is mediated by dual phosphorylation within the motif Thr-Glu-Tyr by MAP kinase kinase (MEK)(3). Following activation, the MAP kinases translocate into the nucleus where they phosphorylate several transduction targets, including transcription factors(4-7). We have previously identified PAC1 as an immediate-early mitogen-inducible tyrosine phosphatase in nuclei of T cells(8). Here we present several lines of evidence indicating that PAC1 is a physiologically relevant MAP kinase phosphatase. Recombinant PAC1 in vitro is a dual-specific Thr/Tyr phosphatase with stringent substrate specificity for MAP kinase. Constitutive expression of PAC1 in vivo leads to inhibition of MAP kinase activity normally stimulated by epidermal growth factor, phorbol myristyl acetate, or T-cell receptor crosslinking. The inactivation of MAP kinase by PAC1 results in inhibition of MAP kinase-regulated reporter gene expression. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. UNIV MASSACHUSETTS,SCH MED,HOWARD HUGHES MED INST,DEPT BIOCHEM & MOLEC BIOL,WORCESTER,MA 01605. NR 25 TC 306 Z9 307 U1 0 U2 3 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD FEB 17 PY 1994 VL 367 IS 6464 BP 651 EP 654 DI 10.1038/367651a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MW688 UT WOS:A1994MW68800056 PM 8107850 ER PT J AU QUINTERO, RA REICH, H PUDER, KS BARDICEF, M EVANS, MI COTTON, DB ROMERO, R AF QUINTERO, RA REICH, H PUDER, KS BARDICEF, M EVANS, MI COTTON, DB ROMERO, R TI UMBILICAL-CORD LIGATION OF AN ACARDIAC TWIN BY FETOSCOPY AT 19 WEEKS OF GESTATION - BRIEF REPORT SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note ID SELECTIVE DELIVERY; ACEPHALIC TWIN; PREGNANCIES; HYSTEROTOMY C1 WYOMING VALLEY GYN ASSOCIATES,KINGSTON,PA. NICHHD,PERINATOL RES BRANCH,BETHESDA,MD. RP QUINTERO, RA (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,CTR FETAL DIAG & THERAPY,DEPT OBSTET & GYNECOL,DETROIT,MI 48201, USA. NR 14 TC 135 Z9 139 U1 0 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 17 PY 1994 VL 330 IS 7 BP 469 EP 471 DI 10.1056/NEJM199402173300705 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA MW480 UT WOS:A1994MW48000005 PM 8289853 ER PT J AU HOEG, JM AF HOEG, JM TI FAMILIAL HYPERCHOLESTEROLEMIA - WHAT THE ZEBRA CAN TEACH US ABOUT THE HORSE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Discussion ID LOW-DENSITY-LIPOPROTEIN; LIVER-TRANSPLANTATION; PLASMA-EXCHANGE; DEFICIENT RABBITS; DRUG-THERAPY; GENE-THERAPY; RECEPTOR; ATHEROSCLEROSIS; CHOLESTEROL; METABOLISM RP HOEG, JM (reprint author), NHLBI,MOLEC DIS BRANCH,CELL BIOL SECT,9000 ROCKVILLE PIKE,BLDG 10,BETHESDA,MD 20892, USA. NR 32 TC 16 Z9 16 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 16 PY 1994 VL 271 IS 7 BP 543 EP 546 DI 10.1001/jama.271.7.543 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA MV423 UT WOS:A1994MV42300038 PM 8301770 ER PT J AU ALAVANJA, MCR SWANSON, C BROWN, C BROWNSON, R AF ALAVANJA, MCR SWANSON, C BROWN, C BROWNSON, R TI LUNG-CANCER - ANOTHER CONSEQUENCE OF A HIGH-FAT DIET SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter C1 MISSOURI DEPT HLTH,DIV CHRON DIS PREVENT & CONTROL,COLUMBIA,MO. RP ALAVANJA, MCR (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,EPN,RM 543,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 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 16 PY 1994 VL 86 IS 4 BP 314 EP 314 DI 10.1093/jnci/86.4.314 PG 1 WC Oncology SC Oncology GA MV706 UT WOS:A1994MV70600020 PM 8158689 ER PT J AU GLICK, BN ROBERTS, WC AF GLICK, BN ROBERTS, WC TI CONGENITALLY BICUSPID AORTIC-VALVE IN MULTIPLE FAMILY MEMBERS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Note ID ACTIVE INFECTIVE ENDOCARDITIS; NECROPSY PATIENTS; STENOSIS; AGE; REGURGITATION; AUTOPSY; DISEASE C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. RP GLICK, BN (reprint author), NHLBI,PATHOL BRANCH,BETHESDA,MD 20892, USA. NR 37 TC 37 Z9 39 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD FEB 15 PY 1994 VL 73 IS 5 BP 400 EP 404 DI 10.1016/0002-9149(94)90018-3 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MX082 UT WOS:A1994MX08200018 PM 8109558 ER PT J AU BIGGAR, RJ CURTIS, RE COTE, TR RABKIN, CS MELBYE, M AF BIGGAR, RJ CURTIS, RE COTE, TR RABKIN, CS MELBYE, M TI RISK OF OTHER CANCERS FOLLOWING KAPOSIS-SARCOMA - RELATION TO ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; HIV; NEOPLASMS; LYMPHOMA, NON-HODGKINS; RECTAL NEOPLASMS; SARCOMA, KAPOSIS AB To evaluate the risk of another cancer among persons who initially developed Kaposi's sarcoma, the authors used data from the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute for the years 1973-1990. In persons under 70 years of age, 4,946 cases of Kaposi's sarcoma were observed during the period 1980-1990 (6,217 person-years of follow-up). On the basis of rates seen during the period prior to the epidemic of acquired immunodeficiency syndrome (AIDS), 169 cases were expected. Therefore, cases of Kaposi's sarcoma in this group were assumed to be AIDS-related, while cases occurring in older persons or during the 1970s were assumed to be non-AIDS-related. Rates were compared with the numbers of cases expected overall and by site on the basis of age-, sex-, and calendar year-specific rates from the SEER data. Among the 4,946 persons with AIDS-related Kaposi's sarcoma, the risk of developing non-Hodgkin's lymphoma through 1990 was increased 198-fold (95% confidence interval 169-232). However, the risk of all other cancers was only marginally increased (1.5-fold;95% confidence interval 0.95-2.3), a risk that was probably biased upward because of ascertainment and misclassification. Among 491 persons with non-AIDS-related Kaposi's sarcoma, the relative risk of all cancers including non-Hodgkin's lymphoma, was 0.9 (upper confidence limit 1.2), and the risk of non-Hodgkin's lymphoma alone was 0.6 (upper 95% confidence limit 3.3). As of 1990, the risk of having another cancer following Kaposi's sarcoma was increased only in persons infected with human immunodeficiency virus, who were at high risk of non-Hodgkin's lymphoma but probably not of other cancers as a whole. C1 NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. STATE SERUM INST,EPIDEMIOL RES UNIT,COPENHAGEN,DENMARK. NR 15 TC 81 Z9 82 U1 0 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 15 PY 1994 VL 139 IS 4 BP 362 EP 368 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MY894 UT WOS:A1994MY89400002 PM 8109570 ER PT J AU ROGOT, E SORLIE, PD BACKLUND, E AF ROGOT, E SORLIE, PD BACKLUND, E TI PROBLEMS IN DICHOTOMIZING CONTINUOUS-VARIABLES - REPLY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter C1 US BUR CENSUS,DIV STAT METHODS,SUITLAND,MD 20233. RP ROGOT, E (reprint author), NHLBI,EPIDEMIOL PROGRAM,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 15 PY 1994 VL 139 IS 4 BP 445 EP 445 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MY894 UT WOS:A1994MY89400012 ER PT J AU KUPFER, C AF KUPFER, C TI THE INTERNATIONAL AGENCY FOR THE PREVENTION OF BLINDNESS SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Editorial Material RP KUPFER, C (reprint author), NEI,BLDG 31,ROOM 6A-03,BETHESDA,MD 20892, USA. NR 0 TC 9 Z9 11 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 15 PY 1994 VL 117 IS 2 BP 253 EP 257 PG 5 WC Ophthalmology SC Ophthalmology GA MV287 UT WOS:A1994MV28700018 PM 7993402 ER PT J AU CASAZZA, JP SOHN, DH PARK, KS SONG, BJ AF CASAZZA, JP SOHN, DH PARK, KS SONG, BJ TI SERUM ACETONE AND LIVER ACETONE MONOOXYGENASE ACTIVITY IN PREGNANT RATS, FETUSES, AND NEONATES - REVERSIBLE PRETRANSLATIONAL REDUCTION OF CYTOCHROME P450IIE1 (P450IIE1) DURING PREGNANCY SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID N-NITROSODIMETHYLAMINE DEMETHYLASE; TRANSCRIPTIONAL REGULATION; PLACENTAL-LACTOGEN; MESSENGER-RNA; DIABETIC RAT; CYP2E1 GENE; ISOZYME 3A; ETHANOL; METABOLISM; EXPRESSION AB Serum acetone in neonates was found to increase from <20 mu M at 20 days gestation to 377 +/- 107 mu M 1 day after birth. This increase in acetone occurs concurrently with the initial expression of liver P450IIE1 in rat (Song et al., 1986, J. Biol. Chem. 261:16689-16697). Treating pregnant rats with drinking water containing 1% acetone did not result in a premature induction of liver acetone monooxygenase, a P450IIE1 catalyzed activity, in fetuses sacrificed at 20 days gestation. The data indicate that increased serum acetone levels are not responsible for the initial induction of P450IIE1 in neonates. However, acetone monooxygenase activity in their mothers was significantly less than acetone-treated females which were not pregnant, indicating a reduced activity of P450IIE1 during pregnancy although its induction by acetone was still observed. Acetone monooxygenase activity in 20 day pregnant rats given untreated drinking water was also less than in nongravid rats. These findings are supported by immunoblot data which show significant and progressive reductions in liver P450IIE1 in both untreated and acetone-treated rats during pregnancy. Northern mRNA blot analysis further revealed that the decreases in P450IIE1 activity and protein content were mainly due to pretranslational suppression with reduced level of its mRNA. However, their levels rapidly returned to the control level after parturition (within 1 day). Repeated administration of several exogenous hormones (estriol, pregnanediol, thyroxine) or peptide hormones (placental lactogen, prolactin, chorionic gonadotropin) failed to suppress P450IIE1 in nonpregnant rats, indicating a possibility of another factor(s) responsible for the P450IIE1 suppression during pregnancy. (C) 1994 Academic Press, Inc. C1 NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20852. NIAAA,METAB LAB,ROCKVILLE,MD 20852. NR 47 TC 12 Z9 12 U1 1 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD FEB 15 PY 1994 VL 309 IS 1 BP 111 EP 116 DI 10.1006/abbi.1994.1092 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MY517 UT WOS:A1994MY51700018 PM 8117100 ER PT J AU TEMUSSI, PA SALVADORI, S AMODEO, P BIANCHI, C GUERRINI, R TOMATIS, R LAZARUS, LH PICONE, D TANCREDI, T AF TEMUSSI, PA SALVADORI, S AMODEO, P BIANCHI, C GUERRINI, R TOMATIS, R LAZARUS, LH PICONE, D TANCREDI, T TI SELECTIVE OPIOID DIPEPTIDES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID CONFORMATIONAL PROPERTIES; RECEPTOR ANTAGONIST; AMPHIBIAN SKIN; NUCLEIC-ACIDS; HIGH-AFFINITY; FORCE-FIELD; PEPTIDE; DELTORPHIN; DERMORPHIN; FEATURES C1 UNIV FERRARA,DIPARTIMENTO SCI FARMACEUT,I-44100 FERRARA,ITALY. UNIV FERRARA,IST FARMACOL,I-44100 FERRARA,ITALY. NIEHS,LMNI,RES TRIANGLE PK,NC 27709. CNR,ICMIB,I80072 ARCO,ITALY. RP TEMUSSI, PA (reprint author), UNIV NAPOLI FEDERICO II,DIPARTIMENTO CHIM,VIA MEZZOCANNONE 4,I-80134 NAPLES,ITALY. RI Picone, Delia/I-5605-2012; Amodeo, Pietro/P-1800-2015; OI Picone, Delia/0000-0002-7582-2581; Amodeo, Pietro/0000-0002-6439-7575; Guerrini, Remo/0000-0002-7619-0918; SALVADORI, Severo/0000-0002-8224-2358 NR 30 TC 85 Z9 87 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 15 PY 1994 VL 198 IS 3 BP 933 EP 939 DI 10.1006/bbrc.1994.1133 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MW332 UT WOS:A1994MW33200017 PM 8117299 ER PT J AU BALEN, P KIMURA, K SIDHU, A AF BALEN, P KIMURA, K SIDHU, A TI SPECIFIC PHOSPHOLIPID REQUIREMENTS FOR THE SOLUBILIZATION AND RECONSTITUTION OF D-1 DOPAMINE-RECEPTORS FROM STRIATAL MEMBRANES SO BIOCHEMISTRY LA English DT Article ID RAT STRIATUM; LIGAND; AGONIST; ANTAGONIST; SYNERGISM; PROTEINS; D1 AB We have reported the solubilization and reconstitution of functional D-1 dopamine receptors from rat striatal tissue, using sodium cholate as detergent [Sidhu, A. (1988) Biochemistry 27, 8768-8776]. Critical to our method of extraction was the absolute requirement for the persistent presence of a crude extract of phospholipids (PLs) from bovine brain, during both solubilization of membranes and reconstitution of the soluble extract into PL vesicles. In the absence of PLs, fewer than 10% of the receptors were recovered, while in the presence of PLs, 40% of the receptors were reconstituted into vesicles. To probe the composition of PLs required by D-1 dopamine receptors during these extraction procedures, specific PLs of a defined composition were used during either solubilization or reconstitution alone or during both solubilization and reconstitution. Phosphatidylcholine (PC), when used during the solublization procedure alone or during both solubilization and reconstitution, resulted in recovery of 41-48% of the D-1 dopamine receptors but was 3.7-fold less effective when present during reconstitution alone (11%). Phosphatidylethanolamine (PE), when used during reconstitution alone, resulted in recovery of nearly 25% of the D-1 dopamine receptors. When PE was present during either solubilization or both solubilization and reconstitution, 6-11% of the receptors were recovered. If PE was used with PC in ratios of 1:1 or 2:1, respectively, 28-38% of the receptors were recovered. When PL vesicles of PE:PC were present in ratios of 1:2 during both solubilization and reconstitution, the maximum theoretical (74-87%) recovery of total receptor binding sites was achieved. These reconstituted receptors were pharmacologically active, with 53.5% of the receptor population present in the high-affinity state. C1 GEORGETOWN UNIV,CHILDRENS MED CTR,DEPT PEDIAT,WASHINGTON,DC 20007. NIH,MOLEC & CELLULAR NEUROBIOL LAB,MEMBRANE BIOCHEM SECT,BETHESDA,MD 20892. RI Kimura, Kazuhiro/A-5029-2012 FU NINDS NIH HHS [NS-29685, NS-30912] NR 18 TC 5 Z9 5 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 15 PY 1994 VL 33 IS 6 BP 1539 EP 1544 DI 10.1021/bi00172a034 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX208 UT WOS:A1994MX20800034 PM 8312274 ER PT J AU HE, RY REID, DM JONES, CE SHULMAN, NR AF HE, RY REID, DM JONES, CE SHULMAN, NR TI SPECTRUM OF IG CLASSES, SPECIFICITIES, AND TITERS OF SERUM ANTIGLYCOPROTEINS IN CHRONIC IDIOPATHIC THROMBOCYTOPENIC PURPURA SO BLOOD LA English DT Article ID MEMBRANE GLYCOPROTEIN-IIB; IIIA COMPLEX; CHRONIC ITP; MONOCLONAL-ANTIBODY; PLATELET-FUNCTION; BLOOD PLATELETS; BOUND IGG; AUTOANTIBODIES; PLASMA; IB RP HE, RY (reprint author), NIDDK,CLIN HEMATOL BRANCH,9000 ROCKVILLE PIKE,BLDG 10,RM 4D51,BETHESDA,MD 20892, USA. NR 48 TC 124 Z9 138 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 1994 VL 83 IS 4 BP 1024 EP 1032 PG 9 WC Hematology SC Hematology GA MW692 UT WOS:A1994MW69200019 PM 8111044 ER PT J AU BUSCH, MP LAYCOCK, M KLEINMAN, SH WAGES, JW CALABRO, M KAPLAN, JE KHABBAZ, RF HOLLINGSWORTH, CG NASS, C JACKSON, CM OWNBY, H HUTCHING, S MURPHY, EL GILCHER, RO SCHREIBER, GB THOMSON, R NEMO, GJ ZUCK, T AF BUSCH, MP LAYCOCK, M KLEINMAN, SH WAGES, JW CALABRO, M KAPLAN, JE KHABBAZ, RF HOLLINGSWORTH, CG NASS, C JACKSON, CM OWNBY, H HUTCHING, S MURPHY, EL GILCHER, RO SCHREIBER, GB THOMSON, R NEMO, GJ ZUCK, T TI ACCURACY OF SUPPLEMENTARY SEROLOGIC TESTING FOR HUMAN T-LYMPHOTROPIC VIRUS TYPE-I AND TYPE-II IN US BLOOD-DONORS SO BLOOD LA English DT Article ID CELL LEUKEMIA-VIRUS; HTLV-I; ENZYME-IMMUNOASSAY; INFECTION; ANTIBODY; CONFIRMATION; IMMUNOBLOT; ASSAY; PCR C1 UNIV CALIF SAN FRANCISCO, DEPT LAB MED, SAN FRANCISCO, CA 94143 USA. WESTAT CORP, MED COORDINATING CTR, ROCKVILLE, MD USA. UNIV CALIF LOS ANGELES, LOS ANGELES, CA 90024 USA. SRA TECHNOL INC, SUPPORTING LAB, ROCKVILLE, MD USA. CTR DIS CONTROL & PREVENT, ATLANTA, GA USA. NHLBI, ROCKVILLE, MD USA. AMER RED CROSS, BLOOD SERV GREATER CHESAPEAKE & POTOMAC REG, CTR BLOOD, HOLLAND LAB, ROCKVILLE, MD USA. AMER RED CROSS, BLOOD SERV SE MICHIGAN REG, CTR BLOOD, DETROIT, MI USA. UNIV CALIF LOS ANGELES, MED CTR,AMER RED CROSS,BLOOD SERV SO CALIF REG, CTR BLOOD, LOS ANGELES, CA USA. OKLAHOMA BLOOD INST, OKLAHOMA CITY, OK USA. HOXWORTH BLOOD CTR, CINCINNATI, OH USA. RP BUSCH, MP (reprint author), UCSF, IRWIN MEM BLOOD CTR, CTR BLOOD, 270 MASONIC AVE, SAN FRANCISCO, CA 94118 USA. FU NHLBI NIH HHS [N01-HB-97077] NR 25 TC 55 Z9 55 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1994 VL 83 IS 4 BP 1143 EP 1148 PG 6 WC Hematology SC Hematology GA MW692 UT WOS:A1994MW69200034 PM 8111054 ER PT J AU SCHAIN, WS DANGELO, TM DUNN, ME LICHTER, AS PIERCE, LJ AF SCHAIN, WS DANGELO, TM DUNN, ME LICHTER, AS PIERCE, LJ TI MASTECTOMY VERSUS CONSERVATIVE SURGERY AND RADIATION-THERAPY SO CANCER LA English DT Article DE BREAST CANCER; CONSERVATIVE SURGERY; RADIATION THERAPY; SURGICAL THERAPY; MASTECTOMY; PSYCHOSOCIAL STUDIES ID PRIMARY BREAST-CANCER; MODIFIED RADICAL-MASTECTOMY; PSYCHOLOGICAL-FACTORS; CHOICE; LUMPECTOMY; IRRADIATION; DEPRESSION; ADJUSTMENT; DISTRESS; TRIAL AB Background. Clinical trials comparing mastectomy to conservative surgery plus radiation therapy in the treatment of breast cancer have provided an opportunity to increase understanding of the biology of this disease and the psychological adaptation of the breast cancer patient. Because these local treatments appear to be equal in terms of survival, the question remains as to whether conservative surgery plus radiation therapy confers a measure of psychological comfort superior to that of mastectomy for women diagnosed with early-stage breast cancer. Methods. One hundred forty-two women participating in a clinical trial randomizing patients to mastectomy or lumpectomy and radiation therapy were prospectively evaluated for psychological response to their respective local therapy. A baseline assessment before randomization and subsequent questionnaires at 6, 12, and 24 months after treatment were completed by patients entered in the clinical trial. Results. At 6 months, mastectomy patients reported significantly less control over events in their lives (P = 0.003) and more problems with sexual relations (P = 0.021) than did their conservatively treated counterparts. In addition, there were marked differences between mastectomy patients and lumpectomy and radiation therapy patients in the degree of distress over their nude bodies, with P = 0.001 at 6 months, P = 0.019 at 12 months, and P = 0.057 at 24 months. Conclusions. From our findings, it appears that breast conservation therapy protects women's perception of their body but does not, over time, contribute to a more positive sexual adjustment. C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NIH,CTR CLIN,BETHESDA,MD 20892. NIH,CANC NURSING SERV,BETHESDA,MD. ORKAND CORP,SILVER SPRING,MD. UNIV MICHIGAN,DEPT RADIAT ONCOL,ANN ARBOR,MI 48109. NR 37 TC 76 Z9 78 U1 1 U2 4 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 1994 VL 73 IS 4 BP 1221 EP 1228 DI 10.1002/1097-0142(19940215)73:4<1221::AID-CNCR2820730416>3.0.CO;2-S PG 8 WC Oncology SC Oncology GA MY538 UT WOS:A1994MY53800015 PM 8313326 ER PT J AU SAMID, D RAM, Z HUDGINS, WR SHACK, S LIU, L WALBRIDGE, S OLDFIELD, EH MYERS, CE AF SAMID, D RAM, Z HUDGINS, WR SHACK, S LIU, L WALBRIDGE, S OLDFIELD, EH MYERS, CE TI SELECTIVE ACTIVITY OF PHENYLACETATE AGAINST MALIGNANT GLIOMAS - RESEMBLANCE TO FETAL BRAIN-DAMAGE IN PHENYLKETONURIA SO CANCER RESEARCH LA English DT Note ID TUMOR; CELLS; HYPERPHENYLALANINEMIA; DIFFERENTIATION; PHENYLALANINE; DERIVATIVES; INHIBITION; ENZYMES; MODEL; ACID AB Phenylacetate, a deaminated metabolite of phenylalanine, has been implicated in damage to immature brain in phenylketonuria. Because primary brain tumors are highly reminiscent of the immature central nervous system, these neoplasms should be equally vulnerable. We shes here that sodium phenylacetate can induce cytostasis and reversal of malignant properties of cultured human glioblastoma cells, when used at pharmacological concentrations that are well tolerated by children and adults. Treated tumor cells exhibited biochemical alterations similar to those observed in phenylketonuria-like conditions, including selective decline in de novo cholesterol synthesis from mevalonate. Because gliomas, but not mature normal brain cells, are highly dependent on mevalonate for production of sterols and isoprenoids vital for cell growth, sodium phenylacetate would be expected to affect tumor growth in vivo while sparing normal tissues. Systemic treatment of rats bearing intracranial gliomas resulted in significant tumor suppression with no apparent toxicity to the host. The data indicate that phenylacetate, acting through inhibition of protein prenylation and other mechanisms, may offer a safe and effective novel approach to treatment of malignant gliomas and perhaps other neoplasms as well. C1 NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. RP SAMID, D (reprint author), NCI,DIV CANC TREATMENT,CLIN PHARMACOL BRANCH,BLDG 10,ROOM 12C103,BETHESDA,MD 20892, USA. NR 31 TC 110 Z9 111 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1994 VL 54 IS 4 BP 891 EP 895 PG 5 WC Oncology SC Oncology GA MW686 UT WOS:A1994MW68600009 PM 8313377 ER PT J AU KOHN, EC FELDER, CC JACOBS, W HOLMES, KA DAY, A FREER, R LIOTTA, LA AF KOHN, EC FELDER, CC JACOBS, W HOLMES, KA DAY, A FREER, R LIOTTA, LA TI STRUCTURE-FUNCTION ANALYSIS OF SIGNAL AND GROWTH-INHIBITION BY CARBOXYAMIDO-TRIAZOLE, CAI SO CANCER RESEARCH LA English DT Article ID MEDIATED CALCIUM ENTRY; INOSITOL PHOSPHATES; TYROSINE PHOSPHORYLATION; TUMOR-METASTASIS; COLON CANCER; CA2+ INFLUX; RECEPTOR; CELLS; PROSTAGLANDINS; TRANSDUCTION AB Evidence is accumulating that calcium homeostasis and calcium-regulated events may be selectively important in generation and maintenance of the malignant phenotype. CAI, a carboxyamido-triazole with a halogenated benzophenone tail, is a novel inhibitor of receptor-operated calcium influx and arachidonic acid release which inhibits malignant proliferation, invasion, and metastasis. The focus of this investigation was structural analysis of CAI and to determine if the inhibition of calcium influx and arachidonic acid release by CAI and its antiproliferative activity were mediated through the same chemical domains. Four families of molecular modifications of the CAI parent were synthesized: (I) modification or substitution of the triazole ring; (II) removal of the substituted benzophenone tail; (III) dehalogenation or partial truncation of the benzophenone moiety; and (IV) removal of the triazole and altered substitutions of the benzophenone tail. Compounds were tested for the inhibition of calcium influx and arachidonic acid release and inhibition of proliferation and colony formation in soft agar using the malignant CHO line transfected with the m5 muscarinic receptor and the A2058 human melanoma cell line. Only CAI and Group I compounds inhibited stimulated calcium influx, arachidonic acid release, and proliferation. Linear regression analysis of the relationship of the 50% inhibitory concentration values for all compounds in inhibition of calcium influx and arachidonate release was statistically significant (r(2) = 0.993). Similarly, a linear relationship was demonstrated between inhibition of calcium influx and inhibition of tumor cell proliferation (r(2) = 0.971). Groups II-IV had minimal or no signal or growth inhibitory activity. This investigation provides the first evidence for a coordinate link between calcium influx, calcium-mediated arachidonic acid release, and malignant proliferation and metastasis and constitutes the initial analysis of structurally important domains of the CAI molecule. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT BIOMED ENGN,RICHMOND,VA 23298. RP KOHN, EC (reprint author), NCI,PATHOL LAB,BLDG 10,ROOM 2A33,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 38 TC 91 Z9 92 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1994 VL 54 IS 4 BP 935 EP 942 PG 8 WC Oncology SC Oncology GA MW686 UT WOS:A1994MW68600017 PM 8313384 ER PT J AU SATHYAMOORTHY, N WANG, TTY PHANG, JM AF SATHYAMOORTHY, N WANG, TTY PHANG, JM TI STIMULATION OF PS2 EXPRESSION BY DIET-DERIVED COMPOUNDS SO CANCER RESEARCH LA English DT Article ID HUMAN-BREAST-CANCER; CELL-LINE MCF-7; NORDIHYDROGUAIARETIC ACID; LIPOXYGENASE INHIBITOR; GENE-EXPRESSION; GROWTH-FACTOR; ESTROGEN; PHYTOESTROGENS; ENTEROLACTONE; LIGNANS AB Epidemiological studies suggest a lowered risk of hormone-dependent cancers among vegetarians, but the basis for this association remains unclear. Vegetables and fruits contain certain compounds,which can be converted to biologically active hormone-like substances, such as lignans and isoflavones, by intestinal flora. The interaction of these compounds with endogenous hormones may be a novel, diet-dependent mechanism in cancer prevention. To explore this possibility, we developed a rapid, specific assay system to screen for compounds with estrogen-like activity in tissue culture. We utilized the estrogen receptor-positive breast cancer cell MCF-7 and monitored the expression of the estrogen-responsive protein pS2 by Northern blots. Our results indicated that the phenolic compounds daidzein, equol, nordihydroguaiaretic acid, enterolactone, and kaempferol were able to elicit an estrogen-like response, while quercetin and enterodiol were not. RP SATHYAMOORTHY, N (reprint author), NCI,FREDERICK CANC RES & DEV CTR,NUTR & MOLEC REGULAT LAB,BLDG 434-2,POB B,FREDERICK,MD 21702, USA. NR 29 TC 115 Z9 118 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1994 VL 54 IS 4 BP 957 EP 961 PG 5 WC Oncology SC Oncology GA MW686 UT WOS:A1994MW68600020 PM 8313386 ER PT J AU POTTER, M MUSHINSKI, EB WAX, JS HARTLEY, J MOCK, BA AF POTTER, M MUSHINSKI, EB WAX, JS HARTLEY, J MOCK, BA TI IDENTIFICATION OF 2 GENES ON CHROMOSOME-4 THAT DETERMINE RESISTANCE TO PLASMACYTOMA INDUCTION IN MICE SO CANCER RESEARCH LA English DT Article ID BALB/C MICE; MOUSE CHROMOSOME-1; SUSCEPTIBILITY; PRISTANE; GENETICS; TUMORS; LOCUS; CELLS; MAP AB BALB/cAn mice are highly susceptible to the induction of plasmacytomas (PCTs) by the i.p. injection of paraffin oils, whereas DBA/2 mice are solidly resistant. To search for genes that control the dominant resistant phenotype of DBA/2, BALB/c.DBA/2 (C.D2) congenic strains were constructed, and the susceptibility and resistance to PCT development were determined. PCT formation takes place over an extended period of 365 days but begins morphologically in focal proliferations of atypical plasma cells (foci) in the reactive oil granuloma that forms on mesenteric surfaces. Cells from some of these foci spread to other locations in oil granuloma tissue, forming new foci. Mice that develop six or more foci appear to be progressing towards eventual overgrowth and replacement of all peritoneal tissues with PCT cells. From Days 100 to 250, between 28 and 56% of PCT-susceptible BALB/cAn mice had 6 or more foci, whereas less than 5% of resistant DBA/2, BALB/c x DBA/2 F-1 (hereafter called CD2F(1)), C57BL/6, and BALB/cJ mice had 6 or more foci. Four C.D2 congenic strains carrying D2 alleles of genes on chromosomes other than chromosome 4 were highly susceptible. Between 0 and 20% of the mice in C.D2-Chr 4 congenic strains C.D2-MIA, C.D2-TF3, C.D2-Fv-1(n/n), C.D2-Pnd7, C.D2-Lgm-1A, C.D2-Lgm-1B, C.D2-Lgm-1C, and C.D2-Lgm-1H developed 6 or more foci from 125 to 260 days, indicating resistance. The segments of DBA/2 chromosome 4 chromatin in C.D2-FV-1(n/n) and C.D2-Pnd7 were discontinuous with those in C.D2-TF3, C.D2-Lgm-1A, C.D2-Lgm-1B, C.D2-Lgm-1C, and C.D2-Lgm-1H, indicating there are at least two genes (Pct(r1) and Pct(r2)) in the distal half of this chromosome that confer resistance. Pct(r1) is located between Ifa and D4Rck41, and Pct(r2) is between Tnfr-1 and Pkcz. Each locus acting alone distinctly conferred a partial resistant phenotype. Pct(r1) and Pct(r2) did not appear to prevent the formation of clonal foci but did appear to limit the ability of the plasma cells in foci to acquire greater autonomy; thus, these genes affect tumor progression. C1 HAZELTON LABS,ROCKVILLE,MD 20850. NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. RP POTTER, M (reprint author), NCI,GENET LAB,BLDG 37,ROOM 2B04,BETHESDA,MD 20892, USA. NR 29 TC 70 Z9 70 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1994 VL 54 IS 4 BP 969 EP 975 PG 7 WC Oncology SC Oncology GA MW686 UT WOS:A1994MW68600022 PM 8313388 ER PT J AU PHILLIPS, PC LEVOW, C CATTERALL, M COLVIN, OM PASTAN, I BREM, H AF PHILLIPS, PC LEVOW, C CATTERALL, M COLVIN, OM PASTAN, I BREM, H TI TRANSFORMING GROWTH-FACTOR-ALPHA - PSEUDOMONAS EXOTOXIN FUSION PROTEIN (TGF-ALPHA-PE38) TREATMENT OF SUBCUTANEOUS AND INTRACRANIAL HUMAN GLIOMA AND MEDULLOBLASTOMA XENOGRAFTS IN ATHYMIC MICE SO CANCER RESEARCH LA English DT Article ID CENTRAL-NERVOUS-SYSTEM; FACTOR RECEPTOR EXPRESSION; MONOCLONAL-ANTIBODY; BRAIN-TUMORS; NUDE-MICE; INTRATHECAL 4-HYDROPEROXYCYCLOPHOSPHAMIDE; NEOPLASTIC MENINGITIS; CHEMOTHERAPY; AMPLIFICATION; SURVIVAL AB Epidermal growth factor receptor (EGFR) is amplified or overexpressed in many malignant gliomas and other primary brain tumors but is low or undetectable in normal brain. In the present study, this differential expression has been exploited for targeted brain tumor therapy using a TGF-alpha-Pseudomonas exotoxin recombinant toxin, TGF-alpha-PE38. In vitro experiments demonstrate that the cytotoxicity of this fusion protein is primarily determined by tumor EGFR expression and that TGF-alpha-PE38 cytotoxicity is abolished by pretreatment with excess epidermal growth factor. Treatment with i.p. TGF-alpha-PE38 in nude mice bearing glioblastoma or medulloblastoma s.c. xenografts produced tumor regres sion and growth delay. For intracranial xenograft implants treated with i.p. TGF-alpha-PE38, significant increases in median survival were noted only for tumors with the highest EGFR expression. However, intracranial tumors treated with a single intratumoral injection of TGF-alpha-PE38 showed increased survival in all xenografts tested. These results indicate that TGF-alpha-PE38 is active against primary human brain tumors ranging from moderate to high EGFR expression. For intracranial tumors, however, the higher survival rates produced by intracranial injection of TGF-alpha-PE38 than by continuous i.p. administration suggest that increased drug clearance or impaired drug delivery reduces the efficacy of systemic TGF-alpha PE38. Direct delivery of TGF-alpha-PE38 into brain tumors by controlled-release biodegradable polymers or intratumoral implanted catheters, or intrathecal administration into the colony stimulating factor of patients with leptomeningeal metastasis, may represent clinically useful applications of recombinant toxin therapy in tumors with high EGFR expression. C1 CHILDRENS HOSP PHILADELPHIA,DIV ONCOL,PHILADELPHIA,PA 19104. JOHNS HOPKINS UNIV,SCH MED,DEPT ONCOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSURG,BALTIMORE,MD 21205. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RP PHILLIPS, PC (reprint author), CHILDRENS HOSP PHILADELPHIA,DIV NEUROL,34TH & CIV CTR BLVD,PHILADELPHIA,PA 19104, USA. FU NCI NIH HHS [CA 52857]; NINDS NIH HHS [NS01279, NS31102] NR 48 TC 70 Z9 74 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1994 VL 54 IS 4 BP 1008 EP 1015 PG 8 WC Oncology SC Oncology GA MW686 UT WOS:A1994MW68600029 PM 8313355 ER PT J AU COHEN, PA COHEN, PJ ROSENBERG, SA MULE, JJ AF COHEN, PA COHEN, PJ ROSENBERG, SA MULE, JJ TI CD4(+) T-CELLS FROM MICE IMMUNIZED TO SYNGENEIC SARCOMAS RECOGNIZE DISTINCT, NON-SHARED TUMOR-ANTIGENS SO CANCER RESEARCH LA English DT Article ID IMMUNOLOGICAL SPECIFICITY; DENDRITIC CELLS; BEARING MICE; MURINE TUMOR; INVITRO; IMMUNOTHERAPY; INTERLEUKIN-2; CULTURE; CLONES AB We have utilized a newly developed culture system to study the properties of antitumor CD4(+) T-cells relevant to the rejection of syngeneic methylcholanthrene sarcomas. Fresh syngeneic dendritic cells prepared from spleen, then pulsed with crude lysates of methylcholanthrene sarcomas, evoke antigen-specific proliferation by CD4(+) but not by CD8(+) T-cells from tumor-immune mice. Unfractionated splenocytes display similar antigen presenting capacity if they are not irradiated before the pulse with tumor lysate. CD4(+) T-cells from mice immunized to individual methylcholanthrene sarcomas proliferate cross-reactively to dendritic cells pulsed with fresh tumor digests, but not to dendritic cells pulsed with cultured tumor cells. This apparent shared recognition of sarcoma lysates was demonstrated to be a result of sensitization to bacterial collagenase during the immunization procedure. Therefore, the murine CD4(+) T-cell response to tumor immunization is similar to the CD8(+) response in that sensitization occurs predominantly to tumor specific transplantation antigens rather than to shared tumor antigens. Strategies to avoid artefactual tumor cross-recognition by CD4(+) T-cells are discussed. C1 NCI,SURG BRANCH,BETHESDA,MD 20814. NCI,DERMATOL BRANCH,BETHESDA,MD 20814. SYSTEMICS,PALO ALTO,CA 94304. NR 19 TC 36 Z9 38 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1994 VL 54 IS 4 BP 1055 EP 1058 PG 4 WC Oncology SC Oncology GA MW686 UT WOS:A1994MW68600036 PM 7906197 ER PT J AU SAITO, T KREITMAN, RJ HANADA, S MAKINO, T UTSUNOMIYA, A SUMIZAWA, T ARIMA, T CHANG, CN HUDSON, D PASTAN, I AKIYAMA, S AF SAITO, T KREITMAN, RJ HANADA, S MAKINO, T UTSUNOMIYA, A SUMIZAWA, T ARIMA, T CHANG, CN HUDSON, D PASTAN, I AKIYAMA, S TI CYTOTOXICITY OF RECOMBINANT FAB AND FV IMMUNOTOXINS ON ADULT T-CELL LEUKEMIA LYMPH-NODE AND BLOOD-CELLS IN THE PRESENCE OF SOLUBLE INTERLEUKIN-2 RECEPTOR SO CANCER RESEARCH LA English DT Article ID PSEUDOMONAS EXOTOXIN; PROGNOSTIC FACTORS; VARIABLE DOMAINS; MALIGNANT-CELLS; SERA; FEATURES; ANTIBODY; DISEASE; JAPAN AB Single-chain immunotoxins anti-Tac(Fv)-PE40 and anti-Tac(Fv)-PE40KDEL, composed of variable domains of the anti-Tac monoclonal antibody and truncated forms of Pseudomonas exotoxin, have shown potent cytotoxic activity against malignant peripheral blood mononuclear cells (PBMCs) from adult T-cell leukemia (ATL) patients originating from the Caribbean. However, several clinically important issues have not previously been addressed. These include the potential of soluble interleukin 2 receptor in ATL patients to block immunotoxin effectiveness, the relative sensitivity of malignant lymph node cells (LNCs) versus PBMCs, the effect of an immunotoxin with a prolonged half-life, and finally whether ATL cells from patients in Japan have toxin sensitivity equal to those of the Caribbean patients. To resolve these questions, we studied 32 malignant PBMC and LNC samples from 30 ATL patients from Japan. PBMC's from 27 of 27 patients were very sensitive with 50% inhibition of protein synthesis achieved with 0.02-0.85 ng/ml (0.3-13 pM) of anti-Tac(Fv)PE40KDEL or anti-Tac(Fv)-PE40, LNCs had sensitivity very similar to that of PBMCs in the five patients tested. The fully recombinant immunotoxin, anti-Tac(Fab)-PE40, which has 8-10 times the t(1/2) alpha and beta compared to the Fv-immunotoxins, was also very cytotoxic toward cells from 27 of 27 patients tested with 50% inhibition of protein synthesis of 0.08-25 ng/ml. It was found that purified soluble interleukin 2 receptor added to the cytotoxicity assay decreased the cytotoxic activity of anti-Tac(Fv)PE40KDEL or anti-Tac(Fab)-PE40, but that 1 x 10(4) units/ml or less had minimal competitive effects. It was found that ATL patients who have responded even incompletely to conventional chemotherapy have soluble interleukin 2 receptor levels lower than this at posttreatment. We conclude that recombinant immunotoxins containing anti-Tac(Fv) are effective against Japanese ATL PBMCs or LNCs and might be most effective if used in vivo after conventional chemotherapy. If it is found in humans that the effectiveness of single-chain recombinant toxins is limited by short half-life, anti-Tac(Fab)-PE40 should be considered as an alternative agent. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. KAGOSHIMA UNIV,FAC MED,DEPT INTERNAL MED 2,KAGOSHIMA 890,JAPAN. KAGOSHIMA UNIV,FAC MED,INST CANC RES,KAGOSHIMA 890,JAPAN. PROT DESIGN LABS INC,MT VIEW,CA 94043. NR 30 TC 16 Z9 16 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1994 VL 54 IS 4 BP 1059 EP 1064 PG 6 WC Oncology SC Oncology GA MW686 UT WOS:A1994MW68600037 PM 8313362 ER PT J AU CZERWINSKI, M MCLEMORE, TL GELBOIN, HV GONZALEZ, FJ AF CZERWINSKI, M MCLEMORE, TL GELBOIN, HV GONZALEZ, FJ TI QUANTIFICATION OF CYP2B7, CYP4B1, AND CYPOR MESSENGER-RNAS IN NORMAL HUMAN LUNG AND LUNG-TUMORS SO CANCER RESEARCH LA English DT Article ID CDNA-DIRECTED EXPRESSION; MICROSOMAL CYTOCHROME-P-450; GENE-EXPRESSION; IDENTIFICATION; OXIDATION; CANCER; MECHANISMS; CARCINOMAS; CHEMICALS; SEQUENCE AB Cytochrome P450 (CYP) enzymes expressed in human lung can metabolize a variety of xenobiotics, drugs, and endogenous compounds. Metabolism of these substrates may lead to their detoxification or activation and may affect the homeostasis of the lung, its susceptibility to disease, response to therapy, and clinical prognosis. We analyzed the expression of CYP2B7, CYP4B1, and NADPH-cytochrome P450 oxidoreductase (OR) mRNAs in normal lung controls, normal lung from Lung cancer patients, and lung tumors using the sensitive technique of RNase protection. The mRNAs of CYP2B7, CYP4B1, and OR were detected in all the normal and a majority of neoplastic tissues. The three mRNAs were quantified and found at an average ratio of 0.89, 4.03, and 0.88% relative to actin mRNA in normal lung, respectively. There was no correlation between the levels of expression of the three mRNAs and the histological diagnosis of tumors. The amounts of each of the three mRNAs varied considerably between patients, but analysis of frequency distribution of the levels of CYP2B7 and CYP4B1 mRNAs did not present evidence for genetic polymorphism as a possible source of the observed interindividual variability. Levels of expression of the two P450 mRNAs were reduced (2.3- and 2.4-fold) in the neoplasms compared to normal lung. The level of OR mRNA expression was uniform with no significant differences between normal and neoplastic tissues, and its interindividual variability was the lowest amongst the three mRNAs studied. All mRNAs had increased interindividual variability in neoplastic tissues. Analysis of the patients' smoking histories and the level of CYP2B7, CYP4B1, and OR mRNAs revealed no evidence for their induction by compounds present in cigarette smoke. This study identities and characterizes lung and lung tumor mRNAs encoding enzymes that may participate in the metabolism of xenobiotics in humans. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. ST JOSEPHS HOSP,DIV PULM,PARIS,TX 75460. NR 28 TC 77 Z9 80 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1994 VL 54 IS 4 BP 1085 EP 1091 PG 7 WC Oncology SC Oncology GA MW686 UT WOS:A1994MW68600041 PM 8313365 ER PT J AU LEVYTOLEDANO, R CARO, LHP ACCILI, D TAYLOR, SI AF LEVYTOLEDANO, R CARO, LHP ACCILI, D TAYLOR, SI TI INVESTIGATION OF THE MECHANISM OF THE DOMINANT-NEGATIVE EFFECT OF MUTATIONS IN THE TYROSINE KINASE DOMAIN OF THE INSULIN-RECEPTOR SO EMBO JOURNAL LA English DT Article DE GROWTH FACTOR RECEPTORS; HYBRID RECEPTORS; INSULIN RECEPTOR SUBSTRATE-I; RECEPTOR ENDOCYTOSIS ID GROWTH-FACTOR RECEPTOR; COOH-TERMINAL TRUNCATION; EXTRACELLULAR DOMAIN; IMPAIRS TRANSPORT; ALPHA-SUBUNIT; BETA-SUBUNIT; CELL-SURFACE; AUTOPHOSPHORYLATION; BINDING; GENE AB Mutations in the tyrosine kinase domain of the insulin receptor cause insulin resistance in a dominant fashion. It has been proposed that formation of hybrid dimers between normal and mutant receptors may explain the dominant negative effect of these mutations. To investigate this mechanism, we expressed two types of human insulin receptors in NIH-3T3 cells; wild type and the tyrosine kinase-deficient Ile(1153) mutant. To distinguish the two types of receptors, 43 amino acids were deleted from the C-terminus of the wild type receptor (Delta 43 truncation). If mutant and wild type receptors assemble in a random fashion, 50% of the receptors would be hybrid oligomers (alpha(2) beta beta(mut)). However, alpha(2) beta beta(mut) hybrids were undetectable. Nevertheless, insulin stimulated the kinase competent Delta 43 receptors to transphosphorylate the kinase-deficient Ile(1153) mutant receptor in co-transfected cells via an intermolecular mechanism. Furthermore, transphosphorylation of the Ile(1153) mutant receptor is sufficient to trigger insulin-stimulated endocytosis. Despite the absence of alpha(2) beta beta(mut) hybrids, expression of the Ile(1153) mutant receptor inhibited the ability of the Delta 43 truncated receptor to mediate insulin-stimulated phosphorylation of insulin receptor substrate-1 (IRS-1). Evidence is presented to support the hypothesis that the Ile(1153) mutant receptor retains the ability to bind IRS-1, and that sequestration of substrate may explain the dominant negative effect of the mutant receptor to inhibit phosphorylation of IRS-1. C1 NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. NR 37 TC 36 Z9 36 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 1994 VL 13 IS 4 BP 835 EP 842 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MX771 UT WOS:A1994MX77100012 PM 8112298 ER PT J AU FRANTZ, B NORDBY, EC BREN, G STEFFAN, N PAYA, CV KINCAID, RL TOCCI, MJ OKEEFE, SJ ONEILL, EA AF FRANTZ, B NORDBY, EC BREN, G STEFFAN, N PAYA, CV KINCAID, RL TOCCI, MJ OKEEFE, SJ ONEILL, EA TI CALCINEURIN ACTS IN SYNERGY WITH PMA TO INACTIVATE I-KAPPA-B/MAD3, AN INHIBITOR OF NF-KAPPA-B SO EMBO JOURNAL LA English DT Article DE CALCINEURIN; CYCLOSPORINE A; INTERLEUKIN-2; TACROLIMUS; TRANSCRIPTION ID T-CELL ACTIVATION; DNA-BINDING ACTIVITY; CYCLOSPORINE-A; GENE-EXPRESSION; TRANSCRIPTION FACTOR; INTERLEUKIN-2 PROMOTER; LYMPHOCYTES-T; PHOSPHATASE-ACTIVITY; GEL-ELECTROPHORESIS; NUCLEAR PROTEINS AB The interleukin-2 (IL-2) promoter consists of several independent T cell receptor (TcR) responsive elements. The induction of promoters dependent on these elements is inhibitable by the immunosuppressants cyclosporin A (CsA) and tacrolimus (FK-506). Calcineurin, a Ca2+/calmodulin-dependent protein phosphatase, is the FK-506- and CsA-sensitive enzyme required for TcR mediated activation of the IL-2 promoter. We report that a constitutively active form of calcineurin partially substitutes for the Ca2+ co-stimulus required to activate the IL-2 promoter elements IL-2A (which binds the factors OAP and Oct-1) and IL-2E (which binds NF-AT), and completely substitutes for the Ca2+ co-stimulus required to stimulate an NF-kappa B-dependent element. Calcineurin stimulates the NF-kappa B element by enhancing inactivation of I kappa B/MAD3, an inhibitor of NF-kappa B, thereby increasing the amount of nuclear NF-kappa B DNA binding activity. These data provide the first demonstration in vivo that activation of a protein phosphatase can inactivate I kappa B, and suggest one possible explanation for mechanism-based toxicities associated with FK-506 and CsA by demonstrating that these drugs can inhibit the calcineurin-dependent activation of a virtually ubiquitous transcription factor. C1 MERCK & CO INC,MERCK SHARP & DOHME RES LABS,DEPT MOLEC IMMUNOL,RAHWAY,NJ 07065. MAYO CLIN & MAYO FDN,DEPT IMMUNOL,ROCHESTER,MN 55905. NIAAA,MOLEC & CELLULAR NEUROBIOL LAB,IMMUNOL SECT,ROCKVILLE,MD 20852. NR 65 TC 289 Z9 291 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 1994 VL 13 IS 4 BP 861 EP 870 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MX771 UT WOS:A1994MX77100015 PM 8112299 ER PT J AU BONNEROT, C MARKS, MS COSSON, P ROBERTSON, EJ BIKOFF, EK GERMAIN, RN BONIFACINO, JS AF BONNEROT, C MARKS, MS COSSON, P ROBERTSON, EJ BIKOFF, EK GERMAIN, RN BONIFACINO, JS TI ASSOCIATION WITH BIP AND AGGREGATION OF CLASS-II MCH MOLECULES SYNTHESIZED IN THE ABSENCE OF INVARIANT CHAIN SO EMBO JOURNAL LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; MHC CLASS-II; ROUGH ENDOPLASMIC-RETICULUM; ANTIGEN RECEPTOR CHAINS; CELL-SURFACE EXPRESSION; BINDING-PROTEIN BIP; VIRUS G-PROTEIN; HLA-DR; INTRACELLULAR-TRANSPORT; T-CELL AB Class II molecules of the major histocompatibility complex (MHC) are composed of two polymorphic glycoprotein chains (alpha and beta), that associate in the ER with a third, non-polymorphic glycoprotein known as the invariant chain (Ii). We have examined the relationship between the intracellular transport and physico-chemical characteristics of various combinations of murine alpha, beta and Ii chains. Biochemical and morphological analyses of transfected fibroblasts expressing class II MHC chains show that both unassembled alpha and beta chains, as well as a large fraction of alpha + beta complexes synthesized in the absence of Ii chain, are retained in the ER in association with the immunoglobulin heavy chain binding protein, BiP. Analyses by sedimentation velocity on sucrose gradients show that most incompletely assembled class II MHC species exist as high molecular weight aggregates in both transfected fibroblasts and spleen cells from mice carrying a disruption of the Ii chain gene. This is in contrast to the sedimentation properties of alpha beta Ii complexes from normal mice, which migrate as discrete, stoichiometric complexes of M(r) similar to 200 000-300 000. These observations suggest that assembly with the Ii chain prevents accumulation of aggregated alpha and beta chains in the ER, which might relate to the known ability of the Ii chain to promote exit of class II MHC molecules from the ER. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. HARVARD UNIV,DEPT CELLULAR & DEV BIOL,CAMBRIDGE,MA 02138. NR 83 TC 100 Z9 103 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 1994 VL 13 IS 4 BP 934 EP 944 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MX771 UT WOS:A1994MX77100024 PM 8112308 ER PT J AU LUETTEKE, NC PHILLIPS, HK QIU, TH COPELAND, NG EARP, HS JENKINS, NA LEE, DC AF LUETTEKE, NC PHILLIPS, HK QIU, TH COPELAND, NG EARP, HS JENKINS, NA LEE, DC TI THE MOUSE WAVED-2 PHENOTYPE RESULTS FROM A POINT MUTATION IN THE EGF RECEPTOR TYROSINE KINASE SO GENES & DEVELOPMENT LA English DT Article DE EGF RECEPTOR; MUTATION; TYROSINE KINASE; IN SITU; HAIR FOLLICLE ID EPIDERMAL GROWTH-FACTOR; SIGNAL TRANSDUCTION; PROTEIN-KINASE; MESSENGER-RNA; BINDING-SITE; FACTOR-ALPHA; RAT-LIVER; TGF-ALPHA; PHOSPHORYLATION; DOMAINS AB Mice harboring the waved-1 (wa-1) and waved-2 (wa-2) mutations exhibit skin and eye abnormalities that are strikingly similar to those of TGF-alpha-deficient mice, and wa-1 and TGF-alpha were recently shown to be allelic. Because the wa-2 mutation was mapped previously to the vicinity of the EGF/TGF-alpha receptor (EGFR) gene on mouse chromosome 11, we hypothesized that the wa-2 phenotype might result from a defect in either the expression or activity of EGER, or both. In the present report, we show that EGFR mRNA and protein of normal size are expressed in wa-2 liver and skin at levels that are comparable to those in the corresponding normal tissues, and that the ability of wa-2 EGFR to bind ligand is unaltered. However, ligand-dependent autophosphorylation of wa-2 EGFR is diminished 5- to 10-fold in vitro, and the ability of wa-2 EGFR to phosphorylate an exogenous substrate is reduced by >90% compared with that of the control receptor. EGF-induced tyrosine phosphorylation, including that of EGFR itself, is also diminished in skin, particularly at lower doses of exogenous EGF. To establish the nature of the wa-2 mutation, we determined the nucleotide sequence of the coding region of normal and wa-2 murine EGFR cDNAs. A comparison of these sequences revealed a single-nucleotide transversion resulting in the substitution of a glycine for a conserved valine residue near the amino terminus of the tyrosine kinase domain. The importance of this mutation was confirmed by showing that its introduction into an otherwise normal EGFR markedly reduced the receptor's tyrosine kinase activity in transfected Chinese hamster ovary cells. Finally, in situ hybridization analysis demonstrated expression of EGFR predominantly in the outer root sheath of active hair follicles in neonatal mice. As we previously localized TGF-cw mRNA to the inner root sheath, this pattern of EGFR expression is consistent with the effect of the wa-2 mutation on hair structure, and together with our previous characterization of TGF-alpha-deficient mice, reveals a critical role for signaling by this ligand/receptor system in skin. C1 UNIV N CAROLINA,SCH MED,DEPT PHARMACOL,CHAPEL HILL,NC 27599. UNIV N CAROLINA,SCH MED,DEPT MICROBIOL & IMMUNOL,CHAPEL HILL,NC 27599. FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21701. RP LUETTEKE, NC (reprint author), UNIV N CAROLINA,SCH MED,LINEBERGER COMPREHENS CANC CTR,CHAPEL HILL,NC 27599, USA. FU NCI NIH HHS [N01-CO-74101, CA-43793]; NIDDK NIH HHS [DK-30002] NR 82 TC 330 Z9 344 U1 1 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD FEB 15 PY 1994 VL 8 IS 4 BP 399 EP 413 DI 10.1101/gad.8.4.399 PG 15 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA MZ288 UT WOS:A1994MZ28800002 PM 8125255 ER PT J AU DUNCAN, R BAZAR, L MICHELOTTI, G TOMONAGA, T KRUTZSCH, H AVIGAN, M LEVENS, D AF DUNCAN, R BAZAR, L MICHELOTTI, G TOMONAGA, T KRUTZSCH, H AVIGAN, M LEVENS, D TI SEQUENCE-SPECIFIC, SINGLE-STRAND BINDING-PROTEIN ACTIVATES THE FAR UPSTREAM ELEMENT OF C-MYC AND DEFINES A NEW DNA-BINDING MOTIF SO GENES & DEVELOPMENT LA English DT Article DE CDNA CLONE; MYC EXPRESSION; DNA-BINDING PROTEIN; DIFFERENTIATION; POTASSIUM PERMANGANATE (KMNO4) ID CHROMATIN STRUCTURE; TRANSCRIPTIONAL ENHANCER; CELLULAR ONCOGENES; ESCHERICHIA-COLI; MESSENGER-RNAS; HL60 CELLS; GENE; EXPRESSION; DIFFERENTIATION; REPLICATION AB The far upstream element (FUSE) of the human c-myc proto-oncogene stimulates expression in undifferentiated cells. A FUSE-binding protein (FBP) is present in undifferentiated but not differentiated cells. Peptide sequences from the purified protein allowed cloning of cDNAs encoding FBP. Expression of FBP mRNA declined upon differentiation, suggesting transcriptional regulation of FBP. Features in the FBP cDNA suggest that FBP is also regulated by RNA processing, translation, and post-translational mechanisms. Both cellular and recombinant FBP form sequence-specific complexes with a single strand of FUSE. Transfection of FBP into human leukemia cells stimulated c-myc-promoter-driven expression from a reporter plasmid in a FUSE-dependent manner. Deletion and insertion mutagenesis of FBP defined a novel single-strand DNA-binding domain. Analysis of the primary and predicted secondary structure of the amino acid sequence reveals four copies of a reiterated unit comprised of a 30-residue direct repeat and an amphipathic alpha-helix separated by an 18- to 21-residue spacer. The third and fourth copies of this repeat-helix unit constitute the minimum single-stranded DNA-binding domain. To determine whether the FUSE site, in vivo, posesses single-strand conformation, and therefore could be bound by FBP, cells were treated with potassium permanganate (KMnO4) to modify unpaired bases. Modification of genomic DNA in vivo revealed hyperreactivity associated with single-stranded DNA in the FUSE sequence and protection on the strand that binds FBP in vitro. The role of single-stranded DNA and single-strand binding proteins in c-myc regulation is discussed. C1 GEORGETOWN UNIV,DEPT PATHOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,DEPT MED,WASHINGTON,DC 20007. RP DUNCAN, R (reprint author), NCI,PATHOL LAB,BETHESDA,MD 20892, USA. RI Levens, David/C-9216-2009; Duncan, Robert/I-8168-2015 OI Levens, David/0000-0002-7616-922X; Duncan, Robert/0000-0001-8409-2501 FU NCI NIH HHS [CA54818] NR 70 TC 252 Z9 255 U1 1 U2 4 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD FEB 15 PY 1994 VL 8 IS 4 BP 465 EP 480 DI 10.1101/gad.8.4.465 PG 16 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA MZ288 UT WOS:A1994MZ28800007 PM 8125259 ER PT J AU HOYHTYA, M FRIDMAN, R KOMAREK, D PORTERJORDAN, K STETLERSTEVENSON, WG LIOTTA, LA LIANG, CM AF HOYHTYA, M FRIDMAN, R KOMAREK, D PORTERJORDAN, K STETLERSTEVENSON, WG LIOTTA, LA LIANG, CM TI IMMUNOHISTOCHEMICAL LOCALIZATION OF MATRIX METALLOPROTEINASE 2 AND ITS SPECIFIC INHIBITOR TIMP-2 IN NEOPLASTIC TISSUES WITH MONOCLONAL-ANTIBODIES SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID IV COLLAGENASE; EXPRESSION; CELLS; CARCINOMA; IDENTIFICATION; ACTIVATION; MEMBRANES; RECEPTOR; ANTIGEN; CANCER AB Matrix metalloproteinase-2 (MMP-2), synthesized as a 631 amino-acid proenzyme, is activated by cleavage of the first 80 amino acids and naturally inhibited by tissue inhibitor of metalloproteinase-2 (TIMP-2). We report here the production of MAbs against MMP-2 and TIMP-2 and their use in localizing the respective antigens on tumor tissues. The anti-MMP-2 MAb recognized the latent and activated MMP-2 mutant protein (mutein) with C-terminal deletion at amino acid 425, indicating that both N- and C-terminal amino acids of MMP-2 are not important for its binding. The binding study of anti-TIMP-2 MAb, using several C-terminally truncated TIMP-2 muteins, showed that the amino acids I I 1- 126 of TIMP-2 are essential for the binding of this antibody, Besides their respective antigens, both MAbs also recognized the MMP-2/TIMP-2 complex. On frozen sections of breast tumor, anti-MMP-2 MAb stained mainly tumor-cell cytoplasm with varying intensity, while anti-TIMP-2 MAb gave a stromal staining of varying intensity and a weak or absent staining of tumor-cell cytoplasm, suggesting different localization of the proteins in these tumors. In addition, in 1/3 of the breast cases both antibodies also localized on tumor-cell membranes. Similar cytoplasmic and stromal but not membrane staining patterns were observed in colon, gastric, endometrial, squamous-cell, prostatic and ovarian carcinoma as well. Since MMP-2 degrades type-IV collagen, the major component of basement membranes, the differences between MMP-2 and TIMP-2 levels and localization in individual tumors may relate to the invasiveness of the tumor and thus provide predictive information. However, this aspect could not be discussed in this study because no biological and clinical parameters such as lymph-node involvement or Dukes' stage of the tumors were available. (C) Wiley-Liss, Inc. C1 ONCOLOGIX INC,GAITHERSBURG,MD 20878. NCI,PATHOL LAB,BETHESDA,MD 20892. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NCI NIH HHS [IR43 CA55440-01A1] NR 21 TC 132 Z9 135 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 15 PY 1994 VL 56 IS 4 BP 500 EP 505 DI 10.1002/ijc.2910560408 PG 6 WC Oncology SC Oncology GA MW893 UT WOS:A1994MW89300007 PM 8112886 ER PT J AU ZHOU, HX AF ZHOU, HX TI MACROMOLECULAR ELECTROSTATIC ENERGY WITHIN THE NONLINEAR POISSON-BOLTZMANN EQUATION SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID RELAXATION AB A fundamental problem in macromolecular electrostatics is the calculation of the electrostatic energy of a macromolecule solvated in an electrolyte solvated in an electrolyte solution, i.e., the work required to charge up the macromolecule in the presence of the electrolytic ions. Through numerical calculations with the nonlinear Poisson-Boltzmann (PB) equation, Sharp and and Honig [J. Phys. Chem. 94, 7684 (1990)] observed that this energy can be obtained with equal accuracy from the charging integral and from their energy-density integral. Here we give an elementary analytical proof of the exact equivalence of the two different formulations of the energy. In order to calculate the macromolecular electrostatic energy, a boundary element method [Biophys. J. 65, 954 (1993)] previously developed for the linearized PB equation is modified to solve the nonlinear PB equation. Illustrative calculations show that for globular proteins under physiological ionic strengths, the electrostatic energy calculated from the linearized PB equation differs very little from that calculated from the nonlinear equation. RP ZHOU, HX (reprint author), NIDDKD,BETHESDA,MD 20892, USA. RI Zhou, Huan-Xiang/M-5170-2016 OI Zhou, Huan-Xiang/0000-0001-9020-0302 NR 36 TC 69 Z9 69 U1 0 U2 0 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0021-9606 J9 J CHEM PHYS JI J. Chem. Phys. PD FEB 15 PY 1994 VL 100 IS 4 BP 3152 EP 3162 DI 10.1063/1.466406 PG 11 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA MX628 UT WOS:A1994MX62800078 ER PT J AU BONOMO, A KEHN, PJ SHEVACH, EM AF BONOMO, A KEHN, PJ SHEVACH, EM TI PREMATURE ESCAPE OF DOUBLE-POSITIVE THYMOCYTES TO THE PERIPHERY OF YOUNG MICE - POSSIBLE ROLE IN AUTOIMMUNITY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL TOLERANCE; NEONATAL THYMECTOMY; ADOPTIVE TRANSFER; OOPHORITIS; REQUIREMENT; DISEASES; ANTIGEN; THYMUS; ELIMINATION; ACTIVATION AB Thymectomy of 3-day-old mice induces organ-specific autoimmune disease. To define a relationship between the development of T cells early in the neonatal period and autoimmunity, we studied the thymus and peripheral lymphoid tissues of 3-day-old mice. Lymph nodes, but not spleens, of 3- to 4-day-old mice contained a significant number of thymus-derived CD4(+)CD8(+) cells that are phenotypically similar to CD4(+)CD8(+) thymocytes in their level of expression of CD3 and HSA. it is likely that the prematurely exported cells are the progenitors of autoreactive T cells because the lymph nodes from 3- to 4-day-old male, but not female, mice which express a transgenic TCR specific for the H-Y Ag contained a large number of CD4(+)CD8(+)Tg(+) as well as CD4(-)CD8(+)Tg(+) T cells. Thus, the neonatal thymus is capable of exporting immature T cells that in the absence of a thymus may differentiate into autoimmune effector cells. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 33 TC 48 Z9 49 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 1994 VL 152 IS 4 BP 1509 EP 1514 PG 6 WC Immunology SC Immunology GA MY844 UT WOS:A1994MY84400001 PM 8120365 ER PT J AU GEORGE, AJT TITUS, JA JOST, CR KURUCZ, I PEREZ, P ANDREW, SM NICHOLLS, PJ HUSTON, JS SEGAL, DM AF GEORGE, AJT TITUS, JA JOST, CR KURUCZ, I PEREZ, P ANDREW, SM NICHOLLS, PJ HUSTON, JS SEGAL, DM TI REDIRECTION OF T-CELL-MEDIATED CYTOTOXICITY BY A RECOMBINANT SINGLE-CHAIN FV MOLECULE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID STAPHYLOCOCCAL PROTEIN-A; ESCHERICHIA-COLI; BISPECIFIC ANTIBODIES; MONOCLONAL-ANTIBODIES; FUSION PROTEINS; FAB-FRAGMENTS; TUMOR-CELLS; LYMPHOCYTES; RECEPTOR; TRANSFERRIN AB We have produced two single-chain Fv (sFv) proteins by bacterial periplasmic secretion, one sFv with specificity for the hapten DNP, and the other for the human transferrin receptor. After solubilization and refolding, we recovered several mg of active sFv per liter of bacterial culture. Each sFv bound to cells bearing the appropriate Ag and could be used to direct targeted cellular cytotoxicity. Targeting relied on a universal bispecific antibody designed to cross-link CD3 on the cytotoxic T cell with a peptide fused to the sFv carboxyl-terminus. The universal bispecific antibody was used in combination with the Ag-specific sFv to redirect human cytotoxic T cells to kill a variety of target cells. Such an approach has a number of advantages that may make it useful for the immunotherapy of cancer and other diseases. C1 NCI, EXPTL IMMUNOL BRANCH, BETHESDA, MD 20892 USA. NINCDS, SURG NEUROL BRANCH, BETHESDA, MD 20892 USA. CREAT BIOMOLECULES INC, HOPKINTON, MA 01748 USA. RI Perez, Pilar/B-4948-2010; OI Perez, Pilar/0000-0003-3557-2247; George, Andrew/0000-0002-2866-0241 NR 55 TC 48 Z9 48 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 EI 1550-6606 J9 J IMMUNOL JI J. Immunol. PD FEB 15 PY 1994 VL 152 IS 4 BP 1802 EP 1811 PG 10 WC Immunology SC Immunology GA MY844 UT WOS:A1994MY84400033 PM 8120389 ER PT J AU GIESE, T DAVIDSON, WF AF GIESE, T DAVIDSON, WF TI CHRONIC TREATMENT OF C3H-LPR/LPR AND C3H-GLD/GLD MICE WITH ANTI-CD8 MONOCLONAL-ANTIBODY PREVENTS THE ACCUMULATION OF DOUBLE-NEGATIVE T-CELLS BUT NOT AUTOANTIBODY PRODUCTION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MRL-LPR/LPR MICE; LPR-LPR MICE; MUTANT-GENE LPR; MP-IPR IPR; AUTOIMMUNE-DISEASE; MRL/LPR MICE; GLD MUTATIONS; LYT-2+ CELLS; B-CELLS; ANTIGEN AB Mice homozygous for Ipr or gld develop autoimmunity and progressive lymphoproliferative disease characterized by the accumulation of an unusual population of functionally impaired B220(+), TCR-alpha/beta(+), CD4(-), CD8(-) double negative (DN) T cells. Although these cells are thymus derived and appear to have undergone thymic negative selection, the identity of their immediate precursors and the mechanisms leading to their accumulation are poorly understood. Here we investigated the role of CD8(+) T cells in the development of lymphoproliferative disease and autoantibody production. We showed that treatment of C3H-lpr or C3H-gld mice with anti-CD8 mAb beginning at 3 wk of age and continuing to 15 wk of age caused a dramatic reduction in lymphadenopathy. The change in lymph node size resulted predominantly from a very significant decrease in both the proportions and the total numbers of B220(+) DN T cells. The proportions of these cells were reduced up to 20-fold and the total numbers per LN up to 400-fold. Although chronic treatment with anti-CD8 mAb had the most profound effects on B220(+) DN T cells, it also decreased the numbers of CD4(+) T cells, CD4(+)B220(+) T cells, and B cells in Ipr and gld LN up to fivefold. In contrast to its impact on lymphoproliferative disease, anti-CD8 mAb therapy had no significant effect on B cell hyperactivity. Comparisons of serum Ig and autoantibody levels in CD8(+) T cell-depleted and control mAb-treated Ipr and gld mice revealed no changes in the elevated concentrations of serum IgM or total IgG and no significant reduction in the levels of circulating autoantibodies specific for thymocytes or dsDNA. The presence of active germinal centers and accumulations of plasma cells in the LN and spleen of anti-CD8 mAb-treated Ipr and gld mice provided further evidence for sustained B cell activation. These results suggest that in Ipr and gld mice, CD8(+) T cells play a crucial role in the accumulation of B220(+) DN T cells and also may contribute to the characteristic increase in the numbers of B cells and CD4(+) T cells in these mice, but have no significant effect on B cell hyperactivity or autoantibody production. C1 NCI,GENET LAB,BETHESDA,MD 20892. NR 58 TC 57 Z9 58 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 1994 VL 152 IS 4 BP 2000 EP 2010 PG 11 WC Immunology SC Immunology GA MY844 UT WOS:A1994MY84400055 PM 8120404 ER PT J AU RACKE, MK QUIGLEY, L CANNELLA, B RAINE, CS MCFARLIN, DE SCOTT, DE AF RACKE, MK QUIGLEY, L CANNELLA, B RAINE, CS MCFARLIN, DE SCOTT, DE TI SUPERANTIGEN MODULATION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS - ACTIVATION OR ANERGY DETERMINES OUTCOME SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MYELIN BASIC-PROTEIN; STAPHYLOCOCCAL ENTEROTOXIN-B; TUMOR-NECROSIS-FACTOR; T-CELL RECEPTORS; AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS; ADOPTIVE TRANSFER; MONOCLONAL-ANTIBODY; LYMPHOCYTE-T; MICE AB Experimental allergic encephalomyelitis (EAE) is an autoimmune disease that can be induced by the adoptive transfer of CD4, myelin basic protein (MBP)-specific T cells. Superantigens activate T cells expressing appropriate TCR V genes. In this study, MBP-specific T cells activated in vitro with a superantigen, staphylococcal enterotoxin B (SEB), could adoptively transfer a severe form of EAE in (PLxSJL)F1 mice, but did not transfer disease in PL/J or SJL/j mice. SEB treatment of donor mice anergized MBP-specific T cells using V beta 8 in (PLxSJL)F1 mice, because subsequent in vitro activation with SEB resulted in a marked decrease in proliferation to SEB and inability to transfer EAE. However, donor cells from (PLxSJL)F1 mice immunized with MBP/CFA that had been exposed to SEB in vivo before MBP stimulation in vitro still produced EAE in recipient mice. To confirm that non-V beta 8 T cells could transfer disease, donor mice were treated with antibody that eliminated V beta 8 T cells; MBP-activated T cells from these mice could still transfer EAE. Finally, EAE induced by SEB-activated T cells was substantially reduced in mice receiving anti-V beta 8 therapy in vivo. The ability of superantigens to activate encephalitogenic T cells may have relevance to human diseases such as multiple sclerosis. C1 ALBERT EINSTEIN COLL MED,DEPT PATHOL NEUROPATHOL,BRONX,NY 10461. NIAMSD,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD 20892. RP RACKE, MK (reprint author), NINCDS,NEUROIMMUNOL BRANCH,BLDG 10,ROOM 5B-16,BETHESDA,MD 20892, USA. FU NINDS NIH HHS [NS 08952, NS 11920] NR 38 TC 34 Z9 35 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 1994 VL 152 IS 4 BP 2051 EP 2059 PG 9 WC Immunology SC Immunology GA MY844 UT WOS:A1994MY84400060 PM 8120406 ER PT J AU GUTMANN, DH COLE, JL COLLINS, FS AF GUTMANN, DH COLE, JL COLLINS, FS TI MODULATION OF NEUROFIBROMATOSIS TYPE-1 GENE-EXPRESSION DURING IN-VITRO MYOBLAST DIFFERENTIATION SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Note DE NEUROFIBROMIN; MUSCLE; TUMOR SUPPRESSOR GENE; RAS ONCOGENE ID N-RAS; SACCHAROMYCES-CEREVISIAE; PROTEIN PRODUCT; IDENTIFICATION; ONCOGENES; SEQUENCE; DOMAIN; LOCUS; CELLS; GAP AB Neurofibromin, the protein product of the neurofibromatosis type 1 (NF1) gene, has two alternate isoforms which are generated by alternative splicing of two exons. One of these isoforms containing exon 48a is expressed at highest levels in muscle. Since neurofibromin is a p21-ras regulator and has been recently shown to be modulated during Schwann cell differentiation, we examined the expression of the NF1 gene product during in vitro muscle differentiation. Previous work demonstrated that C2C12 murine myoblast cell differentiation could be blocked by the introduction of an activated p21-ras protein. Using this model system, we demonstrate that differentiating C2C12 cells upregulate the expression of NF1 mRNA by 2 days of serum starvation concomitant with increased expression of nicotinic acetylcholine receptor mRNA. This upregulation of mRNA expression paralleled an increase in neurofibromin and N-ras levels, but no change in the relative abundance of the isoforms containing exon 23a or exon 48a was observed during in vitro myoblast differentiation. The increase in neurofibromin levels paralleled a decrease in the levels of activated p21-ras as assayed by in vivo P-32-orthophosphate incorporation into p21-ras. These results suggest that in vitro C2C12 cell differentiation is associated with a concomitant increase in NF1 gene expression and decrease in the proportion of activated p21-ras. (C) 1994 Wiley-Liss, Inc. C1 UNIV MICHIGAN,SCH MED,DEPT NEUROL,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. FU NINDS NIH HHS [NS-01590] NR 28 TC 20 Z9 20 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 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD FEB 15 PY 1994 VL 37 IS 3 BP 398 EP 405 DI 10.1002/jnr.490370312 PG 8 WC Neurosciences SC Neurosciences & Neurology GA MV899 UT WOS:A1994MV89900011 PM 8176761 ER PT J AU DYBDAL, NO HARGREAVES, KM MADIGAN, JE GRIBBLE, DH KENNEDY, PC STABENFELDT, GH AF DYBDAL, NO HARGREAVES, KM MADIGAN, JE GRIBBLE, DH KENNEDY, PC STABENFELDT, GH TI DIAGNOSTIC TESTING FOR PITUITARY PARS-INTERMEDIA DYSFUNCTION IN HORSES SO JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION LA English DT Article DE EQUINE SPECIES; CORTISOL; PITUITARY FUNCTION TESTS; PITUITARY GLAND, INTERMEDIATE LOBE ID EQUINE CUSHINGS-DISEASE; ADRENAL-GLAND FUNCTION; PLASMA CONCENTRATIONS; PRO-OPIOMELANOCORTIN; HEALTHY HORSES; STIMULATION; CORTISOL; CORTICOSTEROIDS; INSULIN; ADENOMA AB Pituitary pars intermedia dysfunction is a slowly progressive disorder that afflicts most breeds of horses. Because it shares features with human Cushing disease, it has been referred to as equine Cushing disease. A variety of tests of pituitary-adrenocortical function were performed on horses with evidence of pituitary pars intermedia dysfunction, and results were compared with those in healthy control horses. Diurnal variations in plasma cortisol concentration were not statistically different between control horses and those with pituitary pars intermedia dysfunction. An ACTH stimulation (1 U of natural ACTH gel/kg of body weight, IM) test or a combined dexamethasone suppression test (10 mg, IM) and ACTH stimulation (100 mg of synthetic ACTH, IV) test also failed to distinguish horses with pituitary pars intermedia dysfunction from control horses. A significant (P < 0.001) dose-related suppression of cortisol concentration in response to increasing doses (5, 10, 20, and 40 mu g/kg) of dexamethasone was observed in control horses but not in those with pituitary pars intermedia dysfunction. On the basis of plasma cortisol concentration, the dexamethasone suppression test, using 40 mu g/kg, whether initiated at 5 PM With Sample collection at 15 (8 AM) and 19 (12 PM) hours after dexamethasone administration, reliably distinguished between control horses and those with pituitary pars intermedia dysfunction. Several horses did not have clinical evidence of pituitary pars intermedia dysfunction, but did have abnormal dexamethasone suppression test results. In these horses, adenomatous hypertrophy and hyperplasia of the pars intermedia of the pituitary gland was confirmed at necropsy. C1 UNIV CALIF DAVIS,SCH VET MED,DEPT MED,DAVIS,CA 95616. UNIV CALIF DAVIS,SCH VET MED,DEPT REPROD,DAVIS,CA 95616. NIDR,NAB,BETHESDA,MD 20892. UNIV CALIF DAVIS,SCH VET MED,DEPT PATHOL,DAVIS,CA 95616. RI Hargreaves, Kenneth/F-5308-2010 NR 28 TC 101 Z9 101 U1 5 U2 17 PU AMER VETERINARY MEDICAL ASSOC PI SCHAUMBURG PA 1931 N MEACHAM RD SUITE 100, SCHAUMBURG, IL 60173-4360 SN 0003-1488 J9 J AM VET MED ASSOC JI J. Am. Vet. Med. Assoc. PD FEB 15 PY 1994 VL 204 IS 4 BP 627 EP 632 PG 6 WC Veterinary Sciences SC Veterinary Sciences GA MX072 UT WOS:A1994MX07200023 PM 8163420 ER PT J AU KNUTTEL, A SCHMITT, JM KNUTSON, JR AF KNUTTEL, A SCHMITT, JM KNUTSON, JR TI LOW-COHERENCE REFLECTOMETRY FOR STATIONARY LATERAL AND DEPTH PROFILING WITH ACOUSTOOPTIC DEFLECTORS AND A CCD CAMERA SO OPTICS LETTERS LA English DT Article ID FOURIER-TRANSFORM SPECTROMETER; PHOTODIODE ARRAY AB We describe a new optical low-coherence reflectometer for depth and lateral scanning without moving parts. The reflectometer covers a range of 0.4 and 1 mm in the depth and lateral dimensions, respectively. This level was accomplished by an acousto-optic deflector for lateral scanning and temporal-coherence gating for depth resolution. The ac component of the reflected light was captured by a cooled 16-bit CCD camera with a special readout scheme. As a proof of principle, optical depths of a staggered stack of glass plates were measured. RP KNUTTEL, A (reprint author), NIH,BETHESDA,MD 20892, USA. NR 12 TC 22 Z9 22 U1 0 U2 2 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 SN 0146-9592 J9 OPT LETT JI Opt. Lett. PD FEB 15 PY 1994 VL 19 IS 4 BP 302 EP 304 DI 10.1364/OL.19.000302 PG 3 WC Optics SC Optics GA MY672 UT WOS:A1994MY67200022 PM 19829624 ER PT J AU BRAY, M PRASAD, S DUBAY, JW HUNTER, E JEANG, KT REKOSH, D HAMMARSKJOLD, ML AF BRAY, M PRASAD, S DUBAY, JW HUNTER, E JEANG, KT REKOSH, D HAMMARSKJOLD, ML TI A SMALL ELEMENT FROM THE MASON-PFIZER MONKEY VIRUS GENOME MAKES HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 EXPRESSION AND REPLICATION REV-INDEPENDENT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE RNA TRANSPORT; NUCLEAR EXPORT; RETROVIRAL GENE EXPRESSION; CIS-ACTING RNA ELEMENT ID LATE REPLACEMENT VECTOR; MESSENGER-RNA; HIV-1 REV; NUCLEOTIDE-SEQUENCE; GENE-PRODUCT; PROTEIN; RETROVIRUS; ENV; BINDING; INVITRO AB Replication of human immunodeficiency virus type 1 (HIV-1) is dependent on the viral Rev protein. This protein acts in concert with the cis-acting rev-responsive element present in intron-containing RNAs to facilitate nuclear export of these RNAs. Here we show that a cis-acting 219-nucleotide sequence from an unrelated ''simple'' retrovirus, Mason-Pfizer monkey virus (MPMV), enables Rev-independent HIV-1 replication. This sequence is present in an untranslated region near the 3' end of the MPMV genome. The MPMV element is also able to efficiently substitute for Rev in expression of Gag/Pol and Env proteins from subgenomic constructs. We hypothesize that the MPMV element functions by interacting with a cellular factor that plays a role in mRNA transport analogous to that of the Rev protein. It might be possible to exploit this element in the development of an HIV vaccine. C1 UNIV VIRGINIA, MYLES H THALER CTR AIDS & HUMAN RETROVIRUS RES, CHARLOTTESVILLE, VA 22908 USA. UNIV VIRGINIA, DEPT MICROBIOL, CHARLOTTESVILLE, VA 22908 USA. UNIV ALABAMA, DEPT MICROBIOL, BIRMINGHAM, AL 35294 USA. NIAID, MOLEC MICROBIOL LAB, BETHESDA, MD 20892 USA. SUNY BUFFALO, BUFFALO, NY USA. RI Jeang, Kuan-Teh/A-2424-2008 FU NIAID NIH HHS [AI27290, AI25721, AI25784] NR 32 TC 329 Z9 329 U1 1 U2 7 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 15 PY 1994 VL 91 IS 4 BP 1256 EP 1260 DI 10.1073/pnas.91.4.1256 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000014 PM 8108397 ER PT J AU FORCE, T BONVENTRE, JV HEIDECKER, G RAPP, U AVRUCH, J KYRIAKIS, JM AF FORCE, T BONVENTRE, JV HEIDECKER, G RAPP, U AVRUCH, J KYRIAKIS, JM TI ENZYMATIC CHARACTERISTICS OF THE C-RAF-1 PROTEIN-KINASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MAP KINASE; S6 KINASE; SIGNAL TRANSDUCTION; RAF-1 PROTOONCOGENE; C-JUN; PHOSPHORYLATION; ACTIVATION; PURIFICATION; RECEPTOR; INVITRO AB The c-Raf-1 protein kinase plays a central role in the mitogenic response of cells to growth factors, cytokines, and many oncogenes. Despite the critical importance of this enzyme, very little is known of its biochemical properties or mechanisms of regulation. In these experiments, we used the only candidate physiologic substrate identified as yet for c-Raf-1, mitogen-activated protein kinase kinase (MAPKK), to examine enzymatic characteristics and candidate modulators of c-Raf-1. c-Raf-1 was purified from Sf9 cells infected with recombinant baculovirus encoding a histidine-tagged c-Raf-1. The K-m values of c-Raf-1 for ATP and MAPKK were 11.6 mu M and 0.8 mu M, respectively, and the stoichiometry of phosphorylation of MAPKK by c-Raf-1 was 1.67 mol of phosphate per mol of MAPKK. In contrast to prior reports, Mg2+ was the preferred cation at Mg2+ and Mn2+ concentrations >5 mM. c-Raf-1 substrate specificity was extremely restricted, consistent with the identification of only one candidate physiologic substrate to date and highlighting the necessity of using MAPKK rather than artificial substrates in c-Raf-1 activity assays. Of multiple potential substrates tested, the only one phosphorylated to >20% of the level of MAPKK phosphorylation was myelin basic protein (22%). Heat-denatured MAPKK was phosphorylated at only 2% the level of native MAPKK, indicating that the restricted substrate specificity may be due to tertiary-structural requirements. We also examined whether c-Raf-1 activity is modulated by lipid binding to the cysteine finger region in its regulatory domain. Of multiple mitogen-stimulated or cell-membrane lipids tested, only phosphatidylserine and diacylglycerol in the presence of Ca2+ (2.5 mM) increased c-Raf-1 kinase activity significantly (1.5-fold). The increase is probably not of physiologic significance because it was about two orders of magnitude less than the stimulation of protein kinase C by these lipids. On gelfiltration chromatography, the peak of c-Raf-1 kinase activity and immunoreactivity eluted at a predicted molecular mass of >150 kDa, suggesting that active c-Raf-1 (but not inactive c-Raf-1) exists as a multimeric complex. This complex may not include p21(ras), however, because immunoreactive p21(ras) was not identified in the active fractions. C1 MASSACHUSETTS GEN HOSP,MED SERV,RENAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,DIABET UNIT,BOSTON,MA 02114. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. RP FORCE, T (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,CARDIAC UNIT,BULFINCH 457,BOSTON,MA 02114, USA. OI Force, Thomas/0000-0002-0450-8659 FU NIDDK NIH HHS [DK01986, DK39773] NR 41 TC 79 Z9 79 U1 0 U2 4 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 15 PY 1994 VL 91 IS 4 BP 1270 EP 1274 DI 10.1073/pnas.91.4.1270 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000017 PM 8108400 ER PT J AU CHOO, QL KUO, G RALSTON, R WEINER, A CHIEN, D VANNEST, G HAN, J BERGER, K THUDIUM, K KUO, C KANSOPON, J MCFARLAND, J TABRIZI, A CHING, K MOSS, B CUMMINS, LB HOUGHTON, M MUCHMORE, E AF CHOO, QL KUO, G RALSTON, R WEINER, A CHIEN, D VANNEST, G HAN, J BERGER, K THUDIUM, K KUO, C KANSOPON, J MCFARLAND, J TABRIZI, A CHING, K MOSS, B CUMMINS, LB HOUGHTON, M MUCHMORE, E TI VACCINATION OF CHIMPANZEES AGAINST INFECTION BY THE HEPATITIS-C VIRUS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE IMMUNIZATION ID NON-B-HEPATITIS; NON-A; HEPATOCELLULAR-CARCINOMA; CIRCULATING ANTIBODIES; BLOOD-DONORS; IMMUNITY; GENOME; RISK AB A high incidence of community-acquired hepatitis C virus infection that can lead to the progressive development of chronic active hepatitis, liver cirrhosis, and primary hepatocellular carcinoma occurs throughout the world. A vaccine to control the spread of this agent that represents a major cause of chronic liver disease is therefore needed, Seven chimpanzees (Pan troglodytes) have been immunized with both putative envelope glycoproteins [E1 (gp33) and E2 (gp72)] that were copurified from HeLa cells infected with a recombinant vaccinia virus expression vector. Despite the induction of a weak humoral immune response to these viral glycoproteins in experimentally infected chimpanzees, a strong humoral immune response was obtained in all vaccinees. The five highest responders showed complete protection against an i.v. challenge with homologous hepatitis C virus 1. The remaining two vaccinees became infected, but both infection and disease may have been ameliorated in comparison with four similarly challenged control chimpanzees, all of which developed acute hepatitis and chronic infections. These results provide considerable encouragement for the eventual control of hepatitis C virus infection by vaccination. C1 CHIRON CORP,EMERYVILLE,CA 94608. NYU MED CTR,EXPTL MED & SURG PRIMATES LAB,TUXEDO PK,NY 10987. WHITE SANDS RES CTR,ALAMOGORDO,NM 88310. NIAID,BETHESDA,MD 20892. RI Ralston, Robert/A-6924-2009 NR 35 TC 417 Z9 442 U1 1 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 15 PY 1994 VL 91 IS 4 BP 1294 EP 1298 DI 10.1073/pnas.91.4.1294 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000022 PM 7509068 ER PT J AU BRESNICK, EH FELSENFELD, G AF BRESNICK, EH FELSENFELD, G TI DUAL PROMOTER ACTIVATION BY THE HUMAN BETA-GLOBIN LOCUS-CONTROL REGION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CHROMATIN; DNASE I-HYPERSENSITIVE SITE; ERYTHROID GENE EXPRESSION ID DOMINANT CONTROL REGION; TRANSGENIC MICE; CHROMATIN STRUCTURE; ERYTHROID-CELLS; HUMAN-FETAL; GENE; TRANSCRIPTION; EXPRESSION; HEMOGLOBIN; ENHANCER AB The human beta-globin locus control region (LCR) is necessary for high-level and position-independent expression of globin genes in erythroid cells. A variety of mechanisms have been Proposed for the cis-activation of individual members of the beta-globin gene family by the LCR located 10-50 kilobases upstream. It is not known, however, whether a given LCR can activate all developmentally appropriate globin family members on its chromosome or whether, within a given chromosome, the LCR must be committed to activating only a single gene. We have devised an experiment to distinguish between these possibilities. This experiment takes advantage of the fact that if two genes in a cluster are transcriptionally active and their promoters, therefore, are in a conformation hypersensitive to nucleases, restriction enzymes that cleave the promoters will excise the intervening chromatin fragment. The Apa I sites on human fetal (G) gamma- and (A) gamma-globin gene promoters are accessible to cleavage in nuclei from the human erythroleukemia cell line K562, which expresses these genes, but not in HeLa cells. We find that Apa I digestion leads to excision in high yield of the fragment spanning these promoters, showing that a LCR element is capable of sharing its activating function among members of a gene cluster on a single chromosome. C1 NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 25 TC 35 Z9 35 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 15 PY 1994 VL 91 IS 4 BP 1314 EP 1317 DI 10.1073/pnas.91.4.1314 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000026 PM 8108408 ER PT J AU CONNELLY, MA GRADY, RC MUSHINSKI, JF MARCU, KB AF CONNELLY, MA GRADY, RC MUSHINSKI, JF MARCU, KB TI PANG, A GENE ENCODING A NEURONAL GLYCOPROTEIN, IS ECTOPICALLY ACTIVATED BY INTRACISTERNAL A-TYPE PARTICLE LONG TERMINAL REPEATS IN MURINE PLASMACYTOMAS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ADHESION MOLECULE L1; IMMUNOGLOBULIN SUPERFAMILY; DOMAINS; MEMBER; FIBRONECTIN; SEQUENCES; RECOGNITION; HOMOLOGY; GENOME AB Plasmacytomagenesis provides a murine model to decipher progressive genetic events culminating in a B-cell neoplasia. Activation of the c-myc protooncogene by chromosomal translocation is considered an initiating event. Intracisternal A-type particles (IAPs) are defective retroviral-like structures present in the endoplasmic reticulum of plasmacytomas (PCTs). IAP proviral insertions have been documented to engender negative or positive effects on the expression of nearby cellular genes. We have isolated a gene, PANG (plasmacytoma-associated neuronal glycoprotein), that is ectopically transcribed in a number of PCTs due to IAP long terminal repeat (LTR) activation. A full-length PANG cDNA was isolated from an MPC-11 plasma cell tumor cDNA library and encodes a polypeptide of about 113 kDa with six immunoglobulin C2-like and four type III fibronectin-like domains. PANG bears a striking resemblance to axonal glycoproteins TAG-1 and F11 known to function in neuronal outgrowth. An extensive survey revealed a predominant 3.6-kb PANG transcript in 60% (30 of 50) of PCTs as well as unique smaller and larger species. All other normal and transformed lymphoid and nonlymphoid cell lines and normal tissues were negative for PANG expression except for the brain, wherein unique 4.0- and 6.1-kb transcripts were detected. Reverse transcriptase PCR analysis revealed IAP LTR fusion to PANG mRNAs in five PCTs and in a neuroblastoma line. The 5' end of a mouse brain PANG cDNA was identical to the MPC-11 PANG transcript except for the precise replacement of its 5' LTR sequence. C1 SUNY STONY BROOK,DEPT PATHOL,STONY BROOK,NY 11794. SUNY STONY BROOK,DEPT BIOCHEM & CELL BIOL,STONY BROOK,NY 11794. SUNY STONY BROOK,DEPT MICROBIOL,STONY BROOK,NY 11794. NCI,GENET LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA 36246] NR 29 TC 21 Z9 22 U1 1 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 15 PY 1994 VL 91 IS 4 BP 1337 EP 1341 DI 10.1073/pnas.91.4.1337 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000031 PM 8108413 ER PT J AU KLADDE, MP SIMPSON, RT AF KLADDE, MP SIMPSON, RT TI POSITIONED NUCLEOSOMES INHIBIT DAM METHYLATION IN-VIVO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CHROMATIN; DAM METHYLTRANSFERASE; ALPHA-2 OPERATOR; SACCHAROMYCES CEREVISIAE ID NUCLEASE-SENSITIVE REGIONS; PROTEIN-DNA INTERACTIONS; YEAST ALPHA-2 REPRESSOR; SACCHAROMYCES-CEREVISIAE; RESTRICTION ENDONUCLEASE; DIPLOCOCCUS-PNEUMONIAE; CHROMATIN STRUCTURE; CORE PARTICLES; INVIVO; REPLICATION AB Escherichia coli Dam DNA methyltransferase can methylate genomic GATC sites when expressed in Saccharomyces cerevisiae. Others have observed changes in the level of methylation at specific sites and suggested that these changes are related to transcriptional state or chromosomal context. To test directly the influence of nucleosome location on the ability of Dam methyltransferase to modify GATC sites in chromatin, we analyzed minichromosomes containing precisely positioned nucleosomes in dam-expressing yeast strains. Levels of methylation at individual GATC sites were rigorously quantified by an oligonucleotide-probing procedure. Within the linker and adjacent 21 bp of nucleosome-associated DNA, GATC sites were highly methylated, whereas methylation was severely inhibited by histone-DNA contacts nearer to the nucleosomal pseudodyad. Other DNA-protein complexes also interfere with Dam methylation. These data are consistent with a model in which nucleosomes exert a repressive influence on the biological functions of DNA by restricting access of trans-acting factors to DNA. RP KLADDE, MP (reprint author), NIH,CELLULAR & DEV BIOL LAB,BLDG 6,ROOM B1-26,BETHESDA,MD 20892, USA. NR 36 TC 56 Z9 57 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 15 PY 1994 VL 91 IS 4 BP 1361 EP 1365 DI 10.1073/pnas.91.4.1361 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000036 PM 8108416 ER PT J AU CROWE, JE MURPHY, BR CHANOCK, RM WILLIAMSON, RA BARBAS, CF BURTON, DR AF CROWE, JE MURPHY, BR CHANOCK, RM WILLIAMSON, RA BARBAS, CF BURTON, DR TI RECOMBINANT HUMAN RESPIRATORY SYNCYTIAL VIRUS (RSV) MONOCLONAL-ANTIBODY FAB IS EFFECTIVE THERAPEUTICALLY WHEN INTRODUCED DIRECTLY INTO THE LUNGS OF RSV-INFECTED MICE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID COTTON RATS; IMMUNODEFICIENCY-VIRUS; F-GLYCOPROTEIN; IMMUNOTHERAPY; LIBRARIES AB Previously, recombinant human respiratory syncytial virus (RSV) monoclonal antibody Fabs were generated by antigen selection from random combinatorial libraries displayed at the tip of filamentous phage. Two such Fabs, which exhibited high binding affinity for RSV F glycoprotein (a major protective antigen), were evaluated for therapeutic efficacy in infected mice just before or at the time of peak virus replication in the lungs. Fab 19, which neutralized RSV infectivity with high efficiency in tissue culture, was effective therapeutically when delivered directly into the lungs by intranasal instillation under anesthesia. In contrast, RSV Fab 126, which failed to neutralize virus in cell culture, did not exhibit a therapeutic effect under these conditions. The amount of Fab 19 required to effect a 5000- to 12,000-fold reduction in titer of RSV in the lungs within 24 hr was rather small. In four separate experiments, a single instillation of 12.9-50 mu g of RSV Fab 19 was sufficient to achieve such a reduction in pulmonary virus in a 25g mouse. The use of Fabs instead of the whole immunoglobulin molecules from which they are derived reduced the protein content of a therapeutic dose. This is important because the protein load that can be delivered effectively into the lungs is limited. The therapeutic effect of a single treatment with Fab 19 was not sustained, so that a rebound in pulmonary virus titer occurred on the 2nd day after treatment. This rebound in pulmonary RSV titer could be prevented by treating infected mice with a single dose of Fab 19 daily for 3 days. These observations suggest that human monoclonal Fabs grown in Escherichia coli may prove useful in the treatment of serious RSV disease as well as diseases caused by other viruses where replication in vivo is limited primarily to the lumenal lining of the respiratory tract. C1 SCRIPPS RES INST, DEPT MOLEC BIOL, LA JOLLA, CA 92037 USA. SCRIPPS RES INST, DEPT IMMUNOL, LA JOLLA, CA 92037 USA. RP CROWE, JE (reprint author), NIAID, INFECT DIS LAB, BLDG 7, ROOM 106, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. RI Crowe, James/B-5549-2009 OI Crowe, James/0000-0002-0049-1079 NR 15 TC 98 Z9 100 U1 1 U2 2 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 15 PY 1994 VL 91 IS 4 BP 1386 EP 1390 DI 10.1073/pnas.91.4.1386 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000041 PM 8108420 ER PT J AU REBAI, N PANTALEO, G DEMAREST, JF CIURLI, C SOUDEYNS, H ADELSBERGER, JW VACCAREZZA, M WALKER, RE SEKALY, RP FAUCI, AS AF REBAI, N PANTALEO, G DEMAREST, JF CIURLI, C SOUDEYNS, H ADELSBERGER, JW VACCAREZZA, M WALKER, RE SEKALY, RP FAUCI, AS TI ANALYSIS OF THE T-CELL RECEPTOR BETA-CHAIN VARIABLE-REGION (V-BETA) REPERTOIRE IN MONOZYGOTIC TWINS DISCORDANT FOR HUMAN-IMMUNODEFICIENCY-VIRUS - EVIDENCE FOR PERTURBATIONS OF SPECIFIC V-BETA SEGMENTS IN CD4(+) T-CELLS OF THE VIRUS-POSITIVE TWINS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MAMMARY-TUMOR VIRUS; MAJOR HISTOCOMPATIBILITY COMPLEX; HTLV-III/LAV ENVELOPE; CLONAL DELETION; LYMPHOCYTES-T; I-E; SUPERANTIGEN; STIMULATION; TOLERANCE; ANTIGENS AB We analyzed the T cell receptor (TCR) V-beta repertoire in human immunodeficiency virus type 1 (HIV-1)-infected individuals at different stages of disease. To circumvent the effect of HLA and other loci on the expressed TCR repertoire, we compared the TCR repertoire in nine pairs of monozygotic twins who were discordant for HIV infection. A semiquantitative polymerase chain reaction (PCR) assay and flow cytometry enabled us to show distinct differences in the V-beta repertoire in the HIV-positive twin compared with the HIV-negative twin. By combining PCR and cytofluorometry, these differences were restricted to a specific set of TCR V-beta segments, with members of the V(beta)13 family perturbed in six out of seven cases and those of the V(beta)21 family perturbed in four out of seven cases studied. Most of the other V-beta families remained unchanged. Our results provide direct evidence for a skewed TCR repertoire in HIV infection. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702. UNIV MONTREAL,DEPT MICROBIOL & IMMUNOL,MONTREAL H3C 3J7,PQ,CANADA. MCGILL UNIV,DEPT MICROBIOL & IMMUNOL,MONTREAL,PQ,CANADA. RP REBAI, N (reprint author), INST RECH CLIN MONTREAL,IMMUNOL LAB,MONTREAL,PQ,CANADA. RI Pantaleo, Giuseppe/K-6163-2016 NR 47 TC 83 Z9 84 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 15 PY 1994 VL 91 IS 4 BP 1529 EP 1533 DI 10.1073/pnas.91.4.1529 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000071 PM 7906416 ER PT J AU CARRIER, F GATIGNOL, A HOLLANDER, MC JEANG, KT FORNACE, AJ AF CARRIER, F GATIGNOL, A HOLLANDER, MC JEANG, KT FORNACE, AJ TI INDUCTION OF RNA-BINDING PROTEINS IN MAMMALIAN-CELLS BY DNA-DAMAGING AGENTS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DNA DAMAGE; RNA-BINDING; HUMAN IMMUNODEFICIENCY VIRUS TYPE 1; RADIATION ID HUMAN-IMMUNODEFICIENCY-VIRUS; NUCLEAR-PROTEIN; TAR ELEMENT; ACTIVATION; TYPE-1; IDENTIFICATION; REGION; KINASE; PHOSPHORYLATION; LOOP AB A technique to detect RNA-binding proteins (RBP) involving hybridization of RNA probe to proteins transferred to a membrane was used to study RBP in different mammalian cells and in cells after genotoxic stress. With this approach, up to 13 proteins of different sizes were detected in crude nuclear extracts by using a viral RNA probe consisting of the trans-activation-responsive (TAR) element of human immunodeficiency virus type 1 (HIV-1). The TAR RNA probe contains a stem-loop structure found in nascent HIV-1 transcripts. A G+C-rich probe with similar structure also bound to many of these RBP. Only a 102-kDa protein Strongly bound to other RNA probes lacking this structure, while a probe with an A+U-rich stem-loop structure fail to bind most RBP, thus indicating a RNA secondary structure preference. The expression of these RBP varied substantially in nine different human and hamster cell lines, with no detectable RBP in two human myeloid lines. Evidence for induction ion of these RBP was found in six of seven lines after treatment with DNA-damaging agents; UV radiation was the most effective agent. In Chinese hamster ovary cells, which showed the strongest response, all five RBP present in untreated cells rapidly increased in activity after UV irradiation, and eight additional RBP were detected. The induction of these RBP by DNA-damaging agents indicates one or more possible roles for these proteins in the cellular response to genotoxic stress and in viral activation after such stress. C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP CARRIER, F (reprint author), NCI,DIV CANC RES,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892, USA. RI Carrier, France/C-3063-2008; Fornace, Albert/A-7407-2008; Jeang, Kuan-Teh/A-2424-2008 OI Fornace, Albert/0000-0001-9695-085X; NR 24 TC 20 Z9 20 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 15 PY 1994 VL 91 IS 4 BP 1554 EP 1558 DI 10.1073/pnas.91.4.1554 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000076 PM 7509078 ER PT J AU CHEN, B JOHANSON, L WIEST, JS ANDERSON, MW YOU, M AF CHEN, B JOHANSON, L WIEST, JS ANDERSON, MW YOU, M TI THE 2ND INTRON OF THE K-RAS GENE CONTAINS REGULATORY ELEMENTS ASSOCIATED WITH MOUSE LUNG-TUMOR SUSCEPTIBILITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE PROTOONCOGENE; DNA-BINDING PROTEINS; TRANSCRIPTIONAL REGULATION ID MICE; PROTOONCOGENE; ACTIVATION; STRAIN; PROMOTER; CANCER; KRAS2; CELLS; A/J; DNA AB We have previously demonstrated the preferential activation of the K-ras gene from the susceptible A/J parent ire lung tumors from F-1 mouse hybrids. In the present study, the mechanism of this observation is further investigated. Higher levels of expression of A/J K ras allele were detected in lung adenomas (30 of 30) from the C3A mouse. In addition, three K-ras alleles, designated as susceptible (K-s), intermediate (K-i), or resistant (K-r), were identified by sequence analysis of the second intron of the K-ras gene from 32 strains of mice. These K-ras alleles are associated with differences in mouse lung tumor susceptibility. All K-r alleles have a tandem 37-bp direct repeat (nt 282-355) in the second intron of the K-ras gene. K-s and K-i alleles have only one copy of the 37-bp sequence (nt 282-318). K-s strains have three base variations at nt 288, 296, and 494, and K-i strains have two base variations at nt 288 and 494 in the second intron of the K-ras gene. Differential protein-binding patterns were observed in gel-mobility-shift experiments between the duplicated 37-bp sequence of the K-r allele and the single 37-bp sequence of the K-s and K-i alleles. DNase I footprinting assay revealed protein binding sites in the second intron of the K-ras gene that correspond to the tandem repeat sequences. Our data suggest that higher expression of the A/J allele relative to C3H allele may be responsible for the allele-specific activation of the K-ras gene in lung tumors from F-1 hybrid mice. C1 MED COLL OHIO,TOLEDO,OH 43699. NIEHS,RES TRIANGLE PK,NC 27709. FU NCI NIH HHS [CA58554] NR 26 TC 86 Z9 86 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 15 PY 1994 VL 91 IS 4 BP 1589 EP 1593 DI 10.1073/pnas.91.4.1589 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MX210 UT WOS:A1994MX21000083 PM 8108449 ER PT J AU CLORE, GM BAX, A OMICHINSKI, JG GRONENBORN, AM AF CLORE, GM BAX, A OMICHINSKI, JG GRONENBORN, AM TI LOCALIZATION OF BOUND WATER IN THE SOLUTION STRUCTURE OF A COMPLEX OF THE ERYTHROID TRANSCRIPTION FACTOR GATA-1 WITH DNA SO STRUCTURE LA English DT Article DE BOUND WATER; GATA-1-DNA COMPLEX; NMR SOLUTION STRUCTURE; PROTEIN HYDRATION ID ATOMIC RESOLUTION; PROTEIN HYDRATION; NMR-SPECTROSCOPY; AQUEOUS-SOLUTION; ROTATING-FRAME; REPRESSOR; MOLECULES; OPERATOR; SPECTRA AB Background: The erythroid specific transcription factor GATA-1 is responsible for the regulation of transcription of erythroid-expressed genes and is an essential component required for the generation of the erythroid lineage. GATA-1 binds specifically as a monomer to the asymmetric consensus target sequence (T/A)GATA-(A/G) found in the cis-regulatory elements of all globin genes and most other erythroid specific genes that have been examined. We have previously determined the solution structure of the complex of the zinc-containing DNA-binding domain of chicken GATA-1 with its cognate DNA target site by multidimensional heteronuclear NMR. From previous studies of complexes between proteins and DNA, water appears to play an important role in DNA-protein recognition by mediating bridging hydrogen bonds between functional groups on the protein and DNA bases. Solvation free energy calculations, however, suggest that hydrophobic interactions should exclude water from parts of the GATA-1:DNA interface. Results: Using water-selective two-dimensional heteronuclear magnetic resonance spectroscopy, we have identified the location of bound water molecules in the specific complex of chicken GATA-1 with DNA. A number of water molecules could be detected between the protein and the phosphate backbone, as well as at the solvent exposed surface of the protein. However, no water molecules could be observed at the interface of the protein with the bases of the DNA. With only one exception, the bound water molecules have a residency time > 200-300 ps. Conclusions: Unlike other protein-DNA complexes, the majority of specific interactions between GATA-1 and the DNA bases in the major groove are hydrophobic in nature. The exclusion of water from the protein-DNA base interface in the major groove supports the view that the specific binding energy is indeed dominated by hydrophobic effects. RP CLORE, GM (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 5,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 24 TC 45 Z9 45 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0969-2126 J9 STRUCTURE JI Structure PD FEB 15 PY 1994 VL 2 IS 2 BP 89 EP 94 DI 10.1016/S0969-2126(00)00011-3 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA NC658 UT WOS:A1994NC65800003 PM 8081746 ER PT J AU SCHULICK, RD MULUK, SC CLERICI, M BERMAS, BL VIA, CS WEIR, MR SHEARER, GM AF SCHULICK, RD MULUK, SC CLERICI, M BERMAS, BL VIA, CS WEIR, MR SHEARER, GM TI VALUE OF IN-VITRO CD4(+) T-HELPER CELL-FUNCTION TEST FOR PREDICTING LONG-TERM LOSS OF HUMAN RENAL-ALLOGRAFTS SO TRANSPLANTATION LA English DT Note ID PATHWAYS C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NIGMS,PHARMACOL RES ASSOCIATE TRAINING PROGRAM,BETHESDA,MD. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. VET AFFAIRS MED CTR,RES SERV,DIV RHEUMATOL & CLIN IMMUNOL,BALTIMORE,MD. UNIV MARYLAND,SCH MED,DEPT MED,DIV NEPHROL,BALTIMORE,MD 21201. NR 7 TC 7 Z9 7 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 1994 VL 57 IS 3 BP 480 EP 482 DI 10.1097/00007890-199402000-00035 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA MX020 UT WOS:A1994MX02000035 PM 7906443 ER PT J AU PAPPU, HR KARASEV, AV ANDERSON, EJ PAPPU, SS HILF, ME FEBRES, VJ ECKLOFF, RMG MCCAFFERY, M BOYKO, V GOWDA, S DOLJA, VV KOONIN, EV GUMPF, DJ CLINE, KC GARNSEY, SM DAWSON, WO LEE, RF NIBLETT, CL AF PAPPU, HR KARASEV, AV ANDERSON, EJ PAPPU, SS HILF, ME FEBRES, VJ ECKLOFF, RMG MCCAFFERY, M BOYKO, V GOWDA, S DOLJA, VV KOONIN, EV GUMPF, DJ CLINE, KC GARNSEY, SM DAWSON, WO LEE, RF NIBLETT, CL TI NUCLEOTIDE-SEQUENCE AND ORGANIZATION OF 8 3' OPEN READING FRAMES OF THE CITRUS TRISTEZA CLOSTEROVIRUS GENOME SO VIROLOGY LA English DT Article ID BEET YELLOWS CLOSTEROVIRUS; HEAT-SHOCK PROTEINS; KDA PROTEIN; VIRUS; RNA; BINDING; GENE; DNA; ALIGNMENT; PLANT C1 UNIV FLORIDA,DEPT PLANT PATHOL,GAINESVILLE,FL 32611. UNIV FLORIDA,DEPT HORT SCI,GAINESVILLE,FL 32611. UNIV CALIF RIVERSIDE,DEPT PLANT PATHOL,RIVERSIDE,CA 92521. US ARS,HORT RES LAB,ORLANDO,FL 32803. UNIV FLORIDA,CTR CITRUS RES & EDUC,LAKE ALFRED,FL 33850. TEXAS A&M UNIV,DEPT BIOL,COLL STN,TX 77843. NIH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BETHESDA,MD 20894. RI Cline, Kenneth/J-6238-2013 NR 46 TC 130 Z9 136 U1 0 U2 7 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 FEB 15 PY 1994 VL 199 IS 1 BP 35 EP 46 DI 10.1006/viro.1994.1095 PG 12 WC Virology SC Virology GA MW946 UT WOS:A1994MW94600004 PM 8116253 ER PT J AU SALTARELLI, MJ SCHOBORG, R PAVLAKIS, GN CLEMENTS, JE AF SALTARELLI, MJ SCHOBORG, R PAVLAKIS, GN CLEMENTS, JE TI IDENTIFICATION OF THE CAPRINE ARTHRITIS-ENCEPHALITIS VIRUS REV PROTEIN AND ITS CIS-ACTING REV-RESPONSIVE ELEMENT SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; TRANS-ACTIVATOR GENE; VIRAL MESSENGER-RNA; HIV-1 REV; NUCLEOTIDE-SEQUENCE; HTLV-III; REGULATORY PROTEINS; MUTATIONAL ANALYSIS; TARGET SEQUENCE; TYPE-1 AFFECTS C1 JOHNS HOPKINS UNIV,SCH MED,DIV COMPARAT MED,BALTIMORE,MD 21205. FREDERICK CANC RES & DEV CTR,HUMAN RETROVIRUS SECT,FREDERICK,MD 21702. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. RI Schoborg, Robert/A-2055-2010 FU NIAID NIH HHS [AI-09394, AI-28748]; NINDS NIH HHS [NS-23039] NR 52 TC 23 Z9 23 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 0042-6822 J9 VIROLOGY JI Virology PD FEB 15 PY 1994 VL 199 IS 1 BP 47 EP 55 DI 10.1006/viro.1994.1096 PG 9 WC Virology SC Virology GA MW946 UT WOS:A1994MW94600005 PM 8116254 ER PT J AU HOSHINO, Y NISHIKAWA, K BENFIELD, DA GORZIGLIA, M AF HOSHINO, Y NISHIKAWA, K BENFIELD, DA GORZIGLIA, M TI MAPPING OF ANTIGENIC SITES INVOLVED IN SEROTYPE-CROSS-REACTIVE NEUTRALIZATION ON GROUP A ROTAVIRUS OUTERCAPSID GLYCOPROTEIN VP7 SO VIROLOGY LA English DT Note ID OUTER CAPSID PROTEIN; AMINO-ACID-SEQUENCE; MONOCLONAL-ANTIBODIES; RHESUS ROTAVIRUS; EPITOPES; RESPONSES; PROTECTION; INFECTION; IDENTIFICATION; SPECIFICITIES C1 S DAKOTA STATE UNIV,DEPT VET SCI,BROOKINGS,SD 57007. RP HOSHINO, Y (reprint author), NIAID,LID,EPIDEMIOL SECT,BLDG 7,ROOM 105,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI Benfield, David/0000-0001-6492-3830 NR 29 TC 24 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 0042-6822 J9 VIROLOGY JI Virology PD FEB 15 PY 1994 VL 199 IS 1 BP 233 EP 237 DI 10.1006/viro.1994.1117 PG 5 WC Virology SC Virology GA MW946 UT WOS:A1994MW94600026 PM 8116249 ER PT J AU CHANG, NC JENKINS, NA GILBERT, DJ COPELAND, NG CHANG, YH CHEN, WM CHANG, AC AF CHANG, NC JENKINS, NA GILBERT, DJ COPELAND, NG CHANG, YH CHEN, WM CHANG, AC TI ASSIGNMENT OF 2 ALPHA-2-ADRENOCEPTOR SUBTYPE GENES TO MURINE CHROMOSOMES SO NEUROSCIENCE LETTERS LA English DT Article DE ALPHA-2 ADRENOCEPTOR GENE; CHROMOSOMAL MAPPING ID LINKAGE MAP; RECEPTOR FAMILY; MOUSE; ORGANIZATION; CLONING; LOCUS AB Subtype-specific probes to the murine homologs of the human ADRA2B and ADRA2C genes were prepared by PCR amplification and used to map these two genes to mouse chromosomes 2 and 5, respectively. Both genes mapped in regions of mouse chromosomes consistent with their map location in humans. These mapping results provide additional insights into the linkage relationships among members of this important gene family. C1 NATL YANG MING MED COLL,INST NEUROSCI,TAIPEI 11221,TAIWAN. NATL YANG MING MED COLL,INST MICROBIOL & IMMUNOL,TAIPEI 11221,TAIWAN. NATL YANG MING MED COLL,INST NEUROSCI,TAIPEI 11221,TAIWAN. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 23 TC 7 Z9 7 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 14 PY 1994 VL 167 IS 1-2 BP 105 EP 108 DI 10.1016/0304-3940(94)91038-3 PG 4 WC Neurosciences SC Neurosciences & Neurology GA MY131 UT WOS:A1994MY13100025 PM 8177505 ER PT J AU BAPTISTA, T WEISS, SRB ZOCCHI, A SITCOSKE, M POST, R AF BAPTISTA, T WEISS, SRB ZOCCHI, A SITCOSKE, M POST, R TI ELECTRICAL KINDLING IS ASSOCIATED WITH INCREASES IN AMYGDALA ACETYLCHOLINE LEVELS - AN IN-VIVO MICRODIALYSIS STUDY SO NEUROSCIENCE LETTERS LA English DT Article DE AMYGDALOID KINDLING; ACETYLCHOLINE; DIAZEPAM; MICRODIALYSIS; RAT ID RATS; RELEASE; SEIZURE AB Using brain microdialysis, acetylcholine (Ach) levels were assessed in the nucleus amygdaloideus lateralis of electrically kindled rats using a cholinesterase inhibitor in the perfusion fluid to prevent Ach breakdown. During kindling development, when the animals displayed afterdischarges lasting more than 30 s but no seizures, a significant increase in Ach levels (+66%) was observed after electrical stimulation. Ach levels were also elevated after a stage 5 kindled seizure (+48%), with no additional increment compared to rats experiencing only afterdischarges. Chronic diazepam administration prevented kindling development and the increment in Ach overflow; however, diazepam itself(following acute administration) tended to decrease Ach levels in the amygdala. These findings are convergent with pharmacological data suggesting that changes in the cholinergic function may be important especially during amygdaloid kindling development. C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. RP BAPTISTA, T (reprint author), UNIV LOS ANDES,DEPT PHYSIOL,MERIDA,VENEZUELA. NR 12 TC 8 Z9 9 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 14 PY 1994 VL 167 IS 1-2 BP 133 EP 136 DI 10.1016/0304-3940(94)91045-6 PG 4 WC Neurosciences SC Neurosciences & Neurology GA MY131 UT WOS:A1994MY13100032 PM 8177511 ER PT J AU BERNART, MW HALLOCK, YF CARDELLINA, JH BOYD, MR AF BERNART, MW HALLOCK, YF CARDELLINA, JH BOYD, MR TI STEREOCHEMISTRY OF ENYNOLS - A CAVEAT ON THE EXCITON CHIRALITY METHOD SO TETRAHEDRON LETTERS LA English DT Article ID ABSOLUTE-CONFIGURATION AB The exciton chirality method, as applied to secondary allylic alcohols, cannot be extended to secondary alcohols flanked by two chromophores. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. NR 14 TC 24 Z9 25 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD FEB 14 PY 1994 VL 35 IS 7 BP 993 EP 994 DI 10.1016/S0040-4039(00)79947-3 PG 2 WC Chemistry, Organic SC Chemistry GA MW024 UT WOS:A1994MW02400009 ER PT J AU WOLFFE, AP ALMOUZNI, G BOUVET, P DIMITROV, S HAYES, JJ LANDSBERGER, N PRUSS, D URA, K AF WOLFFE, AP ALMOUZNI, G BOUVET, P DIMITROV, S HAYES, JJ LANDSBERGER, N PRUSS, D URA, K TI HISTONE MODULATED TRANSCRIPTION - STRUCTURAL AND DEVELOPMENTAL ASPECTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. NR 7 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 11 EP 11 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500031 ER PT J AU BLANCO, J SEGARS, J MEDIN, J MINUCCI, S OZATO, K AF BLANCO, J SEGARS, J MEDIN, J MINUCCI, S OZATO, K TI C-TERMINAL TRUNCATION OF RXR-BETA INHIBITS RETINOIC ACID-INDUCED TRANSCRIPTION IN EMBRYONAL CARCINOMA-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RI Minucci, Saverio/J-9669-2012 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 28 EP 28 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500091 ER PT J AU CHUNG, JH WHITELY, M FELSENFELD, G AF CHUNG, JH WHITELY, M FELSENFELD, G TI A 5' ELEMENT OF THE CHICKEN BETA-GLOBIN DOMAIN SERVES AS TRANSCRIPTIONAL INSULATOR IN HUMAN ERYTHROID-CELLS AND PROTECTS AGAINST POSITION EFFECT IN DROSOPHILA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 28 EP 28 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500094 ER PT J AU HAAS, NB JOHNSON, PF BURCH, JBE AF HAAS, NB JOHNSON, PF BURCH, JBE TI THE DNA-BINDING SITE-SPECIFICITY OF BZIP TRANSCRIPTION FACTORS IS DETERMINED BY A COMBINATORIAL CODE THAT INVOLVES BOTH THE BASIC AND FORK REGIONS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. RI Johnson, Peter/A-1940-2012 OI Johnson, Peter/0000-0002-4145-4725 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 31 EP 31 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500103 ER PT J AU KASHANCHI, F PIRAS, G RADONOVICH, MF DUVALL, JF FATTAEY, A BRADY, JN AF KASHANCHI, F PIRAS, G RADONOVICH, MF DUVALL, JF FATTAEY, A BRADY, JN TI DIRECT INTERACTION OF HUMAN TFIID WITH THE HIV-1 TRANSACTIVATOR TAT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,CTR CANC,CHARLESTON,MA 02129. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 32 EP 32 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500110 ER PT J AU MISHRA, BB MUCHMORE, AV AF MISHRA, BB MUCHMORE, AV TI FOS-JUN HETERO-DIMERIZATION AND BINDING TO DNA IS INHIBITED BY MAN-5 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 TEMPLE UNIV,SCH MED,PHILADELPHIA,PA 19140. NCI,METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 35 EP 35 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500120 ER PT J AU OHTAKAMARUYAMA, C WANG, XY CHEPELINSKY, AB AF OHTAKAMARUYAMA, C WANG, XY CHEPELINSKY, AB TI AP2 TRANSCRIPTION FACTOR IS INVOLVED IN THE TRANSCRIPTION OF THE LENS MIP GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY 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 WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 50 EP 50 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500180 ER PT J AU RICHARDSON, JC LEE, DC WISTOW, GJ AF RICHARDSON, JC LEE, DC WISTOW, GJ TI THE GENE RECRUITMENT OF AN ENZYME CRYSTALLIN - A LENS-SPECIFIC ALTERNATIVE PROMOTER IN ZETA-CRYSTALLIN SO JOURNAL OF CELLULAR BIOCHEMISTRY 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 WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 52 EP 52 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500188 ER PT J AU TSAIMORRIS, CH GENG, Y XIE, L BUCZKO, E DUFAU, M AF TSAIMORRIS, CH GENG, Y XIE, L BUCZKO, E DUFAU, M TI TRANSCRIPTIONAL REGULATION OF LH RECEPTOR GENE-EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,ERRB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 54 EP 54 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500197 ER PT J AU BURKE, LP MORTIN, MA AF BURKE, LP MORTIN, MA TI RNA-POLYMERASE-II MUTANTS CAUSE A UBX-LIKE PHENOTYPE BY AN EFFECT OCCURRING PRIOR TO THE ELONGATION STEP IN TRANSCRIPTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. RI Burke, Lillian/A-7334-2008 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 56 EP 56 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500203 ER PT J AU KASHANCHI, F PIRAS, G RADONOVICH, M DUVALL, J BRADY, JN AF KASHANCHI, F PIRAS, G RADONOVICH, M DUVALL, J BRADY, JN TI ANALYSIS OF HTLV-I TRANSCRIPTION IN-VITRO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 56 EP 56 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500202 ER PT J AU HANSEN, U RIMSKY, S BATSON, SC BUSTIN, M DING, HF AF HANSEN, U RIMSKY, S BATSON, SC BUSTIN, M DING, HF TI CHROMOSOMAL PROTEIN HMG-14 INCREASES THE RATE OF TRANSCRIPTIONAL ELONGATION BY RNA-POLYMERASE-II ON CHROMATIN TEMPLATES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. NCI,BETHESDA,MD 20892. RI Bustin, Michael/G-6155-2015 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 59 EP 59 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500216 ER PT J AU KRAH, R GELLERT, M MENZEL, R AF KRAH, R GELLERT, M MENZEL, R TI THE REGULATION OF TRANSCRIPTION AND DNA SUPERCOILING - A CORRELATION BETWEEN PROMOTER STRENGTH AND THE ANTITERMINATION ABILITY OF MUTANT GYRA PROMOTERS IN ESCHERICHIA-COLI SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,MOLEC BIOL LAB,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB,PRINCETON,NJ 08543. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 62 EP 62 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500225 ER PT J AU MARAIA, RJ KENAN, D KEENE, J AF MARAIA, RJ KENAN, D KEENE, J TI LA RELEASES NASCENT TRANSCRIPT AND RNA-POLYMERASE-III FROM PAUSED TERMINATION COMPLEXES THEREBY PROMOTING MULTIPLE REINITIATIONS - THE ROLES OF LA IN ALU EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 63 EP 63 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500229 ER PT J AU WOLFFE, AP ALMOUZNI, G BOUVET, P DIMITROV, S HAYES, JJ LANDSBERGER, N PRUSS, D URA, K AF WOLFFE, AP ALMOUZNI, G BOUVET, P DIMITROV, S HAYES, JJ LANDSBERGER, N PRUSS, D URA, K TI HISTONE MODULATED TRANSCRIPTION - STRUCTURAL AND DEVELOPMENTAL ASPECTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. RI dimitrov, stefan/M-7697-2013 NR 7 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 82 EP 82 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500290 ER PT J AU BAILER, SM MILLER, MW BERLIN, WK LUBAS, WA STARR, CM HANOVER, JA AF BAILER, SM MILLER, MW BERLIN, WK LUBAS, WA STARR, CM HANOVER, JA TI NUCLEAR-PORE PROTEIN P62 EXPRESSED IN BACULOVIRUS SYSTEM AND ESCHERICHIA-COLI SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 88 EP 88 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500306 ER PT J AU CASPARY, WJ KORBER, C SCHIFFMANN, D SPENCER, D STOPPER, H AF CASPARY, WJ KORBER, C SCHIFFMANN, D SPENCER, D STOPPER, H TI 5-AZACYTIDINE INDUCTION OF MICRONUCLEI AND MITOTIC DISTURBANCES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. UNIV WURZBURG,INST TOXICOL,W-8700 WURZBURG,GERMANY. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 93 EP 93 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500327 ER PT J AU DASSO, M SEKI, T AZUMA, Y SEINO, H OHBA, T NISHIMOTO, T AF DASSO, M SEKI, T AZUMA, Y SEINO, H OHBA, T NISHIMOTO, T TI THE ROLE OF RCC1, A REGULATOR OF CHROMOSOME CONDENSATION, IN CELL-CYCLE CONTROL, DNA-REPLICATION AND NUCLEAR FORMATION - STUDIES IN XENOPUS EXTRACTS USING MUTANT RCC1 PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. KYUSHU UNIV,GRAD SCH MED SCI,DEPT MOLEC BIOL,FUKUOKA 812,JAPAN. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 94 EP 94 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500332 ER PT J AU OTRIN, VR TAKAO, M MCLENIGAN, M LEVINE, AS PROTIC, M AF OTRIN, VR TAKAO, M MCLENIGAN, M LEVINE, AS PROTIC, M TI CELLULAR-DISTRIBUTION OF UV-DDB PROTEIN AND UV-DDB ACTIVITY IN PRIMATE CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,DNA REPLICAT REPAIR & MUTAGENESIS SECT,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 96 EP 96 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500338 ER PT J AU SMITH, MR HAMANAKA, R LONGO, DL FERRIS, DK AF SMITH, MR HAMANAKA, R LONGO, DL FERRIS, DK TI THE MURINE HOMOLOG OF THE DROSOPHILA-POLO SERINE/THREONINE KINASE IS REQUIRED FOR DNA-SYNTHESIS AND MITOTIC SPINDLE FORMATION IN NIH 3T3 CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DYNCORP,PRI,BCDP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,LLB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 96 EP 96 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500340 ER PT J AU BRESNICK, EH FELSENFELD, G AF BRESNICK, EH FELSENFELD, G TI ACTIVATION OF MULTIPLE PROMOTERS ON A SINGLE CHROMOSOME BY THE HUMAN BETA-GLOBIN LOCUS-CONTROL REGION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 98 EP 98 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500346 ER PT J AU ADACHI, Y COPELAND, TD AFONINA, E HATANAKA, M OROSZLAN, S PAVLAKIS, GN AF ADACHI, Y COPELAND, TD AFONINA, E HATANAKA, M OROSZLAN, S PAVLAKIS, GN TI POSSIBLE MECHANISM OF NUCLEOLAR TRANSLOCATION AND ACTIVATION OF HIV-1 REV PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS SECT,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,DEPT MOLEC VIROL & CARCINOGENESIS,FREDERICK,MD 21702. KYOTO UNIV,INST VIRUS RES,SAKYO KU,KYOTO 606,JAPAN. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 111 EP 111 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500399 ER PT J AU BRAY, M ERNST, R PRASAD, S JEANG, KT REKOSH, D HAMMARSKJOLD, ML AF BRAY, M ERNST, R PRASAD, S JEANG, KT REKOSH, D HAMMARSKJOLD, ML TI SMALL ELEMENT FROM THE MASON-PFIZER MONKEY VIRUS GENOME HIV-I EXPRESSION AND REPLICATION REV-INDEPENDENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV VIRGINIA,MYLES H THALER CTR AIDS & RETROVIRUS RES,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,DEPT MICROBIOL,CHARLOTTESVILLE,VA 22908. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 114 EP 114 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500410 ER PT J AU WERNER, MH CLORE, GM GRONENBORN, AM NASH, HA AF WERNER, MH CLORE, GM GRONENBORN, AM NASH, HA TI SYMMETRY AND ASYMMETRY IN THE FUNCTION OF ESCHERICHIA-COLI INTEGRATION HOST FACTOR - IMPLICATIONS FOR TARGET IDENTIFICATION BY DNA-BINDING PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,PHYS CHEM LAB,BETHESDA,MD 20892. NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 129 EP 129 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500460 ER PT J AU TAFURI, SR FINK, D WOLFFE, AP AF TAFURI, SR FINK, D WOLFFE, AP TI CHARACTERIZATION OF THE RNA-BINDING PROPERTIES OF THE XENOPUS TRANSCRIPTION FACTOR, FRGY2 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 WARNER LAMBERT PARKE DAVIS,SIGNAL TRANSDUCT,ANN ARBOR,MI 48105. US FDA,DIV CELL BIOL,BETHESDA,MD 20892. NIH,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 139 EP 139 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500497 ER PT J AU SAROFF, HA AF SAROFF, HA TI THE ENERGETICS OF PROTEIN-DNA INTERACTIONS - ANALYSIS OF THE BINDING ISOTHERMS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,BIOCHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 143 EP 143 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500513 ER PT J AU TAKAO, M OTRIN, VR ABRAMIC, M MOOS, M WOOTON, JC MCLENIGAN, M LEVINE, AS PROTIC, M AF TAKAO, M OTRIN, VR ABRAMIC, M MOOS, M WOOTON, JC MCLENIGAN, M LEVINE, AS PROTIC, M TI CLONING A CDNA-ENCODING A 127 KDA PROTEIN OF THE UV-DAMAGED DNA-BINDING COMPLEX SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract ID PRIMATE CELLS C1 NICHHD,BETHESDA,MD 20892. NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20892. US FDA,DIV CELLULAR & GENE THERAPY,DEV BIOL LAB,BETHESDA,MD 20892. RI Moos, Malcolm/F-3673-2011 OI Moos, Malcolm/0000-0002-9575-9938 NR 3 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 150 EP 150 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500536 ER PT J AU YANG, SW GRANSTON, A NASH, H AF YANG, SW GRANSTON, A NASH, H TI QUANTITATIVE-ANALYSIS OF THE INTERACTION BETWEEN IHF AND DNA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 150 EP 150 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500539 ER PT J AU SLESAREV, A PUSHKIN, A LAKE, J GELLERT, M KRAH, R KOZYAVKIN, S AF SLESAREV, A PUSHKIN, A LAKE, J GELLERT, M KRAH, R KOZYAVKIN, S TI DNA UNLINKING BY A THERMOSTABLE NICKING-CLOSING ENZYME SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,INST MOLEC BIOL,LOS ANGELES,CA 90024. NIDDK,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 154 EP 154 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500553 ER PT J AU ANGOV, E CAMERINIOTERO, RD AF ANGOV, E CAMERINIOTERO, RD TI THE RECA GENE FROM THERMUS-AQUATICUS - CLONING, EXPRESSION AND PURIFICATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 155 EP 155 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500556 ER PT J AU CERRITELLI, SM CROUCH, RJ AF CERRITELLI, SM CROUCH, RJ TI SACCHAROMYCES-CEREVISIAE RNASE H1 HAS 2 DISTINCT DOMAINS, ONE WITH RNASE-H ACTIVITY AND ANOTHER THAT BINDS DOUBLE-STRANDED-RNA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 155 EP 155 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500557 ER PT J AU KOZYAVKIN, SA KRAH, R GELLERT, M LAKE, JA SLESAREV, AI AF KOZYAVKIN, SA KRAH, R GELLERT, M LAKE, JA SLESAREV, AI TI STRUCTURAL HETEROGENEITY OF TYPE-I DNA TOPOISOMERASES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,MOLEC BIOL LAB,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,INST MOLEC BIOL,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 156 EP 156 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500561 ER PT J AU YANCEYWRONA, JE CAMERINIOTERO, RD AF YANCEYWRONA, JE CAMERINIOTERO, RD TI A MODEL DESCRIBING THE SEARCH FOR HOMOLOGY CARRIED OUT BY RECA PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 156 EP 156 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500562 ER PT J AU CARBONE, DP YANUCK, M WIEDENFELD, E CIERNIK, F FERNANDEZVINA, M PENDLETON, CD TSUKUI, T MINNA, JD BERZOFSKY, JA AF CARBONE, DP YANUCK, M WIEDENFELD, E CIERNIK, F FERNANDEZVINA, M PENDLETON, CD TSUKUI, T MINNA, JD BERZOFSKY, JA TI MUTANT P53 TUMOR-SUPPRESSOR PROTEIN AS AN IMMUNOTHERAPEUTIC TARGET SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV TEXAS,SOUTHWESTERN MED CTR,DALLAS,TX 75235. NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 165 EP 165 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500582 ER PT J AU FORNACE, AJ CARRIER, F HOLLANDER, MC SMITH, ML LIEBERMANN, D HOFFMAN, B ZHAN, QM AF FORNACE, AJ CARRIER, F HOLLANDER, MC SMITH, ML LIEBERMANN, D HOFFMAN, B ZHAN, QM TI CHARACTERIZATION OF GROWTH-ARREST GENES INDUCED BY GENOTOXIC STRESS AND ROLES FOR THE TUMOR-SUPPRESSOR P53 IN THEIR REGULATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. TEMPLE UNIV,SCH MED,FELS INST,PHILADELPHIA,PA. RI Carrier, France/C-3063-2008 NR 2 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 168 EP 168 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500589 ER PT J AU GUDAS, JM NGUYEN, H COWAN, KH AF GUDAS, JM NGUYEN, H COWAN, KH TI CELL-CYCLE DEPENDENT EXPRESSION OF MDM-2 IN NORMAL AND IMMORTALIZED HUMAN BREAST EPITHELIAL-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MED BRANCH,MED BREAST CANC SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 168 EP 168 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500592 ER PT J AU HANLEYHYDE, J RAINEY, GJ AF HANLEYHYDE, J RAINEY, GJ TI THE 5'-FLANKING REGION OF THE MURINE CYCLIN D2 GENE CONTAINS E-BOX ELEMENTS THAT BIND MYC AND MAX SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 169 EP 169 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500593 ER PT J AU LEE, JE BECK, TW RAUSCHER, FJ RAPP, UR AF LEE, JE BECK, TW RAUSCHER, FJ RAPP, UR TI ROLE OF RAF IN MALIGNANCY - CONTROL OF RAF GENE-EXPRESSION BY NEGATIVE GROWTH EFFECTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,BCDP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 170 EP 170 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500600 ER PT J AU OWEN, RD BARRETT, JC AF OWEN, RD BARRETT, JC TI ACTION OF TUMOR SUPPRESSORS THAT RESTRICT CUMULATIVE PROLIFERATIVE CAPACITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 172 EP 172 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500605 ER PT J AU GRAY, TA COLLINS, FS AF GRAY, TA COLLINS, FS TI RANDOM OLIGONUCLEOTIDE BINDING-SITE OPTIMIZATION AND NON-NUCLEOSOMAL TARGET ISOLATION FOR THE TRANSCRIPTION FACTOR GATA-1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH MED,MOLEC & CELLULAR BIOL PROGRAM,ANN ARBOR,MI 48109. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 177 EP 177 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500624 ER PT J AU UNGER, T SCHEFFNER, M YEE, CL HOWLEY, PM AF UNGER, T SCHEFFNER, M YEE, CL HOWLEY, PM TI SERINE MUTANTS OF HUMAN P53 IN THE ACTIVATION DOMAIN ARE WILD-TYPE FOR TRANSFORMATION SUPPRESSION AND TRANSACTIVATION FUNCTIONS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 184 EP 184 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500652 ER PT J AU CMARIK, JL HERSCHMAN, H COLBURN, NH AF CMARIK, JL HERSCHMAN, H COLBURN, NH TI THE TIS1 AND TIS21 PRIMARY RESPONSE GENES ARE CANDIDATE TUMOR PROMOTION SUPPRESSOR GENES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. UNIV CALIF LOS ANGELES,SCH MED,INST MOLEC BIOL,BIOMED & ENVIRONM SCI LAB,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOL CHEM,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 187 EP 187 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500663 ER PT J AU MERRICK, BA HE, CY WITCHER, LL PATTERSON, RM SELKIRK, JK AF MERRICK, BA HE, CY WITCHER, LL PATTERSON, RM SELKIRK, JK TI ASSOCIATION OF HUMAN AND MOUSE CYTOPLASMIC P53 WITH HEAT-SHOCK PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 190 EP 190 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500678 ER PT J AU TOPOL, LZ MARX, M CALOTHY, G BLAIR, DG AF TOPOL, LZ MARX, M CALOTHY, G BLAIR, DG TI A REVERTANT OF MOS-TRANSFORMED RAT-CELLS EXHIBITS REDUCED LEVEL OF MAP KINASE-ACTIVITY AND IS RESTRICTED TO RETRANSFORMATION BY SERINE/THREONINE KINASE ONCOGENES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD. CTR UNIV ORSAY,INST CURIE BIOL,F-91405 ORSAY,FRANCE. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 192 EP 192 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500686 ER PT J AU WEINBERG, WC KADIWAR, N AZZOLI, CG MORGAN, DL LITTLES, S YUSPA, SH AF WEINBERG, WC KADIWAR, N AZZOLI, CG MORGAN, DL LITTLES, S YUSPA, SH TI P53-DEFICIENCY AND V-RAS(HA) COOPERATE IN MALIGNANT CONVERSION OF KERATINOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. RI Weinberg, Wendy/A-8920-2009 NR 1 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 193 EP 193 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500687 ER PT J AU LI, CCH DAI, RM LONGO, DL AF LI, CCH DAI, RM LONGO, DL TI P53 PHYSICALLY ASSOCIATES WITH CDK2 IN A CELL CYCLE-DEPENDENT MANNER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DYNCROP INC,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,DIV CANC TREATMENT,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 196 EP 196 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500699 ER PT J AU STACKHOUSE, TM GIARDINA, S LIPAN, J ORCUTT, ML TORY, K DUH, FM LERMAN, M ZBAR, B AF STACKHOUSE, TM GIARDINA, S LIPAN, J ORCUTT, ML TORY, K DUH, FM LERMAN, M ZBAR, B TI CHARACTERIZATION OF THE VONHIPPEL-LINDAU TUMOR-SUPPRESSOR PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. PRI DYNCORP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 197 EP 197 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500704 ER PT J AU BHATIA, K SPANGLER, G HUPPI, K SIWARSKI, D MAGRATH, I AF BHATIA, K SPANGLER, G HUPPI, K SIWARSKI, D MAGRATH, I TI LOSS OF WILD-TYPE C-MYC IN BURKITTS LYMPHOMAS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,GENET MOLEC LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 198 EP 198 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500710 ER PT J AU KRATZKE, RA HOGG, A OTTERSON, GA COXON, AB GERADTS, J COWELL, JK KAYE, FJ AF KRATZKE, RA HOGG, A OTTERSON, GA COXON, AB GERADTS, J COWELL, JK KAYE, FJ TI INCOMPLETE PENETRANCE OF FAMILIAL RETINOBLASTOMA AND BENIGN RETINAL TUMORS ASSOCIATED WITH PARTIAL INACTIVATION OF THE RB PRODUCT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 USN,NCI,MED ONCOL BRANCH,BETHESDA,MD 20889. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20889. IMPERIAL CANC RES FUND,INST CHILD HLTH,LONDON WC1N 1EH,ENGLAND. MOLEC ONCOL INC,GAITHERSBURG,MD 20878. RI kaye, frederic/E-2437-2011 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 200 EP 200 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500718 ER PT J AU REID, AH TSAI, MM WRIGHT, CF VENZON, DJ OLEARY, TJ AF REID, AH TSAI, MM WRIGHT, CF VENZON, DJ OLEARY, TJ TI MDM2 AMPLIFICATION AND P53 MUTATION IN MALIGNANT FIBROUS HISTIOCYTOMA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,DEPT CELLULAR PATHOL,WASHINGTON,DC 20306. NCI,BIOSTAT SECT,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 202 EP 202 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500725 ER PT J AU MCBRIDE, AA WINOKUR, P SARAH, T CARRUTH, M AF MCBRIDE, AA WINOKUR, P SARAH, T CARRUTH, M TI FUNCTIONAL-ANALYSIS OF THE PAPILLOMAVIRUS REGULATORY PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract ID REPLICATION; E1 C1 NCI,BETHESDA,MD 20892. UNIV IOWA HOSP & CLIN,IOWA CITY,IA 52242. WASHINGTON UNIV,ST LOUIS,MO. NR 2 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 210 EP 210 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500749 ER PT J AU BERZOFSKY, JA AF BERZOFSKY, JA TI DESIGNING ANTIVIRAL SYNTHETIC PEPTIDE VACCINES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 212 EP 212 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500753 ER PT J AU LOWY, DR KIRNBAUER, R HUBBERT, NL TAUB, J GREENSTONE, H RODEN, R BECKER, TM WHEELER, CM SCHILLER, JT AF LOWY, DR KIRNBAUER, R HUBBERT, NL TAUB, J GREENSTONE, H RODEN, R BECKER, TM WHEELER, CM SCHILLER, JT TI SELF-ASSEMBLED PAPILLOMAVIRUS STRUCTURAL PROTEINS - POTENTIAL APPLICATION TO VIRAL BIOLOGY, SCREENING ASSAYS, AND VACCINATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. UNIV NEW MEXICO,ALBUQUERQUE,NM 87131. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 212 EP 212 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500754 ER PT J AU GORELICK, RJ OTT, DE SOWDER, RC NIGIDA, SM HENDERSON, LE ARTHUR, LO AF GORELICK, RJ OTT, DE SOWDER, RC NIGIDA, SM HENDERSON, LE ARTHUR, LO TI ON THE SIGNIFICANCE CONSERVED RESIDUES IN THE P6(GAG) REGION OF HIV-1 PR5(GAG) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 213 EP 213 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500759 ER PT J AU HENDERSON, LE SOWDER, RC JOHNSON, DG COREN, LV OTT, DE BESS, JW ARTHUR, LO AF HENDERSON, LE SOWDER, RC JOHNSON, DG COREN, LV OTT, DE BESS, JW ARTHUR, LO TI CELLULAR PROTEINS ASSOCIATED WITH HIV-1 AND SIV VIRIONS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. RI Bess, Jr., Julian/B-5343-2012 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 214 EP 214 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500762 ER PT J AU LANOIX, J LACOSTE, J PEPIN, N RICE, N HISCOTT, J AF LANOIX, J LACOSTE, J PEPIN, N RICE, N HISCOTT, J TI OVERPRODUCTION OF NFKB2 AND C-REL - A MECHANISM FOR HTLV-I TAX-MEDIATED TRANSACTIVATION VIA THE NF-KAPPA-B SIGNALING PATHWAY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MCGILL UNIV,SIR MORTIMER B DAVIS JEWISH HOSP,LADY DAVIS INST MED RES,TERRY FOX MOLEC ONCOL GRP,MONTREAL,PQ,CANADA. MCGILL UNIV,DEPT MICROBIOL & IMMUNOL,MONTREAL,PQ,CANADA. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 214 EP 214 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500761 ER PT J AU REITZ, M ROBERTGUROFF, M DIMARZOVERONESE, F LOUIE, A WATKINS, B GUPTA, G LUSSO, P GALLO, RC AF REITZ, M ROBERTGUROFF, M DIMARZOVERONESE, F LOUIE, A WATKINS, B GUPTA, G LUSSO, P GALLO, RC TI CONFORMATIONAL ASPECTS OF V3 IN HIV-1 NEUTRALIZATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,LTCB,BETHESDA,MD 20892. LOS ALAMOS NATL LAB,LOS ALAMOS,NM. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 217 EP 217 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500772 ER PT J AU DOWHANICK, J MCBRIDE, A HOWLEY, PM AF DOWHANICK, J MCBRIDE, A HOWLEY, PM TI THE TRANSACTIVATION AND DNA-BINDING DOMAINS OF E2 ARE REQUIRED FOR GROWTH SUPPRESSION OF HPV POSITIVE CELL-LINES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 221 EP 221 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500787 ER PT J AU GOLDSTEIN, DJ WANG, LM LI, WQ AARONSON, S SCHLEGEL, R PIERCE, J AF GOLDSTEIN, DJ WANG, LM LI, WQ AARONSON, S SCHLEGEL, R PIERCE, J TI THE BPV-1 E5 ONCOPROTEIN COOPERATES WITH THE BETA-TYPE, BUT NOT THE ALPHA-TYPE, PDGF RECEPTOR TO INDUCE TRANSFORMATION OF A MURINE MYELOID CELL-LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,SCH MED,DEPT OBSTET & GYNECOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20007. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 221 EP 221 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500790 ER PT J AU CLEMENS, KE MAVROMATIS, KO YEE, CL MUNGER, K AF CLEMENS, KE MAVROMATIS, KO YEE, CL MUNGER, K TI STRUCTURE-FUNCTION ANALYSIS OF THE CARBOXY-TERMINAL DOMAIN OF THE HUMAN PAPILLOMAVIRUS E7 ONCOPROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 225 EP 225 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500804 ER PT J AU MIETZ, JA HOWLEY, PM AF MIETZ, JA HOWLEY, PM TI WILD-TYPE P53 STIMULATES EXPRESSION OF GENES INVOLVED IN THE DIFFERENTIATION OF HUMAN EPITHELIAL-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 225 EP 225 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500803 ER PT J AU ROMANCZUK, H HOWLEY, PM AF ROMANCZUK, H HOWLEY, PM TI THE E1 AND E2 REGULATORY GENES OF HUMAN PAPILLOMAVIRUS TYPE-16 REPRESS VIRAL IMMORTALIZATION CAPACITY BY SEVERAL MECHANISMS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 226 EP 226 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500810 ER PT J AU JUDDE, JG JAIN, VK MAGRATH, IT AF JUDDE, JG JAIN, VK MAGRATH, IT TI ROLE OF EPSTEIN-BARR-VIRUS IN THE PATHOGENESIS OF BURKITTS-LYMPHOMA - TRANSACTIVATION OF C-MYC PROMOTER AND IG ENHANCERS BY EBNA-1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,LYMPHOMA BIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 231 EP 231 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500828 ER PT J AU AKIYAMA, SK YAMADA, KM AF AKIYAMA, SK YAMADA, KM TI INTERACTION OF FIBRONECTIN WITH ITS INTEGRIN CELL-SURFACE RECEPTOR - CHARACTERIZATION OF THE SYNERGISTIC SITE OF THE FIBRONECTIN CELL-BINDING DOMAIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 247 EP 247 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500876 ER PT J AU TENNENBAUM, T GLICK, AB BELANGER, AJ TAMURA, R QUARANTA, V YUSPA, SH AF TENNENBAUM, T GLICK, AB BELANGER, AJ TAMURA, R QUARANTA, V YUSPA, SH TI A SPLICE VARIANT OF ALPHA-6 INTEGRIN IS ASSOCIATED WITH MALIGNANT CONVERSION IN MOUSE SKIN TUMORIGENESIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI, LCCTP, BETHESDA, MD 20892 USA. Scripps Res Inst, DEPT CELL BIOL, LA JOLLA, CA 92037 USA. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 256 EP 256 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500913 ER PT J AU ELSON, HF BLUMENTHAL, R AF ELSON, HF BLUMENTHAL, R TI MEMBRANE-FUSION INHIBITED BY A TRANSDOMINANT MUTATION IN THE HIV-1 ENVELOPE GLYCOPROTEIN GP120-GP41 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD FEB 13 PY 1994 SU 18C BP 260 EP 260 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY175 UT WOS:A1994MY17500926 ER PT J AU LAI, ME MAZZOLENI, AP ARGIOLU, F DEVIRGILIS, S BALESTRIERI, A PURCELL, RH CAO, A FARCI, P AF LAI, ME MAZZOLENI, AP ARGIOLU, F DEVIRGILIS, S BALESTRIERI, A PURCELL, RH CAO, A FARCI, P TI HEPATITIS-C VIRUS IN MULTIPLE EPISODES OF ACUTE HEPATITIS IN POLYTRANSFUSED THALASSEMIC CHILDREN SO LANCET LA English DT Note ID NON-B-HEPATITIS; NON-A AB We investigated the course of distinct episodes of acute non-A, non-B (NANB) hepatitis in three polytransfused thalassaemic children. In each case, the first episode was associated with the appearance of serum hepatitis C virus (HCV) RNA and anti-HCV seroconversion. The second episode was accompanied by the reappearance of HCV viraemia, which in two patients was due to reinfection with a different HCV strain and in the third could be the result of either reactivation of primary infection or reinfection with a new but closely related strain. Thus HCV infection may not induce protective immunity, which has implications for vaccine development. C1 UNIV CAGLIARI,INST CLIN & BIOL DEV AGE,CAGLIARI,ITALY. UNIV CAGLIARI,CTR THALASSAEMIA,CAGLIARI,ITALY. NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892. RP LAI, ME (reprint author), UNIV CAGLIARI,INST INTERNAL MED,VIA SAN GIORGIO 12,I-09124 CAGLIARI,ITALY. NR 9 TC 248 Z9 252 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 12 PY 1994 VL 343 IS 8894 BP 388 EP 390 DI 10.1016/S0140-6736(94)91224-6 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA MW283 UT WOS:A1994MW28300010 PM 7905553 ER PT J AU AKSAMIT, RR BACKLUND, PS MOOS, M CARYK, T GOMI, T OGAWA, H FUJIOKA, M CANTONI, GL AF AKSAMIT, RR BACKLUND, PS MOOS, M CARYK, T GOMI, T OGAWA, H FUJIOKA, M CANTONI, GL TI THE ROLE OF CYSTEINE-78 IN FLUOROSULFONYLBENZOYLADENOSINE INACTIVATION OF RAT-LIVER S-ADENOSYLHOMOCYSTEINE HYDROLASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID L-HOMOCYSTEINE HYDROLASE; AMINO-ACID SEQUENCE; SITE-DIRECTED MUTAGENESIS; DICTYOSTELIUM-DISCOIDEUM; COENZYME BINDING; CDNA SEQUENCE; PROTEINS; PURIFICATION; RESIDUES; ENZYME AB Inactivation of rat liver S-adenosylhomocysteine hydrolase by the site-directed reagent 5'-p-fluorosulfonyl-benzoyladenosine (FSBA) is associated with the formation of a disulfide bond between Cys-78 and Cys-112 (Takata, Y., and Fujioka, M. (1984) Biochemistry 23, 4357-4362; Gomi, T., Ogawa,H., and Fujioka, M. (1986) J. Biol. Chem. 261, 13422-13425). To characterize the inactivation mechanism more precisely, the properties of four hydrolase proteins mutated at Cys-78 or Cys-112 were compared to those of the wild-type enzyme. When Cys-78 was mutated to either a serine or an alanine, proteins with greatly reduced enzymatic activity were obtained, large effects on kinetic constants were observed, and enzymatic activity was not affected by incubation with FSBA. When Cys-112 was mutated to either a serine or an alanine, the activity was similar to the wild-type protein, only small changes in the kinetic constants were observed, and the enzyme was inactivated more rapidly upon incubation with FSBA. FSBA inactivation of the C112A mutant protein was accompanied by the formation of a disulfide between Cys-78 and Cys-52. The data indicate that FSBA initially reacts with Cys-78 and that Cys-78 has an important role in the structure of the enzyme. C1 US FDA,CTR BIOL EVALUAT & RES,DEV BIOL LAB,BETHESDA,MD 20892. TOYAMA MED & PHARMACEUT UNIV,FAC MED,DEPT BIOCHEM,SUGITANI,TOYAMA 93001,JAPAN. RP AKSAMIT, RR (reprint author), NIMH,GEN & COMPARAT BIOCHEM LAB,BLDG 36,RM 3D06,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Moos, Malcolm/F-3673-2011 OI Moos, Malcolm/0000-0002-9575-9938 NR 43 TC 20 Z9 20 U1 0 U2 3 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 11 PY 1994 VL 269 IS 6 BP 4084 EP 4091 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW989 UT WOS:A1994MW98900031 PM 8307967 ER PT J AU LEE, NH EARLEHUGHES, J FRASER, CM AF LEE, NH EARLEHUGHES, J FRASER, CM TI AGONIST-MEDIATED DESTABILIZATION OF M1 MUSCARINIC ACETYLCHOLINE-RECEPTOR MESSENGER-RNA - ELEMENTS INVOLVED IN MESSENGER-RNA STABILITY ARE LOCALIZED IN THE 3'-UNTRANSLATED REGION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BETA-ADRENERGIC RECEPTORS; PROTEIN-KINASE-C; SITE-DIRECTED MUTAGENESIS; MESSENGER-RNA LEVEL; INDUCED DOWN-REGULATION; PITUITARY GH3 CELLS; BETA-2-ADRENERGIC RECEPTOR; COUPLED RECEPTORS; LIGAND-BINDING; HORMONE TRH AB The effects of chronic agonist exposure on receptor number (down-regulation) have been shown, in part, to be due to effects on mRNA levels. Agonist-mediated effects on muscarinic acetylcholine receptor (mAChR) mRNA were investigated in Chinese hamster ovary (CHO) cells stably transfected with mi mAChR gene constructs containing the open reading frame and a series of deletions of the flanking 3'-untranslated region (3'-UTR). Carbachol (CBC) down-regulated m1 mAChRs encoded by the construct m1C1, an mi mAChR transcript containing the entire flanking 3'UTR (nucleotides 1526-2622), in a time dependent fashion with maximal decreases occurring by 12 h. Steady-state levels of m1C1 mRNA declined in a parallel fashion beginning 6 h after CBC pretreatment. Similar findings were obtained with m1C2, a construct which is missing all but 261 bases of flanking 3'-UTR (nucleotides (nt) 1526-1786). Since the rate of mRNA degradation represents an important potential regulatory mechanism to control the level of gene expression, we investigated the effects of CBC treatment on m1C1 and m1C2 mRNA stability. The half-life of either transcript in untreated cells was approximately 14 h, whereas m1C1 and m1C2 transcript half-lives decreased to similar to 3 h in cells treated with CBC. Agonist-induced destabilization of m1C2 mRNA could be mimicked by phorbol esters in a concentration-dependent manner and blocked by the protein kinase inhibitor, H-7. In contrast, mi mAChR mRNA constructs missing nt 1526-1786 of the 3'-UTR (m1C3 and m1C4) did not undergo agonist or phorbol ester-induced destabilization. In the neuroblastoma cell line IMR-32, endogenous mi mAChR mRNA was down-regulated and destabilized following CBC treatment. These results demonstrate that agonist-induced mRNA destabilization is a potential mechanism for regulating mi mAChR levels. Furthermore, deletion studies identify a 261 base region of the 3'-UTR having the potential to form stable stem-loop structures which likely harbors element(s) responsible for message destabilization. C1 NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20892. RP LEE, NH (reprint author), INST GENOM RES,DEPT MOLEC & CELLULAR BIOL,GAITHERSBURG,MD 20878, USA. NR 43 TC 65 Z9 66 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 11 PY 1994 VL 269 IS 6 BP 4291 EP 4298 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW989 UT WOS:A1994MW98900062 PM 8307995 ER PT J AU HOU, XY JOHNSON, AC ROSNER, MR AF HOU, XY JOHNSON, AC ROSNER, MR TI IDENTIFICATION OF AN EPIDERMAL GROWTH-FACTOR RECEPTOR TRANSCRIPTIONAL REPRESSOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-BINDING-SITES; DNA-BINDING; STIMULATES TRANSCRIPTION; ENHANCED EXPRESSION; GENE AMPLIFICATION; CARCINOMA-CELLS; PROMOTER; PURIFICATION; ONCOGENE; SEQUENCE AB Identification of the factors controlling transcription of the epidermal growth factor (EGF) receptor gene is essential for understanding regulation of the EGF receptor and its overexpression in human carcinomas. In this study, we have identified a 60-base pair (bp) region (-919 to -860) relative to the AUG translation initiation codon in the EGF receptor 5' promoter that functions as a cis-acting EGF receptor transcriptional repressor (ETR). This fragment also acted as a repressor when linked to the thymidine kinase promoter. Gel mobility shift assays demonstrated that trans-acting factors bind to 60- and 19 bp fragments. Competition and chloramphenicol acetyltransferase assays with oligonucleotides containing mutations and deletions in this region indicate that the TTCGAGGG sequence (-877 to -870) is required for binding as well as repressor activity. While the ETR-protected region contains consensus sequences for the E2F binding site, no competition was observed with an E2F binding fragment. However, DNA-protein blot analysis indicates that both the 60- and 19-bp fragments specifically bind a 128-kDa polypeptide in extracts from HeLa or A431 human epidermoid carcinoma cells. These results suggest that a novel transcription factor(s) negatively regulates EGF receptor gene expression through binding to the ETR element. C1 UNIV CHICAGO,BEN MAY INST,DEPT PHARMACOL & PHYSIOL SCI,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MOLEC GENET & CELL BIOL,CHICAGO,IL 60637. NATL CANC INST,MOLEC BIOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA 35541] NR 45 TC 22 Z9 22 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 11 PY 1994 VL 269 IS 6 BP 4307 EP 4312 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW989 UT WOS:A1994MW98900064 PM 8307997 ER PT J AU CRAXTON, A ERNEUX, C SHEARS, SB AF CRAXTON, A ERNEUX, C SHEARS, SB TI INOSITOL 1,4,5,6-TETRAKISPHOSPHATE IS PHOSPHORYLATED IN RAT-LIVER BY A 3-KINASE THAT IS DISTINCT FROM INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MYOINOSITOL 1,3,4,5,6-PENTAKISPHOSPHATE; CELLS; METABOLISM; PHOSPHATES; TETRAKISPHOSPHATES; 3,4,5,6-TETRAKISPHOSPHATE; PENTAKISPHOSPHATE; EXPRESSION; RECEPTOR; ENZYMES AB Liver homogenates phosphorylated inositol 1,4,5,6-tetrakisphosphate exclusively to inositol 1,3,4,5,6-pentakisphosphate. Approximately 30% of this phosphorylating activity was associated with the particulate fraction of the cell, in contrast to the inositol 3,4,5,6 tetrakisphosphate 1-kinase, which was 90% soluble. This soluble 1-kinase activity was resolved from the soluble activity that phosphorylated inositol 1,4,5,6 tetrakisphosphate by an-ion-exchange chromatography. The two phosphorylating activities were also found to be differentially inhibited by inositol 1,3,4-trisphosphate (IC50 for 3-kinase > 100 mu m; IC50 for 1-kinase < 1 mu M). Thus, we have demonstrated that inositol 1,4,5,6-tetrakisphosphate is phos phorylated directly by a 3-kinase, -and inositol 3,4,5,6 tetrakisphosphate is not an obligatory intermediate, in contrast to one previous model (Oliver, K. G., Putney, J. W., Jr., Obie, J. F., and Shears, S. B. (1992) J. Biol, Chem. 267, 21528-21534). Inositol 1,4,5,6-tetrakisphosphate 3-kinase was inhibited by inositol 1,3,4,6-tetrakisphosphate (IC50, 1 mu M). Soluble inositol 1,4,5,6-tetrakisphosphate 3-kinase and inositol 1,4,5-trisphosphate 3-kinase were resolved by anion exchange chromatography. Furthermore, cDNA clones of two isozymes of inositol 1,4,5-trisphosphate 3-kinase from rat and human brain did not phosphorylate inositol 1,4,5,6-tetrakisphosphate. Thus, these two 3-kinase activities are performed by distinct enzymes. C1 FREE UNIV BRUSSELS,SCH MED,INST INTERDISCIPLINARY RES,B-1070 BRUSSELS,BELGIUM. RP CRAXTON, A (reprint author), NIEHS,CELLULAR & MOLEC PHARMACOL LAB,INOSITOL LIPID SECT,RES TRIANGLE PK,NC 27709, USA. NR 24 TC 23 Z9 24 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 11 PY 1994 VL 269 IS 6 BP 4337 EP 4342 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW989 UT WOS:A1994MW98900069 PM 8308002 ER PT J AU JOHNSON, VG NICHOLLS, PJ AF JOHNSON, VG NICHOLLS, PJ TI HISTIDINE-21 DOES NOT PLAY A MAJOR ROLE IN DIPHTHERIA-TOXIN CATALYSIS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ADP-RIBOSYLTRANSFERASE ACTIVITY; AERUGINOSA EXOTOXIN-A; NAD BINDING-SITE; ESCHERICHIA-COLI; ASPARTIC-ACID; FULL-LENGTH; MUTANT; FRAGMENT; TRANSLATION; EXPRESSION AB It has been proposed that the histidine at position 21 (H21) of the diphtheria toxin A subunit (DTA) plays an important role in the ADP-ribosyltransferase (ADPRT) activity of the toxin. The region of DT encompassing H21 demonstrates sequence similarity with other toxins exhibiting ADPRT activity, is located along the catalytic cleft of DTA, and when H21 is chemically modified, ADPRT activity is abolished. H21 was mutagenized by a polymerase chain reaction-based system whereby all alternative amino acids were substituted in place of the histidine. The majority of the substitutions virtually abolished enzymatic activity, the exception being a mutant in which H21 was replaced with asparagine (DTA-H21N). This mutant demonstrated only a slight increase in K-m and relatively small decreases in both reaction rate (k(cat)) and catalytic efficiency (k(cat)/K-m). Asparagine is a sterically conserved substitution, but its side-chain is unable to replace the imidazole group of histidine in general acid-base mechanisms or to participate in electrostatic interactions. This suggests that H21 is important in maintaining a steric conformation required for catalysis rather than in participating in an electrostatic or acid-base type of exchange. C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. RP JOHNSON, VG (reprint author), US FDA,CBER,DIV BACTERIAL PROD,BACTERIAL TOXINS LAB,BLDG 29,8800 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 35 TC 24 Z9 24 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 11 PY 1994 VL 269 IS 6 BP 4349 EP 4354 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW989 UT WOS:A1994MW98900071 PM 8308004 ER PT J AU HISCOCK, DRR YANAGISHITA, M HASCALL, VC AF HISCOCK, DRR YANAGISHITA, M HASCALL, VC TI NUCLEAR-LOCALIZATION OF GLYCOSAMINOGLYCANS IN RAT OVARIAN GRANULOSA-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FIBROBLAST GROWTH-FACTOR; HEPARAN-SULFATE PROTEOGLYCAN; INTRACELLULAR DEGRADATIVE PATHWAYS; BINDING; LIVER; IDENTIFICATION; TRANSCRIPTION; HEPATOCYTES; METABOLISM; RECEPTOR AB In rat ovarian granulosa cell cultures, internalized cell surface heparan sulfate is processed by either a fast lysosome-mediated pathway or by a slow pathway which generates glycosaminoglycan fragments. Cell-associated dermatan sulfate proteoglycans also undergo processing through analogous pathways, although the slow pathway does not involve endoglycosidic cleavage of the dermatan sulfate chains. In the present study we tested whether intracellular glycosaminoglycan fragments in rat ovarian granulosa cells were transient residents of the nuclei. A technique for isolating nuclei was devised in which cells were lysed with a hypo-osmotic extraction buffer containing detergent. Nuclei were then purified by conventional methods, and final preparations gave excellent recovery of the starting DNA (similar to 90%). The technique was used to isolate glycosaminoglycans from nuclei after cells were metabolically radiolabeled with [S-35]sulfate. The results indicated the possible presence of dermatan sulfate, but not heparan sulfate, glycosaminoglycans at this location. Failure to remove cell surface proteoglycans with trypsin before preparation of nuclei resulted in nuclear contamination with significant amounts of intact dermatan sulfate proteoglycans. Nuclei preparations obtained using traditional homogenization steps from cells either treated without or with trypsin gave identical results except that recoveries of DNA were much lower (similar to 30%). The results demonstrate the difficulty in isolating pure nuclei and therefore also of firm conclusions pertaining to the nuclear association of glycosaminoglycans. RP HISCOCK, DRR (reprint author), NIDR,BONE RES BRANCH,PROTEOGLYCAN CHEM SECT,BETHESDA,MD 20892, USA. NR 30 TC 30 Z9 30 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 11 PY 1994 VL 269 IS 6 BP 4539 EP 4546 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW989 UT WOS:A1994MW98900096 PM 8308024 ER PT J AU REDDY, VY DESROCHERS, PE PIZZO, SV GONIAS, SL SAHAKIAN, JA LEVINE, RL WEISS, SJ AF REDDY, VY DESROCHERS, PE PIZZO, SV GONIAS, SL SAHAKIAN, JA LEVINE, RL WEISS, SJ TI OXIDATIVE DISSOCIATION OF HUMAN ALPHA(2)-MACROGLOBULIN TETRAMERS INTO DYSFUNCTIONAL DIMERS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN ALPHA-2-MACROGLOBULIN; METHIONINE RESIDUES; HALF-MOLECULES; ALPHA-1-PROTEINASE INHIBITOR; NUCLEOPHILIC MODIFICATION; CONFORMATIONAL CHANGE; ALPHA-MACROGLOBULINS; GLUTAMINE-SYNTHETASE; NEUTROPHIL ELASTASE; PROTEINASE-BINDING AB Human alpha(2)-macroglobulin is a broad-spectrum, homotetrameric antiproteinase that can maximally bind up to two proteinase molecules in a ternary complex. Proteinases cleave the inhibitor within a peptide stretch termed the bait region and induce the emergence of internal thiol esters whose nucleophilic scission precede a major conformational change which entraps enzymes within molecular cages. In a previous study, leukocyte generated hypohalous acids and N-haloamines were identified as the first examples of physiologically relevant inactivators of the antiproteolytic activity of alpha(2)-macroglobulin (Reddy, V.Y., Pizzo, S. V., and Weiss, S. J. (1989) J. Biol. Chem. 264, 13801-13809), but the mechanisms whereby the oxidants damaged the inhibitor remained undefined. We now demonstrate that N-chloramines (RNCl) destroy the antiproteolytic activity of alpha(2)-macroglobulin in an unusual biphasic process that results in the formation of inactive alpha(2)-macroglobulin half-molecules. In the first phase, 8 eq of RNCl reacted with each alpha(2)-macroglobulin subunit to generate a partially oxidized antiproteinase containing 8 methionyl sulfoxide residues/monomer. Structure-function analyses demonstrated that the oxidized inhibitor retained its homotetrameric structure as well as its ability to entrap proteinases. In marked contrast, the oxidation of an additional 6 methionyl residues and a single tryptophanyl residue fractured the alpha(2)M homotetramer across its non-covalent axis into two pairs of disulfide-linked dimers. Despite the fact that the oxidized dimers displayed normal bait regions whose cleavage by proteinases initiated thiol ester scission, all antiproteolytic activity was lost. Furthermore, the oxidized dimers were unable to undergo the critical conformational changes normally associated with bait region cleavage or thiol ester scission. Together, these results demonstrate that chlorinated oxidants destroy the antiproteolytic activity of alpha(2)-macroglobulin by attacking a subset of methionyl and tryptophanyl residues whose oxidation mediates the dissociation of the native homotetramer into conformationally locked dimers. C1 DUKE UNIV,MED CTR,DEPT PATHOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT BIOCHEM,DURHAM,NC 27710. UNIV VIRGINIA,HLTH SCI CTR,DEPT PATHOL,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,HLTH SCI CTR,DEPT BIOCHEM,CHARLOTTESVILLE,VA 22908. UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,ANN ARBOR,MI 48109. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RI Levine, Rodney/D-9885-2011 FU NHLBI NIH HHS [HL-28024]; NIAID NIH HHS [AI-23870] NR 68 TC 80 Z9 80 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 11 PY 1994 VL 269 IS 6 BP 4683 EP 4691 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW989 UT WOS:A1994MW98900115 PM 7508448 ER PT J AU ROTH, JS KELLEY, JA CHUN, HG WARD, FT AF ROTH, JS KELLEY, JA CHUN, HG WARD, FT TI SIMULTANEOUS MEASUREMENT OF THE CELL-DIFFERENTIATING AGENT HEXAMETHYLENE BISACETAMIDE AND ITS METABOLITES BY GAS-CHROMATOGRAPHY SO JOURNAL OF CHROMATOGRAPHY B-BIOMEDICAL APPLICATIONS LA English DT Article ID MURINE ERYTHROLEUKEMIA-CELLS; PHASE-I TRIAL; MYELODYSPLASTIC SYNDROME; INDUCE DIFFERENTIATION; MYELOID-LEUKEMIA; RETINOIC ACID; NSC-95580; INFUSION; BIOAVAILABILITY; COMBINATIONS AB Hexamethylene bisacetamide (HMBA) is a potent in vitro differentiating agent that has clinical potential as an anticancer drug both as a single agent and as a component of combination therapy. A sensitive and efficient GC method for the isolation, derivatization, and measurement of both HMBA and its two major metabolites in plasma and urine in a single analysis is described. In situ carbamylation of the biological sample with diethylpyrocarbonate forms the urethane derivative of the basic N-acetyl diaminohexane metabolite and allows analyte isolation and concentration by solid-phase extraction. Subsequent formation of the n-butyl ester of 6-acetamidohexanoic acid, the major metabolite, provides a derivatized biological extract that can be rapidly analyzed by temperature-programmed GC. The quantitative extraction and the efficient derivatization steps provide a limit of quantitation of 0.05 mM (10 mug/ml) for all analytes with a precision better than 8% for the range of in vitro activity (0.1-2.0 mM). This method is amenable to automation and is well-suited for the analysis of clinical samples. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BLDG 37,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,INVEST DRUG BRANCH,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,DEPT MED,HEMATOL ONCOL SERV,WASHINGTON,DC 20307. NR 35 TC 0 Z9 0 U1 0 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR B JI J. Chromatogr. B-Biomed. Appl. PD FEB 11 PY 1994 VL 652 IS 2 BP 149 EP 159 DI 10.1016/0378-4347(93)E0395-7 PG 11 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA ND220 UT WOS:A1994ND22000003 PM 8006099 ER PT J AU FIGG, WD YEH, HJC THIBAULT, A PLUDA, JM ITOH, F YARCHOAN, R COOPER, MR AF FIGG, WD YEH, HJC THIBAULT, A PLUDA, JM ITOH, F YARCHOAN, R COOPER, MR TI ASSAY OF THE ANTIANGIOGENIC COMPOUND TNP-470, AND ONE OF ITS METABOLITES, AGM-1883, BY REVERSED-PHASE HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY IN PLASMA SO JOURNAL OF CHROMATOGRAPHY B-BIOMEDICAL APPLICATIONS LA English DT Article ID ANGIOGENESIS; INHIBITION; HEPARIN; GROWTH AB This paper describes a reversed-phase, high-performance liquid chromatographic (HPLC) method for the isolation, detection, and quantification of TNP-470 (I) and one of its active metabolites, AGM-1883 (II), from plasma. These compounds are initially extracted from plasma with an organic solvent and then separated from one another on a C18 column. Those fractions eluting from the C18 column and containing either I or II are then derivatized through their epoxide moieties with sodium 8-quinolinethiolate (SQT). This derivatization produces fluorescent species that are isolated and quantified by a second reversed-phase HPLC analysis. The assay yields a lower limit of reliable quantification of 2.5 ng/ml and is linear to a concentration at least as high as 160 ng/ml. The inter-assay percent coefficient of variation is less than 18%. C1 NIDDKD,ANALYT CHEM LAB,BETHESDA,MD. NCI,INVEST DRUG BRANCH,DEV CHEMOTHERAPY SECT,BETHESDA,MD 20892. NCI,MED BRANCH,RETROVIRAL DIS SECT,BETHESDA,MD 20892. RP FIGG, WD (reprint author), NCI,CLIN PHARMACOL BRANCH,CLIN PHARMACOKINET LAB,BLDG 10,RM 5A01,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Figg Sr, William/M-2411-2016 NR 10 TC 13 Z9 13 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR B JI J. Chromatogr. B-Biomed. Appl. PD FEB 11 PY 1994 VL 652 IS 2 BP 187 EP 194 DI 10.1016/0378-4347(93)E0388-7 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA ND220 UT WOS:A1994ND22000007 PM 8006103 ER PT J AU SCHUBERT, U HENKLEIN, P BOLDYREFF, B WINGENDER, E STREBEL, K PORSTMANN, T AF SCHUBERT, U HENKLEIN, P BOLDYREFF, B WINGENDER, E STREBEL, K PORSTMANN, T TI THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENCODED VPU PROTEIN IS PHOSPHORYLATED BY CASEIN KINASE-2 (CK-2) AT POSITIONS SER52 AND SER56 WITHIN A PREDICTED ALPHA-HELIX-TURN-ALPHA-HELIX-MOTIF SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Note DE PROTEIN PHOSPHORYLATION; CASEIN KINASE-2 (CK-2); HUMAN IMMUNODEFICIENCY VIRUS TYPE 1 (HIV-1); VPU; PROTEIN STRUCTURE ID INFLUENZA-VIRUS; M2 PROTEIN; HIV-1; DNA; MUTAGENESIS; SPECIFICITY; SEQUENCE; CHANNEL; GENE; BETA C1 HUMBOLDT UNIV BERLIN,MED FAK CHARITE,INST PHARMAKOL & TOXIKOL,BERLIN,GERMANY. UNIV SAARLAND,INST HUMANGENET,HOMBURG,GERMANY. GESELL BIOTECHNOL FORSCH MBH,BEREICH GENET,BRAUNSCHWEIG,GERMANY. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP SCHUBERT, U (reprint author), HUMBOLDT UNIV BERLIN,MED FAK CHARITE,INST MED IMMUNOL,BERLIN,GERMANY. NR 37 TC 124 Z9 126 U1 2 U2 4 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 11 PY 1994 VL 236 IS 1 BP 16 EP 25 DI 10.1006/jmbi.1994.1114 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW687 UT WOS:A1994MW68700003 PM 8107101 ER PT J AU JIN, DJ TURNBOUGH, CL AF JIN, DJ TURNBOUGH, CL TI AN ESCHERICHIA-COLI RNA-POLYMERASE DEFECTIVE IN TRANSCRIPTION DUE TO ITS OVERPRODUCTION OF ABORTIVE INITIATION PRODUCTS SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE RNA POLYMERASE; TRANSCRIPTION INITIATION; PROMOTER CLEARANCE; ABORTIVE INITIATION; PYRBI OPERON ID RIBONUCLEIC-ACID POLYMERASE; RIFAMPICIN INHIBITION; TERNARY COMPLEXES; PYRBI OPERON; TERMINATION; PROMOTER; ELONGATION; PHENOTYPES; MUTATIONS; MECHANISM C1 UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. RP JIN, DJ (reprint author), NCI,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BLDG 37,ROOM 2E14,BETHESDA,MD 20892, USA. FU NIGMS NIH HHS [GM 29466] NR 37 TC 34 Z9 34 U1 0 U2 0 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 11 PY 1994 VL 236 IS 1 BP 72 EP 80 DI 10.1006/jmbi.1994.1119 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW687 UT WOS:A1994MW68700008 PM 7508986 ER PT J AU ALFONSO, PJ CRIPPA, MP HAYES, JJ BUSTIN, M AF ALFONSO, PJ CRIPPA, MP HAYES, JJ BUSTIN, M TI THE FOOTPRINT OF CHROMOSOMAL-PROTEINS HMG-14 AND HMG-17 ON CHROMATIN SUBUNITS SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE CHROMATIN; NON-HISTONES; HMG; HISTONE H1 ID MOBILITY GROUP PROTEIN-14; NUCLEOSOME CORE PARTICLES; HISTONE; DNA; BINDING; TRANSCRIPTION; COMPLEX; DOMAIN; HMG14 C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. RI crippa, massimo/J-6514-2016; Bustin, Michael/G-6155-2015 OI crippa, massimo/0000-0003-3214-9670; NR 39 TC 59 Z9 65 U1 1 U2 2 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 11 PY 1994 VL 236 IS 1 BP 189 EP 198 DI 10.1006/jmbi.1994.1128 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW687 UT WOS:A1994MW68700017 PM 8107104 ER PT J AU PATTERSON, TA ZHANG, ZS BAKER, T JOHNSON, LL FRIEDMAN, DI COURT, DL AF PATTERSON, TA ZHANG, ZS BAKER, T JOHNSON, LL FRIEDMAN, DI COURT, DL TI BACTERIOPHAGE-LAMBDA N-DEPENDENT TRANSCRIPTION ANTITERMINATION - COMPETITION FOR AN RNA SITE MAY REGULATE ANTITERMINATION SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE TRANSCRIPTION ELONGATION; TERMINATION; NUSB; S10; N ID ESCHERICHIA-COLI; PHAGE-LAMBDA; NUSA PROTEIN; RECOGNITION SITE; ANTI-TERMINATION; RIBOSOMAL-RNA; COLIPHAGE-LAMBDA; SECY24 MUTATION; GENE-PRODUCT; NUTL REGION C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHROMOSOME BIOL LAB,FREDERICK,MD 21702. UNIV MICHIGAN,DEPT MICROBIOL & IMMUNOL,ANN ARBOR,MI 48109. RI Friedman, David/G-3198-2015 OI Friedman, David/0000-0002-2741-4671 FU NCI NIH HHS [N01-CO74101]; NIAID NIH HHS [AI1459-10] NR 53 TC 44 Z9 45 U1 0 U2 0 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 11 PY 1994 VL 236 IS 1 BP 217 EP 228 DI 10.1006/jmbi.1994.1131 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW687 UT WOS:A1994MW68700020 PM 8107107 ER PT J AU OBERTO, J SLOAN, SB WEISBERG, RA AF OBERTO, J SLOAN, SB WEISBERG, RA TI A SEGMENT OF THE PHAGE HK022 CHROMOSOME IS A MOSAIC OF OTHER LAMBDOID CHROMOSOMES SO NUCLEIC ACIDS RESEARCH LA English DT Article ID OOP ANTISENSE RNA; BACTERIOPHAGE-LAMBDA; SEQUENCE-ANALYSIS; REPLICATION; PROTEIN; REGION; RECOMBINATION; SPECIFICITY; PROMOTERS; EXCHANGE AB We report the sequence of a region of the PR operon of lambdoid phage HK022 and an analysis of the proteins it encodes. This region has DNA sequence elements and open reading frames that resemble those found in phages lambda, P22, and phi 80. The open reading frames encode homologs of the lambda CII transcription activator, the P22 DNA replication proteins, and a fourth protein of unknown function. C1 NICHHD,MOLEC GENET LAB,MICROBIAL GENET LAB,BETHESDA,MD 20892. NR 22 TC 10 Z9 11 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD FEB 11 PY 1994 VL 22 IS 3 BP 354 EP 356 DI 10.1093/nar/22.3.354 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MX908 UT WOS:A1994MX90800015 PM 8127672 ER PT J AU ONDRIAS, K MISIK, V STASKO, A GERGEL, D HROMADOVA, M AF ONDRIAS, K MISIK, V STASKO, A GERGEL, D HROMADOVA, M TI COMPARISON OF ANTIOXIDANT PROPERTIES OF NIFEDIPINE AND ILLUMINATED NIFEDIPINE WITH NITROSO SPIN TRAPS IN LOW-DENSITY LIPOPROTEINS AND PHOSPHATIDYLCHOLINE LIPOSOMES SO BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM LA English DT Article DE NIFEDIPINE; NITROSO SPIN TRAP; LOW DENSITY LIPOPROTEIN; NITROXIDE RADICAL; LIPID PEROXIDATION; EPR SPECTROSCOPY ID LIPID-PEROXIDATION; CALCIUM-ANTAGONISTS; ENDOTHELIAL-CELLS; FATTY-ACIDS; VITAMIN-E; DEGRADATION; INHIBITION; OXIDATION; PROTECTION; VERAPAMIL AB Illumination nifedipine, a calcium channel blocker, gives a nitroso-compound, 2,6-dimethyl-4-(2-nitrosophenyl)-3,5-pyridine-dicarboxylic acid dimethyl ester (NTP), which has spin trapping properties. The antioxidant ability of NTP was tested in a model of lipid peroxidation in low density lipoproteins (LDL) and phosphatidylchoiine liposomes, and was compared with parent nifedipine and with other nitroso spin traps such as 3,5-dibromo-4-nitrosobenzene-sulfonic acid (BNTB), nitrosobenzene (NTB) and 2-methyl-2-nitrosopropane (MNP). Nifedipine (20-200 mu mol/l) did not inhibit lipid peroxidation either in LDL on in liposomes, whereas its photolytical product NTP was found to be very effective at the same concentrations. The average antioxidant potencies of the nitroso spin traps were similar in both models and decreased in the order: NTP greater than or equal to BNTB > NTB greater than or equal to MNP. As detected by EPR spectroscopy, the studied nitroso compounds formed stable nitroxide radicals in a pseudo-Diels-Alder reaction, as a result of their interaction with unsaturated bonds of lipids in LDL and liposomes. The relative concentrations of thus formed radicals were in the order: NTP much greater than BNTB much greater than NTB approximate to MNP and were related to their antioxidant properties. Thus it seems that the ability of the nitroso-compounds to form nitroxide radicals with unsaturated lipids may play a role in the antioxidant effect of these compounds. C1 NCI, BETHESDA, MD 20892 USA. SLOVAK ACAD SCI, INST EXPTL PHARMACOL, BRATISLAVA 84216, SLOVAK REPUBLIC. SLOVAK UNIV TECHNOL BRATISLAVA, FAC CHEM TECHNOL, BRATISLAVA 81237, SLOVAK REPUBLIC. SLOVAK ACAD SCI, INST EXPTL ENDOCRINOL, BRATISLAVA 83306, SLOVAK REPUBLIC. NR 35 TC 18 Z9 18 U1 2 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0005-2760 J9 BBA-LIPID LIPID MET JI Biochim. Biophys. Acta-Lipids Lipid Metab. PD FEB 10 PY 1994 VL 1211 IS 1 BP 114 EP 119 DI 10.1016/0005-2760(94)90145-7 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MY085 UT WOS:A1994MY08500015 PM 8123675 ER PT J AU WU, CC BRECHBIEL, MW KOZAK, RW GANSOW, OA AF WU, CC BRECHBIEL, MW KOZAK, RW GANSOW, OA TI METAL-CHELATE-DENDRIMER-ANTIBODY CONSTRUCTS FOR USE IN RADIOIMMUNOTHERAPY AND IMAGING SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID MONOCLONAL-ANTIBODIES; CONJUGATION; DTPA; POLYMERS; REAGENT; AGENTS; PROTEINS; ACIDS AB Polyamidoamine dendrimers were modified chemically by reaction with DOTA and DTPA type bifunctional metal chelators and were coupled to monoclonal antibody 2E4 without loss of protein immunoreactivity. Both the DTPA- and DOTA-dendrimer-antibody constructs were easily labeled with Y-90, In-111, Bi-212 or cold Gd(III) suggesting use of this dendrimer-macrocycle for mAb guided radiotherapy or imaging. C1 US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD 20892. RP WU, CC (reprint author), NIH,RADIAT ONCOL BRANCH,CHEM SECT,BETHESDA,MD 20892, USA. NR 34 TC 128 Z9 132 U1 2 U2 11 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD FEB 10 PY 1994 VL 4 IS 3 BP 449 EP 454 DI 10.1016/0960-894X(94)80014-6 PG 6 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA MY646 UT WOS:A1994MY64600013 ER PT J AU MISIK, V RIESZ, P AF MISIK, V RIESZ, P TI FREE-RADICAL FORMATION BY ULTRASOUND IN ORGANIC LIQUIDS - A SPIN-TRAPPING AND EPR STUDY SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID SYNCHRONOUS PICOSECOND SONOLUMINESCENCE; ISOTOPE-EXCHANGE-REACTIONS; AQUEOUS-SOLUTIONS; THERMAL-DECOMPOSITION; NONVOLATILE SOLUTES; PYROLYSIS RADICALS; WATER MIXTURES; SONOCHEMISTRY; SONOLYSIS; CAVITATION AB The 50-kHz sonolysis of a variety of organic liquids, including n-alkanes (C-8-C-16), n-alcohols (C-3-C-8), cyclohexane, toluene, dioxane, and N,N-dimethylformamide, was investigated by EPR and spin trapping. 2,4,6-Tri-tertbutylnitrosobenzene (3tBNB) was found to be a particularly suitable spin trap since primary, secondary, and tertiary alkyl radicals could be distinguished. By comparison with sonolysis of the fully deuterated analogues of the organic liquids (N,N-dimethylformamide-d(7), n-butanol-d(10), cyclohexane-d(12), dioxane-d(8)), the absence of radicals originating from the thermal decomposition of the spin trap (3tBNB) under conditions of the present experiments could be established. When the spin traps 3tBNB and 3,5-dibromo-4-nitrosobenzenesulfonate were compared in the sonolysis of N,N-dimethylformamide and N,N-dimethylformamide-d(7), similar results were obtained. For the homologous series of n-alkanes and n-alcohols spin adduct yields with 3tBNB increase with decreasing solvent vapor pressure. Spin trapping appears to be a promising method for investigating the mechanisms of sonochemical reactions in organic liquids. C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. SLOVAK ACAD SCI,INST EXPTL PHARMACOL,BRATISLAVA 84216,SLOVAKIA. NR 50 TC 18 Z9 18 U1 2 U2 10 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 10 PY 1994 VL 98 IS 6 BP 1634 EP 1640 DI 10.1021/j100057a016 PG 7 WC Chemistry, Physical SC Chemistry GA MW678 UT WOS:A1994MW67800016 ER PT J AU TSUKIYAMA, T BECKER, PB WU, C AF TSUKIYAMA, T BECKER, PB WU, C TI ATP-DEPENDENT NUCLEOSOME DISRUPTION AT A HEAT-SHOCK PROMOTER MEDIATED BY BINDING OF GAGA TRANSCRIPTION FACTOR SO NATURE LA English DT Article ID TUMOR VIRUS PROMOTER; DROSOPHILA-MELANOGASTER; CHROMATIN STRUCTURE; GENE; PROTEINS; DNA; COMPLEX; ACTIVATION; ENCODES; EXTRACTS AB Genetic control elements are usually situated in local regions of chromatin that are hypersensitive to structural probes such as DNase I. We have reconstructed the chromatin structure of the hsp70 promoter using an in vitro nucleosome assembly system. Binding of the GAGA transcription factor on existing nucleosomes leads to nucleosome disruption, DNase I hypersensitivity at the TATA box and heat-shock elements, and rearrangement of adjacent nucleosomes. ATP hydrolysis facilitates this process, suggesting that an energy-dependent pathway is involved in chromatin remodelling. C1 NCI,BIOCHEM LAB,BLDG 37,ROOM 4C-09,BETHESDA,MD 20892. NR 51 TC 521 Z9 522 U1 0 U2 4 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD FEB 10 PY 1994 VL 367 IS 6463 BP 525 EP 532 DI 10.1038/367525a0 PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MV863 UT WOS:A1994MV86300049 PM 8107823 ER PT J AU TRACHTENBERG, AI AF TRACHTENBERG, AI TI OPIATES FOR PAIN - PATIENTS TOLERANCE AND SOCIETY INTOLERANCE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter ID SUICIDE RP TRACHTENBERG, AI (reprint author), NIDA,ROCKVILLE,MD, USA. NR 6 TC 5 Z9 5 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 9 PY 1994 VL 271 IS 6 BP 427 EP 427 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MU491 UT WOS:A1994MU49100018 PM 8295310 ER PT J AU DAVIS, DL DINSE, GE HOEL, DG AF DAVIS, DL DINSE, GE HOEL, DG TI DECREASING CARDIOVASCULAR-DISEASE AND INCREASING CANCER AMONG WHITES IN THE UNITED-STATES FROM 1973 THROUGH 1987 - GOOD-NEWS AND BAD-NEWS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID INDUSTRIALIZED COUNTRIES; TRENDS; MORTALITY; PERIOD; MODELS; RATES; AGE AB Objective.-Trends in cancer mortality, cardiovascular mortality, and cancer incidence are assessed among US whites to determine whether aging of the population and smoking patterns completely account for increased cancer rates from 1973 through 1987. Design.-For mortality, percentage changes in age-specific rates were calculated. For cancer incidence, trends in age-specific rates across time periods and birth cohorts were assessed for several sites. Main Outcome Measures.-National US cardiovascular and cancer mortality rates and incidence rates for smoking-related cancer, breast cancer, and all other types of cancer in 1 0% of the US population covered by the National Cancer Institute's Surveillance, Epidemiology, and End Results Program were analyzed. Results.-From 1973 through 1987, cardiovascular mortality decreased 42% in the age group 0 to 54 years and decreased 33% in the age group 55 to 84 years; concurrently, cancer mortality decreased 17% in the younger group but increased 12% in the older group. By 1987, even though proportionally fewer people in the older age groups died, relatively more of them died of cancer. Men born in the 1940s had twice as much cancer as those born in 1888 through 1897 and more than twice as much cancer not linked to smoking; women born during this period had 50% and 30% more of these same cancers, respectively. Rates of smoking-related cancers in recent cohorts of women were five to six times greater than in those born in 1888 th rough 1897, while rates in men declined. Recent cohorts of women also had more than twice as much breast cancer as those born in 1888 through 1897. Conclusions.-In recent US birth cohorts, our model found that increases in cancer have occurred that are not solely linked to aging of the population and smoking patterns. In light of these results and similar findings in Sweden, changes in carcinogenic hazards in addition to smoking are likely to have occurred and need to be studied further. C1 NIEHS,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709. MED UNIV S CAROLINA,HOLLINGS CANC CTR,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT BIOMETRY & EPIDEMIOL,CHARLESTON,SC 29425. RP DAVIS, DL (reprint author), DEPT HLTH & HUMAN SERV,OFF ASSISTANT SECRETARY HLTH,200 INDEPENDENCE AVE SW,WASHINGTON,DC 20201, USA. NR 20 TC 66 Z9 67 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 9 PY 1994 VL 271 IS 6 BP 431 EP 437 DI 10.1001/jama.271.6.431 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA MU491 UT WOS:A1994MU49100029 PM 8295317 ER PT J AU KOTLOFF, KL JOHNSON, JP NAIR, P HICKMAN, D LIPPINCOTT, P WILSON, PD CLEMENS, JD AF KOTLOFF, KL JOHNSON, JP NAIR, P HICKMAN, D LIPPINCOTT, P WILSON, PD CLEMENS, JD TI DIARRHEAL MORBIDITY DURING THE 1ST 2 YEARS OF LIFE AMONG HIV-INFECTED INFANTS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; LONGITUDINAL DATA-ANALYSIS; PERSISTENT DIARRHEA; SYNDROME AIDS; VIRUS TYPE-1; CHILDREN; WOMEN; ENTEROPATHY; COMMUNITY; PATTERNS AB Objective.-To determine the incidence, cause, and patterns of diarrhea during the first 2 years of life among infants infected perinatally with the human immunodeficiency virus (HIV). Design.-A cohort study in which infants were enrolled shortly after birth and followed up longitudinally using biweekly surveillance for the occurrence of diarrhea. Stool specimens collected at the onset of diarrhea were evaluated for enteropathogens. Infants who were infected with HIV were compared with uninfected infants. Subjects.-Infants born to HIV-infected women at the University of Maryland Hospital, Baltimore, were recruited at 0 to 3 months of age. This analysis included 58 infants enrolled in the cohort and followed up at least 15 months (unless death intervened) whose HIV status was established (18 HIV-infected infants and 40 HIV-uninfected infants). Measurements and Results.-The overall incidence of diarrhea in HIV-infected infants was 3.2 episodes per 12 child-months compared with 1.5 episodes per 12 child-months among HIV-uninfected infants (incidence density ratio, 2.2; P<.05). An enteropathogen was identified in stool specimens collected during 20% of diarrheal episodes occurring in HIV-infected infants and during 25% of diarrheal episodes occurring in HIV-uninfected infants. Episodes that persisted tor 14 days or longer were significantly more common among HIV-infected infants. The peak incidence of diarrhea occurred at 0 to 5 months of age for HIV-infected infants compared with 6 to 11 months for HIV-uninfected infants. Early onset of diarrhea (<6 months old) in HIV-infected infants was associated with the later development of persistent episodes of diarrhea, and those with persistent episodes had more severe HIV infection, characterized by a significantly higher frequency of opportunistic infections and lower CD4+ T-lymphocyte counts by 1 year of age. Conclusions.-Both acute and persistent episodes of diarrhea are major sources of morbidity in HIV-infected infants. Moreover, persistent diarrhea is a marker for rapid progression of HIV disease. C1 UNIV MARYLAND,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DIV TROP PEDIAT,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DIV PEDIAT IMMUNOL,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DIV PEDIAT EDUC,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT EPIDEMIOL,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT PREVENT MED,BALTIMORE,MD 21201. NICHHD,EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP KOTLOFF, KL (reprint author), UNIV MARYLAND,SCH MED,CTR VACCINE DEV,10 S PINE ST,BALTIMORE,MD 21201, USA. RI kotloff, karen/E-7768-2012 OI kotloff, karen/0000-0003-1808-6431 FU NICHD NIH HHS [1R01 HD26691] NR 34 TC 20 Z9 20 U1 0 U2 5 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 9 PY 1994 VL 271 IS 6 BP 448 EP 452 DI 10.1001/jama.271.6.448 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MU491 UT WOS:A1994MU49100032 PM 8295320 ER PT J AU HOSUR, MV BHAT, TN KEMPF, DJ BALDWIN, ET LIU, BS GULNIK, S WIDEBURG, NE NORBECK, DW APPELT, K ERICKSON, JW AF HOSUR, MV BHAT, TN KEMPF, DJ BALDWIN, ET LIU, BS GULNIK, S WIDEBURG, NE NORBECK, DW APPELT, K ERICKSON, JW TI INFLUENCE OF STEREOCHEMISTRY ON ACTIVITY AND BINDING MODES FOR C(2) SYMMETRY-BASED DIOL INHIBITORS OF HIV-1 PROTEASE SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID CRYSTAL-STRUCTURE; COMPLEX AB The incorporation of C-2 Symmetry has become a useful paradigm in the design of active site inhibitors for HIV-1 protease (HIV PR) and has led to the design of a series of highly potent, C-2 symmetry-based, diol-containing inhibitors of HIV PR, one of which, A-77003, has reached clinical trials. However, the stereochemistry of the diol core influences protease inhibition and antiviral activity in a manner that is not well understood. We analyzed the crystal structures of a diastereomeric series of C-2 symmetry-based diol inhibitors, along with a deshydroxy analogue, bound to HIV PR and found that the stereochemistry of the diol core influences the mode of binding to the active site aspartic acids. Diasteromers with similar binding affinity can bind in different, asymmetric and symmetric, modes, while those with different binding affinities can bind in a similar manner. The positional symmetry of an inhibitor with respect to the enzyme C-2 axis may be distinguished from its conformational symmetry. The structural differences between the inhibitor complexes were mainly confined to the central core portion of the diols, can be described by torsional differences about the central three bonds, and primarily affect interactions within the active site pocket formed by Asp 25/125 and Gly 27/127. Some flexibility in the enzyme backbone at Gly 127 was also apparent. Based on these results, we suggest that the binding mode for central hydroxy-bearing, C-2-symmetric inhibitors will be determined by how well the inhibitor can simultaneously optimize hydrogen bonding with the active site carboxylate groups and van der Waals contacts with the neighboring backbone atoms of the active site ''psi''-loops. A symmetric hydrogen-bonding arrangement with either one or tio symmetrically positioned hydroxy groups appears to be preferred over less symmetric configurations. C1 NCI, FCRDC,PRI DYNCORP,FREDERICK BIOMED SUPERCOMP CTR, STRUCT BIOCHEM PROGRAM, FREDERICK, MD 21702 USA. ABBOTT LABS, DIV PHARMACEUT PROD, ABBOTT PK, IL 60064 USA. AGOURON PHARMACEUT, SAN DIEGO, CA 92121 USA. NR 26 TC 125 Z9 126 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD FEB 9 PY 1994 VL 116 IS 3 BP 847 EP 855 DI 10.1021/ja00082a004 PG 9 WC Chemistry, Multidisciplinary SC Chemistry GA MW990 UT WOS:A1994MW99000004 ER PT J AU LIANG, GN GANNETT, P SHI, XL ZHANG, Y CHEN, FX GOLD, B AF LIANG, GN GANNETT, P SHI, XL ZHANG, Y CHEN, FX GOLD, B TI DNA-SEQUENCING WITH THE HYDROPEROXIDE OF TETRAHYDROFURAN SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Note ID ELECTRON-SPIN-RESONANCE; PROBES C1 UNIV NEBRASKA,MED CTR,EPPLEY INST RES CANC & ALLIED DIS,OMAHA,NE 68198. UNIV NEBRASKA,MED CTR,DEPT PHARMACEUT SCI,OMAHA,NE 68198. W VIRGINIA UNIV,DEPT MED CHEM,MORGANTOWN,WV 26506. NCI,EXPTL PATHOL LAB,BETHESDA,MD 20892. RI Shi, Xianglin/B-8588-2012; Gannett, Peter/J-3347-2015; OI Gannett, Peter/0000-0002-7859-5468; Liang, Gangning/0000-0001-8664-922X NR 16 TC 15 Z9 15 U1 1 U2 3 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 9 PY 1994 VL 116 IS 3 BP 1131 EP 1132 DI 10.1021/ja00082a045 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA MW990 UT WOS:A1994MW99000045 ER PT J AU CARROLL, LJ XU, Y THRALL, SH MARTIN, BM DUNAWAYMARIANO, D AF CARROLL, LJ XU, Y THRALL, SH MARTIN, BM DUNAWAYMARIANO, D TI SUBSTRATE-BINDING DOMAINS IN PYRUVATE PHOSPHATE DIKINASE SO BIOCHEMISTRY LA English DT Article ID LIVER MALIC ENZYME; ESCHERICHIA-COLI; ACTIVE-SITE; PHOSPHORYLATED ENZYME; ANALOG BROMOPYRUVATE; LIMITED PROTEOLYSIS; SEQUENCE; RESIDUE; PHOSPHOENOLPYRUVATE; IDENTIFICATION AB Proteolysis of Clostridium symbiosum pyruvate phosphate dikinase (PPDK) in its free or phosphorylated state with subtilisin Carlsberg followed two different cleavage pathways. The major pathway involved initial cleavage of the holoenzyme (93 kDa) into a stable 25-kDa N-terminal fragment and transiently stable 67-kDa C-terminal fragment. The 67-kDa fragment was cleaved to generate a stable 35-kDa fragment and an unstable 30-kDa fragment (containing the catalytic histidine). Proteolytic cleavage via the minor pathway divided the holoenzyme into an unstable 37-kDa N-terminal piece (which was further cleaved to the stable 25-kDa fragment produced in the major pathway) and a transiently stable 55-kDa C-terminal fragment. The 55-kDa fragment was then cleaved to produce the stable 35-kDa fragment produced by the major pathway. The cleavage pattern of PPDK complexed with the ATP analog adenyl imidodiphosphate was identical to that of the free enzyme, only the rate of cleavage as slower. In contrast, proteolysis of the phosphorylenzyme-oxalate complex generated the 55-kDa fragment indicating that oxalate binding induces a change in protein conformation. Treatment of PPDK with [1-C-14] bromopyruvate followed by proteolysis revealed selective radiolabeling of the stable 35-kDa fragment while similar experiments with [C-14]2',3'-dialdehyde adenosine 5'-monophosphate resulted in selective radiolabeling of the stable 25-kDa fragment. These results were interpreted to suggest that PPDK contains several structural domains and that the catalytic histidine, the pyruvate binding site, and the ATP binding site may be located on different domains. C1 UNIV MARYLAND,DEPT CHEM & BIOCHEM,COLL PK,MD 20742. NATL INST MENTAL HLTH,CLIN NEUROSCI BRANCH,MOLEC NEUROGENET UNIT,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM-36260] NR 39 TC 23 Z9 24 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 8 PY 1994 VL 33 IS 5 BP 1134 EP 1142 DI 10.1021/bi00171a012 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MW257 UT WOS:A1994MW25700012 PM 8110745 ER PT J AU LEVY, P LOREAL, O MUNIER, A YAMADA, Y PICARD, J CHERQUI, G CLEMENT, B CAPEAU, J AF LEVY, P LOREAL, O MUNIER, A YAMADA, Y PICARD, J CHERQUI, G CLEMENT, B CAPEAU, J TI ENTEROCYTIC DIFFERENTIATION OF THE HUMAN CACO-2 CELL-LINE IS CORRELATED WITH DOWN-REGULATION OF FIBRONECTIN AND LAMININ SO FEBS LETTERS LA English DT Article DE CACO-2 CELL; ENTEROCYTIC DIFFERENTIATION; FIBRONECTIN; LAMININ; DOWN-REGULATION ID PROTEIN KINASE-C; BASEMENT-MEMBRANE; MULTIDOMAIN PROTEIN; B-CHAINS; A-CHAIN; EXPRESSION; CULTURE; BIOSYNTHESIS; ADHESION; FETAL AB Human intestinal Caco-2 cells were used to examine the expression of fibronectin (FN) and laminin (LN) during enterocytic differentiation. Combination of immunoprecitation, Western and Northern blotting revealed that Caco-2 cells expressed a classical FN and a variant form of LN: besides B1 and B2 chains, LN contained a 350-kDa heavy chain instead of the 400-kDa A chain. Throughout Caco-2 cell differentiation, FN and LN synthesis decreased at both mRNA and protein levels. These data indicate that enterocytic differentiation involves bath transcriptional and/or post-transcriptional down-regulation of FN and LN gene expression. C1 HOP PONTCHAILLOU,INSERM,U49,UNITE RECH HEPATOL,F-35033 RENNES,FRANCE. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. RP LEVY, P (reprint author), UNIV PARIS 06,INSERM,U181,BIOCHIM BIOL CELLULAIRE LAB,27 RUE CHALIGNY,F-75571 PARIS 12,FRANCE. RI Loreal, Olivier/G-3366-2013; Clement, Bruno/E-5546-2016 NR 33 TC 25 Z9 25 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD FEB 7 PY 1994 VL 338 IS 3 BP 272 EP 276 DI 10.1016/0014-5793(94)80282-3 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA MW155 UT WOS:A1994MW15500007 PM 8307193 ER PT J AU CHARY, KVR RASTOGI, VK GOVIL, G MILES, HT AF CHARY, KVR RASTOGI, VK GOVIL, G MILES, HT TI ESTIMATION OF P-31-H-1 AND H-1-H-1 VICINAL COUPLING-CONSTANTS ALONG THE DNA BACKBONE BY 2D HELCO MEASUREMENTS SO JOURNAL OF THE CHEMICAL SOCIETY-CHEMICAL COMMUNICATIONS LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; TWO-DIMENSIONAL NMR; CONFORMATIONAL-ANALYSIS; SPIN SYSTEMS; SPECTROSCOPY; PROTEINS; FRAGMENTS; H-1-NMR; ACIDS AB An accurate method for simultaneous estimation of P-31-H-1 and H-1-H-1 vicinal coupling constants a long the backbone of DNA fragments is described using the two-dimensional heteronuclear long-range correlation (2D HELCO) experiment. C1 NIDDKD,BETHESDA,MD 20892. RP CHARY, KVR (reprint author), TATA INST FUNDAMENTAL RES,CHEM PHYS GRP,HOMI BHABHA RD,BOMBAY 400005,INDIA. NR 24 TC 5 Z9 5 U1 0 U2 0 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK MILTON ROAD, CAMBRIDGE, CAMBS, ENGLAND CB4 4WF SN 0022-4936 J9 J CHEM SOC CHEM COMM JI J. Chem. Soc.-Chem. Commun. PD FEB 7 PY 1994 IS 3 BP 241 EP 242 DI 10.1039/c39940000241 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA MX131 UT WOS:A1994MX13100001 ER PT J AU MORENS, DM GRANDINETTI, A REED, D WHITE, LR AF MORENS, DM GRANDINETTI, A REED, D WHITE, LR TI SMOKING-ASSOCIATED PROTECTION FROM ALZHEIMERS AND PARKINSONS-DISEASE SO LANCET LA English DT Letter C1 BUCK CTR RES AGING,NOVATO,CA. NIA,BETHESDA,MD 20892. RP MORENS, DM (reprint author), UNIV HAWAII,HONOLULU,HI 96822, USA. NR 2 TC 18 Z9 19 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 5 PY 1994 VL 343 IS 8893 BP 356 EP 357 DI 10.1016/S0140-6736(94)91194-0 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MU985 UT WOS:A1994MU98500040 PM 7695666 ER PT J AU TEAL, SB HSU, VW PETERS, PJ KLAUSNER, RD DONALDSON, JG AF TEAL, SB HSU, VW PETERS, PJ KLAUSNER, RD DONALDSON, JG TI AN ACTIVATING MUTATION IN ARF1 STABILIZES COATOMER BINDING TO GOLGI MEMBRANES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID ADP-RIBOSYLATION FACTOR; SENSITIVE G-PROTEIN; BREFELDIN-A; GUANINE-NUCLEOTIDE; COATED VESICLES; BETA-COP; GTP; EXPRESSION; CISTERNAE; TRANSPORT AB The Ras-related protein ADP-ribosylation factor 1 (ARF1) is a low molecular weight GTP binding protein, which in its GTP state supports the binding of coatomer, a cytosolic coat protein complex, to Golgi membranes. To create an ''active'' ARF, we constructed a point mutation in ARF1, Q71I, which was predicted to slow the rate of GTP hydrolysis. We demonstrate that Q71I, in contrast to wild type ARF1, exhibits a 2-3-fold increase in the half-life of ARF-GTP and is able to promote stable coatomer binding to Golgi membranes in the presence of GTP in vitro. Additionally, Q71I is able to support the binding of a significant amount of coatomer to membranes in the absence of added nucleotides, effectively bypassing the brefeldin A (BFA)-sensitive exchange activity. Furthermore, transfection of cells with Q71I, but not ARF1, renders the Golgi association of coatomer resistant to the effects of BFA in vivo. These observations provide compelling evidence that ARF1 is a necessary GTP binding protein that regulates the reversible binding of coat proteins to Golgi membranes and that the effects of BFA on this process in living cells must be a consequence of BFA's inhibition of guanine nucleotide exchange onto ARF1. C1 NICHHD,CELL BIOL & METAB BRANCH,BLDG 18T-101,BETHESDA,MD 20892. OI Teal, Stephanie/0000-0002-0167-1071 NR 24 TC 88 Z9 88 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 4 PY 1994 VL 269 IS 5 BP 3135 EP 3138 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MV631 UT WOS:A1994MV63100004 PM 8106346 ER PT J AU SLESAREV, AI LAKE, JA STETTER, KO GELLERT, M KOZYAVKIN, SA AF SLESAREV, AI LAKE, JA STETTER, KO GELLERT, M KOZYAVKIN, SA TI PURIFICATION AND CHARACTERIZATION OF DNA TOPOISOMERASE-V - AN ENZYME FROM THE HYPERTHERMOPHILIC PROKARYOTE METHANOPYRUS-KANDLERI THAT RESEMBLES EUKARYOTIC TOPOISOMERASE-I SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SITE-SPECIFIC RECOMBINATION; EXTREMELY THERMOPHILIC ARCHAEBACTERIA; ESCHERICHIA-COLI; REVERSE GYRASE; DESULFUROCOCCUS-AMYLOLYTICUS; GENE-PRODUCT; PROTEIN; IDENTIFICATION; MECHANISM; CLEAVAGE AB DNA topoisomerase V is a novel prokaryotic enzyme related to eukaryotic topoisomerase I. The enzyme is a type I DNA topoisomerase and is recognized by polyclonal antibody against human topoisomerase I. We describe its purification from the hyperthermophilic methanogen Methanopyrus kandleri. The enzyme has high activity in crude extracts and is present in at least 1,500 copies/cell. Topoisomerase V migrates as a 110-kDa polypeptide in SDS-polyacrylamide gel electrophoresis and as a 142-kDa globular protein in gel filtration. It is active up to at least 100-degrees-C on both positively and negatively supercoiled DNA and is not inhibited by single-stranded DNA. The enzyme works from 1 to 650 mm NaCl and up to 3.1 m potassium glutamate. It acts processively at low ionic strength and distributively at high NaCl or KCl concentration. Magnesium is not required and does not stimulate the enzymatic activity. Under DNA denaturing conditions, topoisomerase V catalyzes an unlinking reaction which results in substantial reduction in the linking number of closed circular DNA. The driving force for this process is DNA melting. Camptothecin is not nearly as good an inhibitor for topoisomerase V as it is for eukaryotic topoisomerase 1. The unique occurrence of two major type I topoisomerases (reverse gyrase and topoisomerase V) in M. kandleri may shed new light on the evolution of this family of enzymes and supports the concept of a distant but significant relationship between some hyperthermophilic organisms and eukaryotes. C1 UNIV CALIF LOS ANGELES,DEPT BIOL,LOS ANGELES,CA 90024. UNIV REGENSBURG,D-93053 REGENSBURG,GERMANY. NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. RP SLESAREV, AI (reprint author), UNIV CALIF LOS ANGELES,INST MOLEC BIOL,405 HILGARD AVE,LOS ANGELES,CA 90024, USA. NR 73 TC 40 Z9 41 U1 0 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 4 PY 1994 VL 269 IS 5 BP 3295 EP 3303 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MV631 UT WOS:A1994MV63100029 PM 8106368 ER PT J AU WANG, MH YOSHIMURA, T SKEEL, A LEONARD, EJ AF WANG, MH YOSHIMURA, T SKEEL, A LEONARD, EJ TI PROTEOLYTIC CONVERSION OF SINGLE-CHAIN PRECURSOR MACROPHAGE-STIMULATING PROTEIN TO A BIOLOGICALLY-ACTIVE HETERODIMER BY CONTACT ENZYMES OF THE COAGULATION CASCADE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEPATOCYTE GROWTH-FACTOR; AMINO-ACID-SEQUENCE; SCATTER FACTOR; HUMAN-PLASMA; ACTIVATION; PLASMINOGEN; PROTHROMBIN; UROKINASE; CLEAVAGE; HOMOLOGY AB Human serum macrophage stimulating protein (MSP) is a disulfide-linked heterodimer that induces motile and phagocytic activity of mouse resident peritoneal macrophages. It is a member of the family of kringle proteins, which typically exist in extracellular fluid as single chain precursors that are activated by proteolytic cleavage. In this work, we expressed [S-35]cysteine-labeled recombinant pro-MSP in MSP cDNA-transfected Chinese hamster ovary cells and studied proteolytic processing of pro-MSP and the requirement of cleavage for biological activity. In media containing heat-inactivated fetal bovine serum, the protein was secreted as single chain pro-MSP, which was cleaved over a period of hours to the mature heterodimer. Cleavage was prevented by serine protease inhibitors such as leupeptin or aprotinin; it did not occur if cells were cultured in serum-free medium. Nanomolar concentrations of coagulation proteases kallikrein, factor XIIa or factor XIa cleaved pro-MSP to MSP within 30 min. Pro-MSP had no biological activity. After cleavage by kallikrein, biological activity was quantitatively comparable to that of natural MSP isolated from human plasma. These results support our hypothesis that MSP circulates as the biologically inactive precursor and can be activated by enzymes of the intrinsic coagulation cascade. RP WANG, MH (reprint author), NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,IMMUNOPATHOL SECT,BLDG 506,RM 12-71,FREDERICK,MD 21702, USA. NR 22 TC 78 Z9 78 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 4 PY 1994 VL 269 IS 5 BP 3436 EP 3440 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MV631 UT WOS:A1994MV63100048 PM 7508914 ER PT J AU KIM, SJ PARK, K RUDKIN, BB DEY, BR SPORN, MB ROBERTS, AB AF KIM, SJ PARK, K RUDKIN, BB DEY, BR SPORN, MB ROBERTS, AB TI NERVE GROWTH-FACTOR INDUCES TRANSCRIPTION OF TRANSFORMING GROWTH-FACTOR-BETA-1 THROUGH A SPECIFIC PROMOTER ELEMENT IN PC12 CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GENE-PRODUCT; FACTOR-BETA; TRANSACTIVATION; DIFFERENTIATION; IDENTIFICATION; REPRESSION; E1A; FOS; WT1 AB Nerve growth factor (NGF) stimulates the differentiation of PC12 pheochromocytoma cells to those resembling sympathetic neurons. We have investigated whether NGF regulates transforming growth factor (TGF)-beta gene expression and protein secretion in PC12 cells. These cells constitutively express TGF-beta1 mRNA, whereas TGF-beta2 and -beta3 mRNAs are expressed at very low levels. TGF-beta1 gene expression was stimulated greater than 10-fold when PC12 cells were treated with NGF. Sequences between -119 and -98 in the TGF-beta1 promoter, homologous to an Egr-1 binding site, were shown to be important for both basal and NGF-induced promoter activity. We also found that a factor(s) present in nuclear extracts from PC12 cells interacted with the sequences between -119 and -98 and that expression of this factor was induced by NGF treatment. Moreover, specific binding to TGF-beta1 promoter fragments between -119 and -98 was seen using the bacterially expressed transcription factor Egr-1. These results indicate that activation of TGF-beta1 expression is one of the cellular responses of PC12 cells to NGF and suggest that TGF-beta may play a role in the differentiation of sympathetic neurons. C1 NICHHD,GROWTH FACTORS SECT,BETHESDA,MD 20892. RP KIM, SJ (reprint author), NCI,CHEMOPREVENT LAB,BLDG 41,RM C629,BETHESDA,MD 20892, USA. NR 35 TC 85 Z9 90 U1 1 U2 3 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 4 PY 1994 VL 269 IS 5 BP 3739 EP 3744 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MV631 UT WOS:A1994MV63100089 PM 8106419 ER PT J AU CHAE, MY MCDOUGALL, MG DOLAN, ME SWENN, K PEGG, AE MOSCHEL, RC AF CHAE, MY MCDOUGALL, MG DOLAN, ME SWENN, K PEGG, AE MOSCHEL, RC TI SUBSTITUTED O-6-BENZYLGUANINE DERIVATIVES AND THEIR INACTIVATION OF HUMAN O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID RAT MAMMARY-CARCINOMA; ALKYLATING-AGENTS; SENSITIVITY; TUMOR; O6-BENZYLGUANINE; MODULATION; DEPLETION; DNA AB Several new O-6-benzylguanine analogs bearing increasingly bulky substituent groups on the benzene ring or at position 9 were tested for their ability to inactivate the human DNA repair protein, O-6-alkylguanine-DNA alkyltransferase. Substitution on the benzene ring was well tolerated although activity varied considerably with structural changes in groups attached to position 9. For this site, activity was preserved with large or small lipophilic groups while introduction of non-carbohydrate polar groups generally reduced activity regardless of their size. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. UNIV CHICAGO,MED CTR,DIV HEMATOL ONCOL,CHICAGO,IL 60637. PENN STATE UNIV,MILTON S HERSHEY MED CTR,COLL MED,DEPT CELLULAR & MOLEC PHYSIOL,HERSHEY,PA 17033. PENN STATE UNIV,MILTON S HERSHEY MED CTR,COLL MED,DEPT PHARMACOL,HERSHEY,PA 17033. FU NCI NIH HHS [CA-18137, N01-CO-74101, CA-47228] NR 18 TC 76 Z9 77 U1 1 U2 11 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 4 PY 1994 VL 37 IS 3 BP 342 EP 347 DI 10.1021/jm00029a005 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA MW104 UT WOS:A1994MW10400005 PM 8308861 ER PT J AU SMALL, PLC RAMAKRISHNAN, L FALKOW, S AF SMALL, PLC RAMAKRISHNAN, L FALKOW, S TI REMODELING SCHEMES OF INTRACELLULAR PATHOGENS SO SCIENCE LA English DT Editorial Material ID MYCOBACTERIUM-AVIUM; MACROPHAGES C1 STANFORD UNIV,DEPT MICROBIOL & IMMUNOL,STANFORD,CA 94305. RP SMALL, PLC (reprint author), NIAID,ROCKY MT LABS,HAMILTON,MT 59840, USA. NR 13 TC 68 Z9 69 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 4 PY 1994 VL 263 IS 5147 BP 637 EP 639 DI 10.1126/science.8303269 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MU964 UT WOS:A1994MU96400034 PM 8303269 ER PT J AU ZHANG, J DAWSON, VL DAWSON, TM SNYDER, SH AF ZHANG, J DAWSON, VL DAWSON, TM SNYDER, SH TI NITRIC-OXIDE ACTIVATION OF POLY(ADP-RIBOSE) SYNTHETASE IN NEUROTOXICITY SO SCIENCE LA English DT Article ID GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; ADP-RIBOSYLATION; RIBONUCLEOTIDE REDUCTASE; GLUTAMATE NEUROTOXICITY; DNA DAMAGE; CELLS; INHIBITION; POLYMERASE; CALCIUM; NICOTINAMIDE AB Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. NIDA,ADDICT RES CTR,MOLEC NEUROPSYCHIAT SECT,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. OI Dawson, Valina/0000-0002-2915-3970 FU NIDA NIH HHS [DA-271-90-7408, DA-00074, DA-00266] NR 34 TC 964 Z9 1002 U1 0 U2 9 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 4 PY 1994 VL 263 IS 5147 BP 687 EP 689 DI 10.1126/science.8080500 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MU964 UT WOS:A1994MU96400051 PM 8080500 ER PT J AU BASILE, AS DECOSTA, B PAUL, IA AF BASILE, AS DECOSTA, B PAUL, IA TI MULTIPLE [H-3] DTG BINDING-SITES IN GUINEA-PIG CEREBELLUM - EVIDENCE FOR THE PRESENCE OF NONSPECIFIC-BINDING SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE SIGMA-RECEPTOR LIGANDS; DTG (1,3-DI(2-TOLYL)GUANIDINE); (GUINEA-PIG); CEREBELLUM; LIVER ID CENTRAL NERVOUS-SYSTEM; SIGMA-RECEPTOR; RAT-BRAIN; H-3 (+)-PENTAZOCINE; ANTIPSYCHOTIC-DRUGS; HIGH-AFFINITY; PHENCYCLIDINE; ANTAGONISTS; LIGAND; 1,3-DI(2-<5-H-3>TOLYL)GUANIDINE AB The characteristics of the low affinity component of 1,3-di(2-[5-H-3]tolyl)guanidine binding to the guinea pig cerebellum were investigated. Saturation binding assays where a, receptors were masked with dextrallorphan indicated that 1,3-di(2-[5(3)H]tolyl)guanidine bound to cerebellar membranes in a fashion best described by a 1 site + non-specific binding model with a low density of specific binding sites (B-max approximate to 200 fmol/mg protein). Boiling the cerebellar membranes before addition to the saturation assay had no effect on the density of 1,3-di(2-[5-H-3]tolyl)guanidine binding. In contrast, both the K-d and B-max for 1,3-di(2-[5- H-3]tolyl)guanidine binding to liver membranes was significantly reduced by boiling, as was the density of [H-3](+)-pentazocine binding to cerebellum and liver. Thus, a substantial component of 1,3-di(2-[5- 3 H]tolyl)guanidine binding in the guinea pig cerebellum is to non-specific, proteinaceous binding sites with some of the pharmacological characteristics of the sigma(2) binding site. C1 NIDDK,MED CHEM LAB,BETHESDA,MD 20892. RP BASILE, AS (reprint author), NIDDK,NEUROSCI LAB,BLDG 8,ROOM 111,BETHESDA,MD 20892, USA. NR 31 TC 5 Z9 5 U1 0 U2 0 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 3 PY 1994 VL 252 IS 2 BP 139 EP 146 DI 10.1016/0014-2999(94)90589-4 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MW149 UT WOS:A1994MW14900003 PM 8157054 ER PT J AU KUNDRA, V ESCOBEDO, JA KAZLAUSKAS, A KIM, HK RHEE, SG WILLIAMS, LT ZETTER, BR AF KUNDRA, V ESCOBEDO, JA KAZLAUSKAS, A KIM, HK RHEE, SG WILLIAMS, LT ZETTER, BR TI REGULATION OF CHEMOTAXIS BY THE PLATELET-DERIVED GROWTH-FACTOR RECEPTOR-BETA SO NATURE LA English DT Article ID PHOSPHOLIPASE-C-GAMMA; PDGF RECEPTOR; SIGNALING COMPLEX; ASSOCIATION; BINDING; SITES; GAP; PHOSPHORYLATION; KINASE AB CHEMOTAXIS is an important component of wound healing, development, immunity and metastasis, yet the signalling pathways that mediate chemotaxis are poorly understood. Platelet-derived growth factor (PDGF) acts both as a mitogen and a chemoattractant1. Upon stimulation, the tyrosine kinase PDGF receptor-beta (PDGFR-beta) autophosphorylates2 and forms a complex that includes SH2(Src homology 2)-domain-containing proteins such as the phosphatidylinositol-specific phospholipase C-gamma (ref. 3), Ras-GTPase-activating protein (GAP)4, and phosphatidylinositol-3-OH kinase5. Specific tyrosine-to-phenylalanine substitutions in the PDGFR-beta can prevent binding of one SH2-domain-containing protein without affecting binding of other receptor-associated proteins6,7. Here we use phospholipase C-gamma (ref. 8) and PDGFR-beta mutants9-11 to map specific tyrosines involved in both positive and negative regulation of chemotaxis towards the PDGF-BB homodimer. Our results indicate that a delicate balance of migration-promoting (phospholipase C-gamma and phosphatidylinositol-3-OH kinase) and migration-suppressing (GAP) activities are recruited by the PDGFR-beta to drive chemotaxis towards PDGF-BB. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,300 LONGWOOD AVE,BOSTON,MA 02115. UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,CARDIOVASC RES INST,DEPT MED,SAN FRANCISCO,CA 94143. NATL JEWISH CTR IMMUNOL & RESP MED,DENVER,CO 80206. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 19 TC 401 Z9 403 U1 1 U2 6 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD FEB 3 PY 1994 VL 367 IS 6462 BP 474 EP 476 DI 10.1038/367474a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MU679 UT WOS:A1994MU67900058 PM 8107807 ER PT J AU KOKUBO, T GONG, DW WOOTTON, JC HORIKOSHI, M ROEDER, RG NAKATANI, Y AF KOKUBO, T GONG, DW WOOTTON, JC HORIKOSHI, M ROEDER, RG NAKATANI, Y TI MOLECULAR-CLONING OF DROSOPHILA TFIID SUBUNITS SO NATURE LA English DT Article ID MAJOR LATE PROMOTER; RNA POLYMERASE-II; TATA BOX-BINDING; TRANSCRIPTION FACTOR; PREINITIATION COMPLEX; PROTEIN; NUCLEOSOME; COACTIVATORS; INITIATION AB TRANSCRIPTION initiation factor TFIID is a multisubunit complex containing a TATA-box-binding factor (TFIIDtau/TBP) and associated polypeptide factors (TAFs) with sizes ranging from M(r) approximately 20,000 to >200,000 (refs 1-7). As a result of direct promoter interactions8,9, TFIID nucleates the assembly of RNA polymerase II and other initiation factors into a functional preinitiation complex10. Although the native TFIID complex mediates both basal and activator-dependent transcription in reconstituted systems, TBP itself is competent for only basal transcription. Thus, TAFs are essential cofactors for regulated transcription. The complementary DNAs encoding the p230 (M(r) 230,000), p110 and p85 subunits of TFIID have recently been cloned11-18. Here we report the molecular cloning and characterization of the p62, p42, p28 and p22 subunits. These participate in a network of heterogeneous protein-protein interactions within TFIID. Sequence similarities between p62/p42 and the histones H4/H3, respectively, suggest that these subunits have a functional relationship with chromatin. C1 NICHHD,BETHESDA,MD 20892. NINCDS,BETHESDA,MD 20892. NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20892. ROCKEFELLER UNIV,BIOCHEM & MOLEC BIOL LAB,NEW YORK,NY 10021. UNIV TOKYO,INST MOLEC & CELLULAR BIOSCI,BUNKYO KU,TOKYO 113,JAPAN. NR 30 TC 96 Z9 100 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD FEB 3 PY 1994 VL 367 IS 6462 BP 484 EP 487 DI 10.1038/367484a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MU679 UT WOS:A1994MU67900061 PM 7545910 ER PT J AU SLOBODYANSKY, E ANTKIEWICZMICHALUK, L MARTIN, B AF SLOBODYANSKY, E ANTKIEWICZMICHALUK, L MARTIN, B TI PURIFICATION OF A NOVEL DBI PROCESSING PRODUCT, DBI(39-75), AND CHARACTERIZATION OF ITS BINDING-SITE IN RAT-BRAIN SO REGULATORY PEPTIDES LA English DT Article DE DBI(39-75); NEUROPEPTIDE; PREGNENOLONE; CROSS-LINKING; RO5-4864; PK 11195 ID BENZODIAZEPINE RECEPTORS; INHIBITOR DBI; DIAZEPAM; STEROIDOGENESIS; BIOSYNTHESIS AB This report describes the purification and characterization from rat brain of DBI39-75, a novel, biologically active processing product of diazepam binding inhibitor (DBI). We have shown that DBI39-75, in nM concentrations stimulates pregnenolone synthesis in mitochondria of rat brain. Using cross-linking of I-125-DBI39-75 in steroidogenically active concentrations we have demonstrated for the first time that the DBI fragment has a specific high affinity binding site in rat brain. Displacement of [H-3]PK 11195 and [H-3]Ro5-4864 by DBI39-75 indicates more complex interaction than the competitive inhibition. Collectively, the data suggest that the function of DBI39_75 is mediated through a mitochondrial receptor complex which includes binding sites for PK 11195 and Ro5-4864. C1 GEORGETOWN UNIV,MED CTR,FIDIA GEORGETOWN INST NEUROSCI,WASHINGTON,DC 20007. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP SLOBODYANSKY, E (reprint author), GEORGETOWN UNIV,MED CTR,DEPT BIOCHEM & MOLEC BIOL,337 BASIC SCI BLDG,3900 RESERVOIR RD NW,WASHINGTON,DC 20007, USA. NR 14 TC 15 Z9 15 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 3 PY 1994 VL 50 IS 1 BP 29 EP 35 DI 10.1016/0167-0115(94)90188-0 PG 7 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA MW409 UT WOS:A1994MW40900004 PM 8159805 ER PT J AU SCHECHTER, M HARRISON, LH HALSEY, NA TRADE, G SANTINO, M MOULTON, LH QUINN, TC AF SCHECHTER, M HARRISON, LH HALSEY, NA TRADE, G SANTINO, M MOULTON, LH QUINN, TC TI COINFECTION WITH HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I AND HIV IN BRAZIL - IMPACT ON MARKERS OF HIV DISEASE PROGRESSION SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID INTRAVENOUS-DRUG-USERS; HTLV-II; HOMOSEXUAL MEN; LEUKEMIA; INFECTION; RETROVIRUS; AIDS; LYMPHOCYTES; LYMPHOMA; CLINICS AB Objectives.-To study the effect of human T-cell lymphtropic virus type I (HTLV-1) on markers of human immunodeficiency virus (HIV) disease progression. Design.-A retrospective, nested case-control study. Setting.-A university hospital outpatient HIV clinic in Rio de Janeiro, Brazil. Participants.-Human immunodeficiency virus-seropositive adults participating in a prospective HIV cohort study. Main Outcome Measures.-The HIV clinical stage, CD4+ lymphocyte counts, and other laboratory parameters in 27 individuals infected with HIV and HTLV-1 (coinfection) and 99 age-matched, HIV-seropositive, HTLV-seronegative controls (single infection). Results.-Variables independently associated with coinfection included higher CD4+ lymphocyte count (odds ratio [OR], 2.3; 95% confidence limits [CL], 1.3, 4.1), higher CD4+ percentage (OR, 2.0; 95% CL, 1.3, 3.2), beta2-Microglobulin level of 254 nmol/L or more (OR, 6.8; 95% CL, 1.3, 35.4), World Health Organization stages 3 and 4 (OR, 4.4; 95% CL, 1.1, 18.0), and reporting a parenteral risk factor (OR, 7.4; 95% CL, 1.4, 38.9). When stratified by p24 antigenemia, coinfection was associated with an estimated 82% higher CD4+ lymphocyte count (P<.05). Conclusion.-Coinfection was associated with higher CD4+ lymphocyte counts, more advanced clinical disease, and higher beta2-MiCroglobulin levels than HIV infection alone. The higher mean CD4+ lymphocyte count does not appear to offer immunologic benefit. Caution should be exercised when using CD4+ lymphocytes as a surrogate marker in studies of HIV infection in-populations where HTLV-I is prevalent. Further studies are needed to address whether current CD4+ lymphocyte values for the initiation of antiretroviral therapy and chemoprophylaxis against opportunistic infections in HIV infection are appropriate in coinfection. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT INT HLTH,ROOM 5515,615 N WOLFE ST,BALTIMORE,MD 21205. UNIV FED RIO DE JANEIRO,HOSP UNIV CLEMENTINO FRAGA FILHO,DEPT PREVENT MED,INFECT DIS SERV,RIO JANEIRO,BRAZIL. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT BIOSTAT,BALTIMORE,MD 21205. NIAID,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. OI Moulton, Lawrence/0000-0001-7041-7387 NR 40 TC 74 Z9 76 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 2 PY 1994 VL 271 IS 5 BP 353 EP 357 DI 10.1001/jama.271.5.353 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MR983 UT WOS:A1994MR98300029 PM 7904317 ER PT J AU WONG, M GRUBER, J AF WONG, M GRUBER, J TI VIRAL INTERACTIONS WITH THE P53 GENE IN HUMAN CANCER - NCI WORKSHOP SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID HUMAN PAPILLOMAVIRUS TYPE-16; LARGE TUMOR-ANTIGEN; LARGE T-ANTIGEN; RETINOBLASTOMA SUSCEPTIBILITY GENE; WILD-TYPE; MUTANT P53; SIMIAN VIRUS-40; C-MYC; SV40-TRANSFORMED CELLS; TRANSCRIPTION FACTOR RP WONG, M (reprint author), NCI,DIV CANC ETIOL,BIOL CARCINOGENESIS BRANCH,RM 540,EPN,BETHESDA,MD 20892, USA. NR 51 TC 12 Z9 12 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 2 PY 1994 VL 86 IS 3 BP 177 EP 182 DI 10.1093/jnci/86.3.177 PG 6 WC Oncology SC Oncology GA MT437 UT WOS:A1994MT43700008 PM 7904309 ER PT J AU SARTOR, O COOPER, M WEINBERGER, M HEADLEE, D THIBAULT, A TOMPKINS, A STEINBERG, S FIGG, WD LINEHAN, WM MYERS, CE AF SARTOR, O COOPER, M WEINBERGER, M HEADLEE, D THIBAULT, A TOMPKINS, A STEINBERG, S FIGG, WD LINEHAN, WM MYERS, CE TI SURPRISING ACTIVITY OF FLUTAMIDE WITHDRAWAL, WHEN COMBINED WITH AMINOGLUTETHIMIDE, IN TREATMENT OF HORMONE-REFRACTORY PROSTATE-CANCER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ACID-PHOSPHATASE; BREAST-CANCER; CARCINOMA; ANTIGEN; HYDROCORTISONE; RECEPTOR; GROWTH; ANTIANDROGENS; CHEMOTHERAPY; ESTRAMUSTINE AB Background: The best treatment for patients with ''hormone-refractory'' metastatic prostate cancer is unclear, particularly in patients for whom suramin and hydrocortisone have failed. Purpose: We investigated a combination of flutamide withdrawal and aminoglutethimide in suramin- and hydrocortisone-pretreated patients with ''hormone-refractory'' prostate cancer. Methods: Twenty-nine patients with metastatic prostate cancer were treated with simultaneous flutamide withdrawal and aminoglutethimide (250 mg given orally four times daily). All patients were taking flutamide at the time of entry, and previous treatments with medical or surgical castration, flutamide, suramin, and hydrocortisone had failed in all of these patients. Because of suramin-induced adrenal insufficiency, all patients had previously received, and continued to receive, physiological doses of hydrocortisone. Treatment of all nonsurgically castrated patients had previously failed; however, these patients continued to receive depot leuprolide. Results: In 14 (48%) of 29 patients, the prostate-specific antigen (PSA) decreased by more than 80% for 4 or more weeks. Improvements in anemia, thrombocytopenia, soft-tissue masses, bone scans, and symptoms were also noted. Factors associated with response included prolonged flutamide pretreatment, a markedly elevated pretreatment PSA, and the absence of soft-tissue disease. Conclusions: Flutamide withdrawal, when combined with the simultaneous administration of aminoglutethimide, is a therapeutically active approach in patients with ''hormone-refractory'' prostate cancer. Implications: On the basis of these and additional data, we hypothesize that prolonged exposure to flutamide results in the selective proliferation of cancer cells containing a mutant androgen receptor that aberrantly recognizes flutamide metabolites and nonandrogenic steroids as androgenic stimuli. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NCI,SURG BRANCH,DIV CANC TREATMENT,BETHESDA,MD 20892. RI Figg Sr, William/M-2411-2016 NR 42 TC 110 Z9 111 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 2 PY 1994 VL 86 IS 3 BP 222 EP 227 DI 10.1093/jnci/86.3.222 PG 6 WC Oncology SC Oncology GA MT437 UT WOS:A1994MT43700014 PM 7506794 ER PT J AU WINOKUR, G CORYELL, W AKISKAL, HS ENDICOTT, J KELLER, M MUELLER, T AF WINOKUR, G CORYELL, W AKISKAL, HS ENDICOTT, J KELLER, M MUELLER, T TI MANIC-DEPRESSIVE (BIPOLAR) DISORDER - THE COURSE IN LIGHT OF A PROSPECTIVE 10-YEAR FOLLOW-UP OF 131 PATIENTS SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE AFFECTIVE DISORDER; BIPOLAR DISORDER; LONGITUDINAL STUDY ID FAMILY AB For a five-year period, 131 bipolar patients were followed every 6 months; for the next 5 years, they were followed yearly. Each patient was interviewed in a systematic way that gave information about episodes, hospitalizations, cycle lengths and the presence of alcoholism. Women and men were not significantly different in the number of follow-up manic or depressive episodes or hospitalizations. Chronicity from index episode to the end of the 10-year follow-up was uncommon (4%). Alcoholism, which was common in these patients, showed a great diminution at the end of 10 years. Contrary to expectation, cycle lengths showed no systematic decrease in length over the follow-up. In this naturalistic study, treatment intensity was not related to decreasing episodes or to changes in cycle length. The number of episodes in the first 5 years of follow-up was not correlated with the number of episodes in the last 5 years. Cycle lengths in the first 5 years of follow-up were similar in length to the last 5 years of follow-up. A family history of mania in these bipolar patients was associated with more episodes in follow-up than if such a family history were absent. The patients whose alcoholism predated the onset of their affective illness were less likely to have episodes in the follow-up than the patients in whom affective illness predated the onset of the alcoholism. C1 NIMH,COLLABORAT PROGRAM PSYCHOBIOL DEPRESS,BETHESDA,MD. FU NIMH NIH HHS [R01 MH025478] NR 22 TC 104 Z9 104 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-690X J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PD FEB PY 1994 VL 89 IS 2 BP 102 EP 110 DI 10.1111/j.1600-0447.1994.tb01495.x PG 9 WC Psychiatry SC Psychiatry GA MV754 UT WOS:A1994MV75400005 PM 8178659 ER PT J AU HENNINGFIELD, JE AF HENNINGFIELD, JE TI DO THE BENEFITS OF NICOTINE HELP CIGARETTES BEAT THE ADDICTION RAP SO ADDICTION LA English DT Note RP HENNINGFIELD, JE (reprint author), NATL INST DRUG ABUSE,ADDICT RES CTR,CLIN PHARM BRANCH,BALTIMORE,MD 21224, USA. NR 7 TC 9 Z9 9 U1 0 U2 0 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0965-2140 J9 ADDICTION JI Addiction PD FEB PY 1994 VL 89 IS 2 BP 135 EP 136 DI 10.1111/j.1360-0443.1994.tb00865.x PG 2 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA MW074 UT WOS:A1994MW07400002 PM 8173474 ER PT J AU ZOBECK, TS GRANT, BF STINSON, FS BERTOLUCCI, D AF ZOBECK, TS GRANT, BF STINSON, FS BERTOLUCCI, D TI ALCOHOL INVOLVEMENT IN FATAL TRAFFIC CRASHES IN THE UNITED-STATES - 1979-90 SO ADDICTION LA English DT Article AB Trends in alcohol-related traffic crash fatalities for the United States were examined with data from the Fatal Accident Reporting System for the years 1979-90. Alcohol-related traffic crash fatalities have decreased 10% over the 12 years studied, from 20 245 in 1979 to 18 279 in 1990. Fatality rates per 100 million vehicle miles traveled, and per 100 000 population, registered vehicles and licensed drivers have decreased even more sharply. Rates of blood alcohol testing of fatally injured drivers rose substantially among the States, with the nationwide rate increasing from 44% in 1979 to 75% in 1990. Factors that may be affecting these trends are discussed. C1 NIAAA,DIV BIOMETRY & EPIDEMIOL,ROCKVILLE,MD 20857. RP ZOBECK, TS (reprint author), CSR INC,ALCOHOL EPIDEMIOL DATA SYST,1440 EYE ST NW,SUITE 600,WASHINGTON,DC 20005, USA. NR 1 TC 9 Z9 9 U1 0 U2 1 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0965-2140 J9 ADDICTION JI Addiction PD FEB PY 1994 VL 89 IS 2 BP 227 EP 233 DI 10.1111/j.1360-0443.1994.tb00882.x PG 7 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA MW074 UT WOS:A1994MW07400019 PM 8173489 ER PT J AU DSOUZA, MP GEYER, SJ HANSON, CV HENDRY, RM MILMAN, G CHAMOW, S FUNG, M GEYER, S HAIGWOOD, N HANSON, C HENDRY, M HATTORI, T HUISMAN, H SCHUITEMAKER, H KATINGER, H KLIKS, S LEVY, J LAMAN, J LANGEDIJK, H MELOEN, R MCPHEE, D MITCHELL, W NARA, P PAGE, M LING, C PINTER, A POSNER, M POTTS, B FIELD, K RICHMAN, D ROBINSON, J STEIMER, K STOTT, J CORCORAN, T THIRIART, C WAHREN, B WAINBERG, M WEBER, J ZOLLAPAZNER, S BUCHINDER, A AF DSOUZA, MP GEYER, SJ HANSON, CV HENDRY, RM MILMAN, G CHAMOW, S FUNG, M GEYER, S HAIGWOOD, N HANSON, C HENDRY, M HATTORI, T HUISMAN, H SCHUITEMAKER, H KATINGER, H KLIKS, S LEVY, J LAMAN, J LANGEDIJK, H MELOEN, R MCPHEE, D MITCHELL, W NARA, P PAGE, M LING, C PINTER, A POSNER, M POTTS, B FIELD, K RICHMAN, D ROBINSON, J STEIMER, K STOTT, J CORCORAN, T THIRIART, C WAHREN, B WAINBERG, M WEBER, J ZOLLAPAZNER, S BUCHINDER, A TI EVALUATION OF MONOCLONAL-ANTIBODIES TO HIV-1 ENVELOPE BY NEUTRALIZATION AND BINDING ASSAYS - AN INTERNATIONAL COLLABORATION SO AIDS LA English DT Article DE HIV-1; MONOCLONAL ANTIBODIES; IMMUNOADHESIN; NEUTRALIZATION ASSAYS; BINDING ASSAYS ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYPE-1 GP120; GLYCOPROTEIN GP120; PASSIVE-IMMUNIZATION; INFECTED-CELLS; EPITOPES; IDENTIFICATION; CHIMPANZEES; DOMAIN; PROTECTION AB Objective: To characterize a purified panel of monoclonal antibodies (MAb) to epitopes in HIV-1 envelope V3, CD4-binding region, C4 and gp41. Design: Neutralization and/or binding activity data were obtained from 21 laboratories on a coded panel consisting of seven human MAb, seven mouse MAb, recombinant human CD4 immunoadhesin [CD4-immunoglobulin G (IgG)], normal human and normal murine Ig. Methods: Laboratories performed a variety of neutralization assays and antigen binding assays with HIVIIIB, HIVMN and other laboratory strains of HIV-1. Results: For a single MAb, there was up to a 10(3) range of neutralizing antibody titers between laboratories. The range in titers appeared to depend on the sensitivity of the neutralization assay. Two methods were used to consolidate the data from all laboratories, the geometric mean titer (GMT) and the median neutralizing titer (MNT). The panel of MAb were also analyzed by a variety of assays that measure binding activity to native or denatured epitopes. The relative binding activity of the MAb did not appear to correlate with neutralizing activity. Conclusion: Neutralization results from any single laboratory did not correlate with the collective data. The relative potency (rank order) of the MAb in the panel were equivalent when determined by GMT or MNT. These values may be useful to individual laboratories for estimating the sensitivity of their neutralization assays. The study also identified potential reference reagents with which neutralizing activity could be compared. C1 US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD. CALIF DEPT HLTH SERV,VIRAL & RICKETTSIAL LAB,BERKELEY,CA. CHIRON CORP,EMERYVILLE,CA 94608. KYOTO UNIV,KYOTO,JAPAN. NETHERLANDS RED CROSS,AMSTERDAM,NETHERLANDS. UNIV CALIF BERKELEY,BERKELEY,CA. TNO,MED BIOL LAB,AMSTERDAM,NETHERLANDS. CENT DIERGENEESKUNDIG INST,AMSTERDAM,NETHERLANDS. VANDERBILT UNIV,NASHVILLE,TN 37240. NCI,BETHESDA,MD 20892. NATL INST BIOL STAND & CONTROLS,POTTERS BAR EN6 3QG,HERTS,ENGLAND. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. UNIV CONNECTICUT,MED CTR,STORRS,CT. NATL BACTERIOL LAB,STOCKHOLM,SWEDEN. MCGILL UNIV,AIDS CTR,MONTREAL,PQ,CANADA. RP DSOUZA, MP (reprint author), NIAID,DIV AIDS,6003 EXECUT BLVD,SOLAR BLDG,ROOM 2835,BETHESDA,MD 20892, USA. NR 60 TC 30 Z9 30 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 1994 VL 8 IS 2 BP 169 EP 181 PG 13 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NA433 UT WOS:A1994NA43300004 PM 7519019 ER PT J AU LUSSO, P SECCHIERO, P CROWLEY, RW AF LUSSO, P SECCHIERO, P CROWLEY, RW TI IN-VITRO SUSCEPTIBILITY OF MACACA-NEMESTRINA TO HUMAN HERPESVIRUS-6 - A POTENTIAL ANIMAL-MODEL OF COINFECTION WITH PRIMATE IMMUNODEFICIENCY VIRUSES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID LYMPHOCYTES-T; TYPE-1 REPLICATION; INFECTION; HHV-6; TROPISM; HIV-1; CELLS; IDENTIFICATION; EXPRESSION; INDUCTION AB Human herpesvirus 6 (HHV-6), a T lymphotropic herpesvirus, has been suggested as a potential cofactor in the acquired immunodeficiency syndrome (AIDS). Previous studies indicate that HHV-6 has a restricted range of susceptible species. In this study, we tested the in vitro susceptibility to HHV-6 of Macaca nemestrina (pig-tailed macaque), a species that has been found to be infectable by human immunodeficiency virus type I in vivo and that develops an AIDS-like syndrome following simian immunodeficiency virus (SIV) infection. Two different HHV-6 isolates (HHV-6(GS) and HHV-6(BA)), belonging to the two major HHV-6 variants (A and B, respectively), were employed. Both viruses induced a productive and cytopathic infection in phytohemagglutinin-stimulated peripheral blood T lymphocytes from M. nemestrina. In contrast, only HHV-6(BA) (variant B) was able to replicate in lymphocytes from Macaca mulatta (rhesus macaque). Moreover, HHV-6(GS) and SIVsmE660 productively coinfected individual M. nemestrina lymphocytes, resulting in increased levels of SIV replication. Genetic sequences of HHV-6 were not amplified by polymerase chain reaction from peripheral blood mononuclear cells of several adult M. nemestrina, suggesting that these animals, unlike humans, are not commonly infected by HHV-6, or a related virus. Thus, M. nemestrina may represent an optimal animal model system to investigate the in vivo interactions between HHV-6 and the primate immunodeficiency viruses. RP LUSSO, P (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,ROOM 6A09,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI secchiero, paola/G-9689-2015 OI secchiero, paola/0000-0003-4101-7987 NR 44 TC 19 Z9 20 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 PY 1994 VL 10 IS 2 BP 181 EP 187 DI 10.1089/aid.1994.10.181 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA MZ149 UT WOS:A1994MZ14900011 PM 8198870 ER PT J AU LEWIS, MG BELLAH, S MCKINNON, K YALLEYOGUNRO, J ZACK, PM ELKINS, WR DESROSIERS, RC EDDY, GA AF LEWIS, MG BELLAH, S MCKINNON, K YALLEYOGUNRO, J ZACK, PM ELKINS, WR DESROSIERS, RC EDDY, GA TI TITRATION AND CHARACTERIZATION OF 2 RHESUS-DERIVED SIVMAC CHALLENGE STOCKS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID SIMIAN IMMUNODEFICIENCY VIRUS; CELLULAR-LOCALIZATION; CONFERS PROTECTION; LYMPHOID-TISSUES; MACAQUE MONKEYS; VACCINE; INFECTION; RETROVIRUS; CELLS; AIDS AB Simian immunodeficiency virus infection of macaques is a model for human immunodeficiency virus infection of humans. In vivo-titrated stocks of SIV are essential for the utilization of this model for vaccine development. The elicitation of anti-human cell antibodies by some vaccines prepared in human cells and the related protective effects of the vaccine produced in human cells suggest a need for new macaque-derived SIV stocks. Here we describe the titration and characterization of two stocks of SIVmac that were produced in primary rhesus macaque cells. The first virus is SIVmac251, isolated from tissues of macaque 251, and the second is a molecular clone designated as SIVmac239. A 50% rhesus monkey infectious dose (MID(50)) was titrated for each virus stock by intravenous inoculation. An additional five macaques were inoculated with 10 MID(50) of the SIVmac251 stock and were followed for disease outcome. All five monkeys developed antigenemia by 14 days postchallenge. Two of the five monkeys developed strong anti-SIV humoral immunity, whereas three developed little or no humoral immunity. As has been observed previously, the rapidity of disease progression correlated with the lack of a strong antibody response. The three animals with low humoral immunity died within 7 months of challenge, with antigenemia, cachexia, hypoproteinemia, hypoalbuminemia, weight loss, and intractable diarrhea, while maintaining their circulating CD4 numbers. One animal died at 1.5 years of more typical simian AIDS. C1 WALTER REED ARMY INST RES,DEPT RETROVIROL,WASHINGTON,DC 20307. NIAID,INFECT DIS LAB,ROCKVILLE,MD 20850. NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. RP LEWIS, MG (reprint author), HENRY M JACKSON FDN,1500 E GUDE DR,ROCKVILLE,MD 20850, USA. FU NCRR NIH HHS [RR00168]; NIAID NIH HHS [AI26507, AI26463] NR 29 TC 79 Z9 79 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 PY 1994 VL 10 IS 2 BP 213 EP 220 DI 10.1089/aid.1994.10.213 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA MZ149 UT WOS:A1994MZ14900015 PM 8198874 ER PT J AU BALAYAN, M BHAMARAPRAVATI, N BURKE, D CHANDLER, DK DESROSIERS, R SCHILD, G SCHULTZ, A SHAW, GM STOTT, J WEISS, R WIGZELL, H DOWDLE, WR GIRARD, M GOUDSMIT, J GUIMARAES, CS KIENY, MP MBIDDE, EK ROSCAMABBING, EW ESPARZA, J HEYMANN, DL HEYWARD, WL KALLINGS, LO MERSON, MH OSMANOV, S SABA, J AF BALAYAN, M BHAMARAPRAVATI, N BURKE, D CHANDLER, DK DESROSIERS, R SCHILD, G SCHULTZ, A SHAW, GM STOTT, J WEISS, R WIGZELL, H DOWDLE, WR GIRARD, M GOUDSMIT, J GUIMARAES, CS KIENY, MP MBIDDE, EK ROSCAMABBING, EW ESPARZA, J HEYMANN, DL HEYWARD, WL KALLINGS, LO MERSON, MH OSMANOV, S SABA, J TI FEASIBILITY OF DEVELOPING LIVE ATTENUATED HIV VACCINES - CONCLUSIONS AND RECOMMENDATIONS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID GENE C1 MOSCOW POLIOMYELITIS & VIRUS ENCEPHALITIS INST,MOSCOW,RUSSIA. MAHIDOL UNIV,BANGKOK 10700,THAILAND. WALTER REED ARMY INST,ROCKVILLE,MD. US FDA,ROCKVILLE,MD 20857. HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. NATL INST BIOL STAND & CONTROLS,POTTERS BAR EN6 3QG,HERTS,ENGLAND. NIAID,DIV AIDS,BETHESDA,MD 20892. UNIV ALABAMA,BIRMINGHAM,AL. INST CANC RES,CHESTER BEATTY LABS,LONDON SW3 6JB,ENGLAND. KAROLINSKA INST,STOCKHOLM,SWEDEN. CTR DIS CONTROL & PREVENT,ATLANTA,GA. INST PASTEUR,PARIS,FRANCE. UNIV AMSTERDAM,AMSTERDAM,NETHERLANDS. INST MED TROP,SAO PAULO,SP,BRAZIL. WHO,STEERING COMM VACCINE DEV,GENEVA,SWITZERLAND. TRANSGENE SA,STRASBOURG,FRANCE. MULAGO HOSP,KAMPALA,UGANDA. WHO,GLOBAL PROGRAMME AIDS,CH-1211 GENEVA 27,SWITZERLAND. OI /0000-0002-5704-8094 NR 9 TC 6 Z9 6 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 PY 1994 VL 10 IS 2 BP 221 EP 222 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA MZ149 UT WOS:A1994MZ14900016 ER PT J AU CHOU, SP AF CHOU, SP TI AN EXAMINATION OF THE ALCOHOL-CONSUMPTION AND PEPTIC-ULCER ASSOCIATION - RESULTS OF A NATIONAL SURVEY SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE ALCOHOL; PEPTIC ULCER; TOBACCO; LOGISTIC REGRESSION ID HELICOBACTER-PYLORI; DUODENAL-ULCER; GASTRIC-ULCER; HEALING RATE; SMOKING; DISEASE; CANCER; POPULATION; NUTRITION; MORTALITY AB Excessive alcohol consumption causes damages to the stomach or duodenum by impairing the integrity of the mucosal barrier. The aim of this study was to estimate the association between alcohol consumption and peptic ulcer, utilizing a large representative sample of the U.S. population, while controlling for cigarette smoking and major sociodemographic variables. Results indicated that alcohol consumption only minimally increased the odds of peptic ulcer. Thus, this study offers little support for the association between ethanol intake and peptic ulcer. RP CHOU, SP (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,ROOM 14C-26,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 37 TC 8 Z9 11 U1 0 U2 2 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 1994 VL 18 IS 1 BP 149 EP 153 DI 10.1111/j.1530-0277.1994.tb00895.x PG 5 WC Substance Abuse SC Substance Abuse GA MZ335 UT WOS:A1994MZ33500024 PM 8198212 ER PT J AU STREISSGUTH, AP SAMPSON, PD OLSON, HC BOOKSTEIN, FL BARR, HM SCOTT, M FELDMAN, J MIRSKY, AF AF STREISSGUTH, AP SAMPSON, PD OLSON, HC BOOKSTEIN, FL BARR, HM SCOTT, M FELDMAN, J MIRSKY, AF TI MATERNAL DRINKING DURING PREGNANCY - ATTENTION AND SHORT-TERM-MEMORY IN 14-YEAR-OLD OFFSPRING - A LONGITUDINAL PROSPECTIVE-STUDY SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE FETAL ALCOHOL EFFECTS; BEHAVIORAL TERATOLOGY; ALCOHOL; ADOLESCENT DEVELOPMENT; ATTENTION ID PRENATAL ALCOHOL EXPOSURE; 3 TRIMESTER EQUIVALENCY; RAT OPTIC-NERVE; FOLLOW-UP; SPATIAL NAVIGATION; REACTION-TIME; 4-YEAR-OLD CHILDREN; SUSTAINED ATTENTION; SCHOOL AGE; ETHANOL AB A large and compelling experimental literature has documented the adverse impact of prenatal alcohol exposure on the developing brain of the offspring. This is the first report of adolescent attention/ memory performance and its relationship with prenatal alcohol exposure in a population-based, longitudinal, prospective study (n 462) involving substantial covariate control and ''blind'' examiners. Prenatal alcohol exposure was significantly related to attention/ memory deficits in a dose-dependent fashion. A latent variable reflecting 13 measures of maternal drinking was correlated 0.26 with a latent variable representing 52 scores from 6 tests measuring various components of attention and short-term memory performance. The number of drinks/occasion was the strongest alcohol predictor. Fluctuating attentional states, problems with response inhibition, and spatial learning showed the strongest association with prenatal alcohol exposure. A latent variable reflecting the pattern of attention/memory deficits observed at 14 years correlated 0.67 with a composite pattern of deficits previously detected on neurobehavioral tests administered during the first 7 years of life. The 14-year attention/memory deficits observed in the present study appear to be the adolescent sequelae of deficits observed earlier in development. As is usual in such studies, not all exposed offspring showed deficits. C1 UNIV WASHINGTON,DEPT STAT,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT PSYCHOL,SEATTLE,WA 98195. UNIV MICHIGAN,CTR HUMAN GROWTH & DEV,ANN ARBOR,MI 48109. NIMH,PSYCHOL & PSYCHOPATHOL LAB,BETHESDA,MD 20892. RP STREISSGUTH, AP (reprint author), UNIV WASHINGTON,SCH MED,DEPT PSYCHIAT & BEHAV SCI,FETAL ALCOHOL & DRUG UNIT,GG-20,SEATTLE,WA 98195, USA. RI Rohlf, F/A-8710-2008 FU NIAAA NIH HHS [AA01455-01-18] NR 80 TC 240 Z9 241 U1 1 U2 12 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 1994 VL 18 IS 1 BP 202 EP 218 DI 10.1111/j.1530-0277.1994.tb00904.x PG 17 WC Substance Abuse SC Substance Abuse GA MZ335 UT WOS:A1994MZ33500033 PM 8198221 ER PT J AU LUNN, G SANSONE, EB DEMEO, M LAGET, M CASTEGNARO, M AF LUNN, G SANSONE, EB DEMEO, M LAGET, M CASTEGNARO, M TI POTASSIUM-PERMANGANATE CAN BE USED FOR DEGRADING HAZARDOUS COMPOUNDS SO AMERICAN INDUSTRIAL HYGIENE ASSOCIATION JOURNAL LA English DT Note ID MUTAGENESIS AB Solutions of potassium permanganate in 3 M sulfuric acid, 1 M sodium hydroxide solution, and water can be used to degrade hazardous compounds. Excess oxidant can be removed by using sodium metabisulfite. Manganese, a carcinogen and mutagen, can be removed from the final reaction mixtures by making these mixtures strongly basic. Aqueous dilution causes the soluble potassium sulfate to dissolve while still allowing the insoluble manganese compounds to be removed by filtration and so reduces the weight of precipitate. In all cases the amount of manganese left in she filtrates was less than 2 ppm and the reaction mixtures were nonmutagenic. When ethanol was used as a test compound, degradation was much more rapid when the solvent was 3 M sulfuric acid or 1 M sodium hydroxide solution than when the solvent was water. However, the variation of the rate of reaction with pH depends on the nature of the substrate. Thus the effectiveness of the various methods may vary for other substrates. Potassium permanganate in sulfuric acid was used to degrade four polycyclic heterocyclic hydrocarbons. Destruction was greater than 99.9% and the final reaction mixtures contained no more than 0.5 ppm manganese and were not mutagenic. By modifying the work-up procedures to remove manganese from the final reaction mixture, procedures previously developed for degrading hazardous compounds can still be employed. C1 FAC PHARM MARSEILLE,MICROBIOL LAB,F-13385 MARSEILLE 5,FRANCE. INT AGCY RES CANC,F-69372 LYON 8,FRANCE. RP LUNN, G (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,ENVIRONM CONTROL & RES PROGRAM,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [NCI NO1-CO-74102] NR 23 TC 7 Z9 7 U1 0 U2 2 PU AMER INDUSTRIAL HYGIENE ASSOC PI FAIRFAX PA 2700 PROSPERITY AVE #250, FAIRFAX, VA 22031-4307 SN 0002-8894 J9 AM IND HYG ASSOC J JI Am. Ind. Hyg. Assoc. J. PD FEB PY 1994 VL 55 IS 2 BP 167 EP 171 DI 10.1202/0002-8894(1994)055<0167:PPCBUF>2.0.CO;2 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA MV494 UT WOS:A1994MV49400011 PM 8160606 ER PT J AU MINNITI, CP TSOKOS, M NEWTON, WA HELMAN, LJ AF MINNITI, CP TSOKOS, M NEWTON, WA HELMAN, LJ TI SPECIFIC EXPRESSION OF INSULIN-LIKE GROWTH FACTOR-II IN RHABDOMYOSARCOMA TUMOR-CELLS SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE IN SITU; INSULIN-LIKE GROWTH FACTORS; RHABDOMYOSARCOMA ID HUMAN-BREAST CANCER; FACTOR MESSENGER-RNA; AUTOCRINE GROWTH; MOTILITY AB Insulin-like growth factor II (IGF-II) acts as autocrine growth and motility factor in human rhabdomyosarcoma cell lines, and Northern blot analysis of tumor biopsy specimens from both alveolar and embryonal rhabdomyosarcoma demonstrates high levels of IGF-II mRNA expression. To determine the frequency and site of expression of IGF-II in these tumors, the authors performed in situ hybridization. All tumor specimens examined expressed the gene for IGF-II, and this expression was localized to the tumor cells themselves and not to the surrounding stroma. These data suggest that the IGF-II autocrine loop may be operating not only in vitro but also in vivo. C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. CHILDRENS HOSP,INTERGRP RHABDOMYOSARCOMA STUDIES PATHOL CTR,COLUMBUS,OH. NR 19 TC 58 Z9 60 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 1994 VL 101 IS 2 BP 198 EP 203 PG 6 WC Pathology SC Pathology GA MW510 UT WOS:A1994MW51000014 PM 8116575 ER PT J AU BROWN, CC KIPNIS, V FREEDMAN, LS HARTMAN, AM SCHATZKIN, A WACHOLDER, S AF BROWN, CC KIPNIS, V FREEDMAN, LS HARTMAN, AM SCHATZKIN, A WACHOLDER, S TI ENERGY ADJUSTMENT METHODS FOR NUTRITIONAL EPIDEMIOLOGY - THE EFFECT OF CATEGORIZATION SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE CONFOUNDING FACTORS (EPIDEMIOLOGY); DIET; EPIDEMIOLOGIC METHODS; MODELS, STATISTICAL; NUTRITION ASSESSMENT ID MISCLASSIFICATION AB The authors discuss the interpretation of four alternative energy adjustment methods (Residual, Standard, Partition, and Nutrient Density) that have been proposed for the analysis of nutritional epidemiology studies. These methods have so far been compared under circumstances where intake of the nutrient of interest is measured as a continuous variable. Because it is common practice to categorize nutrient intakes in the analysis, the authors investigate the effect of such categorization on the interpretation of results from the four methods with the use of computer simulations and statistical theory. They consider four cases: where the nutrient intake is either divided into quartiles or ordered so as to investigate trend over the quartile groups, combined with using an adjusting variable that is either continuous or categorized. The results show: 1) the Residual, Standard, and Partition methods are no longer equivalent as they are in the continuous case; 2) compared with the Standard method, the Residual method appears to be more powerful for detecting trends in relative odds, is more robust to residual confounding when the adjustment Variable is categorized, and provides more meaningful odds ratios; and 3) the Residual and Nutrient Density methods give closely similar results. C1 NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,BETHESDA,MD 20892. NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. NCI,DIV CANC ETIOL,BIOSTAT BRANCH,BETHESDA,MD 20892. RP BROWN, CC (reprint author), NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,EXECUT PLAZA N,SUITE 344,BETHESDA,MD 20892, USA. NR 9 TC 74 Z9 74 U1 0 U2 5 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD FEB 1 PY 1994 VL 139 IS 3 BP 323 EP 338 PG 16 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MX218 UT WOS:A1994MX21800011 PM 8116608 ER PT J AU CHIPEV, CC YANG, JM DIGIOVANNA, JJ STEINERT, PM MAREKOV, L COMPTON, JG BALE, SJ AF CHIPEV, CC YANG, JM DIGIOVANNA, JJ STEINERT, PM MAREKOV, L COMPTON, JG BALE, SJ TI PREFERENTIAL SITES IN KERATIN-10 THAT ARE MUTATED IN EPIDERMOLYTIC HYPERKERATOSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID GENETIC-BASIS; MUTATIONS; SUBDOMAIN; SEQUENCE; LINKAGE; CLUSTER; BULLOSA; PEPTIDE; PCR; END AB Epidermolytic hyperkeratosis (EH) is a rare autosomal dominant skin disease. Recent studies in our laboratory established genetic linkage to the type II keratin gene locus on chromosome 12q in one family with EH and identified a single amino acid mutation in keratin 1 that is responsible for the disease. Other point mutations in the keratin 1 or keratin 10 genes have now been reported in other patients with EH. We have examined a series of probands with EH in order to develop a catalog of mutations in keratin 10. Using direct sequencing of PCR-amplified genomic DNA, we have identified mutations in six families, in which five mutations occur in the beginning of the 1A rod domain of keratin 10-namely, two Arg10 to His, one Arg10 to Cys, an Asn8 to His, and a Tyr14 to Asp. This region contains highly conserved residues among all keratins. An additional mutation (Leu103 to Gln) was found in the conserved region late in the 2B rod domain in keratin 10. We developed several allele-specific assays to assess the frequency of these mutations in the general population. No evidence was found for the presence of such changes in unaffected individuals. In vitro functional assays performed with peptides corresponding to the 1A mutations in these families show severely diminished capacity to disaggregate preformed keratin intermediate filaments, in comparison with a wild-type control peptide. Results from this work support the hypothesis that the beginning of the 1A rod domain segment in keratin 10 contains preferential sites for disease-causing mutation in EH. This should be of considerable use when developing prenatal diagnostic tests and biologically based therapies for this disease. C1 NIAMSD,SKIN BIOL BRANCH,BETHESDA,MD 20892. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 29 TC 58 Z9 59 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 1994 VL 54 IS 2 BP 179 EP 190 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA MU315 UT WOS:A1994MU31500003 PM 7508181 ER PT J AU BOERWINKLE, E BROWN, S SHARRETT, AR HEISS, G PATSCH, W AF BOERWINKLE, E BROWN, S SHARRETT, AR HEISS, G PATSCH, W TI APOLIPOPROTEIN-E POLYMORPHISM INFLUENCES POSTPRANDIAL RETINYL PALMITATE BUT NOT TRIGLYCERIDE CONCENTRATIONS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID CORONARY-ARTERY DISEASE; LOW-DENSITY-LIPOPROTEIN; CHOLESTERYL-ESTER TRANSFER; RECEPTOR-BINDING ACTIVITY; LIPID TRANSFER PROTEINS; APOPROTEIN-E PHENOTYPE; CHYLOMICRON REMNANTS; PLASMA-CLEARANCE; RICH LIPOPROTEINS; HEPATIC LIPASE AB To quantify the effect of the apolipoprotein (ape)E polymorphism on the magnitude of postprandial lipemia, we have defined its role in determining the response to a single high-fat meal in a large sample of (N = 474) individuals taking part in the biethnic Atherosclerosis Risk in Communities Study. The profile of postprandial response in plasma was monitored over 8 h by triglyceride, triglyceride-rich lipoprotein (TGRL)-triglyceride, apo B-48/apo B-100 ratio, and retinyl palmitate concentrations, and the apo E polymorphism was determined by DNA amplification and digestion. The frequency of the apo E alleles and their effects on fasting lipid levels in this sample were similar to those reported elsewhere. Postprandial plasma retinyl palmitate response to a high-fat meal with vitamin A was significantly different among ape E genotypes, with delayed clearance in individuals with an epsilon 2 allele, compared with epsilon 3/3 and epsilon 3/4 individuals. In the sample of 397 Caucasians, average retinyl palmitate response was 1,489 mu g/dl in epsilon 2/3 individuals, compared with 1,037 mu g/dl in epsilon 3/3 individuals and 1,108 mu g/dl in epsilon 3/4 individuals. The apo E polymorphism accounted for 7.1% of the interindividual variation in postprandial retinyl palmitate response, a contribution proportionally greater than its well-known effect on fasting LDL-cholesterol. However, despite this effect on postprandial retinyl palmitate, the profile of postprandial triglyceride response was not significantly different among apo E genotypes. The profile of postprandial response was consistent between the sample of Caucasians and a smaller sample of black subjects. While these data indicate that the removal of remnant particles from circulation is delayed in subjects with the epsilon 2/3 genotype, there is no reported evidence that the epsilon 2 allele predisposes to coronary artery disease (CAD). The results of this study provide not only a reliable estimate of the magnitude of the effect of the apo E polymorphism on various measurements commonly used to characterize postprandial lipemia, but also provide mechanistic insight into the effects of the apo E gene polymorphism on postprandial lipemia and CAD. C1 METHODIST HOSP,DEPT INTERNAL MED,HOUSTON,TX. BAYLOR COLL MED,HOUSTON,TX. NHLBI,EPIDEMIOL & BIOMETRY PROGRAM,BETHESDA,MD. UNIV N CAROLINA,DEPT EPIDEMIOL,CHAPEL HILL,NC. RP BOERWINKLE, E (reprint author), UNIV TEXAS,HLTH SCI CTR,CTR GENET,POB 20334,HOUSTON,TX 77225, USA. FU NHLBI NIH HHS [HL-27341, N01-HC55015, HL-40613] NR 82 TC 82 Z9 84 U1 0 U2 1 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 1994 VL 54 IS 2 BP 341 EP 360 PG 20 WC Genetics & Heredity SC Genetics & Heredity GA MU315 UT WOS:A1994MU31500018 PM 8304350 ER PT J AU POWERS, WF KIELY, JL AF POWERS, WF KIELY, JL TI THE RISKS CONFRONTING TWINS - A NATIONAL PERSPECTIVE SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE TWINS; RELATIVE RISKS; POPULATION-ATTRIBUTABLE RISK; INFANT MORTALITY; NEONATAL MORTALITY ID INFANT-MORTALITY; MULTIPLE BIRTHS; PREGNANCY; EPIDEMIOLOGY; GESTATION; DEATH AB OBJECTIVES: Our objectives were twofold: (1) to report the relative risks and population-attributable risks of twins compared with singletons for several adverse pregnancy outcomes and (2) to describe the association between having been of low or very low birth weight and death in the neonatal, postneonatal, and infant periods for twins compared with singletons. STUDY DESIGN: We performed population-based analysis of all live births and infant deaths from 1985 to 1986 birth cohorts, as reported in the U.S. Linked Birth/infant Death Data Sets. RESULTS: With singletons as the referent group, twins of all races had relative risks for very low birth weight, low birth weight, and neonatal, postneonatal, and infant death of 9.97, 8.61, 7.06, 2.75, and 5.43, respectively. Although twins make up only 2.09% of live births, the population-attributable risks of twins (the proportion of the population's adverse outcome associated with being a twin) for very low birth weight, low birth weight, and neonatal, postneonatal, and infant death was 15.8%, 13.7%, 11.2%, 3.4%, and 8.4%, respectively. CONCLUSIONS: These population-based data show that although twins are relatively infrequent they account for a disproportionately large share of adverse pregnancy outcomes. Given the relative ease with which twins can be identified early in the course of pregnancy, development and testing of interventions to postpone preterm delivery in twin pregnancy should become a national public health priority. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. CTR DIS CONTROL & PREVENT,NATL CTR HLTH STAT,OFF ANAL & EPIDEMIOL,HYATTSVILLE,MD. NR 23 TC 87 Z9 88 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD FEB PY 1994 VL 170 IS 2 BP 456 EP 461 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA MZ738 UT WOS:A1994MZ73800003 PM 8116697 ER PT J AU WALLER, DK MILLS, JL SIMPSON, JL CUNNINGHAM, GC CONLEY, MR LASSMAN, MR RHOADS, GG AF WALLER, DK MILLS, JL SIMPSON, JL CUNNINGHAM, GC CONLEY, MR LASSMAN, MR RHOADS, GG TI ARE OBESE WOMEN AT HIGHER RISK FOR PRODUCING MALFORMED OFFSPRING SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE OBESITY; PREGNANCY; BIRTH DEFECTS; NEURAL TUBE DEFECTS; BODY MASS INDEX ID NEURAL-TUBE DEFECTS; SERUM ALPHA-FETOPROTEIN; PERICONCEPTIONAL USE; MATERNAL WEIGHT; FOLIC-ACID; VITAMINS; ABSENCE AB OBJECTIVE: Our purpose was to determine whether obese women and underweight women have an increased risk of birth defects in their offspring. STUDY DESIGN: A geographically based case-control study of women living in California and Illinois was performed. There were 499 mothers of offspring with neural tube defects, 337 mothers of offspring with other major birth defects, and 534 mothers of offspring without birth defects who participated. RESULTS: Compared with women of normal weight, women who were extremely obese before pregnancy (body mass index greater than or equal to 31 kg/m(2)) showed a significantly increased risk of having an infant with a neural tube defect (odds ratio 1.8, 95% confidence interval 1.1 to 3.0), especially spina bifida (odds ratio 2.6, 95% confidence interval 1.5 to 4.5), after adjustments for age, race, education, and family income. Obese women also had significantly increased risks (p < 0.05) of having an infant with other defects of the central nervous system, great vessel defects, ventral wall defects, or other intestinal defects. CONCLUSION: Our data suggest that offspring of obese women (but not underweight women) are at an increased risk of neural tube defects and several other malformations. If these findings are confirmed, further research will be necessary before it can be concluded that weight reduction before pregnancy will lower the risk of birth defects among obese women. Until then, obese women can address their risk of birth defects with the same measures that are recommended for all women, such as adequate daily intake of folic acid and alpha-fetoprotein screening to identify malformed fetuses. C1 CALIF DEPT HLTH SERV,GENET DIS BRANCH,BERKELEY,CA. NICHHD,BETHESDA,MD. UNIV TENNESSEE,DEPT OBSTET & GYNECOL,MEMPHIS,TN. ROBERT WOOD JOHNSON MED SCH,PISCATAWAY,NJ. RP WALLER, DK (reprint author), UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,POB 20186,HOUSTON,TX 77225, USA. NR 27 TC 176 Z9 176 U1 1 U2 4 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD FEB PY 1994 VL 170 IS 2 BP 541 EP 548 PG 8 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA MZ738 UT WOS:A1994MZ73800016 PM 8116710 ER PT J AU DAUSCH, R SPRING, KR AF DAUSCH, R SPRING, KR TI REGULATION OF NACL ENTRY INTO NECTURUS GALLBLADDER EPITHELIUM BY PROTEIN-KINASE-C SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE SODIUM CHLORIDE COTRANSPORT; PARALLEL SODIUM-HYDROGEN AND CHLORIDE-BICARBONATE EXCHANGE; BUMETANIDE; AMILORIDE; PHORBOL ESTER; KINASE INHIBITOR ID NA+/H+ EXCHANGER; PHORBOL ESTERS; ION-TRANSPORT; MECHANISMS; VOLUME; CELLS; COTRANSPORT; ACTIVATION; INHIBITION AB The role of protein kinase C in the regulation of the mode of NaCl entry into Necturus gallbladder epithelial cells was determined from the rate and magnitude of ouabain-induced cell swelling in the presence of inhibitors. Stimulation of protein kinase C by phorbol ester increased the rate of cell swelling from the control value of 2.9% to 4.7%/min and caused the predominant apical membrane transport mechanism for NaCl to switch from bumetanide-sensitive Na-Cl cotransport to amiloride-sensitive parallel exchange. Na-Cl cotransport could be restored as the predominant mode of NaCl entry by treatment of stimulated tissues with the kinase inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) and calphostin C. Therefore the mechanism of NaCl transport across the apical membrane can be controlled by the activity of protein kinase C. C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. NR 22 TC 8 Z9 8 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1994 VL 266 IS 2 BP C531 EP C535 PN 1 PG 5 WC Physiology SC Physiology GA NA801 UT WOS:A1994NA80100026 PM 8141267 ER PT J AU SWAIN, MG MACARTHUR, L VERGALLA, J JONES, EA AF SWAIN, MG MACARTHUR, L VERGALLA, J JONES, EA TI ADRENAL SECRETION OF BAM-22P, A POTENT OPIOID PEPTIDE, IS ENHANCED IN RATS WITH ACUTE CHOLESTASIS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ENDOGENOUS OPIOIDS; BOVINE ADRENAL MEDULLA DOCOSAPEPTIDE ID IMMUNOREACTIVE MET-ENKEPHALIN; MESSENGER-RNA; MEDULLA; PLASMA; CELLS; CATECHOLAMINES; INCREASES; STRESS AB The adrenal gland is known to produce and release endogenous opioids into the circulation. Bovine adrenal medulla docosapeptide (BAM-22P) is a potent opioid agonist, derived from the proenkephalin A gene, which is present in the adrenal medulla. This study was undertaken to determine whether BAM-22P is released into plasma during acute cholestatic liver injury, which increases plasma total opioid activity. Acute cholestasis was induced by bile duct ligation or administration of the hepatotoxin alpha-naphthylisothiocyanate. Plasma levels of BAM-22P were determined by a sensitive radioimmunoassay, and the specificity of the assay was confirmed using high-performance liquid chromatography. Plasma BAM-22P levels in cholestatic rats were significantly higher than those in control rats. This increase in plasma BAM-22P levels was completely prevented by adrenalectomy. Adrenal steady-state levels of proenkephalin mRNA, as determined by Northern blot hybridization analyses, were also increased significantly in cholestatic rats. These increases in proenkephalin mRNA levels were not paralleled by changes in adrenal BAM-22P peptide levels, which were similar in cholestatic rats and their respective controls. Similar levels of proenkephalin mRNA expression were observed in innervated and denervated adrenal glands from cholestatic rats, suggesting that the increase in adrenal proenkephalin mRNA levels in acute cholestasis is not due to splanchnic nerve activation. Thus acute cholestasis in the rat is associated with adrenal secretion and accumulation in plasma of the highly potent opioid peptide BAM-22P and an augmentation of adrenal proenkephalin mRNA expression. The increase in plasma BAM-22P levels may contribute substantially to the increase in total circulating opioid activity documented in cholestatic rats. C1 NIMH,MOLEC NEUROSCI SECT,BETHESDA,MD 20892. NIDDKD,BETHESDA,MD 20892. RP SWAIN, MG (reprint author), UNIV CALGARY,HLTH SCI CTR,GASTROENTEROL RES GRP,3330 HOSP DR NW,CALGARY T2N 1N4,AB,CANADA. NR 30 TC 25 Z9 26 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1994 VL 266 IS 2 BP G201 EP G205 PN 1 PG 5 WC Physiology SC Physiology GA NA801 UT WOS:A1994NA80100054 PM 8141292 ER PT J AU SOLOMON, MA CORREA, R ALEXANDER, HR KOEV, LA COBB, JP KIM, DK ROBERTS, WC QUEZADO, ZMN SCHOLZ, TD CUNNION, RE HOFFMAN, WD BACHER, J YATSIV, I DANNER, RL BANKS, SM FERRANS, VJ BALABAN, RS NATANSON, C AF SOLOMON, MA CORREA, R ALEXANDER, HR KOEV, LA COBB, JP KIM, DK ROBERTS, WC QUEZADO, ZMN SCHOLZ, TD CUNNION, RE HOFFMAN, WD BACHER, J YATSIV, I DANNER, RL BANKS, SM FERRANS, VJ BALABAN, RS NATANSON, C TI MYOCARDIAL ENERGY-METABOLISM AND MORPHOLOGY IN A CANINE MODEL OF SEPSIS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HIGH-ENERGY PHOSPHATES; ADENOSINE TRIPHOSPHATE; PHOSPHOCREATINE; MYOCARDIAL DEPRESSION; MYOFIBRILLAR LOSS ID HUMAN SEPTIC SHOCK; TUMOR NECROSIS FACTOR; FREE FATTY-ACIDS; OXYGEN-CONSUMPTION; SUBSTRATE UTILIZATION; ESCHERICHIA-COLI; NITRIC-OXIDE; HEART INVIVO; ENDOTOXIN; DYSFUNCTION AB The mechanism responsible for sepsis-induced myocardial depression is not known. To determine if sepsis-induced myocardial depression is caused by inadequate free energy available for work, we studied myocardial energy metabolism in a canine model of sepsis. Escherichia coli-infected (n = 18) or sterile (n = 16) fibrin clots were implanted intraperitoneally into beagles. Myocardial function and structure was assessed using radionuclide ventriculograms, echocardiograms, and light and electron microscopy. The adequacy of energy metabolism was evaluated by comparing catecholamine-induced work increases [myocardial O-2 consumption (MVo(2)) and rate pressure product (RPP)] with a simultaneously obtained estimate of intracellular free energy [phosphocreatine-to-adenosine triphosphate ratio (PCr:ATP)] determined by P-31-magnetic resonance spectroscopy. When compared with control animals, septic animals had a decrease in left ventricular ejection fraction (EF, P < 0.0001) on day 1 and fractional shortening (FS, P < 0.0003) on day 2 after clot implantation. On day 2, neither septic nor control animals had statistically significant decreases in PCr:ATP, despite catecholamine-induced increases in MVo(2), and RPP (mean maximal increases in septic animals 135 +/- 31 and 51 +/- 10%, respectively). Light and electron microscopic findings showed that hearts of septic animals, compared with control animals, had a greater degree of morphological abnormalities. Thus, in a canine model of sepsis with alterations in myocyte ultrastructure and documented myocardial depression (decreased EF and FS), intracellular free energy levels (PCr:ATP) were maintained despite catecholamine-induced increases in myocardial work (increased MVo(2), and RPP), suggesting high-energy synthetic capabilities are not limiting cardiac function. C1 NHLBI,CARDIAC ENERGET LAB,ULTRASTRUCT SECT,BETHESDA,MD 20892. NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NIH,SURG UNIT,VET RESOURCES PROGRAM,BETHESDA,MD 20892. RP SOLOMON, MA (reprint author), NCI,CTR CLIN,DEPT CRIT CARE MED,BLDG 10,RM 7D-43,BETHESDA,MD 20892, USA. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 64 TC 73 Z9 76 U1 0 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD FEB PY 1994 VL 266 IS 2 BP H757 EP H768 PN 2 PG 12 WC Physiology SC Physiology GA NA803 UT WOS:A1994NA80300049 PM 8141377 ER PT J AU CORYELL, W WINOKUR, G SHEA, T MASER, JD ENDICOTT, J AKISKAL, HS AF CORYELL, W WINOKUR, G SHEA, T MASER, JD ENDICOTT, J AKISKAL, HS TI THE LONG-TERM STABILITY OF DEPRESSIVE SUBTYPES SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DEXAMETHASONE SUPPRESSION TEST; BETA-HYDROXYLASE ACTIVITY; UNIPOLAR DEPRESSION; MAJOR DEPRESSION; FOLLOW-UP; DELUSIONAL DEPRESSION; PSYCHOTIC SYMPTOMATOLOGY; NONPSYCHOTIC DEPRESSION; ENDOGENOUS-DEPRESSION; AFFECTIVE-DISORDERS AB Objective: This study used the concept of diagnostic stability to examine the validity of three subtypes of major depression. Method: Patients with major depressive disorder (N=424) were assigned baseline diagnoses according to structured interviews and the Research Diagnostic Criteria. Follow-up evaluations took place at 6-month intervals over the next 5 years and annually for an additional 3 years. During. this period 424, 246, 163, and 96 of the patients who had recovered from the index episode had one, two, three, and four recurrences, respectively, of major depressive disorder. The kappa statistic was used to quantify the likelihood that patients with the psychotic, agitated/retarded, or endogenous subtype of depression in a given episode would again manifest that subtype in subsequent episodes. Results: The psychotic subtype showed the most enduring diagnostic stability across multiple subsequent episodes. Evert after three intervening episodes, patients with baseline psychotic major depression were five times more likely to develop a psychotic depression than were other depressed patients. For all three subtypes, diagnostic stability was greater for contiguous episodes than for noncontiguous episodes. Psychotic, agitated/retarded and endogenous subtypes showed significant stability after control for the bipolar/unipolar and primary/secondary distinctions. The endogenous subtype was stable among patients with primary depression but not among those with secondary depression. Conclusions: The psychotic subtype was the most valid of the subtypes tested from the perspective of diagnostic stability. The fact that stability across adjacent episodes exceeded stability across more distantly spaced episodes may reflect state-dependent determinants, and these are likely to vary by subtype. C1 NIMH,COLLABORAT PROGRAM PSYCHOBIOL DEPRESS,BETHESDA,MD. RP CORYELL, W (reprint author), UNIV IOWA,COLL MED,DEPT PSYCHIAT,500 NEWTON RD,IOWA CITY,IA 52242, USA. NR 47 TC 77 Z9 78 U1 0 U2 3 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 1994 VL 151 IS 2 BP 199 EP 204 PG 6 WC Psychiatry SC Psychiatry GA MV488 UT WOS:A1994MV48800008 PM 8296889 ER PT J AU MUNTANER, C WOLYNIEC, P MCGRATH, J PULVER, AE AF MUNTANER, C WOLYNIEC, P MCGRATH, J PULVER, AE TI PSYCHOTIC INPATIENTS SOCIAL-CLASS AND THEIR 1ST ADMISSION TO STATE OR PRIVATE PSYCHIATRIC BALTIMORE HOSPITALS SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note ID SOCIOECONOMIC-STATUS; HISTORY; HEALTH; CARE AB Social class differences were investigated among patients admitted to public and private psychiatric hospitals. Participants included first admission White psychotic men admitted to Baltimore metropolitan area hospitals between 1983 and 1989. After adjusting for age and diagnosis, patients with low levels of skills/credentials were found to be more likely than patients with higher levels to be admitted to state psychiatric hospitals. These findings underscore the persistence of social class as a determinant of differences in the use of psychiatric care. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,EPIDEMIOL GENET PROGRAM,BALTIMORE,MD 21205. RP MUNTANER, C (reprint author), NIMH,ROOM B1-A 12,FED BLDG,7550 WISCONSIN AVE,BETHESDA,MD 20892, USA. RI Muntaner, C/A-5043-2010 FU NIMH NIH HHS [MH35712] NR 18 TC 14 Z9 14 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC 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 1994 VL 84 IS 2 BP 287 EP 289 DI 10.2105/AJPH.84.2.287 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NB628 UT WOS:A1994NB62800026 PM 8296956 ER PT J AU CUMMINGS, KM PECHACEK, T SHOPLAND, D AF CUMMINGS, KM PECHACEK, T SHOPLAND, D TI THE ILLEGAL SALE OF CIGARETTES TO UNITED-STATES MINORS - ESTIMATES BY STATE SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note ID ENFORCEMENT AB Data available from recent national surveys on the cigarette consumption and purchasing practices of teenage smokers were used to generate state-specific estimates of the number of teenage smokers and cigarette sales to minors. In 1991, approximately 2.7 million teenage cigarette smokers consumed an average of 28.3 million cigarettes per day (516 million packs per year). An estimated 255 million packs of cigarettes were sold illegally to minors in 1991. To make cigarettes and other tobacco products less accessible to minors, policymakers should consider implementing various legislative and economic measures such as banning cigarette vending machines and raising tobacco excise taxes. C1 SUNY BUFFALO,SCH MED,DEPT SOCIAL & PREVENT MED,BUFFALO,NY 14214. NCI,ROCKVILLE,MD. RP CUMMINGS, KM (reprint author), ROSWELL PK CANC INST,DEPT CANC CONTROL & EPIDEMIOL,ELM & CARLTON STS,BUFFALO,NY 14263, USA. NR 25 TC 29 Z9 29 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC 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 1994 VL 84 IS 2 BP 300 EP 302 DI 10.2105/AJPH.84.2.300 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NB628 UT WOS:A1994NB62800030 PM 8296960 ER PT J AU BAILEY, WC WILSON, SR WEISS, KB WINDSOR, RA WOLLE, JM AF BAILEY, WC WILSON, SR WEISS, KB WINDSOR, RA WOLLE, JM TI MEASURES FUR USE IN ASTHMA CLINICAL RESEARCH - OVERVIEW OF THE NIH WORKSHOP SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Editorial Material C1 AMER INST RES,PALO ALTO,CA. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NHLBI,BETHESDA,MD 20892. RP BAILEY, WC (reprint author), UNIV ALABAMA,619 S 19TH ST,BIRMINGHAM,AL 35233, USA. NR 7 TC 19 Z9 19 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 1994 VL 149 IS 2 SU S BP S1 EP S8 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NQ895 UT WOS:A1994NQ89500001 PM 8298765 ER PT J AU WINDSOR, RA AF WINDSOR, RA TI MANAGEMENT OF ASTHMA BY PATIENTS AND FAMILIES - DISCUSSION SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Discussion RP WINDSOR, RA (reprint author), NHLBI,OFF PREVENT EDUC & CONTROL,9000 ROCKVILLE PIKE,BLDG 31,ROOM 4A21,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 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 1994 VL 149 IS 2 SU S BP S67 EP S68 PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NQ895 UT WOS:A1994NQ89500011 ER PT J AU SOUSA, AR LANE, SJ NAKHOSTEEN, JA YOSHIMURA, T LEE, TH POSTON, RN AF SOUSA, AR LANE, SJ NAKHOSTEEN, JA YOSHIMURA, T LEE, TH POSTON, RN TI INCREASED EXPRESSION OF THE MONOCYTE CHEMOATTRACTANT PROTEIN-1 IN BRONCHIAL TISSUE FROM ASTHMATIC SUBJECTS SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; EPITHELIAL-CELLS; CHEMOTACTIC ACTIVITY; GENE JE; CYTOKINE; LEUKOCYTES; ACTIVATION; BASOPHILS; SECRETION; MCP-1/JE AB The expression of the monocyte chemoattractant protein (MCP-1), a member of the chemokine family of low molecular weight cytokines, was assessed by immunohistochemistry in bronchial biopsies from 12 asthmatic and 12 normal subjects. Both a monoclonal antibody (F9) and a polyclonal antibody were employed to detect MCP-1, while the mouse myeloma protein (MOPC21) was used as a negative control. Strong positive reactions for MCP-1 were seen in the bronchial epithelium. Subepithelial macrophages, blood vessels, and bronchial smooth muscle were also stained. Hue-saturation-intensity color image analysis was used to quantify reactions of the monoclonal antibody in the epithelial and subepithelial layers. With the monoclonal antibody, asthmatic biopsies showed 51.8 +/- 3.7% (mean +/- SEM) of the epithelium staining positively, whereas normal subjects reacted much less, with 6.4 +/- 1.9% of the epithelium staining (P < 0.0001); there was no overlap between the two groups. Likewise, staining was increased in the subepithelium of asthmatic airway biopsies, with 11.5 +/- 3.1% and 2.0 +/- 1.0% staining positively in asthmatic and normal subepithelium, respectively, (P < 0.002). There was a significant correlation between staining of the epithelium and subepithelium (r = 0.77, P < 0.001). The polyclonal anti-MCP-1 antibody also gave strong reactions in the epithelium and subepithelium, with 34.0 +/- 7.8% of the asthmatic and 1.6 +/- 1.0% of the normal bronchial epithelium staining positively (P < 0.0001). These increased levels of MCP-1 in the asthmatic airways suggest that they may play a role in macrophage recruitment and activation and thereby contribute to the inflammatory pathology of bronchial asthma. C1 UMDS,GUYS HOSP,DEPT EXPTL PATHOL,4TH FLOOR,MED SCH BLDG,LONDON SE1 9RT,ENGLAND. AUGUSTA TEACHING HOSP,BOCHUM,GERMANY. UMDS,GUYS HOSP,DEPT ALLERGY & ALLIED RESP DISORDERS,LONDON,ENGLAND. NCI,FCRDC,IMMUNOL LAB,FREDERICK,MD 21701. FU Wellcome Trust NR 34 TC 171 Z9 173 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 1994 VL 10 IS 2 BP 142 EP 147 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA MW512 UT WOS:A1994MW51200003 PM 8110469 ER PT J AU ROSE, CE JULIANO, CA TRACEY, DE YOSHIMURA, T FU, SM AF ROSE, CE JULIANO, CA TRACEY, DE YOSHIMURA, T FU, SM TI ROLE OF INTERLEUKIN-1 IN ENDOTOXIN-INDUCED LUNG INJURY IN THE RAT SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID TUMOR NECROSIS FACTOR; HYPOXIC PULMONARY VASOCONSTRICTION; MACROPHAGE INFLAMMATORY PROTEIN-2; HUMAN-ENDOTHELIAL CELLS; RECEPTOR ANTAGONIST; MESSENGER-RNA; EXPRESSION; SHOCK; INHIBITION; CYTOKINES AB The effects of the recombinant interleukin-I receptor antagonist (rIL-1ra) on the systemic vascular and lung injury following intraperitoneal Salmonella enteritidis lipopolysaccharide (LPS) were determined in male Sprague-Dawley rats. Initial experiments identified that maximal mortality occurred with an intraperitoneal LPS dose of 20 mg/kg, and this dose was used in subsequent experiments. Albumin permeability, measured in an ex vivo perfused heart-lung preparation from the rats 2 h after injection of LPS, was increased with endotoxin as was the wet:dry weight ratio. Pretreatment of the rats with intravenous rIL-1ra, 1 to 10 mg/kg, followed by a continuous intravenous infusion at 30 to 50 mug/kg/min resulted in restoration of blood pressure at 100 min following endotoxin administration. Moreover, coadministration of rIL-1ra with endotoxin totally prevented the rise in albumin permeability of the pulmonary vasculature and the increase in wet:dry lung weight ratios observed in rats treated with LPS alone. LPS injected intraperitoneally caused a marked decrease in circulating leukocyte count, an effect not reversed by rIL-1ra. RNA extraction of whole-lung homogenates revealed that mRNA for IL-1beta was constitutively expressed in the absence of endotoxin, but transcripts increased progressively from 0.5 to 2 h after endotoxin administration. Increases in mRNAs for tumor necrosis factor-alpha (TNF-alpha) and for macrophage inflammatory protein-2 (MIP-2), a potent neutrophil chemoattractant, were also observed from 0.5 until 2 h after endotoxin administration. These data identify up-regulation of IL-1beta, TNF-alpha, and MIP-2 in rat lungs after administration of endotoxin and suggest an important role for IL-1 in the systemic hypotension and increase in lung leak of albumin and water with endotoxin. However, other systemic effects, such as leukopenia, appear to be unrelated to IL-1, indicating a need for broader examination of the effects of endotoxin on cytokine production in general. C1 NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. UNIV VIRGINIA,MED CTR,SCH MED,DEPT INTERNAL MED,CHARLOTTESVILLE,VA 22901. UPJOHN CO,KALAMAZOO,MI 49001. FU NCI NIH HHS [CA 34546] NR 33 TC 34 Z9 34 U1 0 U2 1 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 1994 VL 10 IS 2 BP 214 EP 221 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA MW512 UT WOS:A1994MW51200013 PM 8110477 ER PT J AU MOULIAPELAT, JP NGUYEN, LN GLAZIOU, P CHANTEAU, S OTTESEN, EA CARDINES, R MARTIN, PMV CARTEL, JLL AF MOULIAPELAT, JP NGUYEN, LN GLAZIOU, P CHANTEAU, S OTTESEN, EA CARDINES, R MARTIN, PMV CARTEL, JLL TI IVERMECTIN PLUS DIETHYLCARBAMAZINE - AN ADDITIVE EFFECT ON EARLY MICROFILARIAL CLEARANCE SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID EFFICACY AB The effects of ivermectin, diethylcarbamazine (DEC), and the combination of both drugs on levels of microfilaremia (mf) were studied in 30 male Polynesian Wuchereria bancrofti carriers. Microfilarial densities were measured 30 min (H1/2), I hr (HI), and 2, 4, 8, 24, and 96 hr (H2, H4, H8, H24, and H96) after supervised single doses of ivermectin plus DEC (400 mu g/kg plus 1 mg/kg, respectively, 400 mu g/kg plus 3 mg/kg, respectively, and 400 mu g/kg plus 6 mg/kg, respectively), DEC (6 mg/kg) alone, and ivermectin (400 mu g/kg and 100 mu g/kg, respectively) alone given to six groups of five patients each. The results showed that 1) DEC alone or combined with ivermectin induced a rapid clearance of mf after drug intake; at H1/2, the number of circulating microfilariae was reduced to 16%, 8%, 28%, and 31%, respectively, of pretreatment values in the groups receiving ivermectin plus DEC (400 mu g/kg plus 1 mg/kg, 400 mu g/kg plus 3 mg/kg, and 400 mu g/kg plus 6 mg/kg) and DEC (6 mg/kg) alone; 2) ivermectin alone induced a rapid increase of mf densities during the first 2 hr, followed by a sharp decrease from H4 to H96; and 3) between H8 and H96, mf clearance was almost complete with the combination of ivermectin and DEC. A comparison among groups did not show any synergistic interaction between ivermectin and DEC on the clearance of microfilaria, with the effect of each drug being additive to each another. C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RP MOULIAPELAT, JP (reprint author), INST TERR RECH MED LOUIS MALARDE,BP 30 PAPEETE,TAHITI,FR POLYNESIA. NR 12 TC 16 Z9 16 U1 0 U2 2 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD FEB PY 1994 VL 50 IS 2 BP 206 EP 209 PG 4 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA MZ147 UT WOS:A1994MZ14700013 PM 8116814 ER PT J AU GAGE, KL SCHRUMPF, ME BURGDORFER, W SCHWAN, TG AF GAGE, KL SCHRUMPF, ME BURGDORFER, W SCHWAN, TG TI DNA TYPING OF RICKETTSIAE IN NATURALLY INFECTED TICKS USING A POLYMERASE CHAIN REACTION/RESTRICTION FRAGMENT LENGTH POLYMORPHISM SYSTEM SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID SPOTTED-FEVER GROUP; UNITED-STATES; TYPHUS; IDENTIFICATION; CALIFORNIA; SEROTYPES; HEMOLYMPH; MONTANA; VECTORS; FLEAS AB We used the polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP) rickettsial typing system of Regnery and others to rapidly identify rickettsiae in naturally infected ticks. Unlike previously described methods, our PCR assays type rickettsiae directly from tick tissues without first isolating the organisms. We collected 226 adult Dermacentor andersoni ticks in the Bitterroot Mountains of western Montana and analyzed them for possible rickettsial infection by hemolymph test using the Gimenez stain. Thirteen (5.8%) of these ticks were positive by hemolymph test and selected for further analysis using the above PCR/RFLP typing system. The PCR assays performed using the first primer set (RpCS) resulted in amplification of fragments of the predicted size from nine of the 13 hemolymph test-positive tick samples. Only four of these nine tick samples were also positive in similar PCR assays performed with a second primer set (Rr190) that is presumed to be spotted fever group specific. The RFLP analyses of material amplified from these four ticks indicated they were infected with Rickettsia rickettsii (one sample) and R. rhipicephali (three samples). The PCR/RFLP analyses of the five PCR-positive tick samples that were positive only in assays performed with the RpCS primer set indicated that these ticks were infected with R. bellii. The remaining four of 13 hemolymph test-positive tick samples gave negative PCR results with both the RpCS and Rr190 primer sets. Infected hemocytes from these PCR-negative ticks contained organisms of distinctive bacillary morphology that appeared similar to those described previously as long forms, and it is possible that these organisms belong to a genus other than Rickettsia. We also examined established laboratory isolates of tick-borne rickettsiae from different regions of North America to determine whether this typing system produces consistent results. Multiple isolates of R. montana (nine isolates), R. bellii (five isolates), R. rickettsii (Hip-like) (four isolates), and R. canada (two isolates) were tested and no significant variations in PCR/RFLP patterns were observed between members of the same serotypes. However, among the five isolates of R. rhipicephali tested, two slightly different RFLP patterns were noted. Our results suggest that this PCR/RFLP typing scheme has wide applicability for identifying rickettsiae directly from D. andersoni or D. variabilis tick tissues. C1 NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,ARTHROPOD BORNE DIS SECT,HAMILTON,MT 59840. NR 34 TC 30 Z9 32 U1 0 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD FEB PY 1994 VL 50 IS 2 BP 247 EP 260 PG 14 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA MZ147 UT WOS:A1994MZ14700019 PM 7906924 ER PT J AU KEMPNER, ES MILLER, JH AF KEMPNER, ES MILLER, JH TI EFFECT OF ENVIRONMENTAL-CONDITIONS ON RADIATION TARGET SIZE ANALYSES SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID FUNCTIONAL SIZE; ASSIMILATORY NADH; NITRATE REDUCTASE; MOLECULAR-WEIGHT; INACTIVATION; PROTEINS; RECEPTOR; PLASMA RP NIAMSD, PHYS BIOL LAB, BETHESDA, MD 20892 USA. NR 29 TC 21 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0003-2697 EI 1096-0309 J9 ANAL BIOCHEM JI Anal. Biochem. PD FEB 1 PY 1994 VL 216 IS 2 BP 451 EP 455 DI 10.1006/abio.1994.1067 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA MU712 UT WOS:A1994MU71200030 PM 8179203 ER PT J AU LUBARSKY, DA HAHN, C BENNETT, DH SMITH, LR BREDEHOEFT, SJ KLEIN, HG REVES, JG AF LUBARSKY, DA HAHN, C BENNETT, DH SMITH, LR BREDEHOEFT, SJ KLEIN, HG REVES, JG TI THE HOSPITAL COST (1992) OF A SIMPLE PERIOPERATIVE ALLOGENEIC RED-BLOOD-CELL TRANSFUSION SO ANESTHESIA AND ANALGESIA LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT ANESTHESIA,DURHAM,NC. DUKE UNIV,MED CTR,DEPT BIOMETRY,DURHAM,NC. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC. DUKE UNIV,MED CTR,DEPT TRANSFUS MED,DURHAM,NC. NIH,DEPT TRANSFUS MED,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD FEB PY 1994 VL 78 IS 2 SU S BP U142 EP U142 PG 1 WC Anesthesiology SC Anesthesiology GA NA406 UT WOS:A1994NA40600256 ER PT J AU WHEELER, DM KATZ, A RICE, RT HANSFORD, RG AF WHEELER, DM KATZ, A RICE, RT HANSFORD, RG TI VOLATILE ANESTHETIC EFFECTS ON SARCOPLASMIC-RETICULUM CA CONTENT AND SARCOLEMMAL CA FLUX IN ISOLATED RAT CARDIAC CELL-SUSPENSIONS SO ANESTHESIOLOGY LA English DT Article DE ANESTHETICS, VOLATILE, ENFLURANE, HALOTHANE, ISOFLURANE; CALCIUM CHANNEL BLOCKERS, NITRENDIPINE; HEART, CALCIUM CHANNELS, SARCOPLASMIC RETICULUM; IONS, CALCIUM ID SKINNED MYOCARDIAL FIBERS; DECREASE CALCIUM CONTENT; SLOW ACTION-POTENTIALS; GUINEA-PIG VENTRICLE; MEMBRANE CURRENTS; HALOTHANE; ISOFLURANE; MYOCYTES; DEPRESSION; ENFLURANE AB Background: Cardiac cellular Ca metabolism is central to the control of the inotropic state of the heart and is altered in various ways by the volatile anesthetics halothane, enflurane and isoflurane. Specifically, differences among the agents regarding their effect on the uptake and release of Ca from the sarcoplasmic reticulum (SR) have been found, but the nature of such differences is not yet certain. At the sarcolemma, the effects of the anesthetics on the peak Ca current generally are believed to be similar among the three agents, but their impact on other aspects of sarcolemmal Ca transport is less understood. The authors sought to measure the direct action of these agents on SR Ca content and, in the same preparation, to provide a measure of Ca transfer across the sarcolemma during sustained depolarizations. Methods: In stirred suspensions of quiescent rat cardiac cells, the effects were measured of halothane, eflurane, and isoflurane an changes in quin2Ca fluorescence produced by the addition of caffeine (10 mM) and by depolarization with increased extracellular K+. The peak of the fluorescence response to caffeine, which is due to a sudden release of Ca from the SR into the cytoplasm, was used as an index of SR Ca content. Analysis of the fluorescence increase that occurred after increasing extracellular K+ from 5 mM to 30 mw in the presence of caffeine provided a measure of net Ca influx across the sarcolemma during sustained depolarizations. Results: The Ca channel blocker nitrendipine maximally inhibited 77% of the initial net Ca influx during 30 mM K+ depolarization, indicating that most of this influx involves L-type Ca channels. Of the volatile anesthetics, isoflurane (2.6 vol% or 0.57 mM) and enflurane (4.3 vol% or 1.25 mM) inhibited initial net Ca influx during K depolarization significantly more than halothane (1.7 vol% or 0.50 mM), which had no apparent effect. Isoflurane caused no transient change in cytoplasmic Ca concentration and had no effect on the SR Ca content of these quiescent cells. Enflurane (4.3 vol%) caused a significant reduction in SR Ca content. Conclusions: As previously reported, halothane depleted the SR of Ca in quiescent rat cardiac cells, and the present results indicate that enflurane had a similar effect. However, isoflurane did not produce any SR Ca depletion and thus must not significantly alter the balance between SR Ca efflux and uptake in these quiescent cells. The different effects of the three volatile anesthetics on a Ca influx largely carried by L-type Ca channels stand in contrast to the reported findings of similar inhibition of peak I-channel current among the three agents. This result may indicate a differential action (at least in the case of halothane) on peak and steady-state Ca currents. C1 JOHNS HOPKINS MED INST,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. FU NIGMS NIH HHS [R29 GM39568] NR 34 TC 31 Z9 32 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD FEB PY 1994 VL 80 IS 2 BP 372 EP 382 DI 10.1097/00000542-199402000-00017 PG 11 WC Anesthesiology SC Anesthesiology GA MX446 UT WOS:A1994MX44600016 PM 8311319 ER PT J AU BLANK, CA BRANTLY, M AF BLANK, CA BRANTLY, M TI CLINICAL-FEATURES AND MOLECULAR CHARACTERISTICS OF ALPHA-1-ANTITRYPSIN DEFICIENCY SO ANNALS OF ALLERGY LA English DT Review ID HUMAN ALPHA-1-PROTEINASE INHIBITOR; ALPHA-1 ANTI-TRYPSIN; LOWER RESPIRATORY-TRACT; MEDIATED CYTO-TOXICITY; ACUTE ANTERIOR UVEITIS; RHEUMATOID-ARTHRITIS; LIVER-DISEASE; ANTITRYPSIN PHENOTYPES; ALPHA1-ANTITRYPSIN DEFICIENCY; NEUTROPHIL CHEMOATTRACTANT C1 NICHHD,HUMAN GENET BRANCH,GENET DISORDERS SECRETED PROT UNIT,BETHESDA,MD 20892. NR 152 TC 82 Z9 83 U1 0 U2 1 PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY PI ARLINGTON HTS PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 SN 0003-4738 J9 ANN ALLERGY JI Ann. Allergy PD FEB PY 1994 VL 72 IS 2 BP 105 EP 121 PG 17 WC Allergy SC Allergy GA MW627 UT WOS:A1994MW62700002 PM 8109800 ER PT J AU HAND, MM AF HAND, MM TI EMERGENCY DEPARTMENT - RAPID IDENTIFICATION AND TREATMENT OF PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION SO ANNALS OF EMERGENCY MEDICINE LA English DT Article RP HAND, MM (reprint author), NHLBI,NATL HEART ATTACK ALERT PROGRAM,9600 ROCKVILLE PIKE,BLDG 31,ROOM 4A18,BETHESDA,MD 20892, USA. NR 0 TC 127 Z9 128 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0196-0644 J9 ANN EMERG MED JI Ann. Emerg. Med. PD FEB PY 1994 VL 23 IS 2 BP 311 EP 329 PG 19 WC Emergency Medicine SC Emergency Medicine GA MW110 UT WOS:A1994MW11000015 ER PT J AU GREENWALD, P AF GREENWALD, P TI EXPERIENCE FROM CLINICAL-TRIALS IN CANCER PREVENTION SO ANNALS OF MEDICINE LA English DT Article DE ANTINEOPLASTIC AGENTS; DIET; EPIDEMIOLOGY; NEOPLASMS; NUTRITION; RANDOMIZED; CONTROLLED TRIALS ID BREAST-CANCER; EPIDEMIOLOGIC EVIDENCE; DIETARY-FAT; CHEMOPREVENTION RESEARCH; COLON CANCER; RISK; VEGETABLES; CAROTENOIDS; CONSUMPTION; GREENLAND AB Conduct of randomized, controlled, large-scale prevention trials is fundamental to the full assessment of the efficacy of interventions to prevent cancer. Clinical trials in cancer prevention, which include dietary modification and chemoprevention, are based on leads from epidemiological and laboratory studies. Dietary intervention trials involve the modification of overall eating patterns, whereas chemoprevention trials involve the administration of natural or synthetic substances reported to have anticarcinogenic properties, e.g. vitamins, minerals, and pharmaceuticals. Clinical/ metabolic studies can help advance knowledge of the role of diet in the etiology and prevention of cancer by investigating the metabolism of factors thought to influence cancer risk; thus, these studies have the potential to provide a stronger scientific base for progression to randomized, controlled clinical trials. Cancer prevention trials supported by the National Cancer Institute include the Polyp Prevention Trial, which is testing a low-fat, high-fibre, and vegetable- and fruit-enriched eating pattern on the prevention of polyp recurrence, and the Nutrition Intervention Trials of Oesophageal Cancer in Linxian, China, which are testing the efficacy of vitamin-mineral supplements in the prevention of oesophageal cancer in high-risk populations. Results from clinical cancer prevention trials will enable investigators to establish more firmly the relationships between diet and cancer and to translate the information effectively into significant reductions in cancer incidence and mortality. RP GREENWALD, P (reprint author), NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892, USA. NR 38 TC 8 Z9 9 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0785-3890 J9 ANN MED JI Ann. Med. PD FEB PY 1994 VL 26 IS 1 BP 73 EP 80 DI 10.3109/07853899409147331 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA MW077 UT WOS:A1994MW07700013 PM 8166993 ER PT J AU CHARNAS, LR LUCIANO, CA DALAKAS, M GILLIATT, RW BERNARDINI, I ISHAK, K CWIK, VA FRAKER, D BRUSHART, TA GAHL, WA AF CHARNAS, LR LUCIANO, CA DALAKAS, M GILLIATT, RW BERNARDINI, I ISHAK, K CWIK, VA FRAKER, D BRUSHART, TA GAHL, WA TI DISTAL VACUOLAR MYOPATHY IN NEPHROPATHIC CYSTINOSIS SO ANNALS OF NEUROLOGY LA English DT Article ID RENAL FANCONI SYNDROME; INFLAMMATORY MYOPATHY; CYSTEAMINE; CARNITINE; CHILDREN; HYPOTHYROIDISM; COMPLICATIONS; INSUFFICIENCY; DEFICIENCY; FRACTIONS AB Nephropathic cystinosis is a lysosomal storage disorder leading to renal failure by age 10 years. Prolonged patient survival following renal transplantation has allowed the development of previously unknown long-term complications. Muscle involvement has been reported in a single posttransplant cystinosis patient, but the range of clinical, electrophysiologic, and histologic features has not been fully described. Thirteen of 54 post-renal-transplant patients that we examined developed weakness and wasting in the small hand muscles, with or without facial weakness and dysphagia. Tendon reflexes were preserved and sensory examinations were normal. Electrophysiologic studies in 11 affected patients showed normal nerve conduction velocities and preserved sensory action potentials. The voluntary motor units in the affected distal muscles had reduced amplitude and brief duration, confirmed with quantitative electromyography in 4 patients. Biopsy of the severely affected abductor digiti minimi or extensor carpi radialis brevis muscles in 2 patients revealed marked fiber size variability, prominent acid phosphatase-positive vacuoles, and absence of fiber type grouping or inflammatory cells. Crystals of cystine were detected in perimysial cells but not within the muscle cell vacuoles. The muscle cystine content of clinically affected muscles was markedly elevated. We conclude that a distal vacuolar myopathy is a common late complication of untreated nephropathic cystinosis. Although the cause is unclear, the general lysosomal defect in this disease may also affect the lysosomes within muscle fibers. C1 OFF CLIN DIRECTOR,EMG SECT,BETHESDA,MD. NINCDS,MED NEUROL BRANCH,NEUROMUSCULAR DIS SECT,BETHESDA,MD. NCI,SURG BRANCH,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,DEPT HEPAT PATHOL,WASHINGTON,DC 20306. UNIV ALBERTA,DIV NEUROL,EDMONTON,AB,CANADA. JOHNS HOPKINS UNIV,DEPT ORTHOPED SURG,BALTIMORE,MD. JOHNS HOPKINS UNIV,DEPT NEUROL,BALTIMORE,MD. RP CHARNAS, LR (reprint author), NICHHD,HUMAN GENET BRANCH,HUMAN BIOCHEM GENET SECT,BETHESDA,MD 20892, USA. NR 53 TC 45 Z9 46 U1 1 U2 1 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 1994 VL 35 IS 2 BP 181 EP 188 DI 10.1002/ana.410350209 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MW506 UT WOS:A1994MW50600008 PM 8109899 ER PT J AU PICKAR, D LITMAN, RE HONG, WW SU, TP WEISSMAN, EM HSIAO, JK POTTER, WZ AF PICKAR, D LITMAN, RE HONG, WW SU, TP WEISSMAN, EM HSIAO, JK POTTER, WZ TI CLINICAL-RESPONSE TO CLOZAPINE IN PATIENTS WITH SCHIZOPHRENIA SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter RP PICKAR, D (reprint author), NIMH,DIRP,EXPT THERAPEUT BRANCH,9000 ROCKVILLE PIKE,NIH 10-4N214,BETHESDA,MD 20892, USA. NR 9 TC 9 Z9 9 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD FEB PY 1994 VL 51 IS 2 BP 159 EP 160 PG 2 WC Psychiatry SC Psychiatry GA MW118 UT WOS:A1994MW11800008 PM 8297214 ER PT J AU NANCE, WE BROADDUS, WC BAILEY, BJ LEESTMA, JE PERSKY, V LEWIN, M MAYBERG, MA PAUKER, SG THRALL, JH RATNER, N RINTELMANN, WF RUBEN, RJ STOCKMAN, LV WEBB, JS BERLIN, CI BINI, WD BRACKMANN, DE CURTIN, HD ELDRIDGE, R GARETH, D EVANS, R FICKEL, VD GARDNER, G GLASCOCK, ME HOUSE, WF JACKLER, RK KAISERKUPFER, MI KARTUSH, JM LEVINE, RE LINGGOOD, RM LUNSFORD, D MARTUZA, RL MUSIEK, FE NEDZELSKI, JM OJEMANN, RG PARRY, DM ROBERTSON, JT SCHWARTZ, J SEIZINGER, BR SHANNON, RV SOBEL, RA THOMSEN, J WIET, RJ MIYAMOTO, RT BRAY, EA CLIPPER, SE ELLIOTT, JM FERGUSON, JH HALL, WH SCHLESINGER, SL WILSON, MA ADAMS, RD LUNSFORD, LD NAUNTON, RF AF NANCE, WE BROADDUS, WC BAILEY, BJ LEESTMA, JE PERSKY, V LEWIN, M MAYBERG, MA PAUKER, SG THRALL, JH RATNER, N RINTELMANN, WF RUBEN, RJ STOCKMAN, LV WEBB, JS BERLIN, CI BINI, WD BRACKMANN, DE CURTIN, HD ELDRIDGE, R GARETH, D EVANS, R FICKEL, VD GARDNER, G GLASCOCK, ME HOUSE, WF JACKLER, RK KAISERKUPFER, MI KARTUSH, JM LEVINE, RE LINGGOOD, RM LUNSFORD, D MARTUZA, RL MUSIEK, FE NEDZELSKI, JM OJEMANN, RG PARRY, DM ROBERTSON, JT SCHWARTZ, J SEIZINGER, BR SHANNON, RV SOBEL, RA THOMSEN, J WIET, RJ MIYAMOTO, RT BRAY, EA CLIPPER, SE ELLIOTT, JM FERGUSON, JH HALL, WH SCHLESINGER, SL WILSON, MA ADAMS, RD LUNSFORD, LD NAUNTON, RF TI NATIONAL-INSTITUTES-OF-HEALTH CONSENSUS DEVELOPMENT CONFERENCE STATEMENT ON ACOUSTIC NEUROMA, DECEMBER 11-13, 1991 SO ARCHIVES OF NEUROLOGY LA English DT Editorial Material C1 NCI,OFF MED APPLICAT RES,BETHESDA,MD 20892. NR 0 TC 59 Z9 59 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD FEB PY 1994 VL 51 IS 2 BP 201 EP 207 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA MW625 UT WOS:A1994MW62500015 ER PT J AU WEST, S VITALE, S HALLFRISCH, J MUNOZ, B MULLER, D BRESSLER, S BRESSLER, NM AF WEST, S VITALE, S HALLFRISCH, J MUNOZ, B MULLER, D BRESSLER, S BRESSLER, NM TI ARE ANTIOXIDANTS OR SUPPLEMENTS PROTECTIVE FOR AGE-RELATED MACULAR DEGENERATION SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID VITAMIN-E; ALPHA-TOCOPHEROL; OUTER SEGMENT; RAT RETINA; DAMAGE; LIGHT; CHROMATOGRAPHY; DEFICIENCIES; PREVALENCE; CATARACT AB Objectives: The relationships between fasting plasma levels of retinol, ascorbic acid, alpha-tochopherol, and beta-carotene and age-related macular degeneration (AMD) were studied in a population enrolled in the Baltimore longitudinal Study of Aging (BLSA), in which most of the data were collected 2 or more years before assessment of macular status. Design: A total of 976 participants in the study were scheduled for a biennial examination from January 1988 through January 1, 1990, which included taking lens and macular photographs. A total of 827 (85%) of the participants had fundus photographs taken, and most plasma data were available for 82% of those subjects with fundus photographs. Age-related macular degeneration was defined as neovascular changes, geographic and nongeographic atrophy, large or confluent drusen, or hyperpigmentation. A total of 226 cases of AMD were available for analysis. Results: Logistic regression analyses suggested that alpha-tocopherol was associated with a protective effect for AMD, adjusted for age, sex, and nuclear opacity. An antioxidant index, including ascorbic acid, alpha-tocopherol, and beta-carotene, was also protective for AMD. Our conclusions must be tempered with the knowledge that the population under study was basically well nourished, and few individuals had any clinically deficient status. The study cannot exclude the possibility that quite low levels of micronutrients, lower than those observed in this study, might be risk factors for AMD. Conclusions: The data suggest a protective effect for AMD of high plasma values of alpha-tocopherol. An antioxidant index, composed of plasma ascorbic acid, alpha-tocopherol, and beta-carotene, was also protective. The use of vitamin supplements to prevent AMD is not supported by these data, which showed no protective effect of vitamin use. C1 NIA,FRANCIS SCOTT KEY HOSP,GERONTOL RES CTR,BALTIMORE,MD. RP WEST, S (reprint author), JOHNS HOPKINS UNIV HOSP,WILMER OPHTHALMOL INST,DANA CTR PREVENT OPHTHALMOL,WILMER ROOM 116,BALTIMORE,MD 21205, USA. FU NCRR NIH HHS [S10-RR04060]; NEI NIH HHS [EY07359-03] NR 34 TC 129 Z9 134 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD FEB PY 1994 VL 112 IS 2 BP 222 EP 227 PG 6 WC Ophthalmology SC Ophthalmology GA MV882 UT WOS:A1994MV88200026 PM 8311777 ER PT J AU MEDEIROS, LJ JAFFE, E AF MEDEIROS, LJ JAFFE, E TI LOW-GRADE B-CELL LYMPHOMA OF MUCOSA-ASSOCIATED LYMPHOID-TISSUE INVOLVING KIDNEY - REPLY SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Letter C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892. RP MEDEIROS, LJ (reprint author), RHODE ISL HOSP,DEPT PATHOL,593 EDDEY ST,PROVIDENCE,RI 02903, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD FEB PY 1994 VL 118 IS 2 BP 111 EP 112 PG 2 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA MV289 UT WOS:A1994MV28900005 ER PT J AU RUBY, SG HENSON, DE AF RUBY, SG HENSON, DE TI PRACTICE PROTOCOLS FOR SURGICAL PATHOLOGY - A COMMUNICATION FROM THE CANCER COMMITTEE OF THE COLLEGE-OF-AMERICAN-PATHOLOGISTS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article C1 HINSDALE HOSP,DEPT PATHOL & LAB MED,HINSDALE,IL 60521. NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,BETHESDA,MD. NR 9 TC 11 Z9 11 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD FEB PY 1994 VL 118 IS 2 BP 120 EP 121 PG 2 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA MV289 UT WOS:A1994MV28900007 PM 8311647 ER PT J AU HENSON, DE HUTTER, RVP SOBIN, LH BOWMAN, HE AF HENSON, DE HUTTER, RVP SOBIN, LH BOWMAN, HE TI PROTOCOL FOR THE EXAMINATION OF SPECIMENS REMOVED FROM PATIENTS WITH COLORECTAL-CARCINOMA - A BASIS FOR CHECKLISTS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID LARGE BOWEL-CANCER; TUMOR STUDY-GROUP; PROGNOSTIC-SIGNIFICANCE; RESECTABLE ADENOCARCINOMA; CURATIVE RESECTION; VESSEL INVASION; RECTAL-CANCER; COLON CANCER; PATHOLOGY; CLASSIFICATION C1 ST BARNABAS HOSP,DEPT PATHOL,LIVINGSTON,NJ 07039. ARMED FORCES INST PATHOL,DIV GASTROINTESTINAL PATHOL,WASHINGTON,DC. MICHIGAN STATE UNIV,COLL HUMAN MED,DEPT PATHOL,E LANSING,MI 48824. RP HENSON, DE (reprint author), NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 38 TC 30 Z9 30 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD FEB PY 1994 VL 118 IS 2 BP 122 EP 125 PG 4 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA MV289 UT WOS:A1994MV28900008 PM 8311648 ER PT J AU HOLLINGSWORTH, HC PEIPER, SC WEISS, LM RAFFELD, M JAFFE, ES AF HOLLINGSWORTH, HC PEIPER, SC WEISS, LM RAFFELD, M JAFFE, ES TI AN INVESTIGATION OF THE VIRAL PATHOGENESIS OF KIKUCHI-FUJIMOTO DISEASE - LACK OF EVIDENCE FOR EPSTEIN-BARR-VIRUS OR HUMAN HERPESVIRUS TYPE-6 AS THE CAUSATIVE AGENTS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID POLYMERASE CHAIN-REACTION; HISTIOCYTIC NECROTIZING LYMPHADENITIS; HUMAN-IMMUNODEFICIENCY-VIRUS; HODGKINS-DISEASE; INSITU HYBRIDIZATION; GRANULOCYTIC INFILTRATION; NUCLEIC-ACIDS; SOUTHERN BLOT; INFECTION; LYMPHOMA AB Histiocytic necrotizing lymphadenitis of Kikuchi and Fujimoto is a well-defined clinicopathologic entity of unknown cause. Both the Epstein-Barr virus (EBV) and human herpesvirus type 6 (HHV-6) have been suggested as potential etiologic agents. Twenty cases of Kikuchi-Fujimoto disease were studied for the presence of EBV DNA and HHV-6 DNA by the polymerase chain reaction (PCR), and in situ hybridization in the case of EBV. Cellular DNA from sections of formalin-fixed, paraffin-embedded lymph node tissue was amplified using the PCR technique and oligonucleotide primers to the EBV BamH1 W, lymphocyte-determined membrane antigen, or the EBNA-1 region. These studies were performed in three separate laboratories. In addition, 12 cases were examined by in situ hybridization, eight of which had shown at least one positive PCR signal for EBV. The presence of HHV-6 was assessed by PCR using primers to part of the pZVH14 sequence. Biopsy specimens from eight patients (40%) showed a strong positive signal for EBV in at least one laboratory, while an additional three specimens (15%) showed a weaker positive signal. Five cases studied showed rare positive cells by in situ hybridization, and one case had scattered positive cells. All samples lacked HHV-6 genomic templates. These findings indicate that HHV-6 does not play a role in the pathogenesis of Kikuchi-Fujimoto disease and do not implicate EBV as a causal agent for Kikuchi-Fujimoto disease, since EBV was detected in only a fraction of cases with a low number of positive cells detected by in situ hybridization. Further, some discrepancies were identified in the positive results for EBV in samples studied by multiple laboratories. These results indicate that inconsistent results by PCR may occur with very low levels of viral genomes and that different laboratories perform DNA amplification at different efficiencies. Alternatively, laboratory contamination may give rise to false-positive results. Therefore, a positive result for EBV should be interpreted with caution and should be confirmed by repeated study (PCR) or by independent methodology (in situ hybridization). C1 NCI,PATHOL LAB,BETHESDA,MD 20892. UNIV LOUISVILLE,JAMES GRAHAM BROWN CANC CTR,LOUISVILLE,KY 40292. CITY HOPE NATL MED CTR,DUARTE,CA. NR 45 TC 80 Z9 83 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD FEB PY 1994 VL 118 IS 2 BP 134 EP 140 PG 7 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA MV289 UT WOS:A1994MV28900011 PM 8311651 ER PT J AU ZWEIG, MH AF ZWEIG, MH TI APOLIPOPROTEINS AND LIPIDS IN CORONARY-ARTERY DISEASE - ANALYSIS OF DIAGNOSTIC-ACCURACY USING RECEIVER OPERATING CHARACTERISTIC PLOTS AND AREAS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article AB Identification of clinically important coronary artery disease is a current goal in patient treatment. Serum lipid and apolipoprotein concentrations are commonly used to identify individuals who may have significant disease. With data published earlier from 304 men classified by coronary angiography, this study used receiver operating characteristic plots and analysis to examine the ability of 10 lipid or lipoprotein measures to discriminate between subjects with and without coronary artery disease. The analysis illustrated the simple elegance of receiver operating characteristic plots and demonstrated that all 10 measures are, at best, only moderately accurate. RP ZWEIG, MH (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BETHESDA,MD 20892, USA. NR 3 TC 10 Z9 10 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD FEB PY 1994 VL 118 IS 2 BP 141 EP 144 PG 4 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA MV289 UT WOS:A1994MV28900012 PM 8311652 ER PT J AU DAWISHA, SM GMELIGMEYLING, F STEINBERG, AD AF DAWISHA, SM GMELIGMEYLING, F STEINBERG, AD TI ASSESSMENT OF CLINICAL-PARAMETERS ASSOCIATED WITH INCREASED FREQUENCY OF MUTANT T-CELLS IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS SO ARTHRITIS AND RHEUMATISM LA English DT Article ID LYMPHOCYTES-T; CIRCULATING LYMPHOCYTES; BREAST-CANCER; CLONING ASSAY; INVIVO; MUTATIONS; FIBROBLASTS AB Objective. To determine the clinical features that contribute to an increased frequency of mutant T cells (FMC) in patients with systemic lupus erythematosus (SLE). Methods. During in vivo T cell division, there are errors in replication which give rise to mutations throughout the genome. An estimate of such mutations may be obtained by focusing on mutations in the hprt gene, which can be screened by assessing relative growth of T cell clones in the presence and absence of 6-thio-guanine. In this study, peripheral blood T cell clones from 47 patients with SLE were assessed, and the frequency of mutant T cells (FMC) determined. An attempt was made to correlate the FMC with disease measures. Results. Patients with SLE had a spectrum of FMC values, ranging from normal to almost 1,000 times normal. Total duration of active disease (r(s) = 0.94), past highest disease activity index (r(s) = 0.80), and number of lupus flares (r(s) = 0.76) correlated most strongly (P < 0.0001) with FMC by Spearman's rank order analysis. In contrast, current disease activity index and current anti-DNA level did not correlate with FMC. Similar correlations between FMC and cumulative past lupus disease activity were found by linear regression analysis(r(p) = 0.89 for the correlation between the natural logarithm of FMC and cumulative duration of active disease). By both statistical tests, therapy was found to be only a minor contributor to FMC. Conclusion. In our patient population, a high FMC value appears to reflect cumulative clinical lupus disease activity, involving both intensity and duration of past active disease. C1 MITRE CORP,MCLEAN,VA 22102. NIAMS,ARTHRITIS & RHEUMATISM BRANCH,MCLEAN,VA. NR 26 TC 22 Z9 22 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD FEB PY 1994 VL 37 IS 2 BP 270 EP 277 DI 10.1002/art.1780370217 PG 8 WC Rheumatology SC Rheumatology GA MW509 UT WOS:A1994MW50900016 PM 8129782 ER PT J AU KRUTH, HS SHEKHONIN, B AF KRUTH, HS SHEKHONIN, B TI EVIDENCE FOR LOSS OF APO-B FROM LDL IN HUMAN ATHEROSCLEROTIC LESIONS - EXTRACELLULAR CHOLESTERYL ESTER LIPID PARTICLES LACKING APO-B SO ATHEROSCLEROSIS LA English DT Article DE LDL; ATHEROSCLEROSIS; CHOLESTEROL; CHOLESTERYL ESTER; FILIPIN; LIPOPROTEINS ID LOW-DENSITY LIPOPROTEINS; POLYENE ANTIBIOTICS; AORTIC INTIMA; MAST-CELLS; RICH CORE; DROPLETS; VESICLES; GRANULES; FILIPIN AB Previous studies have demonstrated the accumulation of low density lipoprotein (LDL) in the extracellular spaces of the intima of normal and atherosclerotic human vessels. In this study we have assessed the degree of colocalization in vessels of apolipoprotein B (apo B), the major protein of LDL, with cholesteryl ester, the predominant lipid of LDL. Apo B was detected immunohistochemically and cholesteryl ester was detected after its enzymatic hydrolysis and staining with the fluorescent probe, filipin. Most normal intima showed apo B staining without associated cholesteryl ester staining. This result would be expected with LDL having intact apo B; intact apo B interferes with hydrolysis and filipin staining of LDL cholesteryl ester. Fatty streaks and fibrous plagues showed regions of congruent apo B and cholesteryl ester staining in the extracellular space, suggesting fragmentation of apo B without loss of its immunoreactivity. Still other areas of lesions showed cholesteryl ester staining in the extracellular space without apo B staining. This staining pattern suggests loss of apo B from LDL leaving only the cholesteryl ester-rich core of LDL. Progressive loss of apo B from LDL can explain the patterns of apo B and cholesteryl ester colocalization that occur in vessel wall intima. The distribution of these patterns in normal and atherosclerotic lesions suggests that loss of apo B from the cholesteryl ester core of LDL is associated with lesion development. C1 ACAD MED SCI,CARDIOL RES CTR,INST EXPTL CARDIOL,MOSCOW 121552,RUSSIA. RP KRUTH, HS (reprint author), NHLBI,EXPTL ATHEROSCLEROSIS SECT,BLDG 10,ROOM 5N-113,BETHESDA,MD 20892, USA. NR 28 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0021-9150 J9 ATHEROSCLEROSIS JI Atherosclerosis PD FEB PY 1994 VL 105 IS 2 BP 227 EP 234 DI 10.1016/0021-9150(94)90053-1 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NB968 UT WOS:A1994NB96800012 PM 7516163 ER PT J AU CAUGHEY, B AF CAUGHEY, B TI PROTEASE-RESISTANT PRP ACCUMULATION AND SCRAPIE AGENT REPLICATION - A ROLE FOR SULFATED GLYCOSAMINOGLYCANS SO BIOCHEMICAL SOCIETY TRANSACTIONS LA English DT Article; Proceedings Paper CT 648th Meeting of the Biochemical-Society CY SEP 14-17, 1993 CL QUEENS UNIV, BELFAST, NORTH IRELAND SP BIOCHEM SOC HO QUEENS UNIV ID CREUTZFELDT-JAKOB DISEASE; PRION PROTEIN; SULFATED GLYCOSAMINOGLYCANS; ALZHEIMERS-DISEASE; INCUBATION PERIOD; DEXTRAN SULFATE; AMYLOID PLAQUES; CULTURED-CELLS; MESSENGER-RNA; BRAIN RP CAUGHEY, B (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 52 TC 14 Z9 14 U1 1 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0300-5127 J9 BIOCHEM SOC T JI Biochem. Soc. Trans. PD FEB PY 1994 VL 22 IS 1 BP 163 EP 167 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA929 UT WOS:A1994NA92900034 PM 7911438 ER PT J AU OBRIEN, DA WELCH, JE FULCHER, KD EDDY, EM AF OBRIEN, DA WELCH, JE FULCHER, KD EDDY, EM TI EXPRESSION OF MANNOSE 6-PHOSPHATE RECEPTOR MESSENGER RIBONUCLEIC-ACIDS IN MOUSE SPERMATOGENIC AND SERTOLI CELLS SO BIOLOGY OF REPRODUCTION LA English DT Article ID GROWTH FACTOR-II; ACROSOME BIOGENESIS; NUCLEOTIDE-SEQUENCE; DEHYDROGENASE-C; TESTIS; RNA; CLONING; GENES; MANNOSE-6-PHOSPHATE; POLYADENYLATION AB Spermatogenic and sertoli cells isolated from the mouse synthesize different proportions of the two mannose 6-phosphate receptors (MPR) during overnight culture periods (O'Brien et al., Endocrinology 1989; 125:2973). To determine the relative expression of MPR mRNAs in these cells, poly(A)(+) RNAs were examined by Northern blot analysis using cDNA probes specific for the cation-independent (CI) and cation-dependent (CD) MPRs. A single CI-MPR transcript, similar to 10 kb in size, was present in all tissues and cell types examined. Like the CI-MPR protein, this transcript was more abundant in Sertoli cells than in spermatogenic cells isolated from adult testes. The CD-MPR is the predominant MPR synthesized by pachytene spermatocytes or round spermatids. Multiple CD-MPR transcripts were detected in these cells, including a 2.4-kb CD-MPR mRNA that was indistinguishable from CD-MPR transcripts in somatic tissues and Sertoli cells. Smaller CD-MPR mRNAs of similar to 1.4 and 1.6 kb were prominent in pachytene spermatocytes and round spermatids, respectively, but were faint or undetectable in somatic tissues. These smaller CD-MPR mRNAs did not hybridize with an 0.9-kb restriction fragment derived from the CD-MPR 3' untranslated region (UTR), suggesting that alternate polyadenylation signals are used to produce multiple CD-MPR transcripts in spermatogenic cells. When poly(A) tracts were selectively removed from germ cell RNAs by ribonuclease H treatment, identical 1.3-kb CD-MPR mRNAs were detected in pachytene spermatocytes and round spermatids, indicating that the size difference between the 1.4- and 1.6-kb transcripts is due to variations in poly(A) tail length. These alterations in the 3' UTR of the CD-MPR transcripts may affect mRNA stability or translation during spermatogenesis. C1 UNIV N CAROLINA,DEPT CELL BIOL & ANAT,REPROD BIOL LABS,CHAPEL HILL,NC 27599. NIEHS,REPROD & DEV TOXICOL LAB,GAMETE BIOL SECT,RES TRIANGLE PK,NC 27709. RP OBRIEN, DA (reprint author), UNIV N CAROLINA,DEPT PEDIAT,REPROD BIOL LABS,CB 7500,MACNIDER BLDG,CHAPEL HILL,NC 27599, USA. FU NCI NIH HHS [CA16086]; NICHD NIH HHS [HD26485, R01 HD026485, P30-HD18968] NR 38 TC 18 Z9 18 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD FEB PY 1994 VL 50 IS 2 BP 429 EP 435 DI 10.1095/biolreprod50.2.429 PG 7 WC Reproductive Biology SC Reproductive Biology GA MW521 UT WOS:A1994MW52100027 PM 8142560 ER PT J AU GOLDBERG, EM LESTER, DS BORCHARDT, DB ZIDOVETZKI, R AF GOLDBERG, EM LESTER, DS BORCHARDT, DB ZIDOVETZKI, R TI EFFECTS OF DIACYLGLYCEROLS AND CA2+ ON STRUCTURE OF PHOSPHATIDYLCHOLINE PHOSPHATIDYLSERINE BILAYERS SO BIOPHYSICAL JOURNAL LA English DT Article ID PROTEIN-KINASE-C; DEUTERIUM MAGNETIC-RESONANCE; CALCIUM-ION BINDING; RAT-BRAIN; PHASE-TRANSITION; DIVALENT-CATIONS; ACTIVATION; PHOSPHATIDYLSERINE; MEMBRANES; VESICLES AB The combined effects of the diacylglycerols (DAGs) with the various acyl chains and Ca-2+ on the structure of phosphatidylcholine/phosphatidylserine (4:1 mole/mole) bilayers were studied using H-2- and P-31 NMR. The following DAG- and Ca2+-induced bilayer perturbations were identified. 1) Increased tendency to form nonbilayer lipid phases was induced by diolein or stearoylarachidonoylglycerol, and was synergistically enhanced by the addition of Ca2+. 2) ''Transverse'' bilayer perturbation was induced by dioctanoylglycerol. The addition of this DAG caused increased ordering of the phospholipid acyl side chains in the region adjacent to the headgroup, with the concomitant decrease of the order toward the bilayer interior. 3) Separation of the phosphatidylcholine and phosphatidylserine bilayer components was induced by combinations of relatively high (1:5 mole/mole to phosphatidylserine) Ca2+ and 25 mol% (to the phospholipids) of diolein, stearoylarachidonoylglycerol, or oleoylacetylglycerol. 4) Lateral phase separation of the bilayers on the regions of different fluidities was induced by dipalmitin. These physicochemical effects were correlated with the effects of these DAGs and Ca2+ on the activity of protein kinase C. The increased tendency to form nonbilayer lipid phases and the transverse bilayer perturbations correlated with the increased protein kinase C activity, whereas the actual presence of the nonbilayer lipid phases, as well as the separation of the phosphatidylcholine and phosphatidylserine components, was associated with the decrease in the protein kinase C activity. The lateral phase separation of the bilayer on gel-like and liquid crystalline regions did not have an effect on the activity of the enzyme. These results demonstrate the importance of the physicochemical properties of the membranes in the process of activation of protein kinase C. C1 UNIV CALIF RIVERSIDE,DEPT BIOL,RIVERSIDE,CA 92521. UNIV CALIF RIVERSIDE,DEPT CHEM,RIVERSIDE,CA 92521. NATL INST HLTH,NEURAL SYST SECT,ROCKVILLE,MD 20852. NR 64 TC 60 Z9 60 U1 0 U2 9 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 1994 VL 66 IS 2 BP 382 EP 393 PG 12 WC Biophysics SC Biophysics GA MU275 UT WOS:A1994MU27500016 PM 8161692 ER PT J AU BAHAR, I JERNIGAN, RL AF BAHAR, I JERNIGAN, RL TI STABILIZATION OF INTERMEDIATE DENSITY STATES IN GLOBULAR-PROTEINS BY HOMOGENEOUS INTRAMOLECULAR ATTRACTIVE INTERACTIONS SO BIOPHYSICAL JOURNAL LA English DT Article ID ALPHA-LACTALBUMIN; SOLVATION THERMODYNAMICS; COOPERATIVE TRANSITIONS; COMPUTER-SIMULATION; RANGE INTERACTIONS; FOLDING REACTIONS; BIO-POLYMERS; DENATURATION; MOLECULES; CONFORMATIONS AB On-lattice simulations of two-dimensional self-avoiding chains subject to homogeneous intramolecular attractive interactions were performed as a model for studying various density regimes in globular proteins. For short chains of less than 15 units, all conformations were generated and classified by density. The range of intramolecular interactions was found to increase uniformly with density, and the average number of topological contacts is directly proportional to density. The uniform interaction energy increases the probability of high density states but does not necessarily lead to dominance of the highest density state. Typically, several large peaks appear in the probability distribution of packing densities, their location and amplitude being determined by the balance between entropic effects enhancing more expanded conformations and attractive interactions favoring compact forms. Also, the homogeneous interaction energy affects the distribution of most probable interacting points in favor of the longer range interactions over the short range ones, but in addition it introduces some more detailed preferences even among short range interactions. There are some implications about the characteristics of the intermediate density states and also for the likelihood that the native state does not correspond completely to the lowest energy conformation. C1 NCI,DIV CANC BIOL & DIAG & CTR,MATH BIOL LAB,BETHESDA,MD 20892. BOGAZICI UNIV,DEPT CHEM ENGN,POLYMER RES CTR,BEBEK 80815,TURKEY. TUBITAK,ADV POLYMER MAT RES CTR,BEBEK 80815,TURKEY. RI Jernigan, Robert/A-5421-2012 NR 46 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 1994 VL 66 IS 2 BP 454 EP 466 PG 13 WC Biophysics SC Biophysics GA MU275 UT WOS:A1994MU27500023 PM 8161699 ER PT J AU BAHAR, I JERNIGAN, RL AF BAHAR, I JERNIGAN, RL TI COOPERATIVE STRUCTURAL TRANSITIONS INDUCED BY NONHOMOGENEOUS INTRAMOLECULAR INTERACTIONS IN COMPACT GLOBULAR-PROTEINS SO BIOPHYSICAL JOURNAL LA English DT Article ID COMPUTER-SIMULATION; RANGE INTERACTIONS; LATTICE MODEL; FLUCTUATIONS; SEQUENCES; POLYMERS; CHAINS; WALKS AB The role played by non-homogeneous interactions in stabilizing cooperative structural changes in proteins was investigated by exhaustive simulations of all compact conformations compatible with several well-defined globule-like shapes in three dimensions. Conformational free energies corresponding to the association of residues i and j were computed both for the unperturbed system, all subject to identical intramolecular interactions, and for the perturbed system in which a single pair of residues is probed by changing its interactions with an attractive or repulsive interaction. The high packing density leads to strong coupling between residues so that specific interactions between a given pair of residues are accompanied by considerable enthalpy changes. Relatively weak, about 1-2 kcal/mol, attractive interactions can exert a dramatic effect on the free energy distribution. Usually, central positions in the sequence most affect the conformational characteristics. Some of these interaction pairs appear to be capable of effecting major conformation transitions because of the high level of cooperativity in the dense state. Effects of repulsive interactions, however, do not depend so strongly on residue pair and cause more localized structural changes. This approach can suggest more, or less, sensitive loci for amino acid substitution. C1 NCI,DIV CANC BIOL & DIAG & CTR,MATH BIOL LAB,BETHESDA,MD 20892. BOGAZICI UNIV,DEPT CHEM ENGN,POLYMER RES CTR,BEBEK 80815,TURKEY. TUBITAK,ADV POLYMER MAT RES CTR,BEBEK 80815,TURKEY. RI Jernigan, Robert/A-5421-2012 NR 29 TC 8 Z9 8 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 1994 VL 66 IS 2 BP 467 EP 481 PG 15 WC Biophysics SC Biophysics GA MU275 UT WOS:A1994MU27500024 PM 8161700 ER PT J AU ABUGO, O RIFKIND, JM AF ABUGO, O RIFKIND, JM TI REACTION OF NITROBLUE-TETRAZOLIUM WITH HEMOGLOBIN SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. 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 1994 VL 66 IS 2 BP A360 EP A360 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202092 ER PT J AU ACEVEDO, LD GALDZICKI, Z RAPOPORT, SI AF ACEVEDO, LD GALDZICKI, Z RAPOPORT, SI TI IONIC CURRENTS AND EXCITABILITY IN SEPTAL NEURONS FROM THE TRISOMY-16 MOUSE FETUS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,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 1994 VL 66 IS 2 BP A440 EP A440 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202557 ER PT J AU ANSARI, A JONES, CM HENRY, ER HOFRICHTER, J EATON, WA AF ANSARI, A JONES, CM HENRY, ER HOFRICHTER, J EATON, WA TI IN SEARCH OF A MODEL FOR MYOGLOBIN KINETICS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. NR 1 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 1994 VL 66 IS 2 BP A362 EP A362 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202103 ER PT J AU ARISPE, N DEMAZANCOURT, P ROJAS, E AF ARISPE, N DEMAZANCOURT, P ROJAS, E TI G-PROTEIN INHIBITORY CONTROL OF A K+-SELECTIVE CHANNEL OF LARGE-CONDUCTANCE PRESENT IN ADRENAL CHROMAFFIN GRANULE MEMBRANES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,MPB,LCBG,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 1994 VL 66 IS 2 BP A144 EP A144 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200833 ER PT J AU ASZALOS, A PINE, PS WEAVER, JL SCHOENLEIN, PV GOTTESMAN, MM SZABO, G AF ASZALOS, A PINE, PS WEAVER, JL SCHOENLEIN, PV GOTTESMAN, MM SZABO, G TI BEHAVIOR OF N-ACYLATED DAUNORUBICINS IN MULTIDRUG-RESISTANT AND PARENTAL CANCER-CELLS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 US FDA,CDER,DIV RES & TESTING,WASHINGTON,DC 20204. NCI,CELL BIOL LAB,BETHESDA,MD 20892. MED SCH DEBRECEN,DEBRECEN,HUNGARY. 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 1994 VL 66 IS 2 BP A121 EP A121 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200702 ER PT J AU BARNETT, VA MILLER, CA SCHOENBERG, M AF BARNETT, VA MILLER, CA SCHOENBERG, M TI BIOCHEMICAL AND MECHANICAL EFFECTS OF N-PHENYLMALEIMIDE LABELING OF MYOSIN IN GLYCERINATED RABBIT PSOAS FIBERS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV MINNESOTA,SCH MED,DEPT PHYSIOL,MINNEAPOLIS,MN 55455. NIAMS,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 1994 VL 66 IS 2 BP A406 EP A406 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202362 ER PT J AU BARNOY, S EIDELMAN, O POLLARD, HB AF BARNOY, S EIDELMAN, O POLLARD, HB TI NUCLEOTIDE-BINDING OF CFTR AND ASSOCIATED PROTEINS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,LCBG,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 1994 VL 66 IS 2 BP A421 EP A421 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202449 ER PT J AU BARRY, JA GAWRISCH, K AF BARRY, JA GAWRISCH, K TI DIRECT NMR EVIDENCE FOR SURFACE BINDING OF ETHANOL TO LIPID BILAYERS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA,ROCKVILLE,MD 20852. NR 0 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A386 EP A386 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202239 ER PT J AU BEZRUKOV, SM BRUTYAN, RA VODYANOY, I AF BEZRUKOV, SM BRUTYAN, RA VODYANOY, I TI CONDUCTANCE REDUCTION AND NOISE OF A SINGLE SYMMETRICAL AMPHOTERICIN-B CHANNEL IN THE PRESENCE OF DIFFERENTLY SIZED POLYMERS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD 20892. UNIV MARYLAND,COLL PK,MD 20742. ONR,ARLINGTON,VA 22217. 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 1994 VL 66 IS 2 BP A214 EP A214 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201244 ER PT J AU BLANK, PS WU, X CARLSON, FD AF BLANK, PS WU, X CARLSON, FD TI BIREFRINGENCE OF MUSCLE - CROSS-BRIDGE ORIENTATION IN THE ACTIVE STATE OF MUSCLE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NICHD,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. 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 1994 VL 66 IS 2 BP A191 EP A191 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201112 ER PT J AU BOGDANOV, K PEPE, S TALO, A SPURGEON, HA LEAF, A HALLAQ, H LAKATTA, EG AF BOGDANOV, K PEPE, S TALO, A SPURGEON, HA LEAF, A HALLAQ, H LAKATTA, EG TI DOCOSAHEXAENOIC ACID MODULATES NITRENDIPINE EFFECTS ON CALCIUM CHANNELS AND CONTRACTION IN ADULT-RAT CARDIAC MYOCYTES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 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 1994 VL 66 IS 2 BP A423 EP A423 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202460 ER PT J AU BOGDANOV, K JANCZEWSKI, AM ZIMAN, BD SPURGEON, HA LAKATTA, EG AF BOGDANOV, K JANCZEWSKI, AM ZIMAN, BD SPURGEON, HA LAKATTA, EG TI L-TYPE CALCIUM CURRENT CHARACTERISTICS IN CARDIAC VENTRICULAR MYOCYTES WITH AND WITHOUT THE T-TUBULES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 1 Z9 1 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 1994 VL 66 IS 2 BP A95 EP A95 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200547 ER PT J AU BOSE, SK MUKHOPADAY, A HENDLER, RW SHRAGER, RI AF BOSE, SK MUKHOPADAY, A HENDLER, RW SHRAGER, RI TI POSSIBLE ROLE OF MEMBRANE IN CONTROL OF BACTERIORHODOPSIN (BR) PHOTOCYCLE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NIH,DCRT,APPL STUDIES LAB,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 1994 VL 66 IS 2 BP A43 EP A43 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200242 ER PT J AU BRUTYAN, RA AF BRUTYAN, RA TI POTENTIAL-DEPENDENT IONIC CHANNELS INDUCED BY AMPHOTERICIN-B UPON UNILATERAL INTRODUCTION INTO STEROL-CONTAINING PHOSPHATIDYLCHOLINE BILAYERS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD 20892. YEREVAN BIOTECHNOL INST,YEREVAN 375056,ARMENIA. 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 1994 VL 66 IS 2 BP A222 EP A222 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201291 ER PT J AU CHADWICK, RS DIMITRIADIS, EK AF CHADWICK, RS DIMITRIADIS, EK TI WAVE-DISPERSION IN COCHLEA MICROMECHANICS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,NCRR,BEIP,BIOMECH GRP,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 1994 VL 66 IS 2 BP A169 EP A169 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200981 ER PT J AU CHAEN, S HOROWITS, R PODOLSKY, RJ EPSTEIN, ND FANANAPAZIR, L AF CHAEN, S HOROWITS, R PODOLSKY, RJ EPSTEIN, ND FANANAPAZIR, L TI ATPASE ACTIVITY AND ISOMETRIC FORCE GENERATED BY SINGLE SKELETAL MYOFIBERS IN HYPERTROPHIC CARDIOMYOPATHY ASSOCIATED WITH BETA-MYOSIN HEAVY-CHAIN GENE-MUTATIONS 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 1994 VL 66 IS 2 BP A406 EP A406 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202359 ER PT J AU CHANTURIYA, A WHITTAKER, M ZIMMERBERG, J AF CHANTURIYA, A WHITTAKER, M ZIMMERBERG, J TI FUSION OF SECRETORY GRANULES WITH PLANAR LIPID BILAYER-MEMBRANES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,LTPB,BETHESDA,MD 20892. UNIV LONDON UNIV COLL,DEPT PHYSIOL,LONDON WC1E 6BT,ENGLAND. 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 1994 VL 66 IS 2 BP A284 EP A284 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201644 ER PT J AU CHANTURIYA, AN AF CHANTURIYA, AN TI A COMPARATIVE-STUDY OF PLANAR LIPID-MEMBRANES FORMED BY MONTAL-MUELLER AND MUELLER-RUDIN TECHNIQUES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,LTPB,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 1994 VL 66 IS 2 BP A289 EP A289 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201674 ER PT J AU CHAVEZ, MD GERSHFELD, NL MUDD, CP BERGER, RL AF CHAVEZ, MD GERSHFELD, NL MUDD, CP BERGER, RL TI A NOVEL DIFFERENTIAL STOPPED-FLOW TITRATION CALORIMETER - DETECTION OF CMC AND HEMOGLOBIN-LIGAND INTERACTIONS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. NIAMSD,PHYS BIOL LAB,BETHESDA,MD 20892. BEIB,APPL CLIN ENGN SECT,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 1994 VL 66 IS 2 BP A270 EP A270 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201569 ER PT J AU CHEN, YD TSONG, TY AF CHEN, YD TSONG, TY TI REVERSIBILITY AND EFFICIENCY IN OSCILLATION INDUCED FREE-ENERGY TRANSDUCTION SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,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 1994 VL 66 IS 2 BP A112 EP A112 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200647 ER PT J AU CHERNOMORDIK, LV CHANTURIYA, AN GREEN, J ZIMMERBERG, J AF CHERNOMORDIK, LV CHANTURIYA, AN GREEN, J ZIMMERBERG, J TI MONOLAYER AND COMPLETE FUSION STAGES OF THE LIPOSOME-PLANAR LIPID BILAYER INTERACTION DISSECTED BY MODULATION OF MEMBRANE LIPID-COMPOSITION SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,LTPB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A144 EP A144 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200835 ER PT J AU CHERNOMORDIK, LV LEIKINA, EA ZIMMERBERG, J AF CHERNOMORDIK, LV LEIKINA, EA ZIMMERBERG, J TI LYSOLIPID INHIBITION OF LOW PH-TRIGGERED VIRAL FUSION SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,LTPB,BETHESDA,MD 20892. NR 2 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A6 EP A6 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200028 ER PT J AU CHIZMADZHEV, YA COHEN, FS ZIMMERBERG, J SHCHERBAKOV, A AF CHIZMADZHEV, YA COHEN, FS ZIMMERBERG, J SHCHERBAKOV, A TI MEMBRANE MECHANICS CAN ACCOUNT FOR FUSION PORE DILATION IN STAGES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 FRUMKIN ELECTROCHEM INST,MOSCOW,RUSSIA. RUSH MED COLL,CHICAGO,IL 60612. NICHHD,LTPB,BETHESDA,MD 20892. RI Chizmadzhev, Yuri/L-1984-2013 NR 2 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 1994 VL 66 IS 2 BP A283 EP A283 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201643 ER PT J AU CHOE, Y SHORT, BJ CHEN, HH PREISLER, RS RAU, DC AF CHOE, Y SHORT, BJ CHEN, HH PREISLER, RS RAU, DC TI OSMOTIC SENSITIVITY OF THE B-TO-Z TRANSITION IN DNA SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 TOWSON STATE UNIV,DEPT CHEM,BALTIMORE,MD 21204. NIDDK,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 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 1994 VL 66 IS 2 BP A158 EP A158 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200911 ER PT J AU DING, J TANTILLO, C JESSEN, S JACOBOMOLINA, A LU, X NANNI, RG ZHANG, W CLARK, AD BOYER, P HUGHES, SH ARNOLD, E AF DING, J TANTILLO, C JESSEN, S JACOBOMOLINA, A LU, X NANNI, RG ZHANG, W CLARK, AD BOYER, P HUGHES, SH ARNOLD, E TI 3-DIMENSIONAL STRUCTURES OF HIV-1 REVERSE-TRANSCRIPTASE COMPLEXED WITH A DSDNA TEMPLATE-PRIMER AND A NONNUCLEOSIDE INHIBITOR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 CTR ADV BIOTECHNOL & MED,PISCATAWAY,NJ 08854. RUTGERS STATE UNIV,DEPT CHEM,PISCATAWAY,NJ 08854. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 5 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 1994 VL 66 IS 2 BP A358 EP A358 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202075 ER PT J AU DURELL, SR GUY, HR AF DURELL, SR GUY, HR TI MODELING TRANSMEMBRANE HELICES IN MEMBRANE-PROTEINS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,MATH BIOL LAB,BETHESDA,MD 20892. NR 2 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 1994 VL 66 IS 2 BP A63 EP A63 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200358 ER PT J AU EIDELMAN, O GUAYBRODER, C VERGARA, L POLLARD, HB AF EIDELMAN, O GUAYBRODER, C VERGARA, L POLLARD, HB TI CPX ACTIVATES CHLORIDE EFFLUX FROM CELLS EXPRESSING MUTANT, BUT NOT WILD-TYPE CFTR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,LCBG,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 1994 VL 66 IS 2 BP A421 EP A421 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202446 ER PT J AU FISCHER, D TSAI, CJ LIN, SL WOLFSON, H NUSSINOV, R AF FISCHER, D TSAI, CJ LIN, SL WOLFSON, H NUSSINOV, R TI 3-D, SEQUENCE-ORDER-INDEPENDENT COMPARISONS OF PROTEIN STRUCTURES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 TEL AVIV UNIV,DEPT COMP SCI,IL-69978 TEL AVIV,ISRAEL. NCI,MATH BIOL LAB,FREDERICK,MD 21702. NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21702. RI Wolfson, Haim/A-1837-2011 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 1994 VL 66 IS 2 BP A62 EP A62 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200352 ER PT J AU FISHER, RJ CASASFINET, JR ERICKSON, JW FIVASH, MJ BLADEN, SV PAPAS, TS AF FISHER, RJ CASASFINET, JR ERICKSON, JW FIVASH, MJ BLADEN, SV PAPAS, TS TI DNA-BINDING OF ETS1 PROTEIN AND PEPTIDES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 PRI DYNCORP,FREDERICK,MD 21702. NCI,FCRDC,FREDERICK,MD 21702. RI Fisher, Robert/B-1431-2009 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 1994 VL 66 IS 2 BP A358 EP A358 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202076 ER PT J AU FRISBIE, SM YU, LC AF FRISBIE, SM YU, LC TI AFFINITY OF GTP FOR MYOSIN HEADS IN MUSCLE IS CALCIUM-SENSITIVE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,NIAMS,BETHESDA,MD 20892. NR 2 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 1994 VL 66 IS 2 BP A301 EP A301 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201749 ER PT J AU FUKADA, K TAJIMA, K GERSHFELD, NL AF FUKADA, K TAJIMA, K GERSHFELD, NL TI INFLUENCE OF BILAYER CHARGE AND ELECTROLYTE CONCENTRATION ON T-ASTERISK THE CRITICAL-TEMPERATURE FOR SELF-ASSEMBLY OF THE UNILAMELLAR STATE OF DIMYRISTOYLPHOSPHATIDYLGLYCEROL SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,NIAMS,BETHESDA,MD 20892. NR 1 TC 4 Z9 4 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 1994 VL 66 IS 2 BP A289 EP A289 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201675 ER PT J AU GERTHOFFER, WT SELLERS, JR AF GERTHOFFER, WT SELLERS, JR TI EFFECTS OF PHOSPHORYLATION OF CALPONIN AND CALDESMON ON ACTIN SLIDING VELOCITY SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV NEVADA,SCH MED,DEPT PHARMACOL,RENO,NV 89557. NHLBI,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 1994 VL 66 IS 2 BP A198 EP A198 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201153 ER PT J AU GOLDBERG, EM LESTER, DS BORCHARDT, DB ZIDOVETZKI, R AF GOLDBERG, EM LESTER, DS BORCHARDT, DB ZIDOVETZKI, R TI EFFECTS OF DIACYLGLYCEROLS ON THE CONFORMATION OF PHOSPHATIDYLCHOLINE HEADGROUPS IN MIXED PHOSPHATIDYLCHOLINE PHOSPHATIDYLSERINE BILAYERS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV CALIF RIVERSIDE,DEPT BIOL,RIVERSIDE,CA 92521. UNIV CALIF RIVERSIDE,DEPT CHEM,RIVERSIDE,CA 92521. NIH,NEURAL SYST SECT,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 1994 VL 66 IS 2 BP A174 EP A174 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201006 ER PT J AU GUY, HR DURELL, SR AF GUY, HR DURELL, SR TI MODELS OF THE OUTER VESTIBULES AND SELECTIVITY FILTERS OF NA+, CA2+, AND K+ CHANNELS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,DCBDC,MATH BIOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A248 EP A248 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201441 ER PT J AU HENDLER, RW HARMON, PA LEVIN, IW AF HENDLER, RW HARMON, PA LEVIN, IW TI NEAR-INFRARED SPECTRAL CHANGES OF CYTOCHROME-AA(3) DURING POTENTIOMETRIC TITRATIONS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NIDDK,CHEM PHYS 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 1994 VL 66 IS 2 BP A368 EP A368 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202134 ER PT J AU HENDLER, RW DANCSHAZY, ZS BOSE, SK SHRAGER, RI TOKAJI, ZS AF HENDLER, RW DANCSHAZY, ZS BOSE, SK SHRAGER, RI TOKAJI, ZS TI INFLUENCE OF EXCITATION-ENERGY ON THE BACTERIORHODOPSIN PHOTOCYCLE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. BRC,INST BIOPHYS,SZEGED,HUNGARY. NIH,DCRT,APPL STUDIES 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 1994 VL 66 IS 2 BP A43 EP A43 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200239 ER PT J AU HENDRIKS, R KREULEN, DL AF HENDRIKS, R KREULEN, DL TI EVIDENCE FOR A SODIUM-DEPENDENT OUTWARD CURRENT IN CULTURED STELLATE GANGLION NEURONS OF THE GUINEA-PIG SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,TUCSON,AZ 85724. 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 1994 VL 66 IS 2 BP A254 EP A254 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201473 ER PT J AU HERNE, TM LEVIN, IW AF HERNE, TM LEVIN, IW TI PHASE-BEHAVIOR OF DPPC BILAYERS CONTAINING BILE-SALTS AND BILE-SALT CONJUGATES - RAMAN-SPECTROSCOPIC STUDIES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,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 1994 VL 66 IS 2 BP A173 EP A173 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201001 ER PT J AU HOLTE, LL PETER, SA SINNWELL, T GAWRISCH, K AF HOLTE, LL PETER, SA SINNWELL, T GAWRISCH, K TI INFLUENCE OF SN-2 CHAIN UNSATURATION ON THE H-2 NMR ORDER-PARAMETER PROFILE OF STEARIC-ACID SN-1 CHAINS IN PHOSPHATIDYLCHOLINES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA,ROCKVILLE,MD 20852. 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 1994 VL 66 IS 2 BP A175 EP A175 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201015 ER PT J AU IWASA, KH AF IWASA, KH TI CAN MEMBRANE-PROTEINS DRIVE A CELL SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDCD,BETHESDA,MD 20892. NR 2 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 1994 VL 66 IS 2 BP A168 EP A168 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200976 ER PT J AU JAIMOVICH, E ROJAS, E AF JAIMOVICH, E ROJAS, E TI INTRACELLULAR CA2+ TRANSIENTS INDUCED BY HIGH EXTERNAL K+ AND TETRACAINE IN CULTURED RAT MYOTUBES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV CHILE, DEPT FISIOL & BIOFIS, SANTIAGO 9, CHILE. CTR ESTUDIOS CIENT, SANTIAGO, 20892, CHILE. NIDDK, CELL BIOL & GENET, BETHESDA, MD 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 1994 VL 66 IS 2 BP A243 EP A243 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201413 ER PT J AU JANCZEWSKI, AM BOGDANOV, K ZIMAN, BD SPURGEON, HA LAKATTA, EG AF JANCZEWSKI, AM BOGDANOV, K ZIMAN, BD SPURGEON, HA LAKATTA, EG TI ICA ACTIVATED SARCOPLASMIC-RETICULUM (SR) CA2+ RELEASE IN CARDIAC MYOCYTES IS NOT DIRECTLY DEPENDENT UPON THE ABUNDANCE OF MORPHOLOGICAL COUPLINGS BETWEEN THE SR AND SARCOLEMMA (SL) SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,GRC,BALTIMORE,MD 21224. 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 1994 VL 66 IS 2 BP A91 EP A91 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200522 ER PT J AU JEGLITSCH, G REIN, K BADEN, DG ADAMS, DJ AF JEGLITSCH, G REIN, K BADEN, DG ADAMS, DJ TI BREVETOXIN-3 (PBTX-3) AND ITS DERIVATIVES MODULATE SINGLE SODIUM-CHANNELS IN RAT SENSORY NEURONS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,NIEHS,CTR MARINE FRESHWATER BIOMED SCI,MIAMI,FL 33152. UNIV MIAMI,SCH MED,RSMAS,MIAMI,FL 33152. UNIV MIAMI,SCH MED,DEPT MOLEC & CELL PHARMACOL,MIAMI,FL 33152. NR 2 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A323 EP A323 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201877 ER PT J AU JIN, AJ NOSSAL, R AF JIN, AJ NOSSAL, R TI TRISKELION STRUCTURE AND CLATHRIN LATTICE TRANSFORMATIONS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,DCRT,PHYS SCI LAB,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 1994 VL 66 IS 2 BP A285 EP A285 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201654 ER PT J AU JONES, CM HENRY, ER HU, Y CHAN, CK LUCK, SD BHUYAN, A RODER, H HOFRICHTER, J EATON, WA AF JONES, CM HENRY, ER HU, Y CHAN, CK LUCK, SD BHUYAN, A RODER, H HOFRICHTER, J EATON, WA TI FAST EVENTS IN PROTEIN-FOLDING INITIATED BY NANOSECOND LASER PHOTOLYSIS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. FOX CHASE CANC CTR,INST CANC RES,PHILADELPHIA,PA 19111. NR 0 TC 0 Z9 0 U1 3 U2 6 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 1994 VL 66 IS 2 BP A397 EP A397 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202308 ER PT J AU JONES, CM HENRY, ER ANSARI, A HOFRICHTER, J EATON, WA AF JONES, CM HENRY, ER ANSARI, A HOFRICHTER, J EATON, WA TI CAN THE KINETICS OF HEMOGLOBIN BE EXPLAINED BY A 2-STATE ALLOSTERIC MODEL SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. NR 1 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 1994 VL 66 IS 2 BP A362 EP A362 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202100 ER PT J AU KAPLAN, D BLANK, PS CHO, MS STEINBERG, I ZIMMERBERG, J AF KAPLAN, D BLANK, PS CHO, MS STEINBERG, I ZIMMERBERG, J TI CALCIUM SENSITIVITY OF EXOCYTOSIS IN-VITRO IS HETEROGENEOUS - A RAPID-FLOW STUDY SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,LTPB,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 1994 VL 66 IS 2 BP A284 EP A284 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201647 ER PT J AU KEMPNER, ES MILLER, JH AF KEMPNER, ES MILLER, JH TI EFFECT OF ENVIRONMENTAL-CONDITIONS ON RADIATION TARGET SIZE ANALYSES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS,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 1994 VL 66 IS 2 BP A344 EP A344 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202003 ER PT J AU KIM, SJ KNUTSON, JR WU, C AF KIM, SJ KNUTSON, JR WU, C TI FLUORESCENCE PROPERTIES OF DNA-BINDING DOMAINS OF DROSOPHILA HEAT-SHOCK FACTOR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NHLBI,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 1994 VL 66 IS 2 BP A163 EP A163 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200945 ER PT J AU KIM, SJ TSUKIYAMA, T LEWIS, MS WU, C AF KIM, SJ TSUKIYAMA, T LEWIS, MS WU, C TI THERMODYNAMIC ANALYSIS OF THE INTERACTION BETWEEN THE DROSOPHILA HEAT-SHOCK FACTOR DNA-BINDING DOMAIN AND ITS COGNATE SEQUENCE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,LB,BETHESDA,MD 20892. NIH,NCRR,BEIP,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 1994 VL 66 IS 2 BP A35 EP A35 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200195 ER PT J AU KOENIG, BW GAWRISCH, K FERRETTI, JA AF KOENIG, BW GAWRISCH, K FERRETTI, JA TI NMR STRUCTURE DETERMINATION OF A PEPTIDE FRAGMENT CORRESPONDING TO THE C-TERMINUS OF GP41 OF HIV-1 IN A MEMBRANE MIMETIC ENVIRONMENT SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. NIAAA,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 1994 VL 66 IS 2 BP A37 EP A37 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200203 ER PT J AU KOSHINUMA, M NAKAMURA, A TAJIMA, K GERSHFELD, NL AF KOSHINUMA, M NAKAMURA, A TAJIMA, K GERSHFELD, NL TI THE CRITICAL MICELLE CONCENTRATION OF DIMYRISTOYLPHOSPHATIDYLGLYCEROL SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, NIAMS, BETHESDA, MD 20892 USA. NR 1 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 EI 1542-0086 J9 BIOPHYS J JI Biophys. J. PD FEB PY 1994 VL 66 IS 2 BP A289 EP A289 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201677 ER PT J AU KOZLOV, M LEIKIN, S RAND, RP AF KOZLOV, M LEIKIN, S RAND, RP TI ENERGETICS OF THE REENTRANT HEXAGONAL-LAMELLAR PHASE-TRANSITION IN PHOSPHOLIPIDS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 FREE UNIV BERLIN,W-1000 BERLIN 33,GERMANY. NIH,BETHESDA,MD 20892. BROCK UNIV,ST CATHARINES L2S 3A1,ONTARIO,CANADA. NR 0 TC 5 Z9 5 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 1994 VL 66 IS 2 BP A299 EP A299 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201737 ER PT J AU KUDRYASHOVA, I TUCKER, RW REED, JC HANSFORD, RG AF KUDRYASHOVA, I TUCKER, RW REED, JC HANSFORD, RG TI PROTOONCOGENE BCL-2 MAINTAINS THAPSIGARGIN-SENSITIVE CA2+ POOL IN JURKAT CELLS AND INHIBITS APOPTOSIS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,DEPT ONCOL,BALTIMORE,MD 21205. LA JOLLA CANC RES FDN,LA JOLLA,CA 92037. 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 1994 VL 66 IS 2 BP A148 EP A148 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200852 ER PT J AU KUHN, HJ KRAFT, T YU, LC BRENNER, B AF KUHN, HJ KRAFT, T YU, LC BRENNER, B TI CROSS-BRIDGE STIFFNESS AND FREE-ENERGY FUNCTIONS DERIVED FROM NUCLEOTIDE TITRATION IN SKINNED MUSCLE-FIBERS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV ULM,W-7900 ULM,GERMANY. MED SCH HANNOVER,HANNOVER,GERMANY. NIH,BETHESDA,MD 20892. NR 4 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 1994 VL 66 IS 2 BP A304 EP A304 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201767 ER PT J AU LEE, L BUTZOW, JJ TARIEN, E FRAZIER, T EICHHORN, GL AF LEE, L BUTZOW, JJ TARIEN, E FRAZIER, T EICHHORN, GL TI ON THE MECHANISM OF FIDELITY IN RNA-SYNTHESIS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,GERONTOL RES CTR,CELLULAR & MOLEC BIOL LAB,BALTIMORE,MD 21224. 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 1994 VL 66 IS 2 BP A372 EP A372 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202159 ER PT J AU LEE, SP PORTER, DK CHIRIKJIAN, JG KNUTSON, JR HAN, MK AF LEE, SP PORTER, DK CHIRIKJIAN, JG KNUTSON, JR HAN, MK TI THE DEVELOPMENT OF A FLUORESCENCE ASSAY FOR THE BAMHI RESTRICTION-ENDONUCLEASE UTILIZING MODIFIED OLIGONUCLEOTIDES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,DEPT BIOCHEM,WASHINGTON,DC 20007. NHLBI,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 1994 VL 66 IS 2 BP A163 EP A163 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200942 ER PT J AU LEIKIN, S RAU, DC PARSEGIAN, VA AF LEIKIN, S RAU, DC PARSEGIAN, VA TI TEMPERATURE-FAVORED ASSEMBLY OF PROTEINS - A HYDROPHOBIC OR A HYDROPHILIC EFFECT SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,DCRT,BETHESDA,MD 20892. NIDDK,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 1994 VL 66 IS 2 BP A73 EP A73 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200418 ER PT J AU LEWIS, EN LESTER, DS LEVIN, IW AF LEWIS, EN LESTER, DS LEVIN, IW TI DRUG-INDUCED CHANGES OF PURKINJE-CELLS WITHIN THE CEREBELLAR CORTEX OF RAT BRAINS - A VIBRATIONAL IMAGING MICROSCOPIC STUDY SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDKD,BETHESDA,MD 20892. US FDA,CDER,DRT,LAUREL,MD 20708. 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 1994 VL 66 IS 2 BP A373 EP A373 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202163 ER PT J AU LIN, SL FISCHER, D WOLFSON, H NUSSINOV, R AF LIN, SL FISCHER, D WOLFSON, H NUSSINOV, R TI SURFACE DESCRIPTION AND BIOMOLECULAR RECOGNITION (DOCKING) SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,MATH BIOL LAB,FREDERICK,MD 21702. TEL AVIV UNIV,DEPT COMP SCI,IL-69978 TEL AVIV,ISRAEL. NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21702. RI Wolfson, Haim/A-1837-2011 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 1994 VL 66 IS 2 BP A62 EP A62 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200356 ER PT J AU LIVINGSTONE, JR SHIRE, SJ KELLEY, RF AF LIVINGSTONE, JR SHIRE, SJ KELLEY, RF TI THE EFFECT OF A TYR-] GLU MUTATION ON THE THERMODYNAMICS OF HETEROLOGOUS AND HOMOLOGOUS ASSOCIATION OF LIGHT AND HEAVY DOMAINS OF THE HUMANIZED 4D5 ANTI-P185(HER2)ANTIBODY SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,FCRDC,FREDERICK,MD 21702. GENENTECH INC,PROT ENGN,S SAN FRANCISCO,CA 94080. GENENTECH INC,PHARMACEUT RES & DEV,S SAN FRANCISCO,CA 94080. 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 1994 VL 66 IS 2 BP A13 EP A13 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200073 ER PT J AU LOCKWICH, T HONG, I AMBUDKAR, I AF LOCKWICH, T HONG, I AMBUDKAR, I TI CA2+ PERMEABILITY OF RAT PAROTID-GLAND BASOLATERAL MEMBRANE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDR,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 1994 VL 66 IS 2 BP A54 EP A54 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200309 ER PT J AU LUSTIG, B JERNIGAN, RL AF LUSTIG, B JERNIGAN, RL TI CONFORMATIONS OF SMALL RNA STRUCTURES - RIBOZYMES AND TRANSFER-RNA SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,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 1994 VL 66 IS 2 BP A232 EP A232 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201348 ER PT J AU MACGREGOR, RB WU, JQ AF MACGREGOR, RB WU, JQ TI PRESSURE, CHAIN-LENGTH, AND THE THERMAL TRANSITIONS OF DNA SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV TORONTO,FAC PHARM,TORONTO M5S 1A1,ONTARIO,CANADA. NIDDK,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 1994 VL 66 IS 2 BP A296 EP A296 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201717 ER PT J AU MAGER, S MIN, C HENRY, DJ CHAVKIN, C HOFFMAN, BJ DAVIDSON, N LESTER, HA AF MAGER, S MIN, C HENRY, DJ CHAVKIN, C HOFFMAN, BJ DAVIDSON, N LESTER, HA TI CONDUCTING STATES OF A MAMMALIAN SEROTONIN TRANSPORTER SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 CALTECH,DIV BIOL 15629,PASADENA,CA 91125. UNIV WASHINGTON,DEPT PHARMACOL SJ30,SEATTLE,WA 98195. NIMH,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 1994 VL 66 IS 2 BP A337 EP A337 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201957 ER PT J AU MAHANEY, JE FROEHLICH, JP THOMAS, DD AF MAHANEY, JE FROEHLICH, JP THOMAS, DD TI CONFORMATIONAL TRANSITIONS OF THE SARCOPLASMIC-RETICULUM CA2+ PUMP STUDIED BY RAPID MIXING AND TIME-RESOLVED EPR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV MINNESOTA,SCH MED,DEPT BIOCHEM,MINNEAPOLIS,MN 55455. NIA,BALTIMORE,MD 21224. RI Thomas, David/B-4257-2012 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 1994 VL 66 IS 2 BP A200 EP A200 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201163 ER PT J AU MAKAROV, AA PROTASEVICH, II GRISHINA, IB HARTLEY, RW ESIPOVA, NG YAKOVLEV, GI AF MAKAROV, AA PROTASEVICH, II GRISHINA, IB HARTLEY, RW ESIPOVA, NG YAKOVLEV, GI TI ENERGETICAL DOMAINS IN GLOBULAR-PROTEINS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 ENGELHARDT MOLEC BIOL INST,MOSCOW 117894,RUSSIA. NIDDK,BETHESDA,MD 20892. RI Makarov, Alexander/P-5279-2016 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 1994 VL 66 IS 2 BP A178 EP A178 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201030 ER PT J AU MAKHATADZE, GI GRONENBORN, AM PRIVALOV, PL AF MAKHATADZE, GI GRONENBORN, AM PRIVALOV, PL TI THERMODYNAMICS OF INTERLEUKIN-1-BETA UNFOLDING SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. NIDDK,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 1994 VL 66 IS 2 BP A181 EP A181 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201051 ER PT J AU MAKHOV, A HANNAH, J BRENNAN, M TRUS, B KOCSIS, E CONWAY, J WINGFIELD, P SIMON, M STEVEN, A AF MAKHOV, A HANNAH, J BRENNAN, M TRUS, B KOCSIS, E CONWAY, J WINGFIELD, P SIMON, M STEVEN, A TI FILAMENTOUS HEMAGGLUTININ OF BORDETELLA-PERTUSSIS - MONOMERIC HAIRPIN MODEL OF A BACTERIAL ADHESIN SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS,BETHESDA,MD 20892. US FDA,DBP,BETHESDA,MD 20892. NIH,DCRT,BETHESDA,MD 20892. NIH,OD,BETHESDA,MD 20892. BROOKHAVEN NATL LAB,UPTON,NY 11973. 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 1994 VL 66 IS 2 BP A341 EP A341 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201983 ER PT J AU MALINCHIK, S YU, L AF MALINCHIK, S YU, L TI STUDIES OF THE CONFIGURATIONS OF WEAKLY ATTACHED AND FORCE-GENERATING CROSSBRIDGES - MODELING OF EQUATORIAL X-RAY-DIFFRACTION PATTERNS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 2 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A190 EP A190 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201106 ER PT J AU MARGOLIS, LB GLUSHAKOVA, SE BAIBAKOV, BA COLLIN, C ZIMMERBERG, JJ AF MARGOLIS, LB GLUSHAKOVA, SE BAIBAKOV, BA COLLIN, C ZIMMERBERG, JJ TI LOCOMOTION OF TUMOR-CELLS IN LIVING TISSUES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. NINCDS,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 1994 VL 66 IS 2 BP A276 EP A276 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201604 ER PT J AU MASON, JT BATENJANY, M OLEARY, TJ LEVIN, IW AF MASON, JT BATENJANY, M OLEARY, TJ LEVIN, IW TI INTERDIGITATED BILAYERS WITH 3 OR 4 CHAINS PER HEADGROUP - SURFACE HYDRATION PROPERTIES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 AFIP,DEPT CELLULAR PHYSIOL,WASHINGTON,DC 20306. NIH,CHEM PHYS SECT,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 1994 VL 66 IS 2 BP A173 EP A173 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201003 ER PT J AU MINTON, AP AF MINTON, AP TI EFFECTS OF MACROMOLECULAR CROWDING ON MOLECULAR RECOGNITION SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 1994 VL 66 IS 2 BP A68 EP A68 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200388 ER PT J AU MITCHELL, DC LITMAN, BJ AF MITCHELL, DC LITMAN, BJ TI EFFECT OF ETHANOL ON RECEPTOR CONFORMATION CHANGE - PHOSPHOLIPID ACYL-CHAIN UNSATURATION AUGMENTS ABILITY OF ETHANOL TO ENHANCE BOTH META-II FORMATION AND ACYL-CHAIN PACKING FREE-VOLUME SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UNIV VIRGINIA,HSC,DEPT BIOCHEM,CHARLOTTESVILLE,VA 22908. NIAAA,MEMBRANE BIOCHEM & BIOPHYS LAB,ROCKVILLE,MD 20852. NR 0 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A48 EP A48 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200271 ER PT J AU MIYASHITA, Y SOLLOTT, SJ KINSELLA, JL LAKATTA, EG FROEHLICH, JP AF MIYASHITA, Y SOLLOTT, SJ KINSELLA, JL LAKATTA, EG FROEHLICH, JP TI ISOPROTERENOL DEPLETES SR CA2+ IN ARTERIAL SMOOTH-MUSCLE CELLS - DIFFERENTIAL EFFECT OF AGING SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,BALTIMORE,MD 21224. 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 1994 VL 66 IS 2 BP A152 EP A152 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200880 ER PT J AU MORISHIGE, K TAKAHASHI, N KOYAMA, H ZANELLI, JS KURACHI, Y FINDLAY, I JENKINS, NA COPELAND, NG PETERSON, C MORI, N AF MORISHIGE, K TAKAHASHI, N KOYAMA, H ZANELLI, JS KURACHI, Y FINDLAY, I JENKINS, NA COPELAND, NG PETERSON, C MORI, N TI MOLECULAR-CLONING, FUNCTIONAL EXPRESSION AND LOCALIZATION OF AN INWARD RECTIFIER POTASSIUM CHANNEL IN THE MOUSE-BRAIN SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. UNIV TOURS,F-37041 TOURS,FRANCE. NCI,FREDERICK CANC RES & DEV CTR,BETHESDA,MD 20892. UNIV SO CALIF,LOS ANGELES,CA 90089. RI Findlay, Ian/P-5049-2016 OI Findlay, Ian/0000-0003-0650-2602 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 1994 VL 66 IS 2 BP A105 EP A105 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200605 ER PT J AU NIEBYLSKI, CD SALEM, N AF NIEBYLSKI, CD SALEM, N TI TIME-RESOLVED FLUORESCENCE ANISOTROPY AND DIFFERENTIAL SCANNING CALORIMETRY OF A SERIES OF MIXED-ACID PHOSPHATIDYLCHOLINE BILAYERS - EFFECT OF SN-2 ACYL-CHAIN LENGTH AND DEGREE OF UNSATURATION SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA,DICBR,MEMBRANE BIOCHEM & BIOPHYS,FLUORESCENCE STUDIES,ROCKVILLE,MD 20852. NR 0 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A56 EP A56 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200319 ER PT J AU PARSEGIAN, VA RAU, DC COHEN, JA AF PARSEGIAN, VA RAU, DC COHEN, JA TI THEORETICAL AND EXPERIMENTAL STUDIES OF REPULSIVE INTERACTIONS IN 3-DIMENSIONAL MACROMOLECULAR SUSPENSIONS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NIH,DCRT,BETHESDA,MD 20892. UNIV PACIFIC,SAN FRANCISCO,CA 94115. 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 1994 VL 66 IS 2 BP A396 EP A396 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202303 ER PT J AU PEARCE, RJ FUKUYAMA, R GALDZICKI, Z EHRENSTEIN, G RAPOPORT, SI AF PEARCE, RJ FUKUYAMA, R GALDZICKI, Z EHRENSTEIN, G RAPOPORT, SI TI ALZHEIMERS-DISEASE BETA-AMYLOID AFFECTS INHERENT CHANNEL ACTIVITY OF PC12 CELLS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINCDS,CNB,BETHESDA,MD 20892. NIA,LNS,BETHESDA,MD 20892. NR 4 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A430 EP A430 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202499 ER PT J AU PLONSKY, I ZIMMERBERG, J AF PLONSKY, I ZIMMERBERG, J TI DIRECT MEASUREMENT OF FUSION PORE CONDUCTANCE DURING VIRUS-INDUCED CELL-CELL FUSION SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,LTPB,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 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 1994 VL 66 IS 2 BP A388 EP A388 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202254 ER PT J AU PODGORNIK, R JONSSON, B AF PODGORNIK, R JONSSON, B TI POLYELECTROLYTE MEDIATED INTERACTIONS BETWEEN OPPOSITELY CHARGED PLANAR SURFACES AND MICELLAR AGGREGATES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,DCRT,LSB,BETHESDA,MD 20892. CHEM CTR LUND,S-22007 LUND,SWEDEN. RI Podgornik, Rudolf/C-6209-2008 OI Podgornik, Rudolf/0000-0002-3855-4637 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 1994 VL 66 IS 2 BP A292 EP A292 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201696 ER PT J AU PODGORNIK, R RAU, DC PARSEGIAN, VA AF PODGORNIK, R RAU, DC PARSEGIAN, VA TI PARAMETRIZATION OF DIRECT AND SOFT STERIC-UNDULATORY FORCES BETWEEN DNA DOUBLE-HELICAL POLYELECTROLYTES IN SOLUTIONS OF SEVERAL DIFFERENT ANIONS AND CATIONS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,DCRT,LSB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A297 EP A297 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201722 ER PT J AU RANSON, MR STONE, AL PORTER, DK CHEN, RF AF RANSON, MR STONE, AL PORTER, DK CHEN, RF TI BASIC FIBROBLAST GROWTH-FACTOR - INTRINSIC FLUORESCENCE CHANGES UPON BINDING OF SURAMIN AND HEPARIN SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NIMH,BETHESDA,MD 20892. NHLBI,CELLULAR 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 1994 VL 66 IS 2 BP A165 EP A165 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200955 ER PT J AU RAU, DC GARNER, MM AF RAU, DC GARNER, MM TI HYDRATION EFFECTS ON DNA-PROTEIN INTERACTIONS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD 20892. NICHHD,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 1994 VL 66 IS 2 BP A370 EP A370 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202150 ER PT J AU REMETA, DP KRUMBIEGEL, M BLUMENTHAL, R GINSBURG, A AF REMETA, DP KRUMBIEGEL, M BLUMENTHAL, R GINSBURG, A TI THERMODYNAMICS OF ACID-INDUCED CONFORMATIONAL-CHANGES IN THE INFLUENZA-VIRUS HEMAGGLUTININ SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NCI,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 1994 VL 66 IS 2 BP A177 EP A177 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201025 ER PT J AU RIFKIND, JM MANOHARAN, PT ABUGO, O AF RIFKIND, JM MANOHARAN, PT ABUGO, O TI LIGAND POCKET CONFORMATION OF PARTIALLY LIGANDED HEMOGLOBIN PROBED BY EPR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA,ALLGEMEIN CHIRURG RES CTR,BALTIMORE,MD 21224. INDIAN INST TECHNOL,MADRAS 600036,TAMIL NADU,INDIA. 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 1994 VL 66 IS 2 BP A11 EP A11 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200062 ER PT J AU SHAH, AM MEBAZAA, A CUDA, G XIAO, R SELLERS, JR ROBOTHAM, JL LAKATTA, EG AF SHAH, AM MEBAZAA, A CUDA, G XIAO, R SELLERS, JR ROBOTHAM, JL LAKATTA, EG TI ENDOTHELIAL-CELL FACTOR(S) MEDIATE MATCHING OF CARDIAC CONTRACTION AND OXYGENATION SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,CARDIOVASC SCI LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV HOSP,PULM ANESTHESIOL LAB,BALTIMORE,MD 21205. NHLBI,BETHESDA,MD 20892. UNIV WALES COLL MED,DEPT CARDIOL,CARDIFF CF4 4XN,S GLAM,WALES. RI Cuda, Giovanni/F-5359-2012 OI Cuda, Giovanni/0000-0001-6313-1866 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 1994 VL 66 IS 2 BP A83 EP A83 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200477 ER PT J AU SHEN, F TRIEZENBERG, SJ PORTER, D KNUTSON, JR HENSLEY, P AF SHEN, F TRIEZENBERG, SJ PORTER, D KNUTSON, JR HENSLEY, P TI FLUORESCENCE ANALYSIS OF THE TRANSCRIPTIONAL ACTIVATION DOMAIN OF THE HERPESVIRUS PROTEIN VP16 REVEALS A HIGHLY FLEXIBLE STRUCTURE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 MICHIGAN STATE UNIV,DEPT BIOCHEM,E LANSING,MI 48824. NHLBI,LCB,BETHESDA,MD 20892. SMITHKLINE BEECHAM,DEPT MACROMOLEC SCI,KING OF PRUSSIA,PA. 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 1994 VL 66 IS 2 BP A241 EP A241 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201401 ER PT J AU SHLYAKHTENKO, LS APPELLA, E KUTYAVIN, I HARRINGTON, RE LYUBCHENKO, YL AF SHLYAKHTENKO, LS APPELLA, E KUTYAVIN, I HARRINGTON, RE LYUBCHENKO, YL TI 3-WAY DNA JUNCTIONS ARE STRONGLY BENT - CYCLIZATION STUDIES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 SRI INT,MENLO PK,CA 94025. ARIZONA STATE UNIV,DEPT MICROBIOL,TEMPE,AZ 85287. MICROPROBE CORP,BOTHELL,WA 98021. NCI,DEPT BIOCHEM,BETHESDA,MD 20892. UNR,RENO,NV 89557. NR 0 TC 1 Z9 1 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 1994 VL 66 IS 2 BP A24 EP A24 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200134 ER PT J AU SIDOROVA, N RAU, DC AF SIDOROVA, N RAU, DC TI NETROPSIN BINDING TO SPECIFIC DNA-SEQUENCES - COUPLING OF ENERGY AND WATER RELEASE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD 20892. ENGELHARDT MOLEC BIOL INST,MOSCOW,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 1994 VL 66 IS 2 BP A184 EP A184 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201068 ER PT J AU SMITH, PD COLE, J FRIAUF, WS FREDERICKSON, H HENDLER, RW AF SMITH, PD COLE, J FRIAUF, WS FREDERICKSON, H HENDLER, RW TI 100KHZ OPTICAL MULTICHANNEL ANALYZER SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,NCRR,BETHESDA,MD 20892. NHLBI,DCRT,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 1994 VL 66 IS 2 BP A376 EP A376 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202185 ER PT J AU SMOLEN, P SHERMAN, A AF SMOLEN, P SHERMAN, A TI OSCILLATIONS OF GLYCOLYSIS, ATP, AND CALCIUM IN THE PANCREATIC BETA-CELL SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,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 1994 VL 66 IS 2 BP A265 EP A265 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201539 ER PT J AU SOKOLOFF, AV WHALLEY, T ZIMMERBERG, J AF SOKOLOFF, AV WHALLEY, T ZIMMERBERG, J TI CHARACTERIZATION OF THIOL-GROUPS REQUIRED FOR THE GTP-DEPENDENT FUSION OF RAT-LIVER MICROSOMES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,LTPB,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 1994 VL 66 IS 2 BP A284 EP A284 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201649 ER PT J AU STEINBACH, PJ BROOKS, BR AF STEINBACH, PJ BROOKS, BR TI THE GLASS-TRANSITION IN MYOGLOBIN SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,DCRT,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 1994 VL 66 IS 2 BP A363 EP A363 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202105 ER PT J AU SWIDER, E LEE, WL SUICU, DJ COPELAND, TD TAKAHASHI, M MCENERY, MW AF SWIDER, E LEE, WL SUICU, DJ COPELAND, TD TAKAHASHI, M MCENERY, MW TI IMMUNOLOGICAL IDENTIFICATION OF A BRAIN-SPECIFIC 58-KDA PROTEIN THAT COPURIFIES WITH THE N-TYPE VDCC SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract ID SYNAPTIC VESICLES C1 CASE WESTERN RESERVE UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 20892. MITSUBISHI KASEI INST,TOKYO,JAPAN. NR 4 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 1994 VL 66 IS 2 BP A255 EP A255 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201476 ER PT J AU TAKAHASHI, M SNOWMAN, AM OMORI, A ITO, T BEGG, CM COPELAND, TD MCENERY, MW AF TAKAHASHI, M SNOWMAN, AM OMORI, A ITO, T BEGG, CM COPELAND, TD MCENERY, MW TI ASSOCIATION OF RAT-BRAIN OMEGA-CONOTOXIN GVIA RECEPTOR WITH SPECIFIC ISOFORMS OF NA/K-ATPASE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 MITSUBISHI KASEI INST LIFE SCI,TOKYO,JAPAN. JHU,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. CASE WESTERN RESERVE UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROG,FREDERICK,MD 21702. 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 1994 VL 66 IS 2 BP A54 EP A54 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200304 ER PT J AU TSAO, DHH GRUSCHUS, JM WANG, LH NIRENBERG, M FERRETTI, JA AF TSAO, DHH GRUSCHUS, JM WANG, LH NIRENBERG, M FERRETTI, JA TI NMR SOLUTION STRUCTURE OF THE NK-2 HOMEODOMAIN AND ITS INTERACTIONS WITH DNA SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,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 1994 VL 66 IS 2 BP A34 EP A34 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200188 ER PT J AU TSONG, TY XIE, TD MARSZALEK, P CHEN, YD AF TSONG, TY XIE, TD MARSZALEK, P CHEN, YD TI ABSORPTION OF FREE-ENERGY FROM FLUCTUATING ELECTRIC-FIELDS BY A MEMBRANE ION-PUMP TO PERFORM CHEMICAL WORK SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract ID ACTIVATION; NOISE C1 HONG KONG UNIV SCI & TECHNOL,DEPT BIOCHEM,HONG KONG,HONG KONG. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NIDDKD,BETHESDA,MD. NR 4 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 1994 VL 66 IS 2 BP A236 EP A236 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201376 ER PT J AU VERGARA, L STOJILKOVIC, SS ROJAS, E AF VERGARA, L STOJILKOVIC, SS ROJAS, E TI PHASE-RESETTING OF THE GNRH-INDUCED OSCILLATIONS OF CALCIUM-DEPENDENT POTASSIUM CURRENTS BY SINGLE DEPOLARIZING PULSES IN RAT PITUITARY GONADOTROPHS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK,LCBG,BETHESDA,MD 20892. NICHHD,ERRB,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 1994 VL 66 IS 2 BP A249 EP A249 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201447 ER PT J AU VOGEL, SS SHAFI, NI ZIMMERBERG, J AF VOGEL, SS SHAFI, NI ZIMMERBERG, J TI THE CALCIUM-DEPENDENCE OF TRIGGERED EXOCYTOSIS STUDIED USING CAGED CALCIUM - A ROLE FOR GRANULE HETEROGENEITY SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHHD,LTPB,BETHESDA,MD 20892. RI Vogel, Steven/A-3585-2012 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 1994 VL 66 IS 2 BP A145 EP A145 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200840 ER PT J AU WEAVER, JL MCKINNEY, L SCHOENLEIN, PV GOLDENBERG, S GOTTESMAN, MM ASZALOS, A AF WEAVER, JL MCKINNEY, L SCHOENLEIN, PV GOLDENBERG, S GOTTESMAN, MM ASZALOS, A TI VOLUME REGULATION AND MDR1 PROTEIN FUNCTION IN MDR1-TRANSFECTED AND PARENTAL CELL-LINES SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 US FDA,CDER,DRT,WASHINGTON,DC 20204. AFRRI,DEPT PHYSIOL,BETHESDA,MD. MED COLL GEORGIA,DEPT ANAT & CELL BIOL,AUGUSTA,GA 30912. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 1 TC 3 Z9 3 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 1994 VL 66 IS 2 BP A217 EP A217 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201265 ER PT J AU WRIGHT, JM PEOPLES, RW WEIGHT, FF AF WRIGHT, JM PEOPLES, RW WEIGHT, FF TI MULTIPLE EFFECTS OF ETHANOL ON NMDA RECEPTOR-CHANNEL KINETICS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA,ROCKVILLE,MD 20852. 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 1994 VL 66 IS 2 BP A255 EP A255 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201480 ER PT J AU WU, J LU, Y SCHEURING, E MILLER, LM XIE, A NASH, TE CHANCE, MR AF WU, J LU, Y SCHEURING, E MILLER, LM XIE, A NASH, TE CHANCE, MR TI ZINC-FINGER IDENTIFICATION IN GIARDIA-LAMBLIA BY EXAFS SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. 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 1994 VL 66 IS 2 BP A395 EP A395 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202295 ER PT J AU XIAO, JM KNUTTEL, A PACKARD, BS KNUTSON, JR AF XIAO, JM KNUTTEL, A PACKARD, BS KNUTSON, JR TI FREQUENCY-DOMAIN FLUORESCENCE LIFETIME MICROSCOPE WITH GHZ RESPONSE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. US FDA,CBER,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 1994 VL 66 IS 2 BP A161 EP A161 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46200930 ER PT J AU XU, S MALINCHIK, S GILROY, D BRENNER, B YU, L AF XU, S MALINCHIK, S GILROY, D BRENNER, B YU, L TI INTEGRATED-INTENSITIES OF MYOSIN LAYER LINES ARE NOT AFFECTED BY WEAK ATTACHMENT OF CROSS-BRIDGES TO ACTIN AT 20-DEGREES-C SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. HANNOVER MED SCH,HANNOVER,GERMANY. NR 2 TC 2 Z9 2 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 1994 VL 66 IS 2 BP A190 EP A190 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201103 ER PT J AU YOO, SH AF YOO, SH TI PH-DEPENDENT INTERACTION OF CHROMOGRANIN-A WITH INTEGRAL MEMBRANE-PROTEINS OF THE SECRETORY VESICLE INCLUDING A 260 KDA PROTEIN REACTIVE TO THE INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR ANTIBODY SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDCD,CELLULAR BIOL LAB,BETHESDA,MD 20892. NR 1 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 1994 VL 66 IS 2 BP A384 EP A384 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46202228 ER PT J AU YOO, SH LEWIS, MS AF YOO, SH LEWIS, MS TI PH-DEPENDENT INTERACTION OF AN INTRALUMINAL LOOP OF THE INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR WITH CHROMOGRANIN-A SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDCD,LCB,BETHESDA,MD 20892. NCRR,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 1994 VL 66 IS 2 BP A257 EP A257 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201492 ER PT J AU ZHOU, HX AF ZHOU, HX TI ROLE OF ELECTROSTATIC INTERACTIONS IN THE COMPLEX-FORMATION OF CYTOCHROME-C PEROXIDASE AND CYTOCHROMES-C SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDKD,CHEM PHYS 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 1994 VL 66 IS 2 BP A290 EP A290 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201685 ER PT J AU ZOLKIEWSKI, M NOSWORTHY, NJ GINSBURG, A AF ZOLKIEWSKI, M NOSWORTHY, NJ GINSBURG, A TI INTERMEDIATE STATES IN THE UNFOLDING OF DODECAMERIC GLUTAMINE-SYNTHETASE FROM ESCHERICHIA-COLI SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,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 1994 VL 66 IS 2 BP A180 EP A180 PN 2 PG 1 WC Biophysics SC Biophysics GA MU462 UT WOS:A1994MU46201044 ER PT J AU TASAKI, I BYRNE, PM AF TASAKI, I BYRNE, PM TI DISCONTINUOUS VOLUME TRANSITIONS INDUCED BY CALCIUM SODIUM-ION EXCHANGE IN ANIONIC GELS AND THEIR NEUROBIOLOGICAL IMPLICATIONS SO BIOPOLYMERS LA English DT Article AB Discontinuous volume transitions in poly(acrylic acid) gels were studied by determining equilibrium swelling curves of small gel beads immersed in salt solutions containing varying concentrations of Ca2+ and Na+. Reversible contractions of gel membranes associated with Ca2+-Na+ exchange were examined using both isometric and isotonic recording devices. A discontinuous change in electric conductance was demonstrated in association with Ca2+-Na+ exchange in gel membranes. These experimental findings provide a sound physicochemical basis for elucidating the mechanism of nerve excitation. (C) 1994 John Wiley & Sons, Inc. RP NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA. NR 21 TC 34 Z9 35 U1 0 U2 1 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0006-3525 EI 1097-0282 J9 BIOPOLYMERS JI Biopolymers PD FEB PY 1994 VL 34 IS 2 BP 209 EP 215 DI 10.1002/bip.360340207 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MW133 UT WOS:A1994MW13300006 PM 8142589 ER PT J AU HUANG, LM JEANG, KT AF HUANG, LM JEANG, KT TI LONG-RANGE JUMPING OF INCOMPLETELY EXTENDED POLYMERASE CHAIN FRAGMENTS GENERATES UNEXPECTED PRODUCTS SO BIOTECHNIQUES LA English DT Note ID REPEAT; DNA C1 NIAID,MOLEC MICROBIOL LAB,MOLEC VIROL SECT,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 NR 9 TC 8 Z9 9 U1 0 U2 1 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD FEB PY 1994 VL 16 IS 2 BP 242 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MV768 UT WOS:A1994MV76800017 PM 8179886 ER PT J AU KASTENSPORTES, C ZAKNOEN, S STEIS, RG CHAN, WC WINTON, EF WALDMANN, TA AF KASTENSPORTES, C ZAKNOEN, S STEIS, RG CHAN, WC WINTON, EF WALDMANN, TA TI T-CELL RECEPTOR GENE REARRANGEMENT IN T-CELL LARGE GRANULAR LEUKOCYTE LEUKEMIA - PREFERENTIAL-V-ALPHA BUT DIVERSE-J-ALPHA USAGE IN ONE OF 5 PATIENTS SO BLOOD LA English DT Article ID CHRONIC LYMPHOCYTIC-LEUKEMIA; GAMMA-LYMPHOPROLIFERATIVE DISORDERS; NATURAL-KILLER CELLS; BETA-CHAIN; INTERLEUKIN-2 RECEPTOR; RHEUMATOID-ARTHRITIS; ANTIGEN RECEPTOR; CYTOCHROME-C; EXPRESSION; SUPERANTIGEN C1 GEORGIA HEMATOL ONCOL CLIN,ATLANTA,GA. UNIV NEBRASKA,DEPT PATHOL,OMAHA,NE 68182. EMORY UNIV,ATLANTA,GA 30322. RP KASTENSPORTES, C (reprint author), NCI,METAB BRANCH,BLDG 10,ROOM 4N104,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 46 TC 28 Z9 28 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 1 PY 1994 VL 83 IS 3 BP 767 EP 775 PG 9 WC Hematology SC Hematology GA MU302 UT WOS:A1994MU30200021 PM 8298138 ER PT J AU TOSATO, G SGADARI, C TAGA, K JONES, KD PIKE, SE ROSENBERG, A SECHLER, JMG MAGRATH, IT LOVE, LA BHATIA, K AF TOSATO, G SGADARI, C TAGA, K JONES, KD PIKE, SE ROSENBERG, A SECHLER, JMG MAGRATH, IT LOVE, LA BHATIA, K TI REGRESSION OF EXPERIMENTAL BURKITTS-LYMPHOMA INDUCED BY EPSTEIN-BARR-VIRUS IMMORTALIZED HUMAN B-CELLS SO BLOOD LA English DT Article ID TUMOR-NECROSIS-FACTOR; NUDE-MICE; GENE-TRANSFER; FACTOR-ALPHA; REDUCED TUMORIGENICITY; T-CELLS; EXPRESSION; LINES; INVIVO; IMMUNITY C1 US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL PROD,BETHESDA,MD 20014. US FDA,CTR FOOD SAFETY & APPL NUTR,BETHESDA,MD 20014. NCI,PEDIAT ONCOL BRANCH,BETHESDA,MD 20892. RI Sgadari, Cecilia/H-4302-2016 OI Sgadari, Cecilia/0000-0003-0364-4912 NR 47 TC 31 Z9 31 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 1 PY 1994 VL 83 IS 3 BP 776 EP 784 PG 9 WC Hematology SC Hematology GA MU302 UT WOS:A1994MU30200022 PM 8298139 ER PT J AU BIECHE, I CHAMPEME, MH MATIFAS, F CROPP, C CALLAHAN, R LIDEREAU, R AF BIECHE, I CHAMPEME, MH MATIFAS, F CROPP, C CALLAHAN, R LIDEREAU, R TI 2 DISTINCT REGIONS INVOLVED IN 1P DELETION IN HUMAN PRIMARY BREAST-CANCER SO BULLETIN DU CANCER LA English DT Article DE BREAST CANCER; CHROMOSOME 1P; LOSS OF HETEROZYGOSITY; TUMOR-SUPPRESSOR GENE ID CELL-LINE; CHROMOSOME; CARCINOMA; IP AB Alteration of chromosome 1 is the most consistent cytogenetic abnormality found in human breast carcinoma. Cytogenetic studies have shown independent alterations on the two arms of chromosome 1; increased copy number of the long arm and loss of the short arm of chromosome 1. We carried out deletion analysis of the 1p region by using restriction fragment length polymorphism markers mapping to the long (six markers) and short arm (22 markers). Thirty-five of the 74 (47%) human breast tumors tested showed somatic loss of heterozygosity at one or more loci on the short arm. Two commonly deleted regions, 1p13-p21 and 1p32-pter, were identified. Our findings suggest that two tumor suppressor genes involved in the development of human breast carcinoma may occur on the short arm of the chromosome 1. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. RP BIECHE, I (reprint author), CTR RENE HUGUENIN,ONCOVIRO LAB,F-92211 ST CLOUD,FRANCE. NR 15 TC 4 Z9 5 U1 0 U2 2 PU JOHN LIBBEY EUROTEXT LTD PI MONTROUGE PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE SN 0007-4551 J9 B CANCER JI Bull. Cancer PD FEB PY 1994 VL 81 IS 2 BP 108 EP 113 PG 6 WC Oncology SC Oncology GA MU271 UT WOS:A1994MU27100004 PM 7894115 ER PT J AU BOLLINGER, BK LASKIN, WB KNIGHT, CB AF BOLLINGER, BK LASKIN, WB KNIGHT, CB TI EPITHELIOID HEMANGIOENDOTHELIOMA WITH MULTIPLE-SITE INVOLVEMENT - LITERATURE-REVIEW AND OBSERVATIONS SO CANCER LA English DT Article DE EPITHELIOID HEMANGIOENDOTHELIOMA; MULTIFOCAL VASCULAR TUMORS; INTRACYTOPLASMIC LUMINA; FACTOR VIII-RELATED ANTIGEN ID EXTRASKELETAL MYXOID CHONDROSARCOMA; LIVER-TRANSPLANTATION; MONOCLONAL-ANTIBODY; SOFT-TISSUE; BONE; TUMOR; LUNG; RECEPTORS; ESTROGEN AB This report is a case of epithelioid hemangioendothelioma presenting as multiple lytic lesions of the ilium with radiographic findings of diffuse, bilateral lung involvement and biopsy-proven scalp involvement. Histologically, the tumor within bone and skin exhibited cords and nests of plump, epithelioid-appearing cells exhibiting rudimentary vascular differentiation within a myxohyaline stroma. Aggressive histologic features were not present. Immunohistochemical reactivity for Factor VIII-related antigen, Q-bend 10 (CD34), and cytokeratin were demonstrated. Ultrastructural studies revealed abundant intermediate cytoplasmic filaments, pinocytotic vacuoles, and Weibel-Palade bodies. The concurrent bone, skin, and lung involvement, low-grade histologic type, and female sex of the patient aroused speculation about the role of hormones in the development and possible treatment of the tumor, but estrogen and progesterone receptors were not detected. Despite intense combination chemotherapy, the patient died of widely metastatic disease. This report demonstrates the aggressive potential of histologically low-grade epithelioid hemangioendothelioma and the need for a thorough evaluation for metastases. C1 NATL NAVAL MED CTR, NCI, NAVY MED ONCOL BRANCH, BETHESDA, MD USA. RP BOLLINGER, BK (reprint author), NATL NAVAL MED CTR, DEPT PATHOL & LAB MED, BETHESDA, MD 20814 USA. NR 30 TC 81 Z9 82 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 0008-543X J9 CANCER JI Cancer PD FEB 1 PY 1994 VL 73 IS 3 BP 610 EP 615 DI 10.1002/1097-0142(19940201)73:3<610::AID-CNCR2820730318>3.0.CO;2-3 PG 6 WC Oncology SC Oncology GA MU681 UT WOS:A1994MU68100017 PM 7507796 ER PT J AU MURRAY, JL ROSENBLUM, MG ZHANG, HZ PODOLOFF, DA KASI, LP CURLEY, SA CHAN, JC ROH, M HOHN, DC BREWER, H CUNNINGHAM, JE THOMPSON, LB BHADKAMKAR, V PINSKY, CM FOGLER, WE AF MURRAY, JL ROSENBLUM, MG ZHANG, HZ PODOLOFF, DA KASI, LP CURLEY, SA CHAN, JC ROH, M HOHN, DC BREWER, H CUNNINGHAM, JE THOMPSON, LB BHADKAMKAR, V PINSKY, CM FOGLER, WE TI COMPARATIVE TUMOR-LOCALIZATION OF WHOLE IMMUNOGLOBULIN-G ANTICARCINOEMBRYONIC ANTIGEN MONOCLONAL-ANTIBODIES IMMU-4 AND IMMU-4 F(AB')2 IN COLORECTAL-CANCER PATIENTS SO CANCER LA English DT Article; Proceedings Paper CT 9th Conference on Radioimmunodetection and Radioimmunotherapy of Cancer CY SEP 17-19, 1992 CL PRINCETON, NJ DE ANTICARCINOEMBRYONIC ANTIGEN; MONOCLONAL ANTIBODIES; ANTIBODY FRAGMENTS; COLON CANCER ID FRAGMENTS; CARCINOMA; MICE; BIODISTRIBUTION; PARAMETERS; DIAGNOSIS; AFFINITY; THERAPY; IN-111 AB Background, Previous studies in the literature have suggested that radiolabeled F(ab')(2) fragments might be superior to whole immunoglobulin G (IgG) for imaging and therapy of cancer because of their greater penetration in tumors. To test this hypothesis, the authors compared tumor and normal tissue uptake along with plasma clearance of I-125-labeled monoclonal antibody (MoAb) IMMU-4 whole IgG with its I-131-labeled F(ab')(2) fragment. Methods. Five patients with either liver metastases from colorectal cancer (n = 4) or intact primary tumors (n = 1) received a combination of I-125-IMMU-4 IgG (2 mCi/1 mg) plus I-131-IMMU-4 F(ab')(2) (10 mCi/1 mg) as a single 1-hour intravenous infusion on day 1. Serial blood samples were taken for up to 72 hours postinfusion to determine plasma clearance of each MoAb. On days 3-9, patients underwent exploratory laparotomy in which biopsies of tumor as well as normal tissues (liver, normal colon, lymph node, and blood) were obtained. Tissues were weighed and counted in a gamma counter, and the percent of injected dose per kilogram (%ID/kg) of each antibody, along with the radiolocalization index (RI), was computed (RI = %ID/kg tumor . %ID/kg normal tissue). Results. Tumor uptake of both antibodies (2.3 +/- 0.53 %ID/kg) was significantly higher than that of normal tissues (0.56 +/- 0.12; P < 0.001), except for blood (2.8 +/- 0.83), resulting in an RI greater than or equal to 3. There were no significant differences in uptake (%ID/g) between F(ab')(2) and IgG (F[ab'](2) = 2.0 +/-: 0.57; IgG = 2.6 +/- 0.94). The mean +/- SD of plasma T1/2 was slightly shorter for F(ab')(2) (28.8 +/- 7.2 hours) than for IgG (45.9 +/- 16.7; P = 0.08). Conclusion. In short, the biodistribution and pharmacokinetics of IMMU-4 F(ab')(2) were comparable to those of IMMU-4-IgG. C1 IMMUNOMED INC,MORRIS PLAINS,NJ. NCI,CLIN TRIALS EVALUAT PROGRAM,BETHESDA,MD. RP MURRAY, JL (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,1515 HOLCOMBE BLVD,BOX 041,HOUSTON,TX 77030, USA. FU NCI NIH HHS [N01-CM97610] NR 29 TC 17 Z9 17 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 1 PY 1994 VL 73 IS 3 SU S BP 850 EP 857 DI 10.1002/1097-0142(19940201)73:3+<850::AID-CNCR2820731316>3.0.CO;2-S PG 8 WC Oncology SC Oncology GA MV418 UT WOS:A1994MV41800015 PM 8306270 ER PT J AU SCHOTT, ME SCHLOM, J SILER, K MILENIC, DE EGGENSPERGER, D COLCHER, D CHENG, R KRUPER, WJ FORDYCE, W GOECKELER, W AF SCHOTT, ME SCHLOM, J SILER, K MILENIC, DE EGGENSPERGER, D COLCHER, D CHENG, R KRUPER, WJ FORDYCE, W GOECKELER, W TI BIODISTRIBUTION AND PRECLINICAL RADIOIMMUNOTHERAPY STUDIES USING RADIOLANTHANIDE-LABELED IMMUNOCONJUGATES SO CANCER LA English DT Article; Proceedings Paper CT 9th Conference on Radioimmunodetection and Radioimmunotherapy of Cancer CY SEP 17-19, 1992 CL PRINCETON, NJ DE TUMOR-ASSOCIATED GLYCOPROTEIN; MONOCLONAL ANTIBODY CC49; RADIOLANTHANIDE IMMUNOCONJUGATES; ANTIBODY TARGETING; BIODISTRIBUTION; PRECLINICAL THERAPY AB Lutetium-177 (Lu-177), samarium-153 (Sm-153), and yttrium-90 (Y-90) are members of the family of elements known as lanthanides or rare earths. Monoclonal antibody CC49, a murine immunoglobulin (Ig) G1, which is reactive with the tumor-associated antigen TAG-72, previously has been shown to react with a wide range of human carcinomas. The authors review here the comparative biodistributions of CC49 IgG and F(ab')(2) fragments labeled with Lu-177, Sm-153, and Y-90 using the bifunctional chelating agent PA-DOTA. The authors also review the results of a biodistribution study comparing iodine-125-labeled and Lu-177-labeled CC49 sFv, and the use of Lu-177-CC49 IgG in an experimental therapy model. Chelation and conjugations gave similar yields, and the labeled proteins showed similar retention of immunoreactivity regardless of the isotope used for both IgG and F(ab')(2). Biodistribution data obtained in athymic mice bearing LS-174T human colon carcinoma xenografts likewise showed no differences among the three radioisotopes for both IgG and F(ab')(2). Femur uptake of radioactivity was lower than previously reported for other radiolanthanide immunoconjugates. Different metabolic patterns were observed for radioiodinated versus radiometal-labeled sFv, particularly in the kidney, where localization of the latter was increased dramatically. Lu-177-CC49 was found to delay the growth of established LS-174T human colon carcinomas in athymic mice at a single dose of 50 mu Ci. Elimination of established tumors was demonstrated over the observation period (77 days) using single administrations of 200 or 350 mu Ci. Dose fractionation experiments revealed that the mice tolerated 750 mu Ci (3 X 250 mu Ci, given weekly), whereas > 50% of the mice died after receiving a single administration of similar to 500 mu Ci. In isotype-matched control experiments, a large differential in the therapeutic effects was observed between Lu-177-labeled control antibody and CC49. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. DOW CHEM CO USA,MIDLAND,MI. NR 7 TC 36 Z9 36 U1 0 U2 4 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 1 PY 1994 VL 73 IS 3 SU S BP 993 EP 998 DI 10.1002/1097-0142(19940201)73:3+<993::AID-CNCR2820731337>3.0.CO;2-7 PG 6 WC Oncology SC Oncology GA MV418 UT WOS:A1994MV41800036 PM 8306291 ER PT J AU MURRAY, JL MACEY, DJ KASI, LP RIEGER, P CUNNINGHAM, J BHADKAMKAR, V ZHANG, HZ SCHLOM, J ROSENBLUM, MG PODOLOFF, DA AF MURRAY, JL MACEY, DJ KASI, LP RIEGER, P CUNNINGHAM, J BHADKAMKAR, V ZHANG, HZ SCHLOM, J ROSENBLUM, MG PODOLOFF, DA TI PHASE-II RADIOIMMUNOTHERAPY TRIAL WITH I-131 CC49 IN COLORECTAL-CANCER SO CANCER LA English DT Article; Proceedings Paper CT 9th Conference on Radioimmunodetection and Radioimmunotherapy of Cancer CY SEP 17-19, 1992 CL PRINCETON, NJ DE RADIOIMMUNOTHERAPY; PHASE II TRIAL; COLORECTAL CANCER ID MONOCLONAL-ANTIBODY B72.3; IMMUNE-RESPONSE; COLON CANCER; TUMOR CELLS; ANTIGEN; CARCINOMA; PHARMACOKINETICS; RADIOANTIBODY; INTERLEUKIN-1; GENERATION AB Background. Radiolabeled CC49, a second generation high affinity monoclonal antibody (MoAb) reactive with tumor-associated glycoprotein 72 (TAG72) has undergone previous Phase I testing in patients with colon cancer. Based on this report, the authors treated 15 refractory metastatic colon cancer patients with I-131-CC49 to determine its overall toxicity and the response to therapy of patients treated with it. Methods. Patients received 75 mCi/m(2 131) I-CC49 (20 mg MoAb) intravenously for a period of 30-60 minutes. Whole body retention was derived from the measured dose-rate of I-131 monitored daily at 1 m using an ion chamber. Two whole-body and static-gamma camera images were taken of patients on days 4 and 7 after the infusion. Results. Nonhematologic toxicity (Grade 1-2) consisted of nausea (two patients), arthralgias (three patients), transient fever and chills (two patients), and transient blood pressure changes (two patients). At 4-5 weeks posttreatment, reversible Grade 3-4 thrombocytopenia was observed in 7 of 15 patients, and reversible Grade 3-4 granulocytopenia was observed in 6 of 15 patients. Twelve of 13 patients tested developed human antimouse antibody (range, 161 to >20,000 ng/ml) at 6-8 weeks postinfusion. Mean +/- SD whole-body half-life (whole-body retention) of I-131-CC49 was 57.3 +/- 13.4 hours. Tumors were seen in all patients. In two of three patients treated a second time, an increased whole body clearance rate correlated with elevated human antimouse antibody, reduced uptake in tumor, and enhanced uptake in the thyroid. Estimated tumor doses ranged from 19-667 rads. Red marrow dose estimated from whole body retention ranged from 60 to 117 rads and correlated with decreases in platelet count. No objective tumor responses (i.e., partial or complete) were observed. Conclusions. Despite minimal toxicity and favorable tumor uptake, efficacy has been limited at this dose and schedule. Cancer 1994; 73:1057-66. C1 NCI,BETHESDA,MD 20892. RP MURRAY, JL (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,1515 HOLCOMBE BLVD,BOX 041,HOUSTON,TX 77030, USA. FU NCI NIH HHS [N01-CM97610] NR 29 TC 88 Z9 89 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 0008-543X J9 CANCER JI Cancer PD FEB 1 PY 1994 VL 73 IS 3 SU S BP 1057 EP 1066 DI 10.1002/1097-0142(19940201)73:3+<1057::AID-CNCR2820731345>3.0.CO;2-3 PG 10 WC Oncology SC Oncology GA MV418 UT WOS:A1994MV41800044 PM 8306248 ER PT J AU HAND, PH KASHMIRI, SVS SCHLOM, J AF HAND, PH KASHMIRI, SVS SCHLOM, J TI POTENTIAL FOR RECOMBINANT IMMUNOGLOBULIN CONSTRUCTS IN THE MANAGEMENT OF CARCINOMA SO CANCER LA English DT Article; Proceedings Paper CT 9th Conference on Radioimmunodetection and Radioimmunotherapy of Cancer CY SEP 17-19, 1992 CL PRINCETON, NJ DE RECOMBINANT IMMUNOGLOBULINS; MONOCLONAL ANTIBODIES; CARCINOMA; DIAGNOSIS; THERAPY ID MONOCLONAL-ANTIBODY B72.3; SINGLE-CHAIN FV; RADIOIMMUNOGUIDED SURGERY; COLORECTAL-CANCER; IMMUNE-RESPONSE; CARCINOEMBRYONIC ANTIGEN; EFFECTOR FUNCTIONS; HUMAN MAMMARY; FC-RECEPTOR; BINDING AB Background. Numerous monoclonal antibodies (MoAb) have been developed and currently are being evaluated in both diagnostic and therapeutic clinical trials. Despite the major advances fostered by MoAb technology, several limitations inherent to the use of MoAb exist. For example, MoAb may not have the desired plasma pharmacokinetics and metabolic properties, and they may be immunogenic, thus reducing the possibility of numerous administrations. Methods. Recombinant DNA technology is used to develop (1) mouse-human chimeric antibodies in which the constant region of a murine antibody is replaced with the human constant region, (2) chimeric antibodies with domain-deletions or alterations in glycosylation, and (3) sFv molecules, i.e., recombinant proteins composed of a V-L , sequence by a designed peptide. Results. This article reviews some of the genetic modifications that can be made with recombinant or chimeric immunoglobulin forms; two anti-TAG-72 MoAb, B72.3 and CC49, are used as examples. The immunoglobulin molecules that have been generated include those with alterations of subclass, domain deletions, and glycosylation, as well as those sFv molecules that have been prepared. The immunochemical and biologic properties of these novel immunoglobulin forms are described. Conclusions. Recombinant DNA technology makes feasible the development of novel immunoglobulin forms. These genetic modifications may result in more useful diagnostic reagents and in the production of more stable immunoconjugates with the characteristics of more efficient tumor cell killing. Cancer 1994; 73:1105-13. RP HAND, PH (reprint author), NCI,TUMOR IMMUNOL & BIOL LAB,BLDG 10,ROOM 8B07,BETHESDA,MD 20892, USA. NR 53 TC 12 Z9 12 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 0008-543X J9 CANCER JI Cancer PD FEB 1 PY 1994 VL 73 IS 3 SU S BP 1105 EP 1113 DI 10.1002/1097-0142(19940201)73:3+<1105::AID-CNCR2820731351>3.0.CO;2-M PG 9 WC Oncology SC Oncology GA MV418 UT WOS:A1994MV41800050 PM 8306254 ER PT J AU ZIMONJIC, DB POPESCU, NC AF ZIMONJIC, DB POPESCU, NC TI AN IMPROVED PROCEDURE FOR CHROMOSOME PREPARATIONS FROM SOLID TURNERS SO CANCER GENETICS AND CYTOGENETICS LA English DT Letter RP ZIMONJIC, DB (reprint author), NCI,BIOL LAB,BETHESDA,MD 20892, USA. NR 3 TC 18 Z9 18 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0165-4608 J9 CANCER GENET CYTOGEN JI Cancer Genet. Cytogenet. PD FEB PY 1994 VL 72 IS 2 BP 161 EP 161 DI 10.1016/0165-4608(94)90136-8 PG 1 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA NN058 UT WOS:A1994NN05800018 PM 8143279 ER PT J AU KARP, JE BRODER, S AF KARP, JE BRODER, S TI NEW DIRECTIONS IN MOLECULAR MEDICINE SO CANCER RESEARCH LA English DT Review ID ACUTE PROMYELOCYTIC LEUKEMIA; ACUTE MYELOID-LEUKEMIA; PROGRAMMED CELL-DEATH; MYB ANTISENSE OLIGODEOXYNUCLEOTIDES; CHRONIC MYELOGENOUS LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; BECKWITH-WIEDEMANN SYNDROME; ENDOTHELIAL GROWTH-FACTOR; PRADER-WILLI SYNDROME; TUMOR-NECROSIS-FACTOR C1 NCI,OFF DIRECTOR,9000 ROCKVILLE PIKE,BLDG 31,ROOM 11A48,BETHESDA,MD 20892. NR 144 TC 32 Z9 33 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 1 PY 1994 VL 54 IS 3 BP 653 EP 665 PG 13 WC Oncology SC Oncology GA MU677 UT WOS:A1994MU67700015 PM 8306327 ER PT J AU ODWYER, PJ MOYER, JD SUFFNESS, M HARRISON, SD CYSYK, R HAMILTON, TC PLOWMAN, J AF ODWYER, PJ MOYER, JD SUFFNESS, M HARRISON, SD CYSYK, R HAMILTON, TC PLOWMAN, J TI ANTITUMOR-ACTIVITY AND BIOCHEMICAL EFFECTS OF APHIDICOLIN GLYCINATE (NSC-303812) ALONE AND IN COMBINATION WITH CISPLATIN IN-VIVO SO CANCER RESEARCH LA English DT Article ID HUMAN OVARIAN-CARCINOMA; DNA POLYMERASE-ALPHA; CELL-LINES; CANCER; REPLICATION; CIS-DIAMMINEDICHLOROPLATINUM(II); CYTOTOXICITY; INHIBITOR; MECHANISM; INVITRO AB Aphidicolin, an inhibitor of DNA polymerases alpha and delta, is cytotoxic in vitro against tumor cells. The poor solubility of aphidicolin has led to the development of aphidicolin glycinate (AG; NSC 303812), a water soluble ester currently in early clinical trials. The antitumor activity of AG was investigated in a series of transplantable murine tumors in vivo. The drug demonstrated activity against the i.p. implanted B16 melanoma, producing maximum increased life spans of 75% following i.p. administration every 3 h for three doses on days 1-9. Treatment schedules involving both single injections per day on days 1-9 and multiple injections per day on days 1, 5, and 9 were less effective, indicating that this antitumor activity is schedule dependent. Similarly, greater activity was observed against the i.p. M5076 sarcoma when three daily injections were given on days 1-9 (57% increased life span) than with a single injection either on days 1-9 (36% increased life span) or on days 1, 5, 9, and 13 (inactive). Further scheduling studies in the s.c. M5076 sarcoma model showed that a 7-day infusion was superior to both a 24-h infusion and a 7-day course of three bolus treatments per day. On the assumption that DNA polymerase inhibition is the basis for this antitumor activity, inhibition of DNA synthesis in BALB/c x DBA/2 F1 mice was investigated by measuring incorporation of [H-3]thymidine (20 muCi, i.v.) into DNA of spleen and jejunum. At 2 h after administration of AG, inhibition of DNA synthesis was dose dependent (median inhibitory dose, 60 mg/kg in both tissues) and was >99% at 300 mg/kg. The inhibition was rapid in onset: AG (100 mg/kg i.p.) produced maximal (>98%) inhibition in both tissues at 30 min. Recovery occurred in the intestine within 16 h; in spleen recovery was delayed to 24 h, and was followed by a rebound incorporation at 48 h (203%). A comparison of the inhibition of thymidine incorporation in tumor cells (B16 melanoma and P388 leukemia) and normal jejunum revealed no significant differences in the extent of inhibition or the rapidity of recovery in these tissues. The rapid recovery of DNA synthesis inhibition supports the use of prolonged infusion schedules in clinical trials, but the lack of evidence of selectivity for tumor cells suggests that AG may be of limited therapeutic value as a single agent. Thus, we evaluated AG in combination with cisplatin in an in vivo model of cisplatin refractory human ovarian cancer. In this model system, AG as a single agent had minimal activity whereas its use in bolus form at 30 mg/kg/dose every 3 h for 4 doses with cisplatin (5 or 8.3 mg/kg) at 90 min after the second AG injection was markedly superior to cisplatin alone. Furthermore, a continuous 7-day infusion of 150 mg/kg/day with cisplatin (8.3 mg/kg) on the second day of the AG infusion was equivalent in efficacy to the maximum tolerated dose of cisplatin (14 mg/kg). These data, in combination with information on the sustained levels of AG which may be achieved in patients support the clinical development of combination therapy with AG and cisplatin/carboplatin in platinum refractory patients. C1 NCI,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NCI,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892. SO RES INST,BIRMINGHAM,AL 35255. RP ODWYER, PJ (reprint author), FOX CHASE CANC CTR,7701 BURHOLME AVE,PHILADELPHIA,PA 19111, USA. FU NCI NIH HHS [CA-06972, CM-07315, N01-CM-73726] NR 24 TC 45 Z9 45 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 1 PY 1994 VL 54 IS 3 BP 724 EP 729 PG 6 WC Oncology SC Oncology GA MU677 UT WOS:A1994MU67700023 PM 8306334 ER PT J AU YANG, JM GOLDENBERG, S GOTTESMAN, MM HAIT, WN AF YANG, JM GOLDENBERG, S GOTTESMAN, MM HAIT, WN TI CHARACTERISTICS OF P388/VMDRC.04, A SIMPLE, SENSITIVE MODEL FOR STUDYING P-GLYCOPROTEIN ANTAGONISTS SO CANCER RESEARCH LA English DT Article ID CONFERS MULTIDRUG RESISTANCE; DNA TOPOISOMERASE-II; HUMAN MDR1 GENE; CELL-LINES; BUTHIONINE SULFOXIMINE; MONOCLONAL-ANTIBODIES; COMPLEMENTARY-DNA; TUMOR-CELLS; EXPRESSION; DRUGS AB Cross-resistance to chemotherapeutic drugs is a significant problem in the treatment of patients with cancer. The discovery that this phenomenon is associated with the overexpression of a membrane glycoprotein, P-glycoprotein, which acts as a drug efflux pump, has provided a new target for drug development. To develop a model for identifying new compounds which can block the function of P-glycoprotein, we infected P388 mouse leukemic cells with a retrovirus containing a cloned human MDR1 complementary DNA. The new cell line, P388/VMDRC.04, incorporated and overexpressed the human gene as evidenced by Southern blots, increased mRNA and protein synthesis, and recognition by the MRK16 monoclonal antibody. P388/VMDRC.04 was cross-resistant to colchicine, vincristine, and doxorubicin, and the degree of resistance correlated with a reduction in cellular drug accumulation. Unlike many cell lines selected for resistance by growth in increasing concentrations of drug for prolonged periods of time, these cells did not show alternative mechanisms of resistance such as increased synthesis of glutathione or alterations in topoisomerase II. In addition, the sensitivity of P388/VMDRC.04 cells was completely restored by cyclosporin A and trans-flupenthixol. P-388/VMDRC.04 cells were subcloned and 10 clones were picked for in vivo evaluation. One subclone grew similarly to parental cells in female BALB/c x DBA/2 F1 mice and showed no responsiveness to therapeutic doses of vincristine or etoposide. The combination of vincristine with cyclosporin A significantly increased the survival of mice inoculated with P388/VMDRC.04 cells. The availability of a cell line that displays the MDR phenotype, overexpresses human P-glycoprotein, but does not contain alterations in at least two well-defined alternative mechanisms of resistance, and that can be grown in simple animal models should facilitate the development of new agents active against this form of chemotherapeutic drug resistance. C1 ROBERT WOOD JOHNSON MED SCH,CANC INST NEW JERSEY,DEPT MED,CABM BLVD,679 HOES LANE,PISCATAWAY,NJ 08854. ROBERT WOOD JOHNSON MED SCH,CANC INST NEW JERSEY,DEPT PHARMACOL,PISCATAWAY,NJ 08854. NCI,CELL BIOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA 43888, CA 08341] NR 37 TC 28 Z9 35 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 1 PY 1994 VL 54 IS 3 BP 730 EP 737 PG 8 WC Oncology SC Oncology GA MU677 UT WOS:A1994MU67700024 PM 7905786 ER PT J AU HURSTING, SD SWITZER, BR FRENCH, JE KARI, FW AF HURSTING, SD SWITZER, BR FRENCH, JE KARI, FW TI INHIBITION OF RAT MONONUCLEAR CELL LEUKEMIA BY CORN-OIL GAVAGE - IN-VIVO, IN-SITU AND IMMUNE COMPETENCE STUDIES SO CARCINOGENESIS LA English DT Article ID GROWTH FACTOR-I; DIETARY-FAT; GROWING-RATS; FISCHER RATS; F344/N RATS; PROTEIN; RESTRICTION; DISEASE; INVITRO; ACIDS AB Corn oil administered by oral gavage decreases the spontaneous incidence of mononuclear cell leukemia (MNCL) in male Fischer rats used as vehicle controls in long-term carcinogenesis experiments. We used an MNCL transplant model, an in situ MNCL cell proliferation assay and immune competence assays to explore mechanism(s) underlying the effects of corn oil gavage on MNCL development in male rats. Relative to non-gavaged or water-gavaged rats, corn oil-gavaged rats had similar to 25% lower MNCL incidence as well as longer MNCL latency and increased survival. There were no differences in body weight or caloric intake between treatment groups, as corn oil-gavaged rats compensated for calories supplied by the gavaged oil by consuming less food. These data indicate that transplanted MNCL cells grew slower in corn oil-gavaged rats than in non-gavaged or water-gavaged rats and suggest that corn oil gavage may exert its effects through a decrease in protein or other nutrients. Five-day proliferation rates of cultured MNCL cells in diffusion chambers implanted in male corn oil-gavaged rats were 40% less than in water-gavaged rats, suggesting nutrition-sensitive endogenous factors mediate the suppression of MNCL cell proliferation in corn oil-gavaged rats. Corn oil-gavaged rats had 54% lower serum growth hormone (GH) levels, and replacement of GH into corn oil-gavaged rats by osmotic minipump infusion increased in situ MNCL cell proliferation to rates observed in water-gavaged animals. Corn oil-gavaged rats also showed enhanced cellular immune competence as measured by mitogen stimulation, natural cytotoxicity and immunofluorescence assays. Taken together, these findings suggest corn oil administered by oral gavage may decrease MNCL development by slowing MNCL cell proliferation, mediated at least in part by altered levels of diffusible factors such as GH, and/or by enhancing immune competence. C1 NIEHS,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,DEPT NUTR,CHAPEL HILL,NC 27599. NR 43 TC 5 Z9 5 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD FEB PY 1994 VL 15 IS 2 BP 193 EP 199 DI 10.1093/carcin/15.2.193 PG 7 WC Oncology SC Oncology GA MW782 UT WOS:A1994MW78200009 PM 8313508 ER PT J AU STARK, AA RUSSELL, JJ LANGENBACH, R PAGANO, DA ZEIGER, E HUBERMAN, E AF STARK, AA RUSSELL, JJ LANGENBACH, R PAGANO, DA ZEIGER, E HUBERMAN, E TI LOCALIZATION OF OXIDATIVE DAMAGE BY A GLUTATHIONE-GAMMA-GLUTAMYL TRANSPEPTIDASE SYSTEM IN PRENEOPLASTIC LESIONS IN SECTIONS OF LIVERS FROM CARCINOGEN-TREATED RATS SO CARCINOGENESIS LA English DT Article ID ALTERED HEPATOCYTE FOCI; RENAL-CELL CARCINOMA; TRANSFERASE TRANSPEPTIDASE; FERRIC NITRILOTRIACETATE; LIPID-PEROXIDATION; SALMONELLA-TYPHIMURIUM; PEROXISOME PROLIFERATION; NEOPLASTIC LESIONS; OXIDASE ACTIVITY; REACTIVE OXYGEN AB Previous studies from our laboratories have shown that catabolism of glutathione (GSH) by gamma-glutamyl transpeptidase (GGT) in the presence of transition metals leads to oxidative damage (OD). This damage is exemplified in vitro by GGT-dependent GSH mutagenesis which involves reactive oxygen species and by GGT-dependent accumulation of lipid peroxidation (LPO) products in systems containing polyunsaturated fatty acid and GSH. In order to test whether catabolism of GSH by membranal GGT in enzyme-altered preneoplastic hepatic lesions can induce oxidative damage in situ, and to test whether the OD is localized in these lesions, 21 day old Fischer rats were treated with 12 mg/kg diethylnitrosamine (DEN) followed by 0.1% or 0.25% phenobarbital (PB) in the diet. Cryostat sections were examined histochemically for GGT-rich hepatic lesions. Adjacent sections were incubated with GSH and iron and examined for areas staining for lipid peroxidation. Distinct LPO-positive areas were shown to correspond well with the GGT-positive hepatic lesions. Promotion with 0.25% PB led to increasing proportions of LPO-positive lesions with time among GGT-positive lesions. The visualization of LPO in GGT-rich hepatic lesions depended on the presence of GSH and iron, and was not observed following chelation of iron by diethyl triaminopentaacetic acid (DTPA), in the presence of acivicin, an inhibitor of GGT, or in the presence of the radical scavenger butylated hydroxytoluene (BHT). The factors affecting GSH-GGT-dependent LPO in the GGT-rich foci were identical to those affecting GSH-GGT-driven LPO in vitro, and were similar to those affecting oxidative GSH-mutagenesis catalyzed by GGT. The results indicate that metabolism of GSH by GGT in preneoplastic liver foci can initiate an oxidative process leading to a radical-rich environment and to oxidative damage. Such damage may contribute to the processes by which cells within such foci progress to malignancy. C1 ARGONNE NATL LAB,DIV BIOL & MED RES,ARGONNE,IL 60439. NIEHS,EXPTL CARCINOGENESIS & MUTAGENESIS BRANCH,RES TRIANGLE PK,NC 27709. RP STARK, AA (reprint author), TEL AVIV UNIV,DEPT BIOCHEM,IL-69978 TEL AVIV,ISRAEL. RI WSU, USTUR/I-1056-2013 NR 49 TC 58 Z9 59 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD FEB PY 1994 VL 15 IS 2 BP 343 EP 348 DI 10.1093/carcin/15.2.343 PG 6 WC Oncology SC Oncology GA MW782 UT WOS:A1994MW78200033 PM 7906207 ER PT J AU RICE, JM DIWAN, BA HU, H WARD, JM NIMS, RW LUBET, RA AF RICE, JM DIWAN, BA HU, H WARD, JM NIMS, RW LUBET, RA TI ENHANCEMENT OF HEPATOCARCINOGENESIS AND INDUCTION OF SPECIFIC CYTOCHROME P450-DEPENDENT MONOOXYGENASE ACTIVITIES BY THE BARBITURATES ALLOBARBITAL, APROBARBITAL, PENTOBARBITAL, SECOBARBITAL AND 5-PHENYLBARBITURIC AND 5-ETHYLBARBITURIC ACIDS SO CARCINOGENESIS LA English DT Article ID TUMOR-PROMOTING ACTIVITIES; RAT-LIVER; N-NITROSODIETHYLAMINE; MESSENGER-RNAS; POSITIVE FOCI; DOSE-RESPONSE; CARCINOGENESIS; SEQUENCE; MICE; DIETHYLNITROSAMINE AB To test predictions that barbiturates which are long-acting sedatives and/or strong inducers of CYP2B-mediated monooxygenase activities would be effective promoters of hepatocarcinogenesis, a series of clinically-useful barbiturates and structural analogs were tested for ability to promote hepatocellular carcinogenesis in male F344/NCr rats initiated with N-nitrosodiethylamine and for efficacy as inducers of CYP2B activity in non-initiated rats of the same sex and strain. The barbiturates were administered in the diet at concentrations equimolar to 500 p.p.m. of the known liver tumor promoter phenobarbital, which served as the positive control for this study. Phenobarbital, which has the longest duration of sedative action of this series of compounds, caused the greatest induction of CYP2B activity, and displayed strong liver tumor promoting effects. Allobarbital and aprobarbital, two intermediate-duration sedatives, were found to promote hepatocarcinogenesis, with allobarbital proving to be as effective as phenobarbital in this respect and aprobarbital being somewhat weaker as a promoter. These intermediate-duration sedatives were each relatively weak CYP2B-type inducers, causing similar to 25% of the induction displayed by phenobarbital. The nonsedatives, 5-phenyl- and 5-ethylbarbituric acids, were essentially inactive as CYP2B-type inducers and were also found to be relatively inactive as promoters of hepatocarcinogenesis. Of the shorter-duration sedatives, pentobarbital was found to promote, and was relatively effective as a CYP2B-type inducer, while secobarbital showed little or no promoting activity and was less effective as an inducer of CYP2B activities. Pentobarbital thus proved an important exception to our hypothesis that only long-acting sedative barbiturates would promote hepatocarcinogenesis. Although both the durations of sedative action and the degrees of CYP2B-type induction exhibited by these compounds correlate with a quantitative parameter for liver tumor-promoting activity (relative promotion index), neither parameter appears to be sufficient, by itself, as a predictor of promoting activity for rat liver. C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV P,FREDERICK,MD 21702. RP RICE, JM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. NR 47 TC 58 Z9 60 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD FEB PY 1994 VL 15 IS 2 BP 395 EP 402 PG 8 WC Oncology SC Oncology GA MW782 UT WOS:A1994MW78200041 PM 8313534 ER PT J AU WOODHOUSE, E HERSPERGER, E STETLERSTEVENSON, WG LIOTTA, LA SHEARN, A AF WOODHOUSE, E HERSPERGER, E STETLERSTEVENSON, WG LIOTTA, LA SHEARN, A TI INCREASED TYPE-IV COLLAGENASE IN IGI-INDUCED INVASIVE TUMORS OF DROSOPHILA SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID TISSUE INHIBITOR; MALIGNANT NEOPLASMS; MELANOGASTER; EXPRESSION; TIMP-2; METALLOPROTEINASES; IDENTIFICATION; PRODUCT; BENIGN; DOMAIN AB Loss of function mutations in the lethal giant larvae (lgl) gene causes neoplastic brain tumors in Drosophila. We have introduced a lacZ reporter gene into lgl mutant cells and used beta-galactosidase expression as a marker to monitor the growth of such tumors following transplantation into wild-type adult hosts. Whereas normal larval brains do not grow when transplanted, mutant brains can develop into enormous tumors that fill the entire abdominal cavity. To investigate whether these tumors are similar to mammalian tumors at the biochemical level, we examined the accumulation of a specific protein which is differentially expressed in mammalian metastatic tumors and is likely to be involved in the invasive and/or metastatic mechanism. Increased accumulation of a 72 kilodalton (kDa) type IV collagenase has been observed in several metastatic human tumors. Using antibodies directed against this human 72 kDa type IV collagenase, we show for the first time that Drosophila has a cross-reacting 49 kDa protein with gelatinase activity. In brains dissected from lgl mutant larvae, the accumulation of this 49 kDa gelatinase of Drosophila is increased compared to the level in brains dissected from wild-type larvae. In tumors derived from mutant brains, all of the cells express this protein. Moreover, the tumor cells that invade host organs express this protein. These data suggest that the metastasis of Drosophila tumor cells is similar to the metastasis of some human tumors at the biochemical level as well as at the cellular level. C1 JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. NCI,PATHOL LAB,TUMOR INVAS & METASTASIS SECT,BETHESDA,MD 20892. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 32 TC 34 Z9 38 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD FEB PY 1994 VL 5 IS 2 BP 151 EP 159 PG 9 WC Cell Biology SC Cell Biology GA MW525 UT WOS:A1994MW52500006 PM 8180128 ER PT J AU PARDHASARADHI, K KUTTY, RK GENTLEMAN, S KRISHNA, G AF PARDHASARADHI, K KUTTY, RK GENTLEMAN, S KRISHNA, G TI EXPRESSION OF MESSENGER-RNA FOR ATRIAL-NATRIURETIC-PEPTIDE RECEPTOR GUANYLATE-CYCLASE (ANPRA) IN HUMAN RETINA SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE ATRIAL NATRIURETIC PEPTIDE RECEPTOR TYPE A; GUANYLATE CYCLASE; POLYMERASE CHAIN REACTION; HUMAN RETINA; NORTHERN BLOT ID HEAT-STABLE ENTEROTOXIN; RAT RETINA; FAMILY AB 1. Guanylate cyclase plays an important role in the visual cycle. Here we report the mRNA expression for the atrial natriuretic peptide receptor type A form of guanylate cyclase (ANPRA) in human retina. 2. Polymerase chain reaction using two sets of primers on the cDNAs reverse-transcribed from human retinal poly(A)(+) RNA amplified two products under two different reaction conditions. The primers used in the reaction were designed from the reported sequence of human placental ANPRA cDNA. 3. Sequencing of the amplified products showed 100% sequence homology to the human placental ANPRA gene. Northern blot analysis indicated the presence of a 4.4-kb ANPRA mRNA in human retina. similar to that present in human brain. C1 NHLBI,CHEM PHARMACOL LAB,DRUG TISSUE INTERACT SECT,BETHESDA,MD 20892. NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 15 TC 7 Z9 8 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD FEB PY 1994 VL 14 IS 1 BP 1 EP 7 DI 10.1007/BF02088585 PG 7 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA NT221 UT WOS:A1994NT22100001 PM 7954658 ER PT J AU NIKODIJEVIC, B SEI, Y SHIN, YM DALY, JW AF NIKODIJEVIC, B SEI, Y SHIN, YM DALY, JW TI EFFECTS OF ATP AND UTP IN PHEOCHROMOCYTOMA PC12 CELLS - EVIDENCE FOR THE PRESENCE OF 3 P-2 RECEPTORS, ONLY ONE OF WHICH SUBSERVES STIMULATION OF NOREPINEPHRINE RELEASE SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE CALCIUM UPTAKE; CALCIUM CHANNELS; PHOSPHOINOSITIDE BREAKDOWN; PHOSPHOLIPASE C; NOREPINEPHRINE RELEASE; NICOTINIC RECEPTORS; FURA-2; ATP ANALOGS; UTP; PURINERGIC RECEPTORS ID NERVE GROWTH-FACTOR; MEDIATED CALCIUM ENTRY; CATECHOLAMINE RELEASE; EXTRACELLULAR ATP; CA2+ INFLUX; CHANNELS; EXPRESSION; SECRETION; CURRENTS; SK-AND-F-96365 AB 1. In pheochromocytoma PC12 cells ATP and, to a lesser extent, 2-methylthioATP stimulate phosphoinositide breakdown, release of intracellular calcium, and influx of external calcium, leading to stimulation of norepinephrine release. In contrast, although UTP also stimulates phosphoinositide breakdown, release of intracellular calcium, and influx of external calcium, there is no stimulation of norepinephrine release. 2. 2-MethylthioATP, presumably acting at P-2y receptors, and UTP, presumably acting at P-2u receptors, in combination elicit a phosphoinositide breakdown greater than that elicited by either alone. Intracellular levels of calcium measured with Fura-2 increase to greater levels with ATP than with UTP and are sustained, while the UTP intracellular levels of calcium rapidly return to basal values. Both ATP and UTP cause a similar influx of (45) Ca2+ presumably by stimulation of a P-2 receptor directly linked to a cation channel. 3. It is proposed that PC12 cells contain two distinct G protein-coupled P-2 receptors that activate phospholipase C and a P-2 receptor linked to a cation channel. The P-2y receptor sensitive to ATP (and to 2-methylthioATP) causes the depletion of a pool of intracellular calcium, sufficient to activate so-called ''receptor-operated calcium entry.'' The sustained elevation of intracellular calcium after ATP treatment is proposed to result in stimulation of norepinephrine release and activation of calcium-dependent potassium channels and sodium-calcium exchange pathways. 4. The P-2u receptor sensitive to UTP (and to ATP) causes only a transient elevation in levels of intracellular calcium, perhaps from a different pool, insufficient to activate so-called receptor-operated calcium entry. Further sequelae do not ensue, and the functional role of the UTP-sensitive P-2u receptor is unknown. C1 NICHHD,BETHESDA,MD 20892. NIDDKD,BETHESDA,MD 20892. NR 41 TC 22 Z9 22 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD FEB PY 1994 VL 14 IS 1 BP 27 EP 47 DI 10.1007/BF02088587 PG 21 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA NT221 UT WOS:A1994NT22100003 PM 7954659 ER PT J AU VISWANATHAN, M DEOLIVEIRA, AM WU, RM CHIUEH, CC SAAVEDRA, JM AF VISWANATHAN, M DEOLIVEIRA, AM WU, RM CHIUEH, CC SAAVEDRA, JM TI [I-125] CGP-42112 REVEALS A NON-ANGIOTENSIN II BINDING-SITE IN 1-METHYL-4-PHENYLPYRIDINE (MPP(+))-INDUCED BRAIN INJURY SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE CGP 42112; 1-METHYL-4-PHENYLPYRIDINE; BRAIN INJURY ID MONONUCLEAR PHAGOCYTES; CHRONIC PARKINSONISM; MAMMALIAN BRAIN; PRIMATE MODEL; RECEPTORS; CGP-42112A; EXPRESSION; NEURONS; MPTP; SKIN AB 1. Intracerebral injection of the oxidative metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridine (MPP(+)), into the substantia nigra of adult rats resulted in a lesion at the injection site. 2. Using autoradiography, we localized specific [I-125]CGP 42112 binding that was not recognized by angiostensin II or angiotensin II AT(1) or AT(2) receptor-selective ligands. 3. Our results suggest that [I-125]CGP 42112 may be binding to activated microglia that appear at the lesion site. C1 NIMH,CLIN SCI LAB,NEUROTOXICOL & NEUROPROTECT UNIT,BETHESDA,MD 20892. RP VISWANATHAN, M (reprint author), NIMH,CLIN SCI LAB,PHARMACOL SECT,BLDG 10,ROOM 2D-45,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 26 TC 12 Z9 12 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD FEB PY 1994 VL 14 IS 1 BP 99 EP 104 DI 10.1007/BF02088592 PG 6 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA NT221 UT WOS:A1994NT22100008 PM 7954664 ER PT J AU LENFANT, C AF LENFANT, C TI FISCAL YEAR 1994 - GREAT EXPECTATIONS SO CIRCULATION LA English DT Editorial Material RP LENFANT, C (reprint author), NHLBI,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 541 EP 542 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200001 PM 8313540 ER PT J AU DILSIZIAN, V ARRIGHI, JA DIODATI, JG QUYYUMI, AA ALAVI, K BACHARACH, SL MARINNETO, JA KATSIYIANNIS, PT BONOW, RO AF DILSIZIAN, V ARRIGHI, JA DIODATI, JG QUYYUMI, AA ALAVI, K BACHARACH, SL MARINNETO, JA KATSIYIANNIS, PT BONOW, RO TI MYOCARDIAL VIABILITY IN PATIENTS WITH CHRONIC CORONARY-ARTERY DISEASE - COMPARISON OF TC-99M-SESTAMIBI WITH THALLIUM REINJECTION AND [F-18] FLUORODEOXYGLUCOSE SO CIRCULATION LA English DT Article DE SCINTIGRAPHY; TOMOGRAPHY; CORONARY DISEASE; MYOCARDIUM; ISCHEMIA ID HEXAKIS 2-METHOXYISOBUTYL ISONITRILE; POSITRON-EMISSION TOMOGRAPHY; LEFT-VENTRICULAR DYSFUNCTION; TC-99M METHOXYISOBUTYL ISONITRILE; VIABLE MYOCARDIUM; BLOOD-FLOW; TL-201 REINJECTION; FILL-IN; REST; REDISTRIBUTION AB Background Tc-99m-sestamibi and thallium imaging have similar accuracy when used for diagnostic purposes, but whether sestamibi provides accurate information regarding myocardial viability in patients with chronic coronary artery disease has not been established. Since there is minimal redistribution of sestamibi over time, it may overestimate nonviable myocardium in patients with left ventricular dysfunction, in whom blood flow may be reduced at rest. Methods and Results We studied 54 patients with chronic coronary artery disease with a mean ejection fraction of 34+/-14%. Patients underwent stress/redistribution/reinjection thallium tomography and, within a mean of 5 days, same-day rest/stress sestamibi imaging using the same exercise protocol and with patients achieving the same exercise duration. Of the 111 reversible thallium defects on either the redistribution or reinjection study, 40 (36%) were determined to be irreversible on the rest/stress sestamibi study, whereas only 3 of 63 irreversible thallium defects despite reinjection (5%) were classified to be reversible by sestamibi imaging. The concordance regarding reversibility of myocardial defects between thallium stress/redistribution/reinjection and same day rest/stress sestamibi studies was 75%. A subgroup of 25 patients also underwent positron emission tomography (PET) studies with O-15-labeled water and [F-18]fluorodeoxyglucose (FDG) at rest after an oral glucose load. As in the overall group of 54 patients, there was concordance between thallium and sestamibi imaging regarding defect reversibility in 51 of 73 regions (70%). In the remaining 22 discordant regions (30%), 18 (82%) appeared irreversible by sestamibi imaging but were reversible by thallium imaging. Myocardial viability was confirmed in 17 of 18 regions, as evidenced by normal FDG uptake (10 regions) or FDG/blood flow mismatch (7 regions) on PET. These regions were present in 16 of the 25 patients studied (64%). We then explored methods to improve the sestamibi results. First, when the 18 discordant regions with irreversible sestamibi defects were further analyzed according to the severity of defects, 14 (78%) demonstrated only mild-to-moderate reduction in sestamibi activity (51% to 85% of normal activity), suggestive of predominantly viable myocardium, and the overall concordance between thallium and sestamibi studies increased to 93%. Second, when an additional 4-hour redistribution image was acquired in 18 patients after the injection of sestamibi at rest, 6 of 16 discordant irreversible regions (38%) on the rest/stress sestamibi study became reversible, thereby increasing the concordance between thallium and sestamibi studies to 82%. Conclusions These data indicate that same-day rest/stress sestamibi imaging will incorrectly identify 36% of myocardial regions as being irreversibly impaired and nonviable compared with both thallium redistribution/reinjection and PET, However, the identification of reversible and viable myocardium can be greatly enhanced with sestamibi if an additional redistribution image is acquired after the rest sestamibi injection or if the severity of reduction in sestamibi activity within irreversible defects is considered. C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. RP DILSIZIAN, V (reprint author), NIH,DEPT NUCL MED,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 55 TC 221 Z9 224 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 578 EP 587 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200008 PM 8313546 ER PT J AU GOLDBERG, RJ BURCHFIEL, CM REED, DM WERGOWSKE, G CHIU, D AF GOLDBERG, RJ BURCHFIEL, CM REED, DM WERGOWSKE, G CHIU, D TI A PROSPECTIVE-STUDY OF THE HEALTH-EFFECTS OF ALCOHOL-CONSUMPTION IN MIDDLE-AGED AND ELDERLY MEN - THE HONOLULU-HEART-PROGRAM SO CIRCULATION LA English DT Article DE ALCOHOL; AGE; MORTALITY; MORBIDITY ID CORONARY-ARTERY DISEASE; JAPANESE MEN; CARDIOVASCULAR-DISEASE; HEMORRHAGIC STROKE; MORTALITY; RISK; HAWAII; CHOLESTEROL; FRAMINGHAM; EXPERIENCE AB Background The study objective was to determine the association between reported alcohol consumption and total mortality, mortality from selected causes, and incident nonfatal chronic disease events in middle-aged (51 to 64 years old) and elderly (65 to 75 years old) men during an approximate 15-year follow-up period. Methods and Results We conducted a prospective epidemiological study of Japanese-American men who were participating in the Honolulu Heart Program and were free from coronary heart disease, cerebrovascular disease, and cancer at baseline examination and at subsequent reexamination 6 years later. Self-reported alcohol consumption was determined twice: at the baseline examination in 1965 through 1968 and at reexamination approximately 6 years later (1971 through 1974). Four primary alcohol consumption groups who reported similar alcohol intake at the time of these two clinical examinations were considered: abstainers and light (1 to 14 mL of alcohol per day), moderate (15 to 39 mL of alcohol per day), and heavy (140 mt of alcohol per day) drinkers. Study end points were also determined in very light (1 to 4.9 mL of alcohol per day) drinkers and in men who reported a change in their alcohol intake between examinations. Longitudinal follow-up was carried out through the end of 1988 with determination of selected fatal and nonfatal events according to alcohol intake. After controlling for several potentially confounding factors, total mortality exhibited a J-shaped pattern in relation to alcohol consumption in middle-aged and elderly men. There was a trend for lower rates of occurrence of combined fatal and nonfatal coronary heart disease events with increasing alcohol consumption in both middle-aged and elderly men. Increasing alcohol consumption was related to an increased risk of fatal and nonfatal strokes in middle-aged men, whereas elderly light and moderate drinkers were at increased risk for fatal and nonfatal strokes. Heavy drinkers were at increased risk for fatal and nonfatal malignant neoplasms in the two age groups examined. Conclusions The results of this long-term prospective study provide a balanced perspective of the health effects of alcohol consumption in middle-aged and elderly men. High levels of alcohol consumption were shown to be related to an increasing risk of diseases of considerable public health importance. These findings suggest that caution be taken in formulating populationwide recommendations for increases in the population levels of alcohol consumed given the associated significant social and biological problems of high consumption levels. C1 KUAKINI MED CTR, HONOLULU HEART PROGRAM, HONOLULU, HI 96817 USA. NHLBI, EPIDEMIOL & BIOMETRY PROGRAM, HONOLULU EPIDEMIOL RES SECT, HONOLULU, HI USA. UNIV MASSACHUSETTS, SCH MED, DEPT MED, WORCESTER, MA USA. FU NHLBI NIH HHS [N01-HC-02901] NR 44 TC 103 Z9 103 U1 1 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 651 EP 659 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200017 PM 8313554 ER PT J AU VAZIRI, SM LARSON, MG BENJAMIN, EJ LEVY, D AF VAZIRI, SM LARSON, MG BENJAMIN, EJ LEVY, D TI ECHOCARDIOGRAPHIC PREDICTORS OF NONRHEUMATIC ATRIAL-FIBRILLATION - THE FRAMINGHAM-HEART-STUDY SO CIRCULATION LA English DT Article DE ATRIAL FIBRILLATION; ECHOCARDIOGRAPHY; EPIDEMIOLOGY ID LEFT-VENTRICULAR MASS; MITRAL-STENOSIS; RISK FACTOR; STROKE; ENLARGEMENT; PREVENTION; WARFARIN; SIZE AB Background Although structural heart disease is often present in patients with nonrheumatic atrial fibrillation, the echocardiographic precursors of atrial fibrillation have not been reported previously. In this elderly, population-based cohort, our objective was to examine prospectively the echocardiographic predictors of nonrheumatic atrial fibrillation. Methods and Results Subjects in the Framingham Heart Study were routinely evaluated with M-mode echocardiography; 1924 subjects, ranging in age from 59 to 90 years, comprised the population at risk. Cox proportional hazards modeling was used to analyze the association of selected echocardiographic features with atrial fibrillation risk after adjustment for age, sex, hypertension, coronary heart disease, congestive heart failure, diabetes, and valvular heart disease. During a mean follow-up interval of 7.2 years, 154 subjects (8.0%) developed atrial fibrillation. Multivariable stepwise analysis identified left atrial size (hazard ratio [HR] per 5-mm increment, 1.39; 95% confidence interval [CI], 1.14 to 1.68), left ventricular fractional shortening (HR per 5% decrement, 1.34; 95% CI, 1.08 to 1.66), and sum of septal and left ventricular posterior wall thicknesses (HR per 4-mm increment, 1.28; 95% CI, 1.03 to 1.60) as independent echocardiographic predictors of atrial fibrillation. For each of the echocardiographic predictors, risk increased progressively over successive quartiles. Moreover, risk increased markedly when highest-risk-quartile measurements for these features were present in combination; the cumulative 8-year age-adjusted atrial fibrillation rates were 7.3% and 17.0%, respectively, when one and two or more highest-risk-quartile features were present, compared with 3.7% when none was present. Conclusions In this elderly, population-based sample, left atrial enlargement, increased left ventricular wall thickness, and reduced left ventricular fractional shortening were predictive of risk for nonrheumatic atrial fibrillation. These echocardiographic precursors offer prognostic information beyond that provided by traditional clinical atrial fibrillation risk factors. C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA 01701. BETH ISRAEL HOSP,DIV CARDIOL,BOSTON,MA. BETH ISRAEL HOSP,DIV CLIN EPIDEMIOL,BOSTON,MA. BOSTON CITY HOSP,DIV CARDIOL,BOSTON,MA. NHLBI,BETHESDA,MD 20892. NR 38 TC 499 Z9 517 U1 1 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 724 EP 730 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200025 PM 8313561 ER PT J AU LAKS, M ARZBAECHER, R BAILEY, J BERSON, A BRILLER, S GESELOWITZ, D AF LAKS, M ARZBAECHER, R BAILEY, J BERSON, A BRILLER, S GESELOWITZ, D TI WILL RELAXING SAFE CURRENT LIMITS FOR ELECTROMEDICAL EQUIPMENT INCREASE HAZARDS TO PATIENTS SO CIRCULATION LA English DT Editorial Material DE ELECTROCARDIOGRAPHY; ELECTROPHYSIOLOGY; FIBRILLATION; EDITORIALS C1 IIT,CHICAGO,IL 60616. NIH,BETHESDA,MD 20892. MED COLL PENN,PHILADELPHIA,PA 19129. CARNEGIE MELLON UNIV,PITTSBURGH,PA 15213. PENN STATE UNIV,UNIV PK,PA 16802. RP LAKS, M (reprint author), UCLA,HARBOR MED CTR,SCH MED,DEPT MED,1000 W CARSON ST,TORRANCE,CA 90509, USA. NR 6 TC 11 Z9 11 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 909 EP 910 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200047 PM 8313582 ER PT J AU BILD, DE HILNER, JE JACOBS, DR LIU, K PERKINS, LL WILLIAMS, OD HULLEY, SB AF BILD, DE HILNER, JE JACOBS, DR LIU, K PERKINS, LL WILLIAMS, OD HULLEY, SB TI 7-YEAR TRENDS IN LIPIDS IN YOUNG-ADULTS - THE CARDIA STUDY SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 934 EP 934 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200070 ER PT J AU THORN, TJ AF THORN, TJ TI CORONARY HEART-DISEASE MORTALITY - THE NARROWING GAP BETWEEN MEN AND WOMEN SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 938 EP 938 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200096 ER PT J AU SHARRETT, AR CHAMBLESS, LE HEISS, G PATSCH, W AF SHARRETT, AR CHAMBLESS, LE HEISS, G PATSCH, W TI POSTPRANDIAL LIPOPROTEINS, ATHEROSCLEROSIS AND OBESITY - THE ARIC STUDY SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1994 VL 89 IS 2 BP 942 EP 942 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW362 UT WOS:A1994MW36200120 ER PT J AU SOUSA, AR LANE, SJ NAKHOSTEEN, J YOSHIMURA, T LEE, TH POSTON, RN AF SOUSA, AR LANE, SJ NAKHOSTEEN, J YOSHIMURA, T LEE, TH POSTON, RN TI UP-REGULATION OF MONOCYTE CHEMOATTRACTANT PROTEIN-1 (MCP-1) IN ASTHMATIC AIRWAYS SO CLINICAL AND EXPERIMENTAL ALLERGY LA English DT Meeting Abstract C1 UMDS,GUYS HOSP,LONDON SE1 9RT,ENGLAND. AUGUSTA TEACHING HOSP,BOCHUM,GERMANY. NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0954-7894 J9 CLIN EXP ALLERGY JI Clin. Exp. Allergy PD FEB PY 1994 VL 24 IS 2 BP 188 EP 188 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA MZ553 UT WOS:A1994MZ55300100 ER PT J AU SAMPSON, M RUDDEL, M ELIN, RJ AF SAMPSON, M RUDDEL, M ELIN, RJ TI EFFECTS OF SPECIMEN TURBIDITY AND GLYCEROL CONCENTRATION ON 9 ENZYMATIC METHODS FOR TRIGLYCERIDE DETERMINATION SO CLINICAL CHEMISTRY LA English DT Article DE BICHROMATIC ANALYSIS; ANALYTICAL ERROR; INTERMETHOD COMPARISON ID SERUM TRIGLYCERIDES; NEED BLANKING AB We compared the effects of specimen turbidity and glycerol concentration on nine enzymatic methods for triglyceride measurement. We assayed 51 specimens with triglyceride concentrations of 0.85-8.21 mmol/L (75-727 mg/dL) and turbidity at 420 nm equivalent to greater than or equal to 0.1 mmol/L (8.8 mg/dL) triglyceride (measured as part of our comparison method). The data were analyzed by multiple regression, which gave coefficients for the effects of glycerol concentration and the change in turbidity during the reaction. The effects of specimen turbidity and glycerol concentration were method-dependent and ranged from 6.20% to -15.67% of the measured result. The magnitude of the turbidity effect (in assays with a significant turbidity interference) was similar to that for glycerol (in assays with a significant glycerol interference). A triglyceride assay with a bichromatic measurement was less subject to interference from turbidity. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT CLIN PATHOL,CLIN CHEM SERV,BETHESDA,MD 20892. NR 13 TC 7 Z9 7 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD FEB PY 1994 VL 40 IS 2 BP 221 EP 226 PG 6 WC Medical Laboratory Technology SC Medical Laboratory Technology GA NA660 UT WOS:A1994NA66000009 PM 8313598 ER PT J AU POTTER, WZ MANJI, HK AF POTTER, WZ MANJI, HK TI CATECHOLAMINES IN DEPRESSION - AN UPDATE SO CLINICAL CHEMISTRY LA English DT Article; Proceedings Paper CT 17th Annual Symposium of the National-Academy-of-Clinical-Biochemistry CY JUL 10, 1993 CL NEW YORK, NY SP NATL ACAD CLIN BIOCHEM DE NOREPINEPHRINE; AFFECTIVE DISORDERS; CELL RECEPTORS; PLATELETS; CEREBROSPINAL FLUID; URINE ID BETA-ADRENERGIC RECEPTORS; GROWTH-HORMONE RESPONSE; LITHIUM-CARBONATE TREATMENT; MAJOR AFFECTIVE-DISORDER; LOCUS COERULEUS NEURONS; URINARY BIOGENIC-AMINES; SINGLE UNIT-ACTIVITY; FREELY MOVING CAT; CEREBROSPINAL-FLUID; PLASMA NOREPINEPHRINE AB Despite extensive research, the biochemical abnormalities underlying the predisposition to and the pathogenesis of affective disorders remain to be clearly established. Efforts to study norepinephrine (NE) output and function have utilized biochemical assays, neuroendocrine challenge strategies, and measures of peripheral blood cell receptors; the cumulative database points to a dysregulation of the noradrenergic system. Depressed patients (in particular, melancholic, unipolar subjects) excrete disproportionately greater amounts of NE and its major extraneuronal metabolite, normetanephrine, than do controls. Depressed patients also show subsensitive neuroendocrine (growth hormone) and biochemical (inhibition of adenylate cyclase) responses to alpha(2)-adrenergic agonists, suggesting that subsensitivity of nerve terminal alpha(2) autoreceptors may underlie the exaggerated plasma NE observed in response to various challenges in affective disorders. Future advances in brain imaging techniques and in the molecular biology of adrenergic receptor-coupled signal transduction systems offer promise for meaningful advances in our understanding of the pathophysiology of affective disorders. RP POTTER, WZ (reprint author), NIMH,EXPTL THERAPEUT BRANCH,CLIN PHARMACOL SECT,BLDG 10,ROOM 2D46,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 105 TC 55 Z9 55 U1 1 U2 1 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD FEB PY 1994 VL 40 IS 2 BP 279 EP 287 PG 9 WC Medical Laboratory Technology SC Medical Laboratory Technology GA NA660 UT WOS:A1994NA66000024 PM 8313609 ER PT J AU REED, T TRACY, RP FABSITZ, RR AF REED, T TRACY, RP FABSITZ, RR TI MINIMAL GENETIC INFLUENCES ON PLASMA-FIBRINOGEN LEVEL IN ADULT MALES IN THE NHLBI TWIN STUDY SO CLINICAL GENETICS LA English DT Article DE FIBRINOGEN; HERITABILITY; TWINS ID ISCHEMIC-HEART-DISEASE; CARDIOVASCULAR RISK-FACTORS; BLOOD-INSTITUTE TWIN; MYOCARDIAL-INFARCTION; HEMOSTATIC FUNCTION; MEN; HERITABILITY; COAGULATION; CONCORDANCE; SPEEDWELL AB Plasma fibrinogen was determined in 189 twins participating at the Indiana center during the third examination of the NHLBI twin study with a mean age of 63 years. Moderate heritability estimates were obtained from 44 complete MZ pairs and 39 complete DZ pairs. After adjustment of fibrinogen levels for age and other confounding variables related to cardiovascular disease risk, the maximum likelihood heritability estimate was only 30% (p=0.03). Plasma fibrinogen was most strongly associated with smoking and the presence of diabetes. Omitting all subjects with diabetes or cardiovascular disease further reduced the heritability estimates slightly, and most path models including genetic parameters provided no significant improvement in fit over a model determined solely by random environmental effects. Our results are consistent with the environment rather than genetic influences having a greater influence on the level of plasma fibrinogen. C1 UNIV VERMONT,DEPT PATHOL,CLIN BIOCHEM RES LAB,BURLINGTON,VT 05405. NHLBI,CLIN & GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP REED, T (reprint author), INDIANA UNIV,SCH MED,DEPT MED & MOLEC GENET,IB 130,975 W WALNUT ST,INDIANAPOLIS,IN 46202, USA. FU NHLBI NIH HHS [N01-HC-55027] NR 48 TC 45 Z9 45 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD FEB PY 1994 VL 45 IS 2 BP 71 EP 77 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA NC691 UT WOS:A1994NC69100004 PM 8004801 ER PT J AU PINCUS, SH AF PINCUS, SH TI IMMUNOTOXINS - CLINICAL POTENTIAL IN THE TREATMENT OF AIDS SO CLINICAL IMMUNOTHERAPEUTICS LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-INFECTED-CELLS; RICIN-A-CHAIN; EXOTOXIN HYBRID PROTEIN; CD4-PSEUDOMONAS EXOTOXIN; T-CELLS; MONOCLONAL-ANTIBODIES; INHIBITORY PROTEINS; SOLUBLE CD4; INVITRO AB Immunotoxins directed against human immunodeficiency virus (HIV) may be of use in treating AIDS by eliminating HIV-infected cells that are actively secreting virus and serving as a nidus for the spread of the infection. These immunotoxins may be directed either toward viral structures expressed on the surface of cells or toward cell populations known to be sites of HIV replication. The HIV envelope proteins gp120 and gp41 are the major antigenic structures expressed on infected cells. They may be targeted with CD4 (the viral receptor) or with monoclonal antibodies. Activated lymphocytes expressing the interleukin-2 receptor are an important reservoir of HIV replication. The efficacy of these immunotoxins has been established in vitro, and mechanisms of enhancement of immunotoxin action have been defined. A CD4-based immunotoxin has completed phase I clinical trials. RP PINCUS, SH (reprint author), NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,903 S 4TH ST,HAMILTON,MT 59840, USA. NR 40 TC 2 Z9 2 U1 0 U2 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1172-7039 J9 CLIN IMMUNOTHER JI Clin. Immunother. PD FEB PY 1994 VL 1 IS 2 BP 89 EP 94 PG 6 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA MX899 UT WOS:A1994MX89900001 ER PT J AU HITRI, A HURD, YL WYATT, RJ DEUTSCH, SI AF HITRI, A HURD, YL WYATT, RJ DEUTSCH, SI TI MOLECULAR, FUNCTIONAL AND BIOCHEMICAL CHARACTERISTICS OF THE DOPAMINE TRANSPORTER - REGIONAL DIFFERENCES AND CLINICAL RELEVANCE SO CLINICAL NEUROPHARMACOLOGY LA English DT Review DE DOPAMINE TRANSPORTER; COCAINE; [H-3] GBR 12935; AGE; PARKINSONS DISEASE; SCHIZOPHRENIA; TOURETTES DISEASE ID POSITRON EMISSION TOMOGRAPHY; BRAIN GABA TRANSPORTER; COCAINE BINDING-SITES; H-3 GBR-12935 BINDING; RAT NUCLEUS-ACCUMBENS; PARKINSONS-DISEASE; GBR-12935 BINDING; TOURETTE SYNDROME; NEURONAL UPTAKE; CHRONIC-SCHIZOPHRENIA AB The carrier molecule that transports dopamine (DA) across the synaptic membrane is known as the dopamine transporter (DAT). Depending on the ionic conditions, DAT may function as a mediator of both the inward directed DA transport known as the ''reuptake'' and the outward directed DA transport known as the ''release.'' The functional significance of DAT is in the regulation of DA neurotransmission by terminating the action of DA in the synapse via reuptake. With use of DAT binding as a presynaptic marker to measure altered DA innervation, abnormalities of the DAT binding have been demonstrated in idiopathic Parkinson's disease, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity, and progressive supranuclear palsy. Moreover, the identification of DAT as the neuronal element that mediates the addictive properties of cocaine highlights its significance in cocaine addiction. Cocaine binding in the brain is heterogeneous, and there is an uneven distribution of the high- and low-affinity binding sites across the anatomical regions. Regional differences in ligand binding are observed by using both [H-3]cocaine and the diphenyl-substituted piperazine derivatives known as the ''GBR series'' of ligands. The identification of compounds that inhibit the binding of cocaine without affecting DA uptake could potentially lead to development of medications for cocaine abuse. Furthermore, clarification of the various binding domains that may be relevant to transporter function in human neuropsychiatric disorders may lead to the development of new medications for schizophrenia, Tourette's disease, and drug addiction. C1 DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV,WASHINGTON,DC. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20007. NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. KAROLINSKA INST,DEPT PSYCHIAT & PSYCHOL,S-10401 STOCKHOLM,SWEDEN. RP HITRI, A (reprint author), DEPT VET AFFAIRS MED CTR,NIDA,RES UNIT,50 IRVING ST NW,WASHINGTON,DC 20422, USA. NR 140 TC 69 Z9 70 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-5664 J9 CLIN NEUROPHARMACOL JI Clin. Neuropharmacol. PD FEB PY 1994 VL 17 IS 1 BP 1 EP 22 DI 10.1097/00002826-199402000-00001 PG 22 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA MT476 UT WOS:A1994MT47600001 PM 8149355 ER PT J AU MONTOYA, ID MANN, DJ ELLISON, PA LANGE, WR PRESTON, KL AF MONTOYA, ID MANN, DJ ELLISON, PA LANGE, WR PRESTON, KL TI IMPATIENT MEDICALLY SUPERVISED OPIOID WITHDRAWAL WITH BUPRENORPHINE ALONE AND IN COMBINATION WITH NALTREXONE SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIDA,ARC,BALTIMORE,MD. NR 0 TC 5 Z9 5 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 131 EP 131 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100032 ER PT J AU PRESTON, KL BIGELOW, GE AF PRESTON, KL BIGELOW, GE TI DISCRIMINATIVE STIMULUS EFFECTS OF HYDROMORPHONE, BUTORPHANOL, AND PENTAZOCINE AFTER PRETREATMENT WITH NALTREXONE OR PLACEBO SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,NIDA,ADDICT RES CTR,BALTIMORE,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 131 EP 131 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100034 ER PT J AU COVI, L MONTOYA, ID HESS, J KREITER, N AF COVI, L MONTOYA, ID HESS, J KREITER, N TI DOUBLE-BLIND COMPARISON OF DESIPRAMINE AND PLACEBO FOR TREATMENT OF COCAINE DEPENDENCE SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIDA,ARC,BALTIMORE,MD. NR 0 TC 4 Z9 4 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 132 EP 132 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100037 ER PT J AU FLEISHAKER, JC CHAMBERS, JH GARZONE, PD WEINGARTNER, HJ AF FLEISHAKER, JC CHAMBERS, JH GARZONE, PD WEINGARTNER, HJ TI COMPARATIVE EFFECTS OF ALPRAZOLAM AND ADINAZOLAM ON MEMORY AND PSYCHOMOTOR PERFORMANCE SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 UPJOHN CO,CLIN PHARMACOKINET UNIT,KALAMAZOO,MI 49007. UNIV PITTSBURGH,PITTSBURGH,PA. NIAAA,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 135 EP 135 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100049 ER PT J AU ANDREASON, PJ GEORGE, DT GEYER, CL SZYMANSKI, H RIO, D MOMENAN, R ZAMETKIN, AJ ECKARDT, M HOMMER, D LINNOILA, M AF ANDREASON, PJ GEORGE, DT GEYER, CL SZYMANSKI, H RIO, D MOMENAN, R ZAMETKIN, AJ ECKARDT, M HOMMER, D LINNOILA, M TI EFFECTS OF THE SEROTONIN AGONIST METACHLOROPHENYLPIPERAZINE ON CEREBRAL METABOLISM IN ALCOHOLICS AND NORMAL VOLUNTEERS SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIAAA,CLIN STUDIES LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 136 EP 136 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100052 ER PT J AU MARTIN, PR ADINOFF, B WEINGARTNER, H ECKARDT, MJ LINNOILA, M AF MARTIN, PR ADINOFF, B WEINGARTNER, H ECKARDT, MJ LINNOILA, M TI FLUVOXAMINE (F) TREATMENT OF ALCOHOL AMNESTIC DISORDER (AAD) SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 VANDERBILT UNIV,DEPT PSYCHIAT,NASHVILLE,TN. VANDERBILT UNIV,DEPT PHARMACOL,NASHVILLE,TN. NIAAA,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 1 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 136 EP 136 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100054 ER PT J AU SCHMIDT, M MATOCHIK, J RISINGER, R ZAMETKIN, A SCHOUTEN, J COHEN, R POTTER, W AF SCHMIDT, M MATOCHIK, J RISINGER, R ZAMETKIN, A SCHOUTEN, J COHEN, R POTTER, W TI EFFECTS OF IDAZOXAN ON REGIONAL BRAIN METABOLISM SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 136 EP 136 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100051 ER PT J AU COX, SR REICHMAN, RC KNUTH, D AF COX, SR REICHMAN, RC KNUTH, D TI CONSIDERATIONS FOR PHASE-1 CONCENTRATION CONTROLLED TRIALS (CCT) IN HIV-INFECTED PATIENTS - ATEVIRDINE (ATV) AS AN EXAMPLE SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 SUNY BUFFALO,BUFFALO,NY. UNIV ROCHESTER,ROCHESTER,NY. NIAID,KALAMAZOO,MI. UPJOHN CO,KALAMAZOO,MI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 157 EP 157 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100138 ER PT J AU AMANTEA, MA YARBORO, C FORREST, A PUCINO, F KLIPPEL, JH AF AMANTEA, MA YARBORO, C FORREST, A PUCINO, F KLIPPEL, JH TI POPULATION PHARMACOKINETICS (PKS) OF IV AND ORAL ONDANSETRON IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS (SLE) SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NIH,DEPT PHARM,BETHESDA,MD. NIAMS,BETHESDA,MD. SUNY BUFFALO,SCH PHARM,BUFFALO,NY 14260. MILLARD FILLMORE HOSP,CLIN PHARMACOKINET LAB,BUFFALO,NY 14209. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 161 EP 161 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100152 ER PT J AU FORREST, A AMANTEA, MA PUCINO, F YARBORO, C KLIPPEL, JH AF FORREST, A AMANTEA, MA PUCINO, F YARBORO, C KLIPPEL, JH TI POPULATION PHARMACODYNAMICS (PDS) OF IV AND PO ONDANSETRON IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS (SLE) SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 SUNY BUFFALO,SCH PHARM,BUFFALO,NY 14260. MILLARD FILLMORE HOSP,CLIN PHARMACOKINET LAB,BUFFALO,NY 14209. NIH,DEPT PHARM,BETHESDA,MD. NIAMS,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 161 EP 161 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100153 ER PT J AU FIGG, WD CHRISTIAN, MC DAVIS, P COOPER, MR COOPER, WA THIBAULT, A MYERS, CE REED, E AF FIGG, WD CHRISTIAN, MC DAVIS, P COOPER, MR COOPER, WA THIBAULT, A MYERS, CE REED, E TI PHARMACOKINETICS OF ORMAPLATIN SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. RI Figg Sr, William/M-2411-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 189 EP 189 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100266 ER PT J AU SARTOR, AO FIGG, WD THIBAULT, A COOPER, MR HEADLEE, D MYERS, CE AF SARTOR, AO FIGG, WD THIBAULT, A COOPER, MR HEADLEE, D MYERS, CE TI A PHASE-I STUDY OF SOMATULINE IN PATIENTS WITH METASTATIC ANDROGEN-RESISTANT PROSTATE-CANCER SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. RI Figg Sr, William/M-2411-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 190 EP 190 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100269 ER PT J AU GRAUMLICH, JF LUDDEN, TM CANTILENA, CC LEVINE, M WELCH, RW WANG, Y DHARIWAL, K PARK, J WASHKO, P LAZAREV, A KING, J CANTILENA, LR AF GRAUMLICH, JF LUDDEN, TM CANTILENA, CC LEVINE, M WELCH, RW WANG, Y DHARIWAL, K PARK, J WASHKO, P LAZAREV, A KING, J CANTILENA, LR TI PHARMACOKINETIC MODEL OF ASCORBIC-ACID IN DEPLETION AND REPLETION SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 UNIFORMED SERV UNIV HLTH SCI,DIV CLIN PHARMACOL,BETHESDA,MD. US FDA,CDER,ROCKVILLE,MD 20857. NIDDK,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1994 VL 55 IS 2 BP 200 EP 200 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MY421 UT WOS:A1994MY42100308 ER PT J AU HOLLERAN, WM GINNS, EI FARTASCH, M ELIAS, PM SIDRANSKY, E AF HOLLERAN, WM GINNS, EI FARTASCH, M ELIAS, PM SIDRANSKY, E TI THE ABNORMAL BARRIER FUNCTION IN SEVERE BETA-GLUCOCEREBROSIDASE DEFICIENCY IS DUE TO MATURATIONAL BLOCKADE OF STRATUM-CORNEUM INTERCELLULAR LAMELLAE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,DERMATOL SERV,SAN FRANCISCO,CA 94121. UNIV CALIF SAN FRANCISCO,DEPT DERMATOL,SAN FRANCISCO,CA 94143. NIMH,MOLEC NEUROGENET SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1994 VL 42 IS 1 BP A6 EP A6 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MR214 UT WOS:A1994MR21400029 ER PT J AU MERICQ, V CASSORLA, F GARCIA, H AVILA, A BORIC, A MERRIAM, GR AF MERICQ, V CASSORLA, F GARCIA, H AVILA, A BORIC, A MERRIAM, GR TI BETA-ADRENERGIC-BLOCKADE ENHANCES THE GROWTH-PROMOTING EFFECT OF GROWTH HORMONE-RELEASING HORMONE IN GH DEFICIENCY - RESULTS AT ONE-YEAR OF THERAPY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV CHILE,INST INVEST MATERNO INFANTIL,SANTIAGO,CHILE. NIH,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. ALVAMC,RES SERV,TACOMA,WA. UNIV WASHINGTON,SCH MED,DIV METAB ENDOCRINOL & NUTR,SEATTLE,WA 98195. RI Mericq, Veronica/F-3927-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1994 VL 42 IS 1 BP A21 EP A21 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MR214 UT WOS:A1994MR21400109 ER PT J AU PARSHAD, R SANFORD, KK PRICE, FM TARONE, RE ROBBINS, JH AF PARSHAD, R SANFORD, KK PRICE, FM TARONE, RE ROBBINS, JH TI A DNA-REPAIR DEFECT IN ALZHEIMER-DISEASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HOWARD UNIV,COLL MED,WASHINGTON,DC 20001. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1994 VL 42 IS 1 BP A98 EP A98 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MR214 UT WOS:A1994MR21400528 ER PT J AU WRIGHT, LL VERTER, J YOUNES, N FANAROFF, AA AF WRIGHT, LL VERTER, J YOUNES, N FANAROFF, AA TI ANTENATAL STEROIDS ARE ASSOCIATED WITH A SUBSTANTIAL REDUCTION IN THE RISK OF MORTALITY AND MORBIDITY IN INFANTS 501-1500 GRAMS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,NEONATAL NETWORK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD FEB PY 1994 VL 42 IS 1 BP A1 EP A1 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MR214 UT WOS:A1994MR21400004 ER PT J AU OLDS, JL AF OLDS, JL TI THE COMPUTATIONAL BRAIN - CHURCHLAND,PS, SEJNOWSKI,TJ SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review RP OLDS, JL (reprint author), NIH,ADAPT SYST LAB,BETHESDA,MD 20892, USA. RI Olds, James/D-2867-2011 NR 12 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD FEB PY 1994 VL 39 IS 2 BP 127 EP 129 PG 3 WC Psychology, Multidisciplinary SC Psychology GA MW781 UT WOS:A1994MW78100001 ER PT J AU BROWN, KE YOUNG, NS LIU, JM AF BROWN, KE YOUNG, NS LIU, JM TI MOLECULAR, CELLULAR AND CLINICAL ASPECTS OF PARVOVIRUS B19 INFECTION SO CRITICAL REVIEWS IN ONCOLOGY/HEMATOLOGY LA English DT Review ID LINKED-IMMUNOSORBENT-ASSAY; IDIOPATHIC THROMBOCYTOPENIC PURPURA; HEMATOPOIETIC PROGENITOR CELLS; COLONY FORMATION INVITRO; MINK DISEASE PARVOVIRUS; HUMAN-SERUM PARVOVIRUS; BONE-MARROW NECROSIS; NON-IMMUNE HYDROPS; ERYTHEMA-INFECTIOSUM; APLASTIC CRISIS C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. NR 255 TC 105 Z9 108 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1040-8428 J9 CRIT REV ONCOL HEMAT JI Crit. Rev. Oncol./Hematol. PD FEB PY 1994 VL 16 IS 1 BP 1 EP 31 DI 10.1016/1040-8428(94)90040-X PG 31 WC Oncology; Hematology SC Oncology; Hematology GA NP672 UT WOS:A1994NP67200001 PM 8074799 ER PT J AU WESTERGAARD, GC SUOMI, SJ AF WESTERGAARD, GC SUOMI, SJ TI THE USE AND MODIFICATION OF BONE TOOLS BY CAPUCHIN MONKEYS SO CURRENT ANTHROPOLOGY LA English DT Article ID CEBUS-APELLA; WILD CHIMPANZEES; TUFTED CAPUCHIN; NATIONAL-PARK RP WESTERGAARD, GC (reprint author), NICHHD,COMPARAT ETHOL LAB,POB 529,POOLESVILLE,MD 20837, USA. NR 18 TC 15 Z9 15 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0011-3204 J9 CURR ANTHROPOL JI Curr. Anthropol. PD FEB PY 1994 VL 35 IS 1 BP 75 EP 77 DI 10.1086/204243 PG 3 WC Anthropology SC Anthropology GA MR030 UT WOS:A1994MR03000013 ER PT J AU SCHARENBERG, AM KINET, JP AF SCHARENBERG, AM KINET, JP TI IS LOCALIZED IMMUNOGLOBULIN-E SYNTHESIS THE PROBLEM SO CURRENT BIOLOGY LA English DT Note ID EPSILON-TRANSCRIPTS; IGE PRODUCTION; INTERLEUKIN-4; LYMPHOKINE; EXPRESSION; SWITCH; LIGAND; CD23 RP SCHARENBERG, AM (reprint author), NIAID,MOLEC ALLERGY & IMMUNOL SECT,TWINBROOK BLDG 2,ROOM 108,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 21 TC 12 Z9 12 U1 0 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD FEB 1 PY 1994 VL 4 IS 2 BP 140 EP 142 DI 10.1016/S0960-9822(94)00032-1 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MX639 UT WOS:A1994MX63900009 PM 7953515 ER PT J AU GHALAYINI, AJ KOUTZ, CA WETSEL, WC HANNUN, YA ANDERSON, RE AF GHALAYINI, AJ KOUTZ, CA WETSEL, WC HANNUN, YA ANDERSON, RE TI IMMUNOLOCALIZATION OF PKC-ZETA IN RAT PHOTORECEPTOR INNER SEGMENTS SO CURRENT EYE RESEARCH LA English DT Article DE PROTEIN KINASE C; PHOTORECEPTORS; IMMUNOLOCALIZATION; RAT; RETINA ID PROTEIN-KINASE-C; ROD OUTER SEGMENTS; PHOSPHORYLATION; PURIFICATION; ISOENZYMES; CELLS AB We have utilized several peptide specific antisera directed against the C-terminals (Wetsel et al, 1992) of several protein kinase C (PKC) isozymes (alpha, beta(1), beta(11), gamma, delta, epsilon, zeta) to delineate the cellular localization of these PKC isozymes in rat retina. Antisera against PKC beta(1), beta(11), gamma, delta and epsilon were non-reactive in frozen rat retina sections, whereas, anti PKC alpha was strongly reactive with the outer plexiform, inner plexiform and nerve fiber cell layers. The most specific localization of immunoreactivity was observed with PKC zeta, which reacted strongly and exclusively with photoreceptor inner segments, but not outer segments. Immunoblot analysis of whole rat retina homogenate showed that anti-PKC alpha recognized an antigen of similar to 80kD and anti-PKC zeta recognized a similar to 72kD protein. Immunolocalization of PKC zeta to photoreceptor inner segments and possible functional significance are discussed. C1 NIEHS,MED & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. DUKE UNIV,MED CTR,DEPT MED,DIV HEMATOL ONCOL,DURHAM,NC 27710. RP GHALAYINI, AJ (reprint author), BAYLOR COLL MED,DEPT OPHTHALMOL,HOUSTON,TX 77030, USA. FU NEI NIH HHS [EY04149, EY00871, EY02520] NR 24 TC 19 Z9 19 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD FEB PY 1994 VL 13 IS 2 BP 145 EP 150 DI 10.3109/02713689409042409 PG 6 WC Ophthalmology SC Ophthalmology GA NA028 UT WOS:A1994NA02800007 PM 8194361 ER PT J AU VERMUND, SH SCHULTZ, AM HOFF, R AF VERMUND, SH SCHULTZ, AM HOFF, R TI PREVENTION OF HIV/AIDS WITH VACCINES SO CURRENT OPINION IN INFECTIOUS DISEASES LA English DT Article AB HIV vaccines are urgently needed to help control the relentlessly expanding epidemic. However, the development of a safe and effective vaccine for this rapidly mutating virus which produces life-long infection is elusive. Feasibility of HIV vaccination has been demonstrated by challenge studies in primates and by the presence of neutralizing antibodies which confer passive protection and can be detected in vitro. Given safety considerations, the first vaccines developed have been recombinant subunit vaccines consisting of viral envelope antigens formulated with adjuvants or incorporated into live vectors, such as vaccinia and avipox. Subunit envelope vaccines have proven to be safe and immunogenic in human phase I trials. Two gp120 subunit products are being considered for phase III trials based on ongoing evaluation of data from a phase II trial, primate-challenge studies, and laboratory studies evaluating the breadth, magnitude, and duration of immunogenic responses, including neutralization against recent isolates. Efficacy trials will be large and complex, involving people at high behavioral risk for infection. Baseline studies with recruitment goals of over 10 000 people are being sponsored in the USA, with many additional vaccine preparedness studies being sponsored in developing nations by international and national authorities. Because high-risk populations will be recruited for trials of many year's duration, new approaches to trial design and community participation will be needed in order for these trials to succeed. Systems must be in place,to ensure that trial participants receive preventive counseling and services to minimize discrimination from vaccine-related seroconversions. Here we document the urgent need for HIV vaccines, provide a brief preclinical and clinical update, and present the plans and considerations for testing HIV vaccine efficacy. RP VERMUND, SH (reprint author), NIAID,DIV AIDS,CLIN RES PROGRAM,VACCINE TRIALS & EPIDEMIOL BRANCH,ROOM 2A42,BETHESDA,MD 20892, USA. OI Vermund, Sten/0000-0001-7289-8698 NR 0 TC 12 Z9 12 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0951-7375 J9 CURR OPIN INFECT DIS JI Curr. Opin. Infect. Dis. PD FEB PY 1994 VL 7 IS 1 BP 82 EP 94 DI 10.1097/00001432-199402000-00014 PG 13 WC Infectious Diseases SC Infectious Diseases GA MW056 UT WOS:A1994MW05600014 ER PT J AU STRATTON, P CIACCO, KH AF STRATTON, P CIACCO, KH TI CERVICAL NEOPLASIA IN THE PATIENT WITH HIV-INFECTION SO CURRENT OPINION IN OBSTETRICS & GYNECOLOGY LA English DT Article AB With heterosexual transmission of HIV becoming the primary mode of transmission to women in the USA, and a high rate of human papillomavirus (HPV) and cervical neoplasia in HIV-infected women, obstetrician-gynecologists have become primary care providers for HIV-infected women. Reports of a high rate of recurrence and progression of cervical neoplasia in this population suggest that gynecologists must strive to identify those women with cervical neoplasia who are HIV infected. Alterations in local immune response of the genital tract caused by HIV infection may be responsible for higher prevalence, recurrence rates, and progression rates of cervical neoplasms in these women. Since cervical cancer may have a more fulminant course in HIV-infected women and has become an AIDS-defining illness, the surveillance and treatment of cervical neoplasia may need to be more aggressive. RP STRATTON, P (reprint author), NICHHD,CPR,CDB,6100 BLDG,ROOM 8B13,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 19 Z9 19 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 1040-872X J9 CURR OPIN OBSTET GYN JI Curr. Opin. Obstet. Gynecol. PD FEB PY 1994 VL 6 IS 1 BP 86 EP 91 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA MV929 UT WOS:A1994MV92900013 PM 8180357 ER EF