FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Merrick, BA Walker, VR He, CY Patterson, RM Selkirk, JK AF Merrick, BA Walker, VR He, CY Patterson, RM Selkirk, JK TI Induction of novel Grp75 isoforms by 2-deoxyglucose in human and murine fibroblasts SO CANCER LETTERS LA English DT Article DE Grp75; heat shock proteins; 2-deoxyglucose; fibroblasts ID MITOCHONDRIAL STRESS-70 PROTEIN; HSP70 FAMILY; HEAT-SHOCK; MOUSE; MORTALIN; MEMBER; IDENTIFICATION; CLONING; PEPTIDE; BINDING AB Grp75 is a stress-inducible mitochondrial chaperone which has a high homology to senescence-related protein. p66(mot) mortalin. In human cells the mortalin gene assigns to the locus of a putative tumor suppressor gene for myeloid malignancies. In order to study expression and localization of Grp75 and p66(mot) in human and murine fibroblast lines, polyclonal antibodies were raised to conserved portions of each sequence. HT1080 and C3H10T1/2 cells were treated with various Grp-inducing agents. A single 75 kDa band was detected by Western blot of cytoplasmic proteins which was not greatly altered after thermal stress or treatment with L-azetidine-2-carboxylic acid or nonactin. However, glucose deprivation by 2-deoxyglucose treatment induced five novel isoforms at 74-75 kDa mass. Mortalin at 66 kDa could not be detected under these treatment conditions. (C) 1997 Elsevier Science Ireland Ltd. RP Merrick, BA (reprint author), NIEHS,MOL CARCINOGENESIS LAB,D4-03,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 16 TC 26 Z9 27 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD NOV 11 PY 1997 VL 119 IS 2 BP 185 EP 190 DI 10.1016/S0304-3835(97)00270-X PG 6 WC Oncology SC Oncology GA YD697 UT WOS:A1997YD69700009 PM 9570370 ER PT J AU Smith, ML Fornace, AJ AF Smith, ML Fornace, AJ TI p53-mediated protective responses to UV irradiation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DECREASED DNA-REPAIR; LI-FRAUMENI SYNDROME; XERODERMA PIGMENTOSUM; SYNDROME FIBROBLASTS; ULTRAVIOLET-LIGHT; TUMOR-SUPPRESSOR; EXCISION-REPAIR; MOUSE CELLS; P53; CANCER RP Smith, ML (reprint author), NCI,MOL PHARMACOL LAB,DIV BASIC SCI,NIH,BLDG 37,ROOM 5D02,BETHESDA,MD 20892, USA. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 55 TC 94 Z9 94 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 NOV 11 PY 1997 VL 94 IS 23 BP 12255 EP 12257 DI 10.1073/pnas.94.23.12255 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YF393 UT WOS:A1997YF39300004 PM 9356435 ER PT J AU Krylov, D Kasai, K Echlin, DR Taparowsky, EJ Arnheiter, H Vinson, C AF Krylov, D Kasai, K Echlin, DR Taparowsky, EJ Arnheiter, H Vinson, C TI A general method to design dominant negatives to B-HLHZip proteins that abolish DNA binding SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE heterodimer; Max; Mitf; Myc; protein design; transcription factor enhancer binding ID HELIX-LOOP-HELIX; C3H10T1/2 CELLS; B/HLH/Z DOMAIN; MYC PROTEINS; BASIC REGION; TRANSCRIPTION; MAX; MICROPHTHALMIA; DIMERIZATION; MUTATIONS AB We describe a method to design dominant-negative proteins (D-N) to the basic helix-loop-helix-leucine zipper (B-HLHZip) family of sequence-specific DNA binding transcription factors, The D-Ns specifically heterodimerize with the B-HLHZip dimerization domain of the transcription factors and abolish DNA binding in an equimolar competition, Thermal denaturation studies indicate that a heterodimer between a Myc R-HLHZip domain and a D-N consisting of a Id-amino acid sequence appended onto the Max dimerization domain (A-Max) is -6.3 kcal.mol(-1) more stable than the Myc:Max heterodimer. One molar equivalent of A-Max can totally abolish the DNA binding activity of a Myc:Max heterodimer. This acidic extension also has been appended onto the dimerization domain of the B-HLHZlp protein Mitf, a member of the transcription factor enhancer binding subfamily, to produce A-Mitf, The heterodimer between A-Mitf and the B-HLHZip domain of Mitf is -3.7 kcal.mol(-1) more stable than the Mitf homodimer, Cell culture studies show that A-Mitf can inhibit Mitf-dependent transactivation both in acidic extension and in a dimerization-dependent manner. A-Max can inhibit Myc-dependent foci formation twice as well as the Max dimerization domain (HLHZip), This strategy of producing D-Ns may be applicable to other B-HLHZlp or B-HLH proteins because it provides a method to inhibit the DNA binding of these transcription factors in a dimerization-specific manner. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NINCDS,LAB DEV NEUROGENET,NIH,BETHESDA,MD 20892. PURDUE UNIV,DEPT BIOL SCI,W LAFAYETTE,IN 47907. NR 31 TC 56 Z9 56 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 11 PY 1997 VL 94 IS 23 BP 12274 EP 12279 DI 10.1073/pnas.94.23.12274 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YF393 UT WOS:A1997YF39300008 PM 9356439 ER PT J AU Tullio, AN Accili, D Ferrans, VJ Yu, ZX Takeda, K Grinberg, A Westphal, H Preston, YA Adelstein, RS AF Tullio, AN Accili, D Ferrans, VJ Yu, ZX Takeda, K Grinberg, A Westphal, H Preston, YA Adelstein, RS TI Nonmuscle myosin II-B is required for normal development of the mouse heart SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HEAVY CHAIN-B; DIFFERENTIAL LOCALIZATION; MESSENGER-RNAS; NEURAL CREST; ISOFORMS; GENE; EXPRESSION; TISSUES; CLONING; IDENTIFICATION AB We used targeted gene disruption in mice to ablate nonmuscle myosin heavy chain B (NMHC-B), one of the two isoforms of nonmuscle myosin II present in all vertebrate cells, Approximately 65% of the NMHC-B-/- embryos died prior to birth, and those that were born suffered from congestive heart failure and died during the first day, No abnormalities were detected in NMHC-B+/- mice. The absence of NMHC-B resulted in a significant increase in the transverse diameters of the cardiac myocytes from 7.8 +/- 1.8 mu m (right ventricle) and 7.8 +/- 1.3 mu m (left ventricle) in NMHC-B+/+ and B+/- mice to 14.7 +/- 1.1 mu m and 13.8 +/- 2.3 mu m, respectively, in NMHC-B-/- mice (in both cases, P < 0.001), The increase in size of the cardiac myocytes was seen as early as embryonic day 12.5 (4.5 +/- 0.2 mu m for NMHC-B+/+ and B+/- vs. 7.2 +/- 0.6 mu m for NMHC-B-/- mice (P < 0.01)), Six of seven NMHC-B-/- newborn mice analyzed by serial sectioning also showed structural cardiac defects, including a ventricular septal defect, an aortic root that either straddled the defect or originated from the right ventricle, and muscular obstruction to right ventricular outflow, Some of the hearts of NMHC-B-/- mice showed evidence for up-regulation of NMHC-A protein, These studies suggest that nonmuscle myosin II-B is required for normal cardiac myocyte development and that its absence results in structural defects resembling, in part, two common human congenital heart diseases, tetralogy of Fallot and double outlet right ventricle. C1 NHLBI,MOL CARDIOL LAB,NIH,BETHESDA,MD 20892. NHLBI,PATHOL SECT,NIH,BETHESDA,MD 20892. NICHHD,DEV ENDOCRINOL BRANCH,NIH,BETHESDA,MD 20892. NICHHD,LAB MAMMALIAN GENES & DEV,NIH,BETHESDA,MD 20892. OI Adelstein, Robert/0000-0002-8683-2144 NR 29 TC 175 Z9 178 U1 0 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 11 PY 1997 VL 94 IS 23 BP 12407 EP 12412 DI 10.1073/pnas.94.23.12407 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YF393 UT WOS:A1997YF39300031 PM 9356462 ER PT J AU Masison, DC Maddelein, ML Wickner, RB AF Masison, DC Maddelein, ML Wickner, RB TI The prion model for [URE3] of yeast: Spontaneous generation and requirements for propagation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DOUBLE-STRANDED-RNA; SACCHAROMYCES-CEREVISIAE; TRANSGENIC MICE; PROTEIN; FUSION; PSI(+); SYSTEM; MUTANT; GENE AB The genetic properties of the non-Mendelian element, [URE3], suggest that it is a prion (infectious protein) form of Ure2p, a mediator of nitrogen regulation in Saccharomyces cerevisiae. Into a ure2 Delta strain (necessarily lacking [URE3]), we introduced a plasmid overproducing Ure2p. This induced the frequent ''spontaneous generation'' of [URE3], with properties identical to the original [URE3], Altering the translational frame only in the prion-inducing domain of URE2 shows that it is Ure2 protein (and not URE2 RNA) that induces appearance of [URE3], The proteinase K-resistance of Ure2p is unique to [URE3] strains and is not seen in nitrogen regulation of normal strains, The prion-inducing domain of Ure2p (residues 1-65) can propagate [URE3] in the absence of the C-terminal part of the molecule, In contrast, the C-terminal part of Ure2p cannot be converted to the prion (inactive) form without the prion-inducing domain covalently attached, These experiments support the prion model for [URE3] and extend our understanding of its propagation. C1 NIDDKD,LAB BIOCHEM & GENET,NIH,BETHESDA,MD 20892. RI MADDELEIN, Marie-Lise/G-5395-2010 NR 32 TC 119 Z9 119 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 NOV 11 PY 1997 VL 94 IS 23 BP 12503 EP 12508 DI 10.1073/pnas.94.23.12503 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YF393 UT WOS:A1997YF39300048 PM 9356479 ER PT J AU Moriya, K Rivera, J Odom, S Sakuma, Y Muramato, K Yoshiuchi, T Miyamoto, M Yamada, K AF Moriya, K Rivera, J Odom, S Sakuma, Y Muramato, K Yoshiuchi, T Miyamoto, M Yamada, K TI ER-27319, an acridone-related compound, inhibits release of antigen-induced allergic mediators from mast cells by selective inhibition of Fc epsilon receptor 1-mediated activation of Syk SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE immunoreceptor tyrosine-based activation motif; secretion ID PROTEIN-TYROSINE KINASE; HIGH-AFFINITY RECEPTOR; BASOPHILIC LEUKEMIA-CELLS; SRC HOMOLOGY-2 DOMAINS; IGE RECEPTOR; RBL-2H3 CELLS; IMMUNOGLOBULIN-E; SIGNAL-TRANSDUCTION; SH2 DOMAINS; GAMMA-CHAIN AB Engagement of the mast cell high-affinity receptor for immunoglobulin E (IgE), Fc epsilon RI, induces tyrosine phosphorylation of Syk, a non-receptor tyrosine kinase, that has been demonstrated as critical for degranulation, Herein we describe a synthetic compound, ER-27319, as a potent and selective inhibitor of antigen or anti-IgE-mediated degranulation of rodent and human mast cells, ER-27319 affected neither Lyn kinase activity nor the antigen-induced phosphorylation of the Fc epsilon RI but did effectively inhibit the tyrosine phosphorylation of Syk and thus its activity, As a consequence, tyrosine phosphorylation of phospholipase C-gamma 1, generation of inositol phosphates, release of arachidonic acid, and secretion of histamine and tumor necrosis factor alpha were also inhibited, ER-27319 did not inhibit the anti-CD3-induced tyrosine phosphorylation of phospholipase C-gamma 1 in Jurkat T cells, demonstrating a specificity for Syk-induced signals, In contrast the tyrosine phosphorylation and activation of Syk, induced by in vitro incubation with the phosphorylated immunoreceptor tyrosine-based activation motif (ITAM) of Fc epsilon RI gamma subunit or by antigen activation of RBL-2H3 cells, was specifically inhibited by ER-27319, However, when ER-27319 was added to immunoprecipitated Syk, derived from activated cells, no effect was seen on Syk activity, ER-27319 did not inhibit the tyrosine phosphorylation of Syk induced by activation in the presence of Ig beta ITAM or the anti-IgM-induced phosphorylation of Syk in human peripheral B cells, Therefore, ER-27319 selectively interferes with the Fc epsilon RI gamma phospho-ITAM activation of Syk in vitro and in intact cells, These results confirm the importance of Syk in Fc epsilon RI-mediated responses in mast cells and demonstrate the mast cell selectivity and therapeutic potential of ER-27319 in the treatment of allergic disease. C1 EISAI & CO LTD,TSUKUBA RES LABS,DEPT DRUG DISCOVERY,TSUKUBA,IBARAKI 30026,JAPAN. NIAMSD,SECT CHEM IMMUNOL,NIH,BETHESDA,MD 20892. NR 31 TC 63 Z9 64 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 11 PY 1997 VL 94 IS 23 BP 12539 EP 12544 DI 10.1073/pnas.94.23.12539 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YF393 UT WOS:A1997YF39300054 PM 9356485 ER PT J AU Nelson, PG Fitzgerald, S Rapoport, SI Neale, EA Galdzicki, Z Dunlap, V Bowers, L vonAgoston, D AF Nelson, PG Fitzgerald, S Rapoport, SI Neale, EA Galdzicki, Z Dunlap, V Bowers, L vonAgoston, D TI Cerebral cortical astroglia from the trisomy 16 mouse, a model for Down syndrome, produce neuronal cholinergic deficits in cell culture SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ALZHEIMERS-DISEASE; DOWN-SYNDROME; SPINAL-CORD; NEURODEGENERATION; ACETYLCHOLINE; INNERVATION; PLASTICITY; MECHANISM; SURVIVAL; PEPTIDE AB Trisomy 21 (Down syndrome) is associated with a high incidence of Alzheimer disease and with deficits in cholinergic function in humans, We used the trisomy 16 (Ts16) mouse model for Down syndrome to identify the cellular basis for the cholinergic dysfunction, Cholinergic neurons and cerebral cortical astroglia, obtained separately from Ts16 mouse fetuses and their euploid littermates, were cultured in various combinations, Choline acetyltransferase activity and cholinergic neuron number were both depressed in cultures in which both neurons and glia were derived from Ts16 fetuses, Cholinergic function of normal neurons was significantly down-regulated by coculture with Ts16 glia, Conversely, neurons from Ts16 animals could express normal cholinergic function when grown with normal glia, These observations indicate that astroglia may contribute strongly to the abnormal cholinergic function in the mouse Ts16 model for Down syndrome, The Ts16 glia could lack a cholinergic supporting factor present in normal glia or contain a factor that down-regulates cholinergic function. C1 NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892. RP Nelson, PG (reprint author), NICHHD,DEV NEUROBIOL LAB,NIH,49 CONVENT DR MSC 4480,BLDG 49,ROOM 5A38,BETHESDA,MD 20892, USA. NR 29 TC 21 Z9 21 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 NOV 11 PY 1997 VL 94 IS 23 BP 12644 EP 12648 DI 10.1073/pnas.94.23.12644 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YF393 UT WOS:A1997YF39300072 PM 9356503 ER PT J AU Tang, Y Mishkin, M Aigner, TG AF Tang, Y Mishkin, M Aigner, TG TI Effects of muscarinic blockade in perirhinal cortex during visual recognition SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE memory; recognition; rhinal cortex; hippocampus; cholinergic-muscarinic transmission ID INFERIOR TEMPORAL CORTEX; SHORT-TERM-MEMORY; PARAHIPPOCAMPAL CORTICES; RHESUS-MONKEYS; HIPPOCAMPAL-FORMATION; SCOPOLAMINE; AMYGDALA; ANTERIOR; NEURONS; FAMILIARITY AB Stimulus recognition in monkeys is severely impaired by destruction or dysfunction of the perirhinal cortex and also by systemic administration of the cholinergic-muscarinic receptor blocker, scopolamine. These two effects are shown here to be linked: Stimulus recognition was found to be significantly impaired after bilateral microinjection of scopolamine directly into the perirhinal cortex, but not after equivalent injections into the laterally adjacent visual area TE or into the dentate gyrus of the overlying hippocampal formation. The results suggest that the formation of stimulus memories depends critically on cholinergic-muscarinic activation of the perirhinal area, providing a new clue to how stimulus representations are stored. C1 NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. NR 29 TC 90 Z9 90 U1 1 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 11 PY 1997 VL 94 IS 23 BP 12667 EP 12669 DI 10.1073/pnas.94.23.12667 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YF393 UT WOS:A1997YF39300076 PM 9356507 ER PT J AU Umegaki, H Chernak, JM Ikari, H Roth, GS Ingram, DK AF Umegaki, H Chernak, JM Ikari, H Roth, GS Ingram, DK TI Rotational behavior produced by adenovirus-mediated gene transfer of dopamine D-2 receptor into rat striatum SO NEUROREPORT LA English DT Article DE ageing; gene therapy; Huntington's disease; motor performance; neurotransmitter receptor; Parkinson's disease; sulpride ID EXPRESSING TYROSINE-HYDROXYLASE; VIRUS VECTORS; PARKINSONS-DISEASE; TURNING BEHAVIOR; BRAIN; PROTECTS; THERAPY; SYSTEM AB WE investigated the expression and functionality of a previously developed adenoviral vector carrying the rat cDNA for the dopamine D-2 receptor (D2R), AdCMV.DopD(2)R Comparative analysis of the autoradiographic images from the striatum injected with AdCMV.DopD(2)R and the contralateral striatum injected with a control vector, AdCMV.Null, in male rats indicated that D2R binding was increased by 40-60% on days 3 and 5 after injection, but then declined to baseline levels by day 21. When injected with apomorphine on days 3 and 7 after vector injection, experimental groups that had received unilateral striatal injections of AdCMV.DopD(2)R exhibited a distinct and significant laterality in rotational behavior. These results provide the first demonstration of an adenovirally mediated, intracerebral delivery of a functional neurotransmitter receptor. C1 NIA,MOL PHYSIOL & GENET SECT,NATHAN W SHOCK LABS,GERONTOL RES CTR,NIH,BALTIMORE,MD 21224. NAGOYA UNIV,SCH MED,DEPT GERIATR,NAGOYA,AICHI 466,JAPAN. NR 33 TC 21 Z9 21 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD NOV 10 PY 1997 VL 8 IS 16 BP 3553 EP 3558 DI 10.1097/00001756-199711100-00027 PG 6 WC Neurosciences SC Neurosciences & Neurology GA YF197 UT WOS:A1997YF19700032 PM 9427325 ER PT J AU Kimberg, DY DEsposito, M Farah, MJ AF Kimberg, DY DEsposito, M Farah, MJ TI Effects of bromocriptine on human subjects depend on working memory capacity SO NEUROREPORT LA English DT Article DE bromocriptine; dopamine; prefrontal cortex; working memory ID FRONTAL-LOBE LESIONS; INDIVIDUAL-DIFFERENCES; PREFRONTAL CORTEX; BEHAVIOR; MODEL AB PHARMACOLOGICAL manipulation of brain dopamine concentration affects visuospatial working memory in humans and in animals, the latter effects localized to the prefrontal cortex. However, the effects of dopamine agonists on humans are poorly understood. We hypothesized that bromocriptine would have an effect on cognitive functions associated with the prefrontal cortex via its effects on cortical dopamine receptors and on subcortical receptors in areas that project to the neocortex. We found that the effect of bromocriptine on young normal subjects depended on the subjects' working memory capacity. High-capacity subjects performed more poorly on the drug, while low-capacity subjects improved. These results demonstrate an empirical link between a dopamine-mediated working memory system and higher cognitive function in humans. C1 NINCDS,COGNIT NEUROSCI SECT,NIH,PHILADELPHIA,PA 19104. HOSP UNIV PENN,DEPT NEUROL,PHILADELPHIA,PA 19104. HOSP UNIV PENN,DEPT PSYCHOL,PHILADELPHIA,PA 19104. RI Kimberg, Daniel/D-1164-2009 FU NIA NIH HHS [AG13483]; NINDS NIH HHS [NS01762] NR 19 TC 265 Z9 265 U1 3 U2 11 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD NOV 10 PY 1997 VL 8 IS 16 BP 3581 EP 3585 DI 10.1097/00001756-199711100-00032 PG 5 WC Neurosciences SC Neurosciences & Neurology GA YF197 UT WOS:A1997YF19700037 PM 9427330 ER PT J AU Rajeswaran, WG Cohen, LA AF Rajeswaran, WG Cohen, LA TI A convenient method of protecting oxindoles SO TETRAHEDRON LETTERS LA English DT Article AB The nitrogens of oxindoles and indole were protected by dichloroacetyl group in refluxing DCE. The deprotection of these protected oxindoles and indole has been carried out under basic condition using triethylamine. (C) 1997 Elsevier Science Ltd. C1 NIDDK,BIOORGAN CHEM LAB,NIH,BETHESDA,MD 20892. NR 7 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 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD NOV 10 PY 1997 VL 38 IS 45 BP 7813 EP 7814 DI 10.1016/S0040-4039(97)10090-9 PG 2 WC Chemistry, Organic SC Chemistry GA YE895 UT WOS:A1997YE89500001 ER PT J AU Jaworski, C Sperbeck, S Graham, C Wistow, G AF Jaworski, C Sperbeck, S Graham, C Wistow, G TI Alternative splicing of Pax6 in bovine eye and evolutionary conservation of intron sequences SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID HOMEOBOX-CONTAINING GENE; PAIRED DOMAIN; CRYSTALLIN GENE; EYELESS GENE; EXPRESSION; LENS; DNA; MUTATIONS; ANIRIDIA; DROSOPHILA AB Pax-g is essential for eye development and for tissue-specific gene expression within the eye. Splicing of an alternative exon (5a) leads to variant DNA binding specificity in Pax6. Here we show that in the mature bovine eye the relative abundance of the alternative Pax6-5a mRNA varies markedly, particularly between the lens and iris. Additional alternative splicing products were identified which may lead to ''domain swapping'' or truncation of Pax6 proteins. Comparison of amphibian (Xenopus) and mammalian (bovine) Pax-6 genes revealed highly conserved intronic sequences flanking exon 5a, including potential lariat sites which may have a role in the mechanism of alternative splicing. (C) 1997 Academic Press. RP Jaworski, C (reprint author), NEI,SECT MOL STRUCT & FUNCT,NIH,BETHESDA,MD 20892, USA. NR 30 TC 46 Z9 46 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 NOV 7 PY 1997 VL 240 IS 1 BP 196 EP 202 DI 10.1006/bbrc.1997.7623 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA YG933 UT WOS:A1997YG93300039 PM 9367909 ER PT J AU Wu, C AF Wu, C TI Chromatin remodeling and the control of gene expression SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID YEAST SWI/SNF COMPLEX; PUTATIVE TRANSCRIPTIONAL ADAPTER; DNA-BINDING PROPERTIES; CELL-FREE SYSTEM; SACCHAROMYCES-CEREVISIAE; HISTONE ACETYLATION; NUCLEOSOME DISRUPTION; IN-VITRO; MULTISUBUNIT COMPLEX; AMINO-TERMINUS RP Wu, C (reprint author), NCI,MOL CELL BIOL LAB,NIH,BLDG 37,RM 5E-26,BETHESDA,MD 20892, USA. NR 110 TC 174 Z9 178 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 NOV 7 PY 1997 VL 272 IS 45 BP 28171 EP 28174 DI 10.1074/jbc.272.45.28171 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900001 PM 9353261 ER PT J AU Lachowicz, A VanGoor, P Katzur, AC Bonhomme, G Stojilkovic, SS AF Lachowicz, A VanGoor, P Katzur, AC Bonhomme, G Stojilkovic, SS TI Uncoupling of calcium mobilization and entry pathways in endothelin-stimulated pituitary lactotrophs SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID THYROTROPIN-RELEASING-HORMONE; FREE CA-2+ CONCENTRATIONS; RAT ANTERIOR-PITUITARY; PROLACTIN SECRETION; INOSITOL PHOSPHATE; NONEXCITABLE CELLS; INDUCED SPIKE; AR42J CELLS; CA2+ ENTRY; OSCILLATIONS AB In cells expressing Ca2+-mobilizing receptors, InsP(3)- induced Ca2+ release from intracellular stores is commonly associated with extracellular Ca2+ influx. Operation of these two Ca2+ signaling pathways mediates thyrotropin-releasing hormone (TRH) and angiotensin II (AII)-induced prolactin secretion from rat pituitary lactotrophs. After an initial hyperpolarization induced by Ca2+ mobilization from the endoplasmic reticulum (ER), these agonists generated an increase in the steady-state firing of action potentials, further facilitating extracellular Ca2+ influx and prolactin release. Like TRH and AII, endothelin-l (ET-1) also induced a rapid release of Ca2+ from the ER and a concomitant spike prolactin secretion during the first 3-5 min of stimulation, However, unlike TRH and AII actions, Ca2+ mobilization was not coupled to Ca2+ influx during sustained ET-1 stimulation, as ET-1 induced a long-lasting abolition of action potential firing, This lead to a depletion of the ER Ca2+ pool, a prolonged decrease in [Ca2+](i), and sustained inhibition of prolactin release. ET-l-induced inhibition and TRH/AII-induced stimulation of Ca2+ influx and hormone secretion were reduced in the presence of the L-type Ca2+ channel blocker, nifedipine, Basal [Ca2+](i) and prolactin release were also reduced in the presence of nifedipine. Furthermore, TRH-induced Ca2+ influx and secretion were abolished by ET-1, as TRH was unable to reactivate Ca2+ influx and prolactin release in ET-l-stimulated cells. Depolarization of the cells during sustained inhibitory action of ET-1, however, increased [Ca2+](i) and prolactin release, These results indicate that L-type Ca2+ channel represents a common Ca2+ influx pathway that controls basal [Ca2+](i) and secretion and is regulated by TRH/AII and ET-1 in an opposite manner, Thus, the receptor-mediated uncoupling of Ca2+ entry from Ca2+ mobilization provides an effective control mechanism in terminating the stimulatory action of ET-1. Moreover, it makes electrically active lactotrophs quiescent and unresponsive to other calcium-mobilizing agonists. C1 NICHHD,ERBB,UCS,NIH,BETHESDA,MD 20892. NR 47 TC 18 Z9 18 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 NOV 7 PY 1997 VL 272 IS 45 BP 28308 EP 28314 DI 10.1074/jbc.272.45.28308 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900026 PM 9353286 ER PT J AU Vito, P Ghayur, T DAdamio, L AF Vito, P Ghayur, T DAdamio, L TI Generation of anti-apoptotic presenilin-2 polypeptides by alternative transcription, proteolysis, and caspase-3 cleavage SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FAMILIAL ALZHEIMERS-DISEASE; T-CELL HYBRIDOMAS; MISSENSE MUTATIONS; ICE/CED-3 PROTEASE; DEATH; ACTIVATION; GENE; APOPAIN/CPP32; REQUIREMENT; ALG-3 AB PS2, the chromosome 1 familial Alzheimer's disease gene, has been shown to be involved in programmed cell death by three complementary experimental approaches, Reduction of PS2 protein levels by antisense RNA protects from apoptosis, whereas overexpression of an Alzheimer's PS2 mutant increases cell death induced by several stimuli, In addition, ALG-3, a truncated PS2 cDNA, encodes an artificial COOH-terminal PS2 segment that dominantly inhibits apoptosis, Here we describe a physiological COOH-terminal PS2 polypeptide (PS2s, Met(298)-Ile(448)) generated by both an alternative PS2 transcript and proteolytic cleavage, We find that PS2s protects transfected cells from Fas-and tumor necrosis factor alpha (TNF alpha)-induced apoptosis, Furthermore, a similar anti-apoptotic COOH-terminal PS2 polypeptide (PS2Ccas) is generated by caspase-3 cleavage at Asp(329). These results suggest that caspase-3 not only activates pro-apoptotic substrates but also generates a negative feedback signal in which PS2Ccas antagonizes the progression of cell death. Thus, whereas PS2 is required for apoptosis, PS2s and PS2Ccas oppose this process, and the balance between PS2 and these COOH-terminal fragments may dictate the cell fate. C1 NIAID,T CELL MOL BIOL UNIT,CELLULAR & MOL IMMUNOL LAB,NIH,BETHESDA,MD 20892. 3 BASF RES CORP,WORCESTER,MA 01605. NR 33 TC 100 Z9 101 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 NOV 7 PY 1997 VL 272 IS 45 BP 28315 EP 28320 DI 10.1074/jbc.272.45.28315 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900027 PM 9353287 ER PT J AU Choi, YH Lee, SJ Nguyen, P Jang, JS Lee, J Wu, ML Takano, E Maki, M Henkart, PA Trepel, JB AF Choi, YH Lee, SJ Nguyen, P Jang, JS Lee, J Wu, ML Takano, E Maki, M Henkart, PA Trepel, JB TI Regulation of cyclin D1 by calpain protease SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RETINOBLASTOMA FAMILY PROTEINS; ACTIVATED NEUTRAL PROTEASE; PROGRAMMED CELL-DEATH; INHIBITOR P27; G1 PHASE; DEGRADATION; PATHWAY; G(1); PROGRESSION; TRANSITION AB Cyclin D1, a critical positive regulator of G(1) progression, has been implicated in the pathogenesis of certain cancers. Regulation of cyclin D1 occurs at the transcriptional and posttranscriptional level. Here we present evidence that cyclin D1 levels are regulated at the posttranscriptional level by the Ca2+-activated protease calpain. Serum starvation of NIH 3T3 cells resulted in rapid loss of cyclin D1 protein that was completely reversible by calpain inhibitors. Actinomycin D and lovastatin induced rapid loss of cyclin D1 in prostate and breast cancer cells that was reversible by calpain inhibitors and not by phenylmethylsulfonyl fluoride, caspase inhibitors, or lactacystin, a specific inhibitor of the 26 S proteasome. Treatment of intact NIH 3T3, prostate, and breast cancer cells with a calpain inhibitor dramatically increased the half-life of cyclin D1 protein, Addition of purified calpain to PC-3-M lysates resulted in Ca2+-dependent cyclin D1 degradation. Transient expression of the calpain inhibitor calpastatin increased cyclin D1 protein in serum-starved NIR 3T3 cells. Cyclins A, E, and El have been reported to be regulated by proteasome-associated proteolysis. The data presented here implicate calpain in cyclin D1 posttranslational regulation. C1 NCI,MED BRANCH,DIV CLIN SCI,NIH,BETHESDA,MD 20892. NCI,DIV BASIC SCI,EXPT IMMUNOL BRANCH,NIH,BETHESDA,MD 20892. NATL KYOTO HOSP,KYOTO 612,JAPAN. NAGOYA UNIV,NAGOYA,AICHI 46401,JAPAN. NR 61 TC 142 Z9 143 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 NOV 7 PY 1997 VL 272 IS 45 BP 28479 EP 28484 DI 10.1074/jbc.272.45.28479 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900048 PM 9353308 ER PT J AU Bhagwat, M Hobbs, LJ Nossal, NG AF Bhagwat, M Hobbs, LJ Nossal, NG TI The 5'-exonuclease activity of bacteriophage T4 RNase H is stimulated by the T4 gene 32 single-stranded DNA-binding protein, but its flap endonuclease is inhibited SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID POLYMERASE-I; REPLICATION; EXONUCLEASE; CLEAVAGE; 3'-EXONUCLEASE; ENCODES; PRIMERS; FAMILY; FEN-1; A737V AB Bacteriophage T4 RNase H is a 5'- to 3'-nuclease that has exonuclease activity on RNA DNA and DNA DNA duplexes and can remove the pentamer RNA primers made by the T4 primase-helicase (Hollingsworth, H, C., and Nossal, N. G. (1991) J. Biol. Chem. 266, 1888-1897; Hobbs, L. J., and Nossal, N. G. (1996) J. Bacteriol. 178, 6772-6777). Here we show that this exonuclease degrades du plex DNA nonprocessively, releasing a single oligonucleotide (nucleotides 1-4) with each interaction with the substrate, Degradation continues nonprocessively until the enzyme stops 8-11 nucleotides from the 3'-end of the substrate, T4 gene 32 single-stranded DNA-binding protein strongly stimulates the exonuclease activity of T4 RNase H, converting it into a processive nuclease that removes multiple short oligonucleotides with a combined length of 10-50 nucleotides each time it binds to the duplex substrate, 32 protein must bind on single-stranded DNA behind T4 RNase H for processive degradation, T4 RNase H also has a flap endonuclease activity that cuts preferentially on either side of the junction between single-and double-stranded DNA in flap and fork DNA structures, In contrast to the exonuclease, the endonuclease is inhibited completely by 32 protein binding to the single strand of the flap substrate, These results suggest an important role for T4 32 protein in controlling T4 RNase II degradation of RNA primers and adjacent DNA during each lagging strand cycle. C1 NIDDK,MOL & CELLULAR BIOL LAB,NIH,BETHESDA,MD 20892. NR 28 TC 21 Z9 21 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 7 PY 1997 VL 272 IS 45 BP 28523 EP 28530 DI 10.1074/jbc.272.45.28523 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900054 PM 9353314 ER PT J AU Bhagwat, M Meara, D Nossal, NG AF Bhagwat, M Meara, D Nossal, NG TI Identification of residues of T4 RNase H required for catalysis and DNA binding SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ESCHERICHIA-COLI; POLYMERASE-I; ENDONUCLEASE; REPLICATION; EXONUCLEASE; MUTAGENESIS; SUBSTRATE; PROTEINS; CLEAVAGE; INVITRO AB Bacteriophage T4 RNase H, which removes the RNA primers that initiate lagging strand fragments, has a 5'-to 3'-exonuclease activity on DNA DNA and RNA DNA duplexes and an endonuclease activity on flap or forked DNA structures (Bhagwat, M., Hobbs, L. J., and Nossal, N. J. (1997) J. Biol. Chem. 272, 28523-28530). It is a member of the RAD2 family of prokaryotic and eukaryotic replication and repair nucleases, The crystal structure of T4 RNase H, in the absence of DNA, shows two Mg2+ ions coordinated to the amino acids highly conserved in this family, It also shows a disordered region proposed to be involved in DNA binding (Mueser, T. C., Nossal, N. G., and Hyde, C. C. Cell (1996) 85, 1101-1112). To identify the amino acids essential for catalysis and DNA binding, we have constructed and characterized three kinds of T4 RNase H mutant proteins based on the possible roles of the amino acid residues: mutants of acidic residues coordinated to each of the two Mg2+ ions (Mg2+ - 1: D19N, D71N, D132N, and D155N; and Mg2+ - 2: D157N and D200N); mutants of conserved basic residues in or near the disordered region (K87A and R90A); and mutants of residues with hydroxyl side chains involved in the hydrogen bonding network (Y86F and S153A), Our studies show that Mg2+- 1 and the residues surrounding it are important for catalysis and that Lys(87) is necessary for DNA binding. C1 NIDDK,MOL & CELLULAR BIOL LAB,NIH,BETHESDA,MD 20892. NR 29 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 NOV 7 PY 1997 VL 272 IS 45 BP 28531 EP 28538 DI 10.1074/jbc.272.45.28531 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900055 PM 9353315 ER PT J AU Glover, CJ Hartman, KD Felsted, RL AF Glover, CJ Hartman, KD Felsted, RL TI Human N-myristoyltransferase amino-terminal domain involved in targeting the enzyme to the ribosomal subcellular fraction SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN MYRISTOYL-COA; DEPENDENT PROTEIN-KINASE; SACCHAROMYCES-CEREVISIAE; ESCHERICHIA-COLI; BOVINE BRAIN; GENE-PRODUCT; RNA-BINDING; SUBSTRATE-SPECIFICITY; TRANSFERASE-ACTIVITY; CANDIDA-ALBICANS AB N-Myristoyltransferase (NMT) catalyzes the cotranslational acylation with myristic acid of the NH2-terminal glycines of a number of cellular and viral proteins. Most of the in vitro NMT activity (60-85%) in isoosmotic cell homogenates of human lymphoblastic leukemia (i.e. CEM and MOLT-4) and cervical carcinoma (i.e. HeLa) cells was shown to be associated with the ribosomal subcellular fractions by differential centrifugation. Also found in the ribosomal fractions was a approximate to 60-kDa protein that was specifically immunoblotted with an anti-human NMT (hNMT) peptide antibody. This approximate to 60-kDa protein was stable in the presence of proteolytic enzyme inhibitors but was gradually converted into a approximate to 46-kDa species when stored in the absence of protease inhibitors. Sucrose density gradient centrifugation of the ribosomal fraction resulted in the hNMT activity sedimenting exactly coincident with the 260 nm absorption profile and exhibiting A(260)/A(260) absorption ratios >1.8, indicating an association of NMT with putative ribosomal particle (s)/subunit(s), The subcellular targeting of hNMT was also examined by immunoblotting subcellular fractions from HeLa cells transfected with plasmids containing FLAG epitope-tagged hNMT inserts corresponding either to the originally assigned hNMT gene or to an alternative open reading frame initiated from an in-frame start site upstream from the assumed hNMT start site. Anti-FLAG immunoblotting of cells transfected with a plasmid containing the larger insert revealed FLAG-NMT primarily in the ribosomal fraction with an apparent molecular mass similar to the approximate to 60-kDa native hNMT. In contrast, immunoblotting of cells transfected with a plasmid containing the smaller insert identified a approximate to 50-kDa FLAG-NMT predominantly in the cytosolic fraction. An analysis of mixtures of CEM ribosomes and serial dilutions of purified recombinant FLAG-NMTs demonstrated that the approximate to 60-kDa FLAG-NMT binds ribosomes with higher affinity than the approximate to 50-kDa FLAG-NMT. These in vivo and-in vitro subcellular targeting and recombinant expression experiments identify a native hNMT that is 10-12 kDa larger than the enzyme predicted by the originally assigned hNMT gene and which is apparently translated from an alternative up stream start site. The data also indicate that although the unique NH2-terminal residues encoded by this larger open reading frame are not required for in vitro catalytic activity, they do provide signal(s) involved in targeting hNMT to the ribosomal subcellular fraction where cotranslational N-myristoylation occurs. RP Glover, CJ (reprint author), NCI,PHARMACOL & EXPT THERAPEUT SECT,NIH,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,FREDERICK,MD 21702, USA. NR 78 TC 65 Z9 67 U1 2 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 NOV 7 PY 1997 VL 272 IS 45 BP 28680 EP 28689 DI 10.1074/jbc.272.45.28680 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900076 PM 9353336 ER PT J AU Yasui, H Butscher, W Cohen, M Spriggs, N Wersto, R Kohn, EC Liotta, L Gardner, K AF Yasui, H Butscher, W Cohen, M Spriggs, N Wersto, R Kohn, EC Liotta, L Gardner, K TI Selective inhibition of mitogen-induced transactivation of the HIV long terminal repeat by carboxyamidotriazole - Calcium influx blockade represses HIV-1 transcriptional activation SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; NF-KAPPA-B; CELL ANTIGEN RECEPTOR; LYMPHOCYTE-T ACTIVATION; DNA-BINDING ACTIVITY; SIGNAL-TRANSDUCTION; CYCLOSPORINE-A; C-REL; MOLECULAR-BIOLOGY; GENE-EXPRESSION AB Carboxyamidotriazole (CAI) is a calcium influx inhibitor that has both antiproliferative and antimetastatic activities, Pretreatment of human T-cells with micromolar concentrations of CAI causes a near complete inhibition of calcium-regulated mitogen-induced transcription from the human immunodeficiency virus (HIV) long terminal repeat (LTR). This inhibition is selective since other mitogen-activated gene regulatory elements, such as the 12-O-tetradecanoylphorbol-13-acetate response element, are not influenced by the drug, HIV LTR transcription inhibition is maximal at 1.0 mu M CAI, requires a pretreatment interval of at least 8 h for optimum inhibition, and shows no acute interference with the growth properties of the cells, Moreover, the inhibition is rapidly reversible upon removal of the drug from the medium, Studies to identify enhancer elements within the HIV LTR that are functionally sensitive to low-dose long-term pretreatment with CAI, indicate that the NF-kappa B-binding sites are among the major targets of drug action, In vitro DNA binding studies with nuclear extracts prepared from mitogen-induced T-cells stimulated in the presence of CAI indicate that the drug differentially influences the calcium-regulated downstream signal transduction pathways necessary for specific NF-KB DNA binding activity at the two KB sites within the HIV LTR, Studies with ionomycin and thapsigargin show that repression is specific for selected modes of inducible calcium entry and indicate that, in T-cells, a major mechanism of CAI action is to modulate calcium influx at a level that is proximal to the regulated release of calcium from intracellular stores, Measurement of calcium influx in CAI-treated cells reveals a dramatic and reversible inhibition of mitogen-induced calcium influx. These results indicate that CAI can be an important and effective pharmacological tool for analysis of the calcium-dependent modulation of HIV LTR transcription. C1 NCI,DEPT PATHOL,PATHOL LAB,NIH,BETHESDA,MD 20892. NR 57 TC 10 Z9 10 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 NOV 7 PY 1997 VL 272 IS 45 BP 28762 EP 28770 DI 10.1074/jbc.272.45.28762 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900087 PM 9353347 ER PT J AU Acs, P Wang, QMJ Bogi, K Marquez, AM Lorenzo, PS Biro, T Szallasi, Z Mushinski, JF Blumberg, PM AF Acs, P Wang, QMJ Bogi, K Marquez, AM Lorenzo, PS Biro, T Szallasi, Z Mushinski, JF Blumberg, PM TI Both the catalytic and regulatory domains of protein kinase C chimeras modulate the proliferative properties of NIH 3T3 cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HIGH-AFFINITY RECEPTOR; SIGNAL-TRANSDUCTION; PHORBOL ESTER; TYROSINE PHOSPHORYLATION; RAT FIBROBLASTS; PKC-DELTA; BETA-II; ALPHA; EPSILON; EXPRESSION AB Protein kinase C (PKC) isozymes exhibit important differences in terms of their regulation and biological functions, Not only may some PKC isoforms be active and others not for a given response, but the actions of different isoforms may even be antagonistic, In NIH 3T3 cells, for example, PKC delta arrests cell growth whereas PKC epsilon stimulates it, To probe the contribution of the regulatory and the catalytic domains of PKC isozymes to isozyme-specific responses, we prepared chimeras between the regulatory and the catalytic domains of PKC alpha, -delta, and -epsilon. These chimeras, which preserve the overall structure of the native PKC enzymes, were stably expressed in mouse fibroblasts. A major objective was to characterize the growth properties of the cells that overexpress the various PKC constructs. Our data demonstrate that both the regulatory and the catalytic domains play roles in cell proliferation, The regulatory domain of PKC epsilon enhanced cell growth in the absence or presence of phorbol 12-myristate 13-acetate (PMA), and, in the presence of PMA, all chimeras with the PKC epsilon regulatory domain also gave rise to colonies in soft agar; the role of the catalytic domain of PKC epsilon was evident in the PMA-treated cells that overexpressed the PKC chimera containing the delta regulatory and the epsilon catalytic domains (PKC delta/epsilon). The important contribution of the PKC epsilon catalytic domain to the growth of PKC delta/epsilon-expressing cells was also evident in terms of a significantly increased saturation density in the presence of PMA, their formation of foci upon PMA treatment, and the induction of anchorage-independent growth. Aside from the growth-promoting effect of PKC epsilon, we have shown that most chimeras with PKC alpha and -delta regulatory domains inhibit cell growth. These results underscore the complex contributions of the regulatory and catalytic domains to the overall behavior of PKC. C1 NCI,MOL MECH TUMOR PROMOT SECT,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,NIH,BETHESDA,MD 20892. NCI,GENET LAB,NIH,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT PHARMACOL,BETHESDA,MD 20814. RI Wang, Qiming/B-6064-2012 NR 42 TC 45 Z9 45 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 NOV 7 PY 1997 VL 272 IS 45 BP 28793 EP 28799 DI 10.1074/jbc.272.45.28793 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF219 UT WOS:A1997YF21900091 PM 9353351 ER PT J AU Tait, BD Hagen, S Domagala, J Ellsworth, EL Gajda, C Hamilton, HW Prasad, JVNV Ferguson, D Graham, N Hupe, D Nouhan, C Tummino, PJ Humblet, C Lunney, EA Pavlovsky, A Rubin, J Gracheck, SJ Baldwin, ET Bhat, TN Erickson, JW Gulnik, SV Liu, BS AF Tait, BD Hagen, S Domagala, J Ellsworth, EL Gajda, C Hamilton, HW Prasad, JVNV Ferguson, D Graham, N Hupe, D Nouhan, C Tummino, PJ Humblet, C Lunney, EA Pavlovsky, A Rubin, J Gracheck, SJ Baldwin, ET Bhat, TN Erickson, JW Gulnik, SV Liu, BS TI 4-hydroxy-5,6-dihydropyrones .2. Potent non-peptide inhibitors of HIV protease SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID STRUCTURE-BASED DESIGN; IMMUNODEFICIENCY-VIRUS PROTEASE; NONPEPTIDIC INHIBITORS; 5,6-DIHYDRO-4-HYDROXY-2-PYRONES; BINDING; MODE AB The 4-hydroxy-5,6-dihydropyrone template was utilized as a flexible scaffolding from which to build potent active site inhibitors of HIV protease. Dihydropyrone Ic (5,6-dihydro-4-hydroxy-6-phenyl-3-[(2-phenylethyl)thio]-2H-pyran-2-one) was modeled in the active site of HIV protease utilizing a similar binding mode found for the previously reported 4-hydroxybenzopyran-2-ones. Our model led us to pursue the synthesis of 6,6-disubstituted dihydropyrones with the aim of filling S-1 and S-2 and thereby increasing the potency of the parent dihydropyrone Ic which did not fill S-2. Toward this end we attached various hydrophobic and hydrophilic side chains at the 6-position of the dihydropyrone to mimic the natural and unnatural amino acids known to be effective substrates at P-2 and P-2'. Parent dihydropyrone Ic (IC50 = 2100 nM) was elaborated into compounds with greater than a 100-fold increase in potency [18c, IC50 = 5 nM, 5-(3,6-dihydroxy-6-hydroxy-6-oxo-2-phenyl-5-[2-phenylethyl)thio]-2H-pyran-2-yl)pentanoic acid and 12c, IC50 = 51 nM, 5,6-dihydro-4-hydroxy-6-phenyl-6-(2-phenylethyl)thio]-2H-pyran-2-one]. Optimization of the 3-position fragment to fill S-1' and S-2' afforded potent HIV protease inhibitor 49 [IC50 = 10 nM, 3-[(2-tert-butyl-5-methylphenyl)sulfanyl]-5,6-dihydro-4-hydroxy-6-phenyl-6-(2-phenylethyl)-2H-pyran-2-one]. The resulting low molecular weight compounds (<475) have one or no chiral centers and are readily synthesized. C1 WARNER LAMBERT PARKE DAVIS,PARKE DAVIS PHARMACEUT RES DIV,DEPT BIOCHEM,ANN ARBOR,MI 48105. WARNER LAMBERT PARKE DAVIS,PARKE DAVIS PHARMACEUT RES DIV,DEPT BIOMOL STRUCT & DRUG DESIGN,ANN ARBOR,MI 48105. NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PRI,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702. RP Tait, BD (reprint author), WARNER LAMBERT PARKE DAVIS,PARKE DAVIS PHARMACEUT RES DIV,DEPT CHEM,2800 PLYMOUTH RD,ANN ARBOR,MI 48105, USA. NR 36 TC 58 Z9 59 U1 1 U2 8 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 NOV 7 PY 1997 VL 40 IS 23 BP 3781 EP 3792 DI 10.1021/jm970615f PG 12 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA YF149 UT WOS:A1997YF14900012 PM 9371244 ER PT J AU Critchlow, SE ODea, MH Howells, AJ Couturier, M Gellert, M Maxwell, A AF Critchlow, SE ODea, MH Howells, AJ Couturier, M Gellert, M Maxwell, A TI The interaction of the F plasmid killer protein, CcdB, with DNA gyrase: Induction of DNA cleavage and blocking of transcription SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE supercoiling; quinolone; RNA polymerase; topoisomerase ID SEX FACTOR-F; ESCHERICHIA-COLI; A-PROTEIN; B-PROTEIN; LETD CCDB; TOPOISOMERASE POISONS; QUINOLONE DRUGS; NALIDIXIC-ACID; CELL-DIVISION; HOST-CELL AB We have studied the interaction of the F plasmid killer protein CcdB with its intracellular target DNA gyrase. We confirm that CcdB fan induce DNA cleavage by gyrase anti show that this cleavage reaction requires ATP hydrolysis when the substrate is linear DNA, but is independent of hydrolysis when negatively supercoiled DNA is used. The 64 kDa domain of the gyrase A protein, which can catalyse DNA cleavage in the presence of the B protein and quinolone drugs, is unable to cleave DNA in the presence of CcdB unless the C-terminal 33 kDa domain of the gyrase A protein is also present. CcdB-induced DNA cleavage by gyrase requires a minimum length of DNA (> similar to 160 bp), whereas in the presence of quinolone drugs gyrase can cleave much shorter DNA molecules. We show that CcdB, Like quinolones, can form a complex with gyrase which can block transcription by RNA polymerase. A model for the interaction of CcdB with gyrase involving the trapping of a post-strand-passage intermediate is suggested. We conclude that CcdB can stabilise a cleavage complex between DNA gyrase and DNA in a manner distinct from quinolones but, like the quinolone-induced cleavage complex, the CcdB-stabilised complex can also form a barrier to the passage of polymerases. (C) 1997 Academic Press Limited. C1 UNIV LEICESTER,DEPT BIOCHEM,LEICESTER LE1 7RH,LEICS,ENGLAND. NIDDK,MOL BIOL LAB,NIH,BETHESDA,MD 20892. FREE UNIV BRUSSELS,DEPT BIOL MOL,LAB GENET PROCARYOTES,B-1640 RHODE ST GENESE,BELGIUM. FU Wellcome Trust NR 59 TC 58 Z9 58 U1 0 U2 5 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 NOV 7 PY 1997 VL 273 IS 4 BP 826 EP 839 DI 10.1006/jmbi.1997.1357 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YH129 UT WOS:A1997YH12900007 PM 9367775 ER PT J AU Johnston, NL Cerevnak, J Shore, AD Torrey, EF Yolken, RH AF Johnston, NL Cerevnak, J Shore, AD Torrey, EF Yolken, RH TI Multivariate analysis of RNA levels from postmortem human brains as measured by three different methods of RT-PCR SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE postmortem human brain; pH; RNA; RT-PCR; psychiatric disorders; glyceraldehyde phosphate dehydrogenase ID HUNTINGTONS-DISEASE; AGONAL STATE; POST-MORTEM; STABILITY; TISSUE; PREMORTEM; RAT; PH AB The analysis of RNA from postmortem human brain tissue by reverse transcription-polymerase chain reaction (RT-PCR) provides a practical method to measure both normal and abnormal brain gene expression. A major limitation in using human material is that yields can vary dramatically from individual to individual, making comparisons between samples difficult. In this report, we study the association of pH and several pre-and postmortem factors on the RNA yields from 89 postmortem human occipital cortices. Glyceraldehyde phosphate dehydrogenase (GAPdH) mRNA levels were measured by RT-PCR. A major variant in this method is the priming used in the reverse transcription reaction. Three different methods of reverse transcription were performed and the resultant levels of products compared against the pre-and postmortem factors and pH. The levels of GAPdH correlated significantly to pH and pH itself to the rapidity of death (RoD) (agonal state) indicating that premortem factors may play the greatest role in determining postmortem RNA levels. The three methods of priming showed different sensitivities, most notably that oligo dT priming alone is vulnerable to long freezer intervals (FI). We conclude that premortem factors are the major affectors of RNA levels variations and that the polyA tail region of the molecule appears to be adversely affected by extended freezer storage. (C) 1997 Elsevier Science B.V. C1 JOHNS HOPKINS UNIV,DEPT PEDIAT,STANLEY FDN NEUROVIROL LAB,BALTIMORE,MD 21287. NIMH,ST ELIZABETHS HOSP,WASHINGTON,DC 20032. JOHNS HOPKINS UNIV,JOHNS HOPKINS SCH HYG & PUBL HLTH,HLTH SERV RES & DEV CTR,BALTIMORE,MD 21287. NR 23 TC 109 Z9 114 U1 1 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 J9 J NEUROSCI METH JI J. Neurosci. Methods PD NOV 7 PY 1997 VL 77 IS 1 BP 83 EP 92 DI 10.1016/S0165-0270(97)00115-5 PG 10 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA YH551 UT WOS:A1997YH55100011 PM 9402561 ER PT J AU Duncan, WC Johnson, KA Wehr, TA AF Duncan, WC Johnson, KA Wehr, TA TI Increase of 5HT and VIP immunoreactivity within the hamster (Mesocricetus auratus) SCN during chronic MAOI treatment SO NEUROSCIENCE LETTERS LA English DT Article DE serotonin; vasoactive intestinal peptide; monoamine oxidase inhibitor; suprachiasmatic nucleus ID VASOACTIVE INTESTINAL POLYPEPTIDE; RAT SUPRACHIASMATIC NUCLEUS; CHRONIC CLORGYLINE TREATMENT; CIRCADIAN-RHYTHMS; SYRIAN-HAMSTERS; NEUROPEPTIDE-Y; SEROTONIN; LIGHT; PEPTIDE; NEURONS AB The effects of chronic treatment with the monoamine oxidase inhibitor (MAOI), clorgyline (CLG;2 mg/kg per day) on serotonin (5HT) and vasoactive intestinal peptide (VIP) immunoreactivity (IR) within the hamster suprachiasmatic nucleus (SCN) were examined. Optical densities of 5HT IR and VIP IR were increased by MAOI treatment. VIP IR was increased in both the ventrolateral and dorsal regions of the SCN, suggesting that VIP content was increased within both perikarya and terminals of VIP neurons. The results suggest that previously described effects of MAOIs on the mammalian circadian system may be mediated in part, by their effects on serotonergic input to VIP neurons within the SCN. (C) 1997 Elsevier Science Ireland Ltd. RP Duncan, WC (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,NIH,BETHESDA,MD 20892, USA. NR 24 TC 3 Z9 3 U1 0 U2 1 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 NOV 7 PY 1997 VL 236 IS 3 BP 159 EP 162 DI 10.1016/S0304-3940(97)00787-8 PG 4 WC Neurosciences SC Neurosciences & Neurology GA YH841 UT WOS:A1997YH84100010 PM 9406761 ER PT J AU Torrey, EF Miller, J Rawlings, R Yolken, RH AF Torrey, EF Miller, J Rawlings, R Yolken, RH TI Seasonality of births in schizophrenia and bipolar disorder: a review of the literature SO SCHIZOPHRENIA RESEARCH LA English DT Review DE seasonality; schizophrenia; bipolar disorder ID HIGH-RISK SAMPLE; SOUTHERN-HEMISPHERE; FAMILY HISTORY; MENTAL DISORDER; WINTER-BORN; PSYCHIATRIC-PATIENTS; VENTRICULAR ENLARGEMENT; ABNORMAL SEASONALITY; INFECTIOUS-DISEASES; GENERAL POPULATION AB More than 250 studies, covering 29 Northern and five Southern Hemisphere countries, have been published on the birth seasonality of individuals who develop schizophrenia and/or bipolar disorder. Despite methodological problems, the studies are remarkably consistent in showing a 5-8% winter-spring excess of births for both schizophrenia and mania/bipolar disorder. This seasonal birth excess is also found in schizoaffective disorder (December-March), major depression (March-May), and autism (March) but not in other psychiatric conditions with the possible exceptions of eating disorders and antisocial personality disorder. The seasonal birth pattern also may shift over time, Attempts to correlate the seasonal birth excess with specific features of schizophrenia suggest that winter-spring births are probably related to urban births and to a negative family history. Possible correlations include lesser severity of illness and neurophysiological measures. There appears to be no correlation with gender, social class, race, measurable pregnancy and birth complications, clinical subtypes, or neurological, neuropsychological, or neuroimaging measures. Virtually no correlation studies have been done for bipolar disorder. Regarding the cause of the birth seasonality, statistical artifact and parental procreational habits are unlikely explanations. Seasonal effects of genes, subtle pregnancy and birth complications, light and internal chemistry, toxins, nutrition, temperature/weather, and infectious agents or a combination of these are all viable possibilities. (C) 1997 Elsevier Science B.V. C1 NIAAA, CLIN STUDIES LAB, BETHESDA, MD 20892 USA. JOHNS HOPKINS UNIV, MED CTR, STANLEY FDN, NEUROVIROL LAB, BALTIMORE, MD 21205 USA. RP Torrey, EF (reprint author), NIMH, STANLEY FDN RES PROGRAMS, CTR NEUROSCI, ST ELIZABETHS HOSP, 2700 MARTIN LUTHER KING JR AVE SE, WASHINGTON, DC 20032 USA. NR 240 TC 391 Z9 397 U1 6 U2 41 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD NOV 7 PY 1997 VL 28 IS 1 BP 1 EP 38 DI 10.1016/S0920-9964(97)00092-3 PG 38 WC Psychiatry SC Psychiatry GA YH935 UT WOS:A1997YH93500001 PM 9428062 ER PT J AU Tjandra, N Bax, A AF Tjandra, N Bax, A TI Direct measurement of distances and angles in biomolecules by NMR in a dilute liquid crystalline medium SO SCIENCE LA English DT Article ID QUANTITATIVE J-CORRELATION; PHOSPHOLIPID MICELLES; HUMAN UBIQUITIN; PROTEINS; RELAXATION; SPECTROSCOPY; RESOLUTION AB In isotropic solution, internuclear dipolar couplings average to zero as a result of rotational diffusion. By dissolving macromolecules in a dilute aqueous nematic discotic liquid-crystalline medium containing widely spaced magnetically oriented particles, a tunable degree of solute alignment with the magnetic field can be created while retaining the high resolution and sensitivity of the regular isotropic nuclear magnetic resonance (NMR) spectrum. Dipolar couplings between H-1-H-1, H-1-C-13, H-1-N-15, and C-13-C-13 pairs in such an oriented macromolecule no longer average to zero, and are readily measured. Distances and angles derived from dipolar couplings in human ubiquitin are in excellent agreement with its crystal structure. The approach promises to improve the accuracy of structures determined by NMR, and extend the size limit. C1 NIDDKD,CHEM PHYS LAB,NIH,BETHESDA,MD 20892. RP Tjandra, N (reprint author), NHLBI,BIOPHYS CHEM LAB,NIH,BLDG 10,BETHESDA,MD 20892, USA. NR 31 TC 1286 Z9 1300 U1 11 U2 106 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD NOV 7 PY 1997 VL 278 IS 5340 BP 1111 EP 1114 DI 10.1126/science.278.5340.1111 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YE652 UT WOS:A1997YE65200048 PM 9353189 ER PT J AU Mishra, L Tully, RE Monga, SPS Yu, P Cai, T Makalowski, W Mezey, E Pavan, WJ Mishra, B AF Mishra, L Tully, RE Monga, SPS Yu, P Cai, T Makalowski, W Mezey, E Pavan, WJ Mishra, B TI Praja1, a novel gene encoding a RING-H2 motif in mouse development SO ONCOGENE LA English DT Article DE Praja1 gene; PRAJA1 protein; RING-H2 domain; molecular cloning; liver development; chromosome localization; explant cultures ID ZINC-FINGER; PROTEIN; DOMAIN; FAMILY; GRANIN AB As part of a cloning strategy to identify genes involved in early mouse liver development we have isolated Praja1, a gene with similar sequences to the Drosophila melanogaster gene goliath (gl) which is involved in the fate of mesodermal cells ultimately forming gut musculatures, fat body, and the heart, Praja1 is a 2.1 kb gene encoding a putative 396 amino acid ORF and includes a COOH-terminal RING-H2 domain, Using the Jackson Laboratory BSS panel, we have localized Praja1 on chromosome X at 36 cM, which may be a candidate gene for mouse sla (sex linked sideroblastic anemia), near the X inactivation center gene, Xist, Northern blot analysis demonstrated three transcripts (3.1, 2.6 and 2.1 kb) in mRNA from adult mouse tissues brain, liver, and kidney as well as in mRNA from developing mouse embryos (days 7, 11, 15 and 17 post coitus, p.c.). In vitro transcription/translation yielded a product with an M-r of 59 kD, Immunohistochemical staining of in vitro liver explant cultures using a heterologous antibody against praja1 demonstrated cytoplasmic staining of cuboidal cells that have hepatocyte morphology and organization, The presence of the RING-H2 domain, a proline-rich region at the COOH-end, and regions rich in acidic amino acids, leads to the hypothesis that the Praja1 product is possibly involved in mediating protein-protein interactions, possibly as part of a protein sorting or transport pathway, This is strengthened by the similarity of Praja1 to rat Neurodap1, whose product has been shown to localize to the endoplasmic reticulum and golgi in brain. C1 NATL HUMAN GENOME RES INST,LAB GENET DIS RES,CLIN GENE THERAPY BRANCH,NIH,BETHESDA,MD. NATL CTR BIOTECHNOL INFORMAT,NIH,BETHESDA,MD. JOHNS HOPKINS SCH MED,BALTIMORE,MD. RP Mishra, L (reprint author), VET ADM MED CTR,LAB DEV MOL BIOL,WASHINGTON,DC 20422, USA. RI Makalowski, Wojciech/I-2843-2016 NR 23 TC 33 Z9 34 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD NOV 6 PY 1997 VL 15 IS 19 BP 2361 EP 2368 DI 10.1038/sj.onc.1201405 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA YE157 UT WOS:A1997YE15700010 PM 9393880 ER PT J AU Kovalchuk, AL Muller, JR Janz, S AF Kovalchuk, AL Muller, JR Janz, S TI Deletional remodeling of c-myc-deregulating chromosomal translocations SO ONCOGENE LA English DT Article DE BALB/c plasmacytomas; chromosomal translocation; deregulation of c-myc; isotype switching ID IMMUNOGLOBULIN HEAVY-CHAIN; CLASS SWITCH RECOMBINATION; MURINE PLASMACYTOMA; ABERRANT REARRANGEMENT; ENHANCER ELEMENT; IGH 3'-ENHANCER; B-CELLS; REGION; LOCUS; GENE AB Evidence is presented for the existence of a novel remodeling-by-deletion mechanism that alters the fine structure of c-myc-deregulating chromosomal translocations in t(12;15)-positive BALB/c plasmacytomas. DNA sequence analysis of the t(12;15) in five primary tumors revealed the co-existence of precursor cells harboring genetic recombinations between the immunoglobulin heavy-chain mu locus (Igh mu) and c-myc with clonally related progenitors containing rearrangements between the immunoglobulin heavy-chain alpha locus (Igh alpha) and c-myc. Clonal relatedness was based upon unique junction fragments between the snitch region of Igh mu and c-myc. S mu/c-myc junctions are thus useful clonotypic markers for monitoring the conversion of Igh mu/c-myc-positive tumor precursor clones into Igh alpha/c-myc-positive plasmacytomas. Aberrant isotype switch recombination appears to be the most likely mechanism effecting this conversion event (other possibilities are discussed) which may help to explain the preferred usage of the Igh alpha locus in recombinations with c-myc in t(12;15)-positive plasma cell tumors in BALB/c mice. C1 NCI,GENET LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892. NR 44 TC 36 Z9 36 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD NOV 6 PY 1997 VL 15 IS 19 BP 2369 EP 2377 DI 10.1038/sj.onc.1201409 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA YE157 UT WOS:A1997YE15700011 PM 9393881 ER PT J AU Irvine, KR Chamberlain, RS Shulman, EP Surman, DR Rosenberg, SA Restifo, NP AF Irvine, KR Chamberlain, RS Shulman, EP Surman, DR Rosenberg, SA Restifo, NP TI Enhancing efficacy of recombinant anticancer vaccines with prime/boost regimens that use two different vectors SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID T-CELL MEMORY; ESTABLISHED PULMONARY METASTASES; FOWLPOX VIRUS; IMMUNE-RESPONSES; ANTIGEN; DNA; IMMUNIZATION; IDENTIFICATION; IMMUNOTHERAPY; ENHANCEMENT AB Background: The identification of tumor-associated antigens and the cloning of DNA sequences encoding them have enabled the development of anticancer vaccines, Such vaccines target tumors by stimulating an immune response against the antigens, One method of vaccination involves the delivery of antigen-encoding DNA sequences, and a number of recombinant vectors have been used for this purpose, To optimize the efficacy of recombinant vaccines, we compared primary and booster treatment regimens that used a single vector (i.e., homologous boosting) with regimens that used two different vectors (i.e., heterologous boosting), Methods: Pulmonary tumors (experimental metastases) were induced in BALB/c mice inoculated with CT26.CL25 murine colon carcinoma cells, which express recombinant bacterial beta-galactosidase (the model antigen). Protocols for subsequent vaccination used three vectors that encoded beta-galactosidase-vaccinia (cowpox) virus, fowlpox virus, naked bacterial plasmid DNA, Mouse survival was evaluated in conjunction with antibody and cytotoxic T-lymphocyte responses to beta-galactosidase. Results: Heterologous boosting resulted in significantly longer mouse survival than homologous boosting (all P<.00001, two-sided), Potent antigen-specific cytotoxic T lymphocytes were generated following heterologous boosting with poxvirus vectors, This response was not observed with any of the homologous boosting regimens, Mice primed with recombinant poxvirus vectors generated highly specific antibodies against viral proteins, Conclusions: The poor efficacy of homologous boosting regimens with viral vectors was probably a consequence of the induction of a strong antiviral antibody response, Heterologous boosting augmented antitumor immunity by generating a strong antigen-specific cytotoxic T-lymphocyte response, These data suggest that heterologous boosting strategies may be useful in increasing the efficacy of recombinant DNA anticancer vaccines that have now entered clinical trials. C1 NCI,SURG BRANCH,DIV CLIN SCI,NIH,BETHESDA,MD 20892. RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z99 CA999999, Z01 BC010763-01] NR 30 TC 127 Z9 130 U1 1 U2 3 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 NOV 5 PY 1997 VL 89 IS 21 BP 1595 EP 1601 DI 10.1093/jnci/89.21.1595 PG 7 WC Oncology SC Oncology GA YD840 UT WOS:A1997YD84000011 PM 9362157 ER PT J AU Olivero, OA Anderson, LM Diwan, BA Haines, DC Harbaugh, SW Moskal, TJ Jones, AB Rice, JM Riggs, CW Logsdon, D Yuspa, SH Poirier, MC AF Olivero, OA Anderson, LM Diwan, BA Haines, DC Harbaugh, SW Moskal, TJ Jones, AB Rice, JM Riggs, CW Logsdon, D Yuspa, SH Poirier, MC TI Transplacental effects of 3'-azido-2',3'-dideoxythymidine (AZT): Tumorigenicity in mice and genotoxicity in mice and monkeys SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; FETAL MOUSE SUSCEPTIBILITY; ZIDOVUDINE TREATMENT; CHILDHOOD-CANCER; DNA; CARCINOGENESIS; RETROVIRUS; 3-METHYLCHOLANTHRENE; TRANSMISSION; ASSOCIATION AB Background: When given during pregnancy, the drug 3'-azido-2',3'-dideoxythymidine (AZT) substantially reduces maternal-fetal transmission of human immunodeficiency virus type 1 (HIV-1), However, AZT has been shown to be carcinogenic in adult mice after lifetime oral administration, In this study, we assessed the transplacental tumorigenic and genotoxic effects of AZT in the offspring of CD-I mice and Erythrocebus patas monkeys given AZT orally during pregnancy, Methods: Pregnant mice were given daily doses of either 12.5 or 25.0 mg AZT on days 12 through 18 of gestation (last 37% of gestation period), Pregnant monkeys were given a daily dose of 10.0 mg AZT 5 days a week for the last 9.5-10 weeks of gestation (final 41%-43% of gestation period), AZT incorporation into nuclear and mitochondrial DNA and the length of chromosomal end (telomere) DNA were examined in multiple tissues of newborn mice and fetal monkeys, Additional mice were followed from birth and received no further treatment until subjected to necropsy and complete pathologic examination at 1 year of age, An anti-AZT radioimmunoassay was used to monitor AZT incorporation into DNA. Results: At 1 year of age, the offspring of AZT-treated mice exhibited statistically significant, dose-dependent increases in tumor incidence and tumor multiplicity in the lungs, liver, and female reproductive organs, AZT incorporation into nuclear and mitochondrial DNA was detected in multiple organs of transplacentally exposed mice and monkeys, Shorter chromosomal telomeres were detected in liver and brain tissues from most AZT-exposed newborn mice but not in tissues from fetal monkeys, Conclusions: AZT is genotoxic in fetal mice and monkeys and is a moderately strong transplacental carcinogen in mice examined at 1 year of age, Careful long-term follow-up of AZT-exposed children would seem to be appropriate. C1 NATL CANC INST,COMPARAT CARCINOGENESIS LAB,DIV BASIC SCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. RP Olivero, OA (reprint author), NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,DIV BASIC SCI,NIH,BLDG 37,RM 3B15,MSC-4255,BETHESDA,MD 20892, USA. NR 39 TC 173 Z9 176 U1 0 U2 2 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 NOV 5 PY 1997 VL 89 IS 21 BP 1602 EP 1608 DI 10.1093/jnci/89.21.1602 PG 7 WC Oncology SC Oncology GA YD840 UT WOS:A1997YD84000012 PM 9362158 ER PT J AU Fisher, B Dignam, J AF Fisher, B Dignam, J TI Five versus more than five years of tamoxifen therapy for breast cancer patients with negative lymph nodes and estrogen receptor-positive tumors - Response SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter C1 UNIV PITTSBURGH,SCH MED,DEPT SURG,PITTSBURGH,PA 15261. UNIV PITTSBURGH,DEPT BIOSTAT,PITTSBURGH,PA 15261. RP Fisher, B (reprint author), UNIV PITTSBURGH,SCH MED,NATL SURG ADJUVANT BREAST & BOWEL PROJECT,3550 TERRACE ST,RM 914,PITTSBURGH,PA 15261, USA. NR 5 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 NOV 5 PY 1997 VL 89 IS 21 BP 1632 EP 1632 PG 1 WC Oncology SC Oncology GA YD840 UT WOS:A1997YD84000025 ER PT J AU Bahar, I Erman, B Haliloglu, T Jernigan, RL AF Bahar, I Erman, B Haliloglu, T Jernigan, RL TI Efficient characterization of collective motions and interresidue correlations in proteins by low-resolution simulations SO BIOCHEMISTRY LA English DT Article ID MOLECULAR-DYNAMICS SIMULATIONS; MONTE-CARLO SIMULATIONS; BACTERIOPHAGE-T4 LYSOZYME; T4 LYSOZYME; LATTICE MODEL; FLEXIBILITY; STABILITY; MUTANT; NMR AB A low-resolution model is used together with recently developed knowledge-based potentials for exploring the dynamics of proteins. Configurations are generated using a Monte Carlo/Metropolis scheme combined with a singular value decomposition technique (SVD). The approach is shown to characterize the cooperative motions in good detail, at least 1 order of magnitude faster than atomic simulations. Trajectories are partitioned into modes, and the slowest ones are analyzed to elucidate the dominant mechanism of collective motions. Calculations performed for bacteriophage T4 lysozyme, a two-domain enzyme, demonstrate that the structural elements within each domain are subject to strongly coupled motions, whereas the motions of the two domains with respect to each other are strongly anticorrelated. This type of motion, evidenced by the synchronous fluctuations of the domain centroids by up to +/-4.0 Angstrom in opposite directions, is comparable to the movements observed by recent spin-labeling experiments in solution. The potential of mean force governing these fluctuations is shown to be anharmonic. The beta-sheet region at the N-terminal domain and the helix E in the C-terminal domain are identified as regions important for mediating cooperative motions and, in particular, for the opening and closing of the active-site cleft between the domains. Residues Leu66-Phe67 in the central helix C stop the propagation of correlated motions between the domains. There is a correlation between the groups involved in highly cooperative motions revealed by simulations and the highly protected regions during unfolding measured by pulsed H/D exchange and 2-D NMR. C1 NCI,MOL STRUCT SECT,LAB EXPT COMPUTAT BIOL,DIV BASIC SCI,NIH,BETHESDA,MD 20892. BOGAZICI UNIV,POLYMER RES CTR,TR-80815 BEBEK,ISTANBUL,TURKEY. BOGAZICI UNIV,SCH ENGN,TR-80815 BEBEK,ISTANBUL,TURKEY. TUBITAK,ADV POLYMER MAT RES CTR,TR-80815 BEBEK,ISTANBUL,TURKEY. RI Jernigan, Robert/A-5421-2012; OI ERMAN, BURAK/0000-0002-2496-6059 NR 47 TC 60 Z9 62 U1 4 U2 11 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD NOV 4 PY 1997 VL 36 IS 44 BP 13512 EP 13523 DI 10.1021/bi971611f PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YE774 UT WOS:A1997YE77400008 PM 9354619 ER PT J AU Guetta, V Quyyumi, AA Prasad, A Panza, JA Waclawiw, M Cannon, RO AF Guetta, V Quyyumi, AA Prasad, A Panza, JA Waclawiw, M Cannon, RO TI The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women SO CIRCULATION LA English DT Article DE atherosclerosis; coronary disease; nitric oxide; endothelium; hormones ID LOW-DENSITY-LIPOPROTEIN; SMOOTH-MUSCLE CELLS; CULTURED ENDOTHELIAL-CELLS; L-ARGININE; HYPERCHOLESTEROLEMIC HUMANS; REPLACEMENT THERAPY; SUPEROXIDE ANION; INDUCED RELEASE; RELAXING FACTOR; SEX-HORMONES AB Background At physiological concentrations, 17 beta-estradiol selectively enhances endothelium-dependent coronary vasodilation by an unknown mechanism in postmenopausal women. Methods and Results To assess the contribution of nitric oxide (NO) to the vascular effects of estradiol, we measured coronary epicardial and microvascular responses to intracoronary acetylcholine (range, 3 to 300 mu g/min for 2 minutes) before and after intracoronary estradiol 75 ng/min for 15 minutes in 20 estrogen-deficient women, 16 of whom had angiographic evidence of atherosclerosis or risk factors for atherosclerosis. This testing was repealed after inhibition of NO synthesis with intracoronary N-G-monomethyl-L-arginine (L-NMMA) 64 mu mol/min for 5 minutes. Estradiol increased acetylcholine-stimulated coronary flow from 54+/-48% (mean+/-SD) above baseline values before estradiol infusion to 100-63% above baseline values (P=.007) and decreased coronary resistance from 32+/-21% to 46+/-15% below baseline values (P=.007) at a coronary sinus estradiol concentration of 1725+/-705 pmol/L (470+/-192 pg/mL). Estradiol also tended to lessen the severity of acetylcholine-induced epicardial coronary artery vasoconstriction from 8+/-11% to 3+/-11% below baseline values (P=.123). However, during L-NMMA infusion, estradiol no longer potentiated the effects of acetylcholine on coronary flow dynamics; coronary flow increased 39+/-46% above baseline values and coronary resistance decreased 19+/-30% below baseline values (both P<.001 versus pre-L-NMMA responses). The epicardial diameter decreased 8+/-11% below baseline values (P=.06 versus pre-L-NMMA response). Conclusions The effects of estradiol at physiological concentrations on endothelium-dependent coronary vasodilator responsiveness in postmenopausal women are mediated by enhanced bioavailability of NO, which may be responsible in part for the cardioprotective effects of estrogen. C1 NHLBI,CARDIOL BRANCH,NIH,BETHESDA,MD 20892. NHLBI,OFF BIOSTAT RES,NIH,BETHESDA,MD 20892. NR 66 TC 198 Z9 200 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 4 PY 1997 VL 96 IS 9 BP 2795 EP 2801 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YF295 UT WOS:A1997YF29500012 PM 9386140 ER PT J AU Muller, JE Kaufmann, PG Luepker, RV Weisfeldt, ML Deedwania, PC Willerson, JT AF Muller, JE Kaufmann, PG Luepker, RV Weisfeldt, ML Deedwania, PC Willerson, JT TI Mechanisms precipitating acute cardiac events - Review and recommendations of an NHLBI workshop SO CIRCULATION LA English DT Review DE NHLBI; cardiovascular diseases; coronary disease; epidemiology; prevention ID ACUTE MYOCARDIAL-INFARCTION; CORONARY-ARTERY DISEASE; CIRCADIAN VARIATION; RISK-FACTORS; MORTALITY; DEPRESSION; ISCHEMIA; PLAQUES; ABSENCE; WOMEN C1 NHLBI,BETHESDA,MD 20892. UNIV KENTUCKY,MED CTR,LEXINGTON,KY 40506. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. UNIV CALIF SAN FRANCISCO,SCH MED,SAN FRANCISCO,CA 94143. UNIV TEXAS,SCH MED,HOUSTON,TX. NR 35 TC 77 Z9 80 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 4 PY 1997 VL 96 IS 9 BP 3233 EP 3239 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YF295 UT WOS:A1997YF29500069 PM 9386197 ER PT J AU Brinton, LA Benichou, J Gammon, MD Brogan, DR Coates, R Schoenberg, JB AF Brinton, LA Benichou, J Gammon, MD Brogan, DR Coates, R Schoenberg, JB TI Ethnicity and variation in breast cancer incidence SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID RISK-FACTORS; ATTRIBUTABLE RISK; BLACK-WOMEN; WHITE AB A breast cancer case-control study in Atlanta and 5 counties of central New Jersey involving interviews with 960 white and 281 black cases younger than 54 years of age enabled assessment of reasons for the varying incidence rates among these 2 ethnic groups. Of interest was why rates of breast cancer are higher among older white women, a trend that is reversed among very young women (<40 years). Calculation of the prevalence of exposure to classic and speculative risk factors and associated relative risks enabled derivation of population attributable risks (PARs) for the various combinations of age and ethnic groups. A higher PAR was derived for older (40-54 years) white (62%) than black (54%) women, which appeared to account for the observed difference in incidence between the 2 ethnic groups. Most of the difference in PARs between older whites and blacks was accounted for by whites having fewer births, later ages at first birth and slightly higher risks associated with reproductive and menstrual factors. Consideration of only well-established breast cancer risk factors showed a PAR among older whites of 57%, an estimate comparable to those previously published. Slightly higher overall PARs were derived when analyses considered several speculative but modifiable risk factors, including years of use of oral contraceptives, body size and alcohol consumption. Many of the analyses among younger women (20-39 years) were limited by available numbers, but it appeared that very little disease occurrence in young black women was associated with the factors studied. (C) 1997 Wiley-Liss, Inc. C1 UNIV ROUEN,SCH MED,ROUEN,FRANCE. COLUMBIA UNIV,SCH PUBL HLTH,DIV EPIDEMIOL,NEW YORK,NY. EMORY UNIV,DEPT BIOSTAT,ROLLINS SCH PUBL HLTH,ATLANTA,GA 30322. CTR DIS CONTROL & PREVENT,DIV CANC PREVENT & CONTROL,ATLANTA,GA. NEW JERSEY DEPT HLTH & SENIOR SERV,APPL CANCER EPIDEMIOL PROGRAM,TRENTON,NJ. RP Brinton, LA (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,DIV CANC EPIDEMIOL & GENET,EXECUT PLAZA N,ROOM 443,BETHESDA,MD 20892, USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 20 TC 67 Z9 67 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 NOV 4 PY 1997 VL 73 IS 3 BP 349 EP 355 DI 10.1002/(SICI)1097-0215(19971104)73:3<349::AID-IJC8>3.0.CO;2-# PG 7 WC Oncology SC Oncology GA YE849 UT WOS:A1997YE84900008 PM 9359481 ER PT J AU Bergman, AC Linder, C Sakaguchi, K StenLinder, M Alaiya, AA Franzen, B Shoshan, MC Bergman, T Wiman, B Auer, G Appella, E Jornvall, H Linder, S AF Bergman, AC Linder, C Sakaguchi, K StenLinder, M Alaiya, AA Franzen, B Shoshan, MC Bergman, T Wiman, B Auer, G Appella, E Jornvall, H Linder, S TI Increased expression of alpha-enolase in c-jun transformed rat fibroblasts without increased activation of plasminogen SO FEBS LETTERS LA English DT Article DE two-dimensional gel electrophoresis; mass spectrometry; cell transformation; plasminogen activation ID METASTATIC PHENOTYPE; CELLS; PHOSPHORYLATION; ONCOGENES; PLASMA; GENE AB Two-dimensional gel electrophoresis was used to identify polypeptides differentially expressed between normal and c-jun transformed rat fibroblasts, The level of a 49 kDa polypeptide was 3-fold elevated in c-jun transformed cells, Sequence analysis by ion trap mass spectrometry identified the polypeptide as rat alpha-enolase, Enolase functions as a cell surface receptor for plasminogen, suggesting that upregulation may increase plasminogen activation and cell surface proteolysis important for tumor growth, However, no difference was observed between normal and transformed cells in formation of plasmin, suggesting that upregulation of alpha-enolase may contribute to an increased metabolic capacity, but not to increased plasminogen activation, (C) 1997 Federation of European Biochemical Societies. C1 KAROLINSKA HOSP & INST,RADIUMHEMMETS RES LAB,DEPT PATHOL & ONCOL,S-17176 STOCKHOLM,SWEDEN. NCI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. KAROLINSKA HOSP & INST,DEPT CLIN CHEM,DEPT PATHOL & ONCOL,S-17176 STOCKHOLM,SWEDEN. KAROLINSKA HOSP & INST,UNIT CELL & MOL ANAL,DEPT PATHOL & ONCOL,S-17176 STOCKHOLM,SWEDEN. RP Bergman, AC (reprint author), KAROLINSKA INST,DEPT MED BIOCHEM & BIOPHYS,S-17177 STOCKHOLM,SWEDEN. NR 23 TC 16 Z9 16 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD NOV 3 PY 1997 VL 417 IS 1 BP 17 EP 20 DI 10.1016/S0014-5793(97)01247-7 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA YF214 UT WOS:A1997YF21400004 PM 9395066 ER PT J AU Capasso, A Amodeo, P Balboni, G Guerrini, R Lazarus, LH Temussi, PA Salvadori, S AF Capasso, A Amodeo, P Balboni, G Guerrini, R Lazarus, LH Temussi, PA Salvadori, S TI Design of mu selective opioid dipeptide antagonists SO FEBS LETTERS LA English DT Article DE antagonism; peptide; opioid selectivity; conformation ID CONFORMATIONAL-ANALYSIS; RECEPTOR ANTAGONIST; NUCLEIC-ACIDS; FORCE-FIELD; POTENT; DERMORPHIN; PEPTIDES; PROTEINS; AGONISTS; ANALOGS AB We have recently designed potent delta selective opioid antagonist dipeptides on the basis of a simple conformational analysis. Following a similar procedure me found a mu selective dipeptide antagonist, 2,6-dimethyl-Tyr-D-Phe-NH2. Although its selectivity is not as high as those of the quoted delta selective dipeptides it has good in vitro activity and looks very promising for further development since the 2,6-dimethyl-Tyr-D-Phe message, like the delta selective 2,6-dimethyl-Tyr-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid counterpart, seems able to impart antagonism to longer peptides. (C) 1997 Federation of European Biochemical Societies. C1 UNIV NAPLES FEDERICO II,DIPARTIMENTO CHIM,I-80134 NAPLES,ITALY. UNIV SALERNO,DIPARTIMENTO SCI FARMACEUT,I-84084 SALERNO,ITALY. CNR,ICMIB,I-80072 ARCO,NAPLES,ITALY. UNIV FERRARA,DIPARTIMENTO SCI FARMACEUT,I-44100 FERRARA,ITALY. NIEHS,LMNI,RES TRIANGLE PK,NC 27709. RI Amodeo, Pietro/P-1800-2015; OI Amodeo, Pietro/0000-0002-6439-7575; CAPASSO, Anna/0000-0002-6579-7802; Guerrini, Remo/0000-0002-7619-0918 NR 27 TC 21 Z9 22 U1 0 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 NOV 3 PY 1997 VL 417 IS 1 BP 141 EP 144 DI 10.1016/S0014-5793(97)01271-4 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA YF214 UT WOS:A1997YF21400030 PM 9395092 ER PT J AU SchartonKersten, T Contursi, C Masumi, A Sher, A Ozato, K AF SchartonKersten, T Contursi, C Masumi, A Sher, A Ozato, K TI Interferon consensus sequence binding protein-deficient mice display impaired resistance to intracellular infection due to a primary defect in interleukin 12 p40 induction SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TOXOPLASMA-GONDII INFECTION; REGULATORY FACTOR FAMILY; IFN-GAMMA PRODUCTION; PERITONEAL-MACROPHAGES; TRANSCRIPTION FACTOR; INDUCIBLE GENES; IMMUNE-RESPONSE; NITRIC-OXIDE; ICSBP GENE; IN-VIVO AB Mice lacking the transcription factor interferon consensus sequence binding protein (ICSBP), a member of the interferon regulatory factor family of transcription proteins, were infected with the intracellular protozoan, Toxoplasma gondii. ICSBP-deficient mice exhibited unchecked parasite replication in vivo and rapidly succumbed within 14 d after inoculation with an avirulent Toxoplasma strain. In contrast, few intracellular parasites were observed in wild-type littermates and these animals survived for at least 60 d alter infection. Analysis of cytokine synthesis in vitro and in vivo revealed a major deficiency in the expression of both interferon (IFN)-gamma and interleukin (IL)-12 p40 in the T. gondii exposed ICSBP-/- animals. In related experiments, macrophages from uninfected ICSBP-/- mice were shown to display a selective impairment in the mRNA expression of IL-12 p40 but not IL-1 alpha, IL-1 beta, IL-1Ra, IL-6, IL-10, or TNF-alpha in response to live parasites, parasite antigen, lipopolysaccharide, or Staphylococcus aureus. This selective defect in IL-12 p40 production was observed regardless of whether the macrophages had been primed with IFN-gamma. We hypothesize that the impaired synthesis of IL-12 p40 in ICSBP-/- animals is the primary lesion responsible for the loss in resistance to T. gondii because IFN-gamma-induced parasite killing was unimpaired in vitro and, more importantly, administration of exogenous IL-12 in vivo significantly prolonged survival of the infected mice. Together these findings implicate ICSBP as a major transcription factor which directly or indirectly regulates IL-12 p40 gene activation and, as a consequence, IFN-gamma-dependent host resistance. C1 NICHHD, LMGR, NIH, BETHESDA, MD 20892 USA. NIAID, PARASIT DIS LAB, IMMUNOL SECT, BETHESDA, MD 20892 USA. NR 55 TC 162 Z9 164 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 3 PY 1997 VL 186 IS 9 BP 1523 EP 1534 DI 10.1084/jem.186.9.1523 PG 12 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA YE942 UT WOS:A1997YE94200013 PM 9348310 ER PT J AU Giese, NA Gabriele, L Doherty, TM Klinman, DM TadesseHeath, L Contursi, C Epstein, SL Morse, HC AF Giese, NA Gabriele, L Doherty, TM Klinman, DM TadesseHeath, L Contursi, C Epstein, SL Morse, HC TI Interferon (IFN) consensus sequence-binding protein, a transcription factor of the IFN regulatory factor family, regulates immune responses in vivo through control of interleukin 12 expression SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MURINE PERITONEAL-MACROPHAGES; CHRONIC MYELOGENOUS LEUKEMIA; CELL-MEDIATED-IMMUNITY; LEISHMANIA-MAJOR; GENE-EXPRESSION; MESSENGER-RNA; IN-VIVO; T-HELPER-1 CELLS; VIRUS-INFECTION; DENDRITIC CELLS AB Mice with a null mutation of the gene encoding interferon consensus sequence-binding protein (ICSBP) develop a chronic myelogenous leukemia-like syndrome and mount impaired responses to certain viral and bacterial infections. To gain a mechanistic understanding of the contributions of ICSBP to humoral and cellular immunity, we characterized the responses of control and ICSBP-/- mice to infection with influenza A (flu) and Leishmania major (L. major). Mice of both genotypes survived infections with flu, but differed markedly in the isotype distribution of antiflu antibodies. In sera of normal mice, immunoglobulin (Ig)G2a antibodies were dominant over IgG1 antibodies, a pattern indicative of a T helper cell type 1 (Th1)-driven response. In sera of ICSBP-/- mice, however, IgG1 antibodies dominated over IgG2a antibodies, a pattern indicative of a Th2-driven response. The dominance of IgG1 and ISE over IgG2a was detected in the sera of uninfected mice as well. A seeming Th2 bias of ICSBP-deficient mice was also uncovered in their inability to control infection with L. major, where resistance is known to be dependent on IL-12 and IFN-gamma as components of a Th1 response. Infected ICSBP-deficient mice developed fulminant, disseminated leishmaniasis as a result of failure to mount a Th1-mediated curative response, although T cells remained capable of secreting IFN-gamma and macrophages of producing nitric oxide. Compromised Th1 differentiation in ICSBP-/- mice could not be attributed to hyporesponsiveness of CD4(+) T cells to interleukin (IL)-12; however, the ability of uninfected and infected ICSBP-deficient mice to produce IL-12 was markedly impaired. This indicates that ICSBP is a deciding factor in Th responses governing humoral and cellular immunity through its role in regulating IL-12 expression. C1 NIAID,PARASITOL LAB,NIH,BETHESDA,MD 20892. NICHHD,LAB MOL GROWTH REGULAT,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,DIV VIROL,BETHESDA,MD 20852. US FDA,CTR BIOL EVALUAT & RES,DIV CELL & GENE THERAPIES,BETHESDA,MD 20852. RP Giese, NA (reprint author), NIAID,LIP,NIH,7 CTR DR,MSC 0760,BETHESDA,MD 20892, USA. OI Morse, Herbert/0000-0002-9331-3705 NR 74 TC 124 Z9 126 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 3 PY 1997 VL 186 IS 9 BP 1535 EP 1546 DI 10.1084/jem.186.9.1535 PG 12 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA YE942 UT WOS:A1997YE94200014 PM 9348311 ER PT J AU Leung, DYM Hamid, Q Vottero, A Szefler, SJ Surs, W Minshall, E Chrousos, GP Klemm, DJ AF Leung, DYM Hamid, Q Vottero, A Szefler, SJ Surs, W Minshall, E Chrousos, GP Klemm, DJ TI Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID STEROID-RESISTANT ASTHMA; BINDING; FEATURES; ISOFORM AB In many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression The molecular oasis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition. C1 NATL JEWISH MED & RES CTR,DIV CLIN PHARMACOL,DENVER,CO 80206. UNIV COLORADO,HLTH SCI CTR,DEPT PEDIAT,DENVER,CO 80262. MCGILL UNIV,MEAKINS CHRISTIE LABS,MONTREAL,PQ,CANADA. MCGILL UNIV,DEPT PATHOL,MONTREAL,PQ,CANADA. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP Leung, DYM (reprint author), NATL JEWISH MED & RES CTR,DIV ALLERGY IMMUNOL,1400 JACKSON ST,DENVER,CO 80206, USA. FU NCRR NIH HHS [M01 RR000051]; NHLBI NIH HHS [R37 HL037260, HL36577, HL37260, P01 HL036577]; NIAMS NIH HHS [AR41256, R01 AR041256] NR 21 TC 300 Z9 323 U1 4 U2 6 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 3 PY 1997 VL 186 IS 9 BP 1567 EP 1574 DI 10.1084/jem.186.9.1567 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA YE942 UT WOS:A1997YE94200017 PM 9348314 ER PT J AU Soderstrom, CA Dischinger, PC Smith, GS Hebel, JR McDuff, DR Gorelick, DA Kerns, TJ Ho, SM Read, KM AF Soderstrom, CA Dischinger, PC Smith, GS Hebel, JR McDuff, DR Gorelick, DA Kerns, TJ Ho, SM Read, KM TI Alcoholism at the time of injury among trauma center patients: Vehicular crash victims compared with other patients SO ACCIDENT ANALYSIS AND PREVENTION LA English DT Article DE trauma; alcoholism; vehicular crashes; unintentional injuries; violence ID DRUG-USE; UNITED-STATES; PREVALENCE; DRIVERS; DEPENDENCE; MARIJUANA; ABUSE AB A structured in-depth interview employing standardized criteria was used to determine the prevalence of lifetime and current alcohol dependence (alcoholism) in unselected consecutive patients admitted to a regional Level I trauma center. Of 629 patients, 157 (25.0%) were current alcoholics at the time of injury. An additional 87 (13.8%) were diagnosed as lifetime non-current alcoholics. There was no significant difference in the rates of current alcohol dependence among patients injured in vehicular crashes (23.5%), other unintentional trauma victims (29.3%), and those injured as a result of violence (24.6%). Of BAC+ (blood alcohol concentration positive) patients, 54.5% were current alcoholics. However, 14.4% of alcohol-negative patients were also diagnosed as alcohol dependent. (C) 1997 Elsevier Science Ltd. C1 UNIV MARYLAND, SCH MED, DEPT EPIDEMIOL, BALTIMORE, MD 21201 USA. UNIV MARYLAND, SCH MED, DEPT PSYCHIAT, BALTIMORE, MD 21201 USA. NATL INST DRUG ABUSE, ADDICT RES CTR, BALTIMORE, MD 21224 USA. RP Soderstrom, CA (reprint author), UNIV MARYLAND, MED CTR, DEPT SURG & TRAUMATOL, R ADAMS COWLEY SHOCK TRAUMA CTR, COLLEGE PK, MD 20742 USA. OI Smith, Gordon/0000-0002-2911-3071 FU NIAAA NIH HHS [R01 AA09050] NR 32 TC 17 Z9 17 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0001-4575 EI 1879-2057 J9 ACCIDENT ANAL PREV JI Accid. Anal. Prev. PD NOV PY 1997 VL 29 IS 6 BP 715 EP 721 DI 10.1016/S0001-4575(97)00040-7 PG 7 WC Ergonomics; Public, Environmental & Occupational Health; Social Sciences, Interdisciplinary; Transportation SC Engineering; Public, Environmental & Occupational Health; Social Sciences - Other Topics; Transportation GA YD872 UT WOS:A1997YD87200002 PM 9370007 ER PT J AU Bujacz, G Miller, M Harrison, R Thanki, N Gilliland, GL Ogata, CM Kim, SH Wlodawer, A AF Bujacz, G Miller, M Harrison, R Thanki, N Gilliland, GL Ogata, CM Kim, SH Wlodawer, A TI Structure of monellin refined to 2.3 angstrom resolution in the orthorhombic crystal form SO ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY LA English DT Article ID INTENSELY SWEET PROTEIN; AMINO-ACID-SEQUENCE; DIOSCOREOPHYLLUM-CUMMINSII; MACROMOLECULAR STRUCTURES; THAUMATIN-I; PURIFICATION; PRINCIPLE; INHIBITOR; CYSTATIN AB The structure of orthorhombic crystals of monellin, a sweet protein extracted from African serendipity berries, has been solved by molecular replacement and refined to 2.3 Angstrom resolution. The final R factor was 0.150 for a model with excellent geometry. A monellin molecule consists of two peptides that are non-covalently bound, with chain A composed of three beta-strands interconnected by loop regions and chain B composed of two beta-strands interconnected by an alpha-helix. The N terminus of chain A is in close proximity to the C terminus of chain B. The two molecules in the asymmetric unit are related by a non-crystallographic twofold axis and form a dimer, similar to those previously observed in other crystal forms of both natural and single-chain monellin. The r.m.s. deviation between the C alpha atoms in the two independent molecules is 0.60 Angstrom, while the deviations from the individual molecules in the previously reported monoclinic crystals are 0.50-0.57 Angstrom. This result proves that the structure of monellin is not significantly influenced by crystal packing forces. C1 NIST,CTR ADV RES BIOTECHNOL,ROCKVILLE,MD 20850. UNIV MARYLAND,INST BIOTECHNOL,CTR ADV RES BIOTECHNOL,ROCKVILLE,MD 20850. BROOKHAVEN NATL LAB,HOWARD HUGHES MED INST,UPTON,NY 11973. UNIV CALIF BERKELEY,DEPT CHEM,BERKELEY,CA 94720. UNIV CALIF BERKELEY,LAWRENCE BERKELEY LAB,BERKELEY,CA 94720. RP Bujacz, G (reprint author), NCI,FREDERICK CANC RES & DEV CTR,MACROMOL STRUCT LAB,FREDERICK,MD 21702, USA. RI Miller, Maria/I-1636-2013 OI Miller, Maria/0000-0003-0252-5348 NR 31 TC 11 Z9 13 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0907-4449 J9 ACTA CRYSTALLOGR D JI Acta Crystallogr. Sect. D-Biol. Crystallogr. PD NOV 1 PY 1997 VL 53 BP 713 EP 719 DI 10.1107/S0907444997006860 PN 6 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics; Crystallography SC Biochemistry & Molecular Biology; Biophysics; Crystallography GA YJ649 UT WOS:A1997YJ64900010 PM 15299859 ER PT J AU Guinet, F Diallo, DA Minta, D Dicko, A Sissoko, MS Keita, MM Wellems, TE Doumbo, O AF Guinet, F Diallo, DA Minta, D Dicko, A Sissoko, MS Keita, MM Wellems, TE Doumbo, O TI A comparison of the incidence of severe malaria in Malian children with normal and C-trait hemoglobin profiles SO ACTA TROPICA LA English DT Article DE malaria hypothesis; hemoglobin C; genetic polymorphisms; hemoglobinopathies ID ABNORMAL-HEMOGLOBINS; POPULATION-GENETICS; SUDAN SAVANNA; 2 AREAS; FALCIPARUM; IMMUNOGLOBULINS; ANTIBODIES; NIGERIA; AFRICA; CELLS AB Although a protective effect against malaria has been demonstrated for several hemoglobin variants, no selective factor is established for the high incidence of HbC in regions of West Africa. Here we report a survey of hemoglobin profiles among children admitted with symptomatic and severe malaria to the Gabriel Toure Hospital in Bamako, Mali, where the frequency of the HbC gene is 8-10%. Children with AC and AA profiles presented with severe malaria at comparable rates, indicating lack of protection by the heterozygous state. Two admitted children, one of whom presented with cerebral malaria, were found to have SC profiles. No CC homozygotes were detected in the study cohort. (C) 1997 Elsevier Science B.V. C1 NIAID,NIH,BETHESDA,MD 20892. FAC MED PHARM & ODONTOSTOMATOL,HEMATOL LAB,BAMAKO,MALI. FAC MED PHARM & ODONTOSTOMATOL,MALARIA RES & TRAINING CTR,DEPT EPIDEMIOL PARASIT DIS,BAMAKO,MALI. PEDIAT HOSP,HOP GABRIEL TOURE,BAMAKO,MALI. NR 25 TC 23 Z9 25 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PD NOV PY 1997 VL 68 IS 2 BP 175 EP 182 DI 10.1016/S0001-706X(97)00089-2 PG 8 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA YC382 UT WOS:A1997YC38200004 PM 9386792 ER PT J AU Audrain, J Boyd, NR Roth, J Main, D Caporaso, NE Lerman, C AF Audrain, J Boyd, NR Roth, J Main, D Caporaso, NE Lerman, C TI Genetic susceptibility testing in smoking-cessation treatment: One-year outcomes of a randomized trial SO ADDICTIVE BEHAVIORS LA English DT Article ID QUIT-SMOKING; SOCIAL SUPPORT; SELF-EFFICACY; NICOTINE; INTERVENTION; RELAPSE; METAANALYSIS; PREDICTORS; VALIDATION; POPULATION AB This study evaluated the long-term impact of genetic susceptibility biomarker feedback on smoking behavior change and symptoms of depression in 426 male and female smokers. Smokers were randomized to one of three smoking-cessation interventions: minimal contact quit-smoking counseling (QSC), QSC + exposure biomarker feedback (EBF), and QSC + EBF + biomarker feedback about genetic susceptibility to lung cancer (SBF). The logistic regression model for quit attempt revealed a significant main effect for treatment such that participants in the SBF group were more than two times more likely to make a quit attempt than participants in the QSC group. There was not a significant difference between EBF and QSC participants. The results also revealed a significant effect for baseline stage of change. Those smokers in the preparation stage at baseline were more than three times more likely to make a quit attempt over the 12 months following treatment. The models for 30-day cessation and follow-up smoking rate revealed no significant main or interacting effects for treatment. A repeated measures analysis of variance revealed a significant main effect for time, indicating that an initial increase in depression in the genetic susceptibility group was not maintained over time. Genetic susceptibility feedback has the intended effects on motivation to quit, but it may need to be delivered within a more intensive smoking-cessation treatment for the heightened motivation to translate into smoking cessation. (C) 1997 Elsevier Science Ltd. C1 FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. RP Audrain, J (reprint author), GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,2233 WISCONSIN AVE NW,SUITE 535,WASHINGTON,DC 20007, USA. FU NCI NIH HHS [R01 CA63562] NR 33 TC 79 Z9 79 U1 7 U2 8 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4603 J9 ADDICT BEHAV JI Addict. Behav. PD NOV-DEC PY 1997 VL 22 IS 6 BP 741 EP 751 DI 10.1016/S0306-4603(97)00060-9 PG 11 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA YH870 UT WOS:A1997YH87000003 PM 9426791 ER PT J AU Sloand, EM Young, NS Sato, T Kumar, P Kim, S Weichold, FF Maciejewski, JP AF Sloand, EM Young, NS Sato, T Kumar, P Kim, S Weichold, FF Maciejewski, JP TI Secondary colony formation after long-term bone marrow culture using peripheral blood and bone marrow of HIV-infected patients SO AIDS LA English DT Article DE bone marrow; stem cells; HIV-1; AIDS; progenitors ID HUMAN-IMMUNODEFICIENCY-VIRUS; HEMATOPOIETIC PROGENITOR CELLS; DEFECTIVE INVITRO GROWTH; HEMATOLOGIC MANIFESTATIONS; ENVELOPE GLYCOPROTEIN; MAJOR RESERVOIR; TYPE-1 HIV-1; SUPPRESSION; REPLICATION; INDIVIDUALS AB Objective: To determine if defective bone mat-row function in HIV infection is associated with decreased numbers of progenitor cells or defective stromal cell function. Design: Defective bone marrow function may in part be responsible for the cytopenias so frequently seen in patients with AIDS, Although a number of investigators have reported impaired growth of committed hematopoietic progenitor cells in HIV-1-infected patients, few studies have examined the most primitive hematopoietic stem cells. Our study was designed to determine the function and quality of the most immature hematopoietic progenitor and stem cells in the peripheral blood and bone marrow of HIV-l-infected patients and to assess stromal cell function. Methods: For quantification of these cells we used a modified long-term culture-initiating cell (LTCIC) assay in which the number of secondary colony-forming cells after 5 weeks of stromal culture served as a measure of LTCIC. Stromal cells from normal controls and HIV-l-infected patients were used for cross-matching experiments. Normal CD34+ cells or those derived iron? HIV-infected patients were plated and colony growth assessed. Results: We found that HIV-1-infected patients had a mean of 0.8 secondary colony forming cells/10(5) peripheral blood mononuclear cells (PBMC), whereas normal controls showed 1.2 secondary colony-forming cells/10(5) PBMC (P = not significant) after long-term culture. Asymptomatic patients showed well preserved numbers of secondary colony-forming cells after long-term culture of PBMC, but a significant reduction was seen in patients with a history of opportunistic infections (P < 0.01), low CD4+ cell count (< 200 x 10(6)/l; P < 0.05), or leukopenia (P < 0.05). Decreased numbers of secondary colony-forming cells have also been found in bone marrow of HIV-l-infected patients with advanced disease. When normal CD34+ cells were cultured on stromal layers from bone marrow of HIV-1-infected patients or normal controls, no differences in the numbers of surviving progenitor cells were found. Conclusions: Our data indicate that the hematopoietic defect in HIV-1 infection involves the most immature hematopoietic cells and becomes evident in advanced disease. Stromal function of HIV-infected patients appears normal. C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,DEPT INFECT DIS,WASHINGTON,DC. NR 32 TC 24 Z9 24 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD NOV PY 1997 VL 11 IS 13 BP 1547 EP 1553 DI 10.1097/00002030-199713000-00002 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA YE146 UT WOS:A1997YE14600002 PM 9365758 ER PT J AU GarzinoDemo, A Arya, SK Devico, AL Cocchi, F Lusso, P Gallo, RC AF GarzinoDemo, A Arya, SK Devico, AL Cocchi, F Lusso, P Gallo, RC TI C-C chemokine RANTES and HIV long terminal repeat-driven gene expression SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID CD8(+) T-CELLS; VIRUS TYPE-2 HIV-2; TROPIC HIV-1; REPLICATION; INFECTION; RECEPTOR; TRANSCRIPTION; MIP-1-ALPHA; LYMPHOCYTES; MIP-1-BETA AB The C-C chemokines RANTES, MIP-1 alpha, and MIP-1 beta have been characterized as constituents of an HIV-and SIV-suppressive factor released by CD8(+) cells, Furthermore, it has been demonstrated that chemokine receptors cooperate in HIV entry, However, these proteins are also known to have an effect on multiple intracellular signaling cascades that may affect the process of transcription, In the present study we demonstrate that treatment of CD4(+) T cells with these chemokines or with cell supernatants from HTLV-I-immortalized CD8(+) T cells results in significant reduction in the abundance of HIV-l-specific RNA as analyzed by Northern blot hybridization. To examine the possibility that such suppressive factors may inhibit HIV RNA transcription, we studied the effect of RANTES, the most effective HIV-suppressive chemokine, on basal and Tat-induced HIV-directed LTR expression of a reporter gene, Neither recombinant RANTES nor conditioned medium from CD8(+) cells significantly altered HIV-1 LTR-directed chloramphenicol acetyltransferase expression in either transiently or; stably transfected CD4(+) T cell lines, either in the presence or in the absence of Tat, These results suggest that C-C chemokines do not inhibit viral RNA transcription. C1 SCH MED,BALTIMORE,MD 21201. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. SAN RAFFAELE SCI INST,DIBIT,I-20132 MILAN,ITALY. RP GarzinoDemo, A (reprint author), UNIV MARYLAND,INST HUMAN VIROL,CTR MED BIOTECHNOL,INST BIOTECHNOL,725 W LOMBARD ST,BALTIMORE,MD 21201, USA. NR 26 TC 8 Z9 8 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD NOV 1 PY 1997 VL 13 IS 16 BP 1367 EP 1371 DI 10.1089/aid.1997.13.1367 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA YD668 UT WOS:A1997YD66800003 PM 9359655 ER PT J AU Margolis, LB Fitzgerald, W Glushakova, S Hatfill, S Amichay, N Baibakov, B Zimmerberg, J AF Margolis, LB Fitzgerald, W Glushakova, S Hatfill, S Amichay, N Baibakov, B Zimmerberg, J TI Lymphocyte trafficking and HIV infection of human lymphoid tissue in a rotating wall vessel bioreactor SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID THYMIC ORGAN-CULTURE; PATHOGENESIS; MODEL; MICROENVIRONMENT; LOCOMOTION; THERAPY; VIVO AB The pathogenesis of HIV infection involves a complex interplay between both the infected and noninfected cells of human lymphoid tissue, the release of free viral particles, the de novo infection of cells, and the recirculatory trafficking of peripheral blood lymphocytes. To develop an ia vitro model for studying these various aspects of HIV pathogenesis we have utilized blocks of surgically excised human tonsils and a rotating wall vessel (RWV) cell culture system, Here we show that (1) fragments of the surgically excised human lymphoid tissue remain viable and retain their gross cytoarchitecture for at least 3 weeks when cultured in the RWV system; (2) such lymphoid tissue gradually shows a loss of both T and B cells to the surrounding growth medium; however, this cellular migration is reversible as demonstrated by repopulation of the tissue by labeled cells from the growth medium; (3) this cellular migration may be partially or completely inhibited by embedding the blocks of lymphoid tissue in either a collagen or agarose gel matrix; these embedded tissue blocks retain most of the basic elements of a normal lymphoid cytoarchitecture; and (4) both embedded and nonembedded RWV-cultured blocks of human lymphoid tissue are capable of productive infection by HIV-1 of at least three various strains of different tropism and phenotype, as shown by an increase in bath p24 antigen levels and free virus in the culture medium, and by the demonstration of HIV-1 RNA-positive cells inside the tissue identified by in situ hybridization, It is therefore reasonable to suggest that gel-embedded and nonembedded blocks of human lymphoid tissue, cocultured with a suspension of tonsillar lymphocytes in an RWV culture system, constitute a useful model for simulating normal lymphocyte recirculatory traffic and provide a new tool for testing the various aspects of HIV pathogenesis. RP Margolis, LB (reprint author), NICHHD,NASA NIH CTR 3 DIMENS TISSUE CULTURES,LAB CELLULAR & MOL BIOPHYS,NIH,BLDG 10,RM 10D14,BETHESDA,MD 20892, USA. NR 26 TC 27 Z9 27 U1 0 U2 5 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 NOV 1 PY 1997 VL 13 IS 16 BP 1411 EP 1420 DI 10.1089/aid.1997.13.1411 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA YD668 UT WOS:A1997YD66800009 PM 9359661 ER PT J AU Garcia, MC Kim, KY Hough, C Kim, HY AF Garcia, MC Kim, KY Hough, C Kim, HY TI Effects of chronic ethanol on the mobilization of arachidonate and docosahexaenoate stimulated by the type 2A serotonin receptor agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride in C6 glioma cells SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE ethanol; arachidonate; docosahexaenoate; serotonin-2 receptor; C6 glioma cells ID GROWTH-FACTOR; GLIAL-CELLS; PHOSPHOINOSITIDE HYDROLYSIS; GLUTAMATE-RECEPTOR; PRENATAL EXPOSURE; PRIMARY CULTURES; RAT-BRAIN; NEURONS; ASTROCYTES; PROLIFERATION AB We studied the effects of chronic ethanol exposure on the mobilization of polyunsaturated fatty acids stimulated by activation of the type 2A serotonin receptor in C6 glioma cells. In our in vitro model, we prelabeled cells with [H-3]arachidonate and [C-14]docosahexaenoate and subsequently stimulated with the type 2A serotonin receptor agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride. In as early as 10 days of exposure to 20 or 50 mM ethanol, the (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride-stimulated mobilization of [H-3]arachidonic acid ([H-3]AA) and [C-14]docosahexaenoic acid ([C-14]DHA) was significantly inhibited, and this inhibition was accompanied by decreased mobilization of intracellular [Ca2+](i). Exposure to ethanol did not alter significantly the release of [H-3]AA and [C-14]DHA stimulated by the calcium ionophore A23187 nor the incorporation of [H-3]AA and [C-14]DHA into cellular lipids. Decreased mobilization of polyunsaturated fatty acids and calcium in astroglia may contribute to neurotoxicity caused by chronic ethanol exposure. C1 NIAID,SECT MASS SPECTROMETRY,LAB MEMBRANE BIOCHEM & BIOPHYS,NIH,ROCKVILLE,MD 20852. NIMH,MOL NEUROBIOL LAB,NIH,ROCKVILLE,MD 20857. NR 43 TC 7 Z9 7 U1 0 U2 0 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 NOV PY 1997 VL 21 IS 8 BP 1465 EP 1470 PG 6 WC Substance Abuse SC Substance Abuse GA YG096 UT WOS:A1997YG09600018 PM 9394119 ER PT J AU Cohen, SG AF Cohen, SG TI Asthma among the famous - William Tecumesh Sherman (1820-1891) - American (Union) Army General SO ALLERGY AND ASTHMA PROCEEDINGS LA English DT Biographical-Item C1 NIAID, Bethesda, MD 20892 USA. RP Cohen, SG (reprint author), NIAID, Bethesda, MD 20892 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 USA SN 1088-5412 J9 ALLERGY ASTHMA PROC JI Allergy Asthma Proc. PD NOV-DEC PY 1997 VL 18 IS 6 BP 371 EP 377 DI 10.2500/108854197778558016 PG 7 WC Allergy SC Allergy GA YM262 UT WOS:000071046000007 ER PT J AU Cohen, SG AF Cohen, SG TI Asthma among the famous - Woodrow Wilson (1856-1924) - Twenty-eighth president of the United States SO ALLERGY AND ASTHMA PROCEEDINGS LA English DT Biographical-Item C1 NIAID, Bethesda, MD 20892 USA. RP Cohen, SG (reprint author), NIAID, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 USA SN 1088-5412 J9 ALLERGY ASTHMA PROC JI Allergy Asthma Proc. PD NOV-DEC PY 1997 VL 18 IS 6 BP 378 EP 381 PG 4 WC Allergy SC Allergy GA YM262 UT WOS:000071046000008 PM 9429674 ER PT J AU Cohen, SG AF Cohen, SG TI Asthma among the famous - Theodore Roosevelt (1853-1919) - Twenty-sixth president of the United States SO ALLERGY AND ASTHMA PROCEEDINGS LA English DT Biographical-Item C1 NIAID, Bethedsa, MD 20892 USA. RP Cohen, SG (reprint author), NIAID, Bethedsa, MD 20892 USA. NR 7 TC 1 Z9 1 U1 1 U2 2 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 USA SN 1088-5412 J9 ALLERGY ASTHMA PROC JI Allergy Asthma Proc. PD NOV-DEC PY 1997 VL 18 IS 6 BP 382 EP 386 PG 5 WC Allergy SC Allergy GA YM262 UT WOS:000071046000009 PM 9429675 ER PT J AU Cohen, SG AF Cohen, SG TI Asthma among the famous - William Lyon Phelps (1865-1943) - American University professor of English, literary critic, and lecturer SO ALLERGY AND ASTHMA PROCEEDINGS LA English DT Biographical-Item C1 NIAID, Bethesda, MD 20892 USA. RP Cohen, SG (reprint author), NIAID, Bethesda, MD 20892 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 USA SN 1088-5412 J9 ALLERGY ASTHMA PROC JI Allergy Asthma Proc. PD NOV-DEC PY 1997 VL 18 IS 6 BP 387 EP 390 PG 4 WC Allergy SC Allergy GA YM262 UT WOS:000071046000010 PM 9429676 ER PT J AU Cecco, SA Hristova, EN Rehak, NN Elin, RJ AF Cecco, SA Hristova, EN Rehak, NN Elin, RJ TI Clinically important intermethod differences for physiologically abnormal ionized magnesium results SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE ion-selective electrodes; electrolytes; intermethod comparison; ionized magnesium ID ELECTRODES; ANALYZER; CALCIUM; AVL AB We compared physiologically abnormal low and high ionized magnesium (iMg) results determined with the AVL 988-4 (AVL, Graz, Austria) and Nova CRT (Nova Biomedical, Waltham, Mass) ion-selective electrodes (ISEs) in serum samples from randomly selected patients. A result of less than or equal to 0.39 mmol/L with either ISE constituted the low magnesium group and of greater than or equal to 0.65 mmol/L the high magnesium group. Within each group we found significant differences between the iMg results. Major intermethod differences were found for samples with physiologically normal total magnesium concentration: most of the samples in the low magnesium group (83%) had abnormally low results with the Nova ISE, whereas most of the results with the AVL ISE (83%) were normal. In contrast, all results with the AVL ISE for the high magnesium group were abnormally high, but 67% of the results with the Nova ISE were normal. The agreement for the clinical interpretation of iMg results based on the reference interval for each method was only 32%. The differences in iMg results between the two analyzers must be resolved before using the iMg test as measured with ISE for patient care. C1 NIH,CLIN CHEM SECT,DEPT CLIN PATHOL,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD 20892. NR 11 TC 6 Z9 6 U1 0 U2 0 PU AMER SOC CLIN PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON ST, CHICAGO, IL 60612 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD NOV PY 1997 VL 108 IS 5 BP 564 EP 569 PG 6 WC Pathology SC Pathology GA YC418 UT WOS:A1997YC41800012 PM 9353096 ER PT J AU Schendel, DE Stockbauer, JW Hoffman, HJ Herman, AA Berg, CJ Schramm, WF AF Schendel, DE Stockbauer, JW Hoffman, HJ Herman, AA Berg, CJ Schramm, WF TI Relation between very low birth weight and developmental delay among preschool children without disabilities SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE birth weight; child development; infant, very low birth weight ID COGNITIVE-DEVELOPMENT; GESTATIONAL-AGE; SCHOOL-AGE; INFANTS; PRETERM; RISK; METAANALYSIS; BEHAVIOR; HEALTH; COHORT AB The authors examined the relation between very low birth weight (VLBW: <1,500 g) and possible developmental delay (DELAY) in the absence of frank developmental disability among young children. The prevalence of DELAY in a population-based cohort (Missouri resident births born from December 1989 through March 1991) of singleton VLBW children (n = 367) was compared with the prevalence of DELAY among both moderately low birth weight (MLBW: 1,500-2,499 g; n = 553) and normal birth weight (NEW: greater than or equal to 2,500 g; n = 555) singleton control children. DELAY was defined by nine measures of performance on the Denver Developmental Screening Test II at a median adjusted age of 15 months (range: 9-34 months). Subjects were asymptomatic for disabling conditions at developmental follow-up. Apparently well VLBW children were consistently at greater risk for both moderate and severe measures of DELAY and for DELAY across four functional areas than were either the MLBW (adjusted odds ratios: 1.4-2.7) or NEW children (adjusted odds ratios: 2.1-6.3). The greatest prevalence of DELAY tended to be among appropriate-for-gestational age VLBW children who were also the most premature. This study supports developmental follow-up of nondisabled VLBW children because of the significantly elevated risk for DELAY among apparently normal infants. C1 MISSOURI DEPT HLTH,STATE CTR HLTH STAT,BUR HLTH DATA ANAL,ST LOUIS,MO. NICHHD,EPIDEMIOL BRANCH,DIV EPIDEMIOL STAT & PREVENT RES,NIH,BETHESDA,MD 20892. CTR DIS CONTROL & PREVENT,PREGNANCY & INFANT HLTH BRANCH,DIV REPROD HLTH,ATLANTA,GA 30341. NATL INST DEAFNESS & OTHER COMMUN DISORDERS,EPIDEMIOL STAT & DATA SYST BRANCH,OFF DIRECTOR,NIH,BETHESDA,MD 20892. RP Schendel, DE (reprint author), CTR DIS CONTROL & PREVENT,DEV DISABIL DIS,DIV BIRTH DEFECTS & DEV DISABIL,NATL CTR ENVIRONM HLTH,CHAMBLEE,GA 30341, USA. FU NICHD NIH HHS [N01-HD-6-2916] NR 27 TC 30 Z9 32 U1 0 U2 0 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 NOV 1 PY 1997 VL 146 IS 9 BP 740 EP 749 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YF572 UT WOS:A1997YF57200009 PM 9366622 ER PT J AU Marrone, A Shih, JWK Nakatsuji, Y Alter, HJ Lau, D Vergalla, J Hoofnagle, JH AF Marrone, A Shih, JWK Nakatsuji, Y Alter, HJ Lau, D Vergalla, J Hoofnagle, JH TI Serum hepatitis G virus RNA in patients with chronic viral hepatitis SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID PLACEBO-CONTROLLED TRIAL; DISEASE ASSOCIATION; ALPHA-INTERFERON; DOUBLE-BLIND; GBV-C; INFECTION; THERAPY; RIBAVIRIN AB Objectives: The hepatitis G virus (HGV) is a newly described flavivirus that affects a high proportion of patients with chronic viral hepatitis: our objective was to determine what role HGV might play in the course of disease, Methods: We evaluated stored serum samples from 108 patients with chronic hepatitis B and 99 patients with chronic hepatitis C who participated in trials of cu-interferon or ribavirin for the presence of hepatitis B virus (HBV) DNA and, hepatitis C virus (HCV) RNA by branched DNA and for the presence of HGV RNA by polymerase chain reaction (PCR), using primers from the NS5 region of the genome, Results: Initially, 20 (19%) patients with hepatitis B and 11 (11%) with hepatitis C had HGV RNA in their serum, Patients with and without HGV infection were similar with regard to clinical features, laboratory tests, and hepatic histology, HGV RNA levels fell during interferon therapy and became undetectable in those receiving the highest doses; however, HGV RNA levels returned to pretreatment values when therapy was stopped, With ribavirin therapy, HGV RNA levels did not change, Two- to 12-yr follow-up serum samples were available from 17 initially HGV RNA-positive patients, of whom only 10 (59%) were still positive, Conclusions: HGV infection is common among patients with chronic hepatitis B and C but has little effect on the short-term course of disease or response to therapy, HGV RNA levels are suppressed but not eradicated by alpha-interferon and are unaffected by ribavirin treatment, Spontaneous loss of HGV RNA occurs over time in a proportion of patients. C1 NIH,CTR CLIN,DIV TRANSFUS MED,BETHESDA,MD 20892. RP Marrone, A (reprint author), NIDDKD,LIVER DIS SECT,DIGEST DIS BRANCH,BLDG 10,ROOM 9B16,BETHESDA,MD 20892, USA. NR 21 TC 13 Z9 13 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD NOV PY 1997 VL 92 IS 11 BP 1992 EP 1996 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YE270 UT WOS:A1997YE27000008 PM 9362178 ER PT J AU Hazelwood, S Shotelersuk, V Wildenberg, SC Chen, D Iwata, F KaiserKupfer, MI White, JG King, RA Gahl, WA AF Hazelwood, S Shotelersuk, V Wildenberg, SC Chen, D Iwata, F KaiserKupfer, MI White, JG King, RA Gahl, WA TI Evidence for locus heterogeneity in Puerto Ricans with Hermansky-Pudlak syndrome SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID STORAGE POOL DEFICIENCY AB Hermansky-Pudlak syndrome (HPS) consists of oculocutaneous albinism, a platelet storage-pool deficiency, and ceroid lipofuscinosis. In a recent report on the cloning of an HPS gene, all 22 Puerto Rican HPS patients were homozygous for a 16-bp duplication in exon 15. This presumably reflected a founder effect for the HPS mutation in Puerto Rico. Nevertheless, we ascertained two individuals from central Puerto Rico who lacked the 16-bp duplication, exhibited significant amounts of normal-size HPS mRNA by northern blot analysis, and had haplotypes in the HPS region that were different from the haplotype of every 16-bp-duplication patient. Moreover, these two individuals displayed no mutations in their cDNA sequences, throughout the entire HPS gene. Both patients exhibited pigment dilution, impaired visual acuity, nystagmus, a bleeding diathesis, and absent platelet dense bodies, confirming the diagnosis of HPS. These findings indicate that analysis of Puerto Rican patients for the 16-bp duplication in HPS cannot exclude the diagnosis of HPS. In addition, HPS most likely displays locus heterogeneity, consistent with the existence of several mouse strains manifesting both pigment dilution and a platelet storage-pool deficiency. C1 NEI,SECT HUMAN BIOCHEM GENET,HERITABLE DISORDERS BRANCH,NICHHD,BETHESDA,MD 20892. NEI,HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,NIH,BETHESDA,MD 20892. NEI,OPHTHALM GENET & CLIN SERV BRANCH,BETHESDA,MD 20892. UNIV MINNESOTA,DEPT MED,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT PEDIAT,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,INST HUMAN GENET,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT LAB MED,MINNEAPOLIS,MN 55455. NR 19 TC 53 Z9 53 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 NOV PY 1997 VL 61 IS 5 BP 1088 EP 1094 DI 10.1086/301611 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA YH017 UT WOS:A1997YH01700013 PM 9345105 ER PT J AU Mukherjee, AB Ward, JM Zhang, ZJ AF Mukherjee, AB Ward, JM Zhang, ZJ TI A role for uteroglobin in glomerulopathy: Knockout mice as a model system - Reply SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Editorial Material ID PREDOMINANT FIBRONECTIN DEPOSITS; CELL-SURFACE; BINDING; TRANSGLUTAMINASE; ANTIGENICITY; MODULATION; BIOLOGY; RABBIT; MATRIX; SITE RP Mukherjee, AB (reprint author), NICHHD,SECT DEV GENET,HERITABLE DISORDERS BRANCH,NIH,BLDG 10,ROOM 9S241,BETHESDA,MD 20892, USA. NR 27 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD NOV PY 1997 VL 30 IS 5 BP 722 EP 724 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA YD675 UT WOS:A1997YD67500020 ER PT J AU Sibai, BM Ewell, M Levine, RJ Klebanoff, MA Esterlitz, J Catalano, PM Goldenberg, RL Joffe, G AF Sibai, BM Ewell, M Levine, RJ Klebanoff, MA Esterlitz, J Catalano, PM Goldenberg, RL Joffe, G TI Risk factors associated with preeclampsia in healthy nulliparous women SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 17th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 20-25, 1997 CL ANAHEIM, CA SP Soc Perinatal Obstetricians DE risk factors; preeclampsia; nulliparous women ID PRE-ECLAMPSIA; PREGNANCY; HYPERTENSION; ABORTION AB OBJECTIVE: Our goal was to identify risk factors for the development of preeclampsia in nulliparous women enrolled in a multicenter trial comparing calcium supplementation to a placebo. STUDY DESIGN: A total of 4589 women from five centers was studied. Analysis of risk factors for preeclampsia was performed in 4314 who carried the pregnancy to >20 weeks. Baseline systolic and diastolic blood pressure, demographic characteristics, and findings after randomization were examined for the prediction of preeclampsia. Preeclampsia was defined as hypertension (diastolic blood pressure greater than or equal to 90 mm Hg on two occasions 4 hours to 1 week apart) and proteinuria (greater than or equal to 3C0 mg/24 hours, a protein/creatinine ratio greater than or equal to 0.35, one dipstick measurement greater than or equal to 2+ or two dipstick measurements greater than or equal to 1+ at an interval as specified for diastolic blood pressure). RESULTS: Preeclampsia developed in 326 women (7.6%). The first analysis treated each risk factor as a categoric variable in a univariate regression. Maternal age, blood group and Rh factor, alcohol use, previous abortion or miscarriage, private insurance, and calcium supplementation were not statistically significant. Risk factors initially found to be significant were body mass index, systolic blood pressure, diastolic blood pressure, non-white race (African-American and other), clinical center, and smoking. Adjusted odds ratios computed with a logistic regression model revealed that body mass index (odds ratio 3.22 for greater than or equal to 35 kg/m(2) vs <19.8 kg/m(2)), systolic blood pressure (odds ratic 2.66 for greater than or equal to 120 vs <101 mm Hg), diastolic blood pressure (odds ratio 1.72 for greater than or equal to 61 mm Hg vs <60 mm Hg), and clinical center (odds ratio 1.85 for Memphis vs the other clinical centers) were statistically significant predictors of preeclampsia. Results of the final model fit revealed that preeclampsia risk increases significantly (p < 0.0001) with increased body mass index at randomization, as well as with increased systolic and diastolic blood pressure at randomization. Calcium supplementation had no effect on the risks posed by body mass index and blood pressure. Among risk factors developing after randomization, an abnormal result of a glucose screen (plasma glucose greater than or equal to 140 mg/dl 1 hour after a 50 gm glucose challenge) was not found to be associated with a significant risk of preeclampsia. CONCLUSION: These risk factors should be of value in counseling women regarding preeclampsia and should aid in understanding the pathophysiologic characteristics of this syndrome. C1 UNIV ALABAMA,DEPT OBSTET & GYNECOL,BIRMINGHAM,AL 35294. METROHLTH MED CTR,DEPT OBSTET & GYNECOL,CLEVELAND,OH. EMMES CORP,POTOMAC,MD. NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,NIH,BETHESDA,MD 20892. UNIV NEW MEXICO,CTR HLTH SCI,DEPT OBSTET & GYNECOL,ALBUQUERQUE,NM 87131. RP Sibai, BM (reprint author), UNIV TENNESSEE,COLL MED,DEPT OBSTET & GYNECOL,MEMPHIS,TN 38163, USA. FU NICHD NIH HHS [N01-HD-1-3122, N01-HD-1-3121, N01-HD-1-3123] NR 22 TC 314 Z9 324 U1 2 U2 16 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 NOV PY 1997 VL 177 IS 5 BP 1003 EP 1010 DI 10.1016/S0002-9378(97)70004-8 PG 8 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA YJ231 UT WOS:A1997YJ23100004 PM 9396883 ER PT J AU Spong, CY Ghidini, A Walker, CN Ossandon, M Pezzullo, JC AF Spong, CY Ghidini, A Walker, CN Ossandon, M Pezzullo, JC TI Elevated maternal serum midtrimester alpha-fetoprotein levels are associated with fetoplacental ischemia SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 17th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 20-25, 1997 CL ANAHEIM, CA SP Soc Perinatal Obstetricians DE elevated maternal serum alpha-fetoprotein; angiogenin; fetoplacental ischemia AB OBJECTIVE: Elevation of maternal serum alpha-fetoprotein in the second trimester is associated with poor pregnancy outcome, including fetal death, preterm delivery, and fetal growth restriction. We hypothesized that placental ischemia may be the common underlying pathogenesis of these outcomes. Thus we tested angiogenin, a potent inducer of neovascularization, in midtrimester amniotic fluid of patients with elevated maternal serum alpha-fetoprotein values to determine whether alpha-fetoprotein elevation is due to ischemia with subsequent stimulation of angiogenesis. STUDY DESIGN: In this case-control study, patients with elevated maternal serum a-fetoprotein levels (greater than or equal to 2.0 multiples of the median, n = 9) at triple screen were matched with two controls (n = 18) on the basis of year of amniocentesis and maternal age, race, and parity. The median elevation of maternal serum alpha-fetoprotein in the study population was 4.01 multiples of the median (range 2.65 to 7.24 multiples of the median). inclusion criteria were (1) singleton gestation, (2) no evidence of fetal structural or chromosomal anomalies, and (3) genetic amniocentesis. Amniotic fluid was immunoassayed for angiogenin (Quantikine, R&D Systems; sensitivity 0.026 ng/ml, interassay and intraassay coefficients of variation 4.6% and 2.9%, respectively). Statistical analysis included one-way analysis of variance and regression with p < 0.05 significant. Angiogenin and maternal serum alpha-fetoprotein values were normalized with use of natural log transformation for statistical analysis. RESULTS: Angiogenin values were significantly elevated in patients with high maternal serum alpha-fetoprotein levels (median 31.1 [range 9.2 to 54.6] vs 17.1 [range 9.0 to 29.2] ng/ml, p = 0.02). Mean gestational age at sampling, maternal age, and year of amniocentesis were not significantly different between the study and control groups (each p 0.05). As anticipated, there was, a significant increase in preterm deliveries and small-for-gestational-age neonates in the patients with elevated maternal serum alpha-fetoprotein levels (each p < 0.01). CONCLUSIONS: Midtrimester amniotic fluid angiogenin levels are significantly elevated in patients with elevated midtrimester maternal serum alpha-fetoprotein levels. Because angiogenin is a known marker of tissue ischemia, resulting in neovascularization, we hypothesize that elevation of maternal serum alpha-fetoprotein levels at triple screen is due to placental ischemia. C1 GEORGETOWN UNIV,MED CTR,DEPT OBSTET & GYNECOL,WASHINGTON,DC 20057. GEORGETOWN UNIV,MED CTR,DEPT BIOSTAT & BIOMATH,WASHINGTON,DC 20007. RP Spong, CY (reprint author), NICHHD,DEV NEUROBIOL LAB,NIH,BETHESDA,MD 20892, USA. NR 6 TC 19 Z9 20 U1 0 U2 1 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 NOV PY 1997 VL 177 IS 5 BP 1085 EP 1087 DI 10.1016/S0002-9378(97)70019-X PG 3 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA YJ231 UT WOS:A1997YJ23100019 PM 9396898 ER PT J AU Chez, RA Jonas, WB AF Chez, RA Jonas, WB TI The challenge of complementary and alternative medicine SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE alternative medicine; complementary medicine ID CONTROLLED TRIAL; PRIMARY DYSMENORRHEA; CLINICAL-TRIALS; CHRONIC PAIN; ACUPUNCTURE; METAANALYSIS; PREVENTION; THERAPIES; DISEASE; CANCER AB Complementary and alternative medicine can be defined as those medical systems, practices, interventions, and applications that currently are not part of the dominant or conventional medical system. There are more than 300 different topics under the term complementary and alternative medicine that can be divided into seven major categories on the basis of philosophy, approach to the patient, and orientation. Most patients seeking care from complementary and alternative medicine providers do so for the relief of signs and symptoms related to chronic illness while they are under the care of a physician. Clinical data derived from appropriately conducted clinical trials support the use and value of complementary and alternative medicine for selected indications. The challenge for both conventional medicine and complementary and alternative medicine is to fulfill the role of patient advocate by engaging in reciprocal open communication, facilitating the patient's informed choice, avoiding harmful or useless practices, and implementing an integrated evidence-based care plan. C1 UNIV S FLORIDA,TAMPA,FL. NIH,OFF ALTERNAT MED,BETHESDA,MD 20892. NR 44 TC 31 Z9 31 U1 0 U2 3 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 NOV PY 1997 VL 177 IS 5 BP 1156 EP 1161 DI 10.1016/S0002-9378(97)70033-4 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA YJ231 UT WOS:A1997YJ23100033 PM 9396912 ER PT J AU Brinton, LA Gridley, G Persson, I AF Brinton, LA Gridley, G Persson, I TI Endometriosis and non-Hodgkin's lymphoma - Reply SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Letter RP Brinton, LA (reprint author), NCI,DIV CANC EPIDEMIOL & GENET,BETHESDA,MD 20892, USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 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 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD NOV PY 1997 VL 177 IS 5 BP 1275 EP 1275 DI 10.1016/S0002-9378(97)70062-0 PG 1 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA YJ231 UT WOS:A1997YJ23100063 ER PT J AU McCartneyFrancis, NL Mizel, DE FrazierJessen, M Kulkarni, AB McCarthy, JB Wahl, SM AF McCartneyFrancis, NL Mizel, DE FrazierJessen, M Kulkarni, AB McCarthy, JB Wahl, SM TI Lacrimal gland inflammation is responsible for ocular pathology in TGF-beta 1 null mice SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID TGF-BETA ISOFORMS; CELL-ADHESION MOLECULES; SJOGRENS-SYNDROME; ADULT TISSUES; MESSENGER-RNA; FIBRONECTIN PEPTIDES; GROWTH-FACTOR; MRL/LPR MICE; DIFFERENTIAL EXPRESSION; ANTIGEN EXPRESSION AB Mice homozygous for a nonfunctional transforming growth factor-beta 1 gene develop rampant inflammation in vital organs that contributes to a shortened life span. The presence of circulating anti-nuclear antibodies, immune deposits in tissues, leukocyte infiltration, and increased major histocompatibility complex antigen expression resembles an autoimmune-like syndrome. One of the overt symptoms that appears in these mice lacking transforming growth factor-beta 1 is the development of dry crusty eyes that close persistently as their health declines. Histologically, the eyes appear normal with Little or no inflammation. However, inflammatory lesions, predominantly lymphocytic, develop in the lacrimal glands, disrupting their structure and function and severely limiting their ability to generate tears. This histopathology and aberrant function mimic that of Sjogren's syndrome, a human autoimmune disease characterized by dry eyes and dry mouth, Impeding the leukocyte infiltration into the glands with synthetic fibronectin peptides, which block adhesion, not only prevents the inflammatory pathology but also prevents the persistent eye closure characteristic of these mice. C1 NIDR, GENE TARGETING RES & CORE FACIL, NIH, BETHESDA, MD 20892 USA. UNIV MINNESOTA, DEPT LAB MED & PATHOL, MINNEAPOLIS, MN 55455 USA. RP McCartneyFrancis, NL (reprint author), NIDR, ORAL INFECT & IMMUN BRANCH, NIH, 30 CONVENT DR, BETHESDA, MD 20892 USA. NR 55 TC 21 Z9 21 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD NOV PY 1997 VL 151 IS 5 BP 1281 EP 1288 PG 8 WC Pathology SC Pathology GA YD878 UT WOS:A1997YD87800015 PM 9358754 ER PT J AU Dienel, GA Cruz, NF Adachi, KJ Sokoloff, L Holden, JE AF Dienel, GA Cruz, NF Adachi, KJ Sokoloff, L Holden, JE TI Determination of local brain glucose level with [C-14]methylglucose: effects of glucose supply and demand SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE cerebral glucose utilization; brain hexose transport ID 2-DEOXYGLUCOSE LUMPED CONSTANT; RAT-BRAIN; DEOXYGLUCOSE METHOD; TRANSPORT; BLOOD; PHOSPHORYLATION; METHYLGLUCOSE; METABOLITES; BARRIER; CULTURE AB Methylglucose can be used to assay brain glucose levels because the equilibrium brain-to-plasma distribution ratio for methylglucose (C-e*/C-p*) is quantitatively related to brain (C-e) and plasma (C-p) glucose contents. The relationship between C-e and C-e*/C-p* predicted by Michaelis-Menten kinetics has been experimentally confirmed when glucose utilization rate (CMRGlc) is maintained at normal, resting levels and C-p is varied in conscious rats. Theoretically, however, C-e and C-e*/C-p* should change when CMRGlc is altered and C-p is held constant; their relationship in such conditions was, therefore, examined experimentally. Drugs were applied topically to brains of conscious rats with fixed levels of C-p to produce focal alterations in CMRGlc, and C-e and C-e*/C-p* were measured. Plots of C-e as a function of C-e*/C-p* for each C-p produced straight lines; their slopes decreased as C-p increased. The results confirm that a single theoretical framework describes the relationship between C-e and C-e*/C-p* as either glucose supply or demand is altered over a wide range; they also validate the use of methylglucose to estimate local C-e under abnormal conditions. C1 NIMH, CEREBRAL METAB LAB, BETHESDA, MD 20892 USA. UNIV WISCONSIN, SCH MED, DEPT MED PHYS, MADISON, WI 53706 USA. NR 32 TC 21 Z9 21 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD NOV PY 1997 VL 273 IS 5 BP E839 EP E849 PG 11 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA YF556 UT WOS:A1997YF55600002 PM 9374668 ER PT J AU Gabel, SA Cross, HR London, RE Steenbergen, C Murphy, E AF Gabel, SA Cross, HR London, RE Steenbergen, C Murphy, E TI Decreased intracellular pH is not due to increased H+ extrusion in preconditioned rat hearts SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE preconditioning; phosphorus-31 nuclear magnetic resonance ID ISCHEMIA; EXCHANGE; RECOVERY; NA+; GLYCOGENOLYSIS; MECHANISM; CALCIUM; SODIUM; VOLUME; DELAYS AB Ischemic preconditioning reduces intracellular acidification during a subsequent, prolonged period of ischemia. This may reflect decreased anaerobic glycolysis or increased H+ efflux. To distinguish between these hypotheses, we monitored intracellular and extracellular pH during a sustained period of ischemia to determine whether the preconditioned hearts had increased H+ efflux compared with nonpreconditioned hearts. At the end of 20 min of ischemia, intracellular pH in nonpreconditioned hearts was 5.90 +/- 0.08 and extracellular pH was 5.51 +/- 0.21, whereas in preconditioned hearts, intracellular pH was 6.50 +/- 0.06 and extracellular pH was 6.62 +/- 0.06. To investigate whether an Na+/H+ exchange inhibitor would alter the reduced acidification during ischemia, we preconditioned hearts with and without dimethylamiloride (DMA). Intracellular pH during ischemia was similar in preconditioned hearts with and without DMA treatment (pH 6.42 +/- 0.02 vs. 6.45 +/- 0.03, respectively). These data do not support the hypothesis that enhanced proton efflux is responsible for the more alkaline intracellular pH during sustained ischemia in preconditioned hearts. C1 NIEHS, Lab Mol Biophys, Res Triangle Pk, NC 27709 USA. Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA. RP Gabel, SA (reprint author), NIEHS, Lab Mol Biophys, POB 12233, Res Triangle Pk, NC 27709 USA. NR 25 TC 29 Z9 30 U1 0 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD NOV PY 1997 VL 273 IS 5 BP H2257 EP H2262 PG 6 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA YF553 UT WOS:A1997YF55300022 ER PT J AU Johansson, M Rundqvist, B Eisenhofer, G Friberg, P AF Johansson, M Rundqvist, B Eisenhofer, G Friberg, P TI Cardiorenal epinephrine kinetics: evidence for neuronal release in the human heart SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE neuronal epinephrine release ID CARDIAC SYMPATHETIC-NERVES; NORADRENALINE RELEASE; REGIONAL RELEASE; HYPERTENSION; ADRENALINE; NOREPINEPHRINE; CATECHOLAMINES; REMOVAL AB There are experimental data suggesting that epinephrine (Epi) may act as a cotransmitter in sympathetic nerves, stimulating presynaptic beta(2)-receptors and enhancing norepinephrine (NE) release. To examine neuronal Epi release, patients with congestive heart failure and hypertension and healthy subjects were examined with the isotope-dilution method. At baseline, small cardiac and renal Epi spillovers were found in patients. During intense supine exercise, cardiac NE and Epi spillovers increased concomitantly with similar magnitude, whereas no renal Epi spillover could be detected. Blockade of neuronal uptake 1 caused a consistent decrease in both cardiac and renal fractional extractions of NE and Epi. The present study demonstrates baseline cardiorenal Epi release in patients with congestive heart failure and renal Epi release in hypertensive patients. Furthermore, Epi is removed by neuronal uptake in both the heart and kidney, and cardiac Epi spillover increases during exercise. This study, in contrast to other results, provides evidence for cardiac neuronal Epi release. C1 Sahlgrens Univ Hosp, Dept Clin Physiol, S-41345 Gothenburg, SWEDEN. Sahlgrens Univ Hosp, Dept Cardiol, S-41345 Gothenburg, SWEDEN. NINDS, NIH, Bethesda, MD 20892 USA. RP Johansson, M (reprint author), Sahlgrens Univ Hosp, Dept Clin Physiol, S-41345 Gothenburg, SWEDEN. NR 26 TC 18 Z9 18 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD NOV PY 1997 VL 273 IS 5 BP H2178 EP H2185 PG 8 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA YF553 UT WOS:A1997YF55300012 PM 9374751 ER PT J AU Potdar, PD Andrews, KL Nettesheim, P Ostrowski, LE AF Potdar, PD Andrews, KL Nettesheim, P Ostrowski, LE TI Expression and regulation of gamma-glutamyl transpeptidase-related enzyme in tracheal cells SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY LA English DT Article DE glutathione; oxidative stress; pulmonary epithelium ID EPITHELIAL-CELLS; TRANSFERASE TRANSPEPTIDASE; GLUTATHIONE; DIFFERENTIATION; IDENTIFICATION; TOXICITY; RNA AB Glutathione plays an essential role in protecting the pulmonary system from toxic insults. gamma-Glutamyl transpeptidase-related enzyme (GGT-rel) is a novel protein capable of cleaving the gamma-glutamyl peptide bond of glutathione and of converting leukotriene C-4 to leukotriene D-4. A rat homologue of GGT-rel was identified and was found to be highly expressed in cultures of differentiating rat tracheal epithelial (RTE) cells. The 2.6-kb cDNA predicts a 572-amino acid protein with 79% identity to human GGT-rel. GGT-rel was weakly expressed in normal trachea but was strongly induced by epidermal growth factor in cultures of RTE cells. GGT-rel was also highly expressed in lung tumors induced by inhalation of isobutyl nitrite. These results demonstrate that GCT-rel 1) is expressed in normal tracheal cells, 2) can be induced by epidermal growth factor, and 3) is elevated after chemical exposure. The induction of high levels of GGT-rel may play an important role in protecting the lung from oxidative stress or other toxic insults. C1 NIEHS, PULM PATHOBIOL LAB, RES TRIANGLE PK, NC 27709 USA. NR 24 TC 15 Z9 15 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1040-0605 J9 AM J PHYSIOL-LUNG C JI Am. J. Physiol.-Lung Cell. Mol. Physiol. PD NOV PY 1997 VL 273 IS 5 BP L1082 EP L1089 PG 8 WC Physiology; Respiratory System SC Physiology; Respiratory System GA YF568 UT WOS:A1997YF56800023 ER PT J AU Demas, GE Chefer, V Talan, MI Nelson, RJ AF Demas, GE Chefer, V Talan, MI Nelson, RJ TI Metabolic costs of mounting an antigen-stimulated immune response in adult and aged C57BL/6J mice SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article DE energetics; melatonin; thermoregulation; immunoglobulin ID PINEAL-GLAND; COLD TOLERANCE; DEER MICE; MELATONIN; PHOTOPERIOD; SEROTONIN; REPRODUCTION; MOUSE AB Animals must balance their energy budget despite seasonal changes in both energy availability and physiological expenditures. Immunity, in addition to growth, thermoregulation, and cellular maintenance, requires substantial energy to maintain function, although few studies have directly tested the energetic cost of immunity. The present study assessed the metabolic costs of an antibody response. Adult and aged male C5BL/6J mice were implanted with either empty Silastic capsules or capsules filled with melatonin and injected with either saline or keyhole limpet hemocyanin (KLH). O-2 consumption was monitored periodically throughout antibody production using indirect calorimetry. KLH-injected mice mounted significant immunoglobulin G (IgG) responses and consumed more O-2 compared with animals injected with saline. Melatonin treatment increased O-2 consumption in mice injected with saline but suppressed the increased metabolic rate associated with an immune response in KLH-injected animals. Melatonin had no effect on immune response to KLH. Adult and aged mice did not differ in antibody response or metabolic activity Aged mice appear unable to maintain sufficient heat production despite comparable O-2 production to adult mice. These results suggest that mounting an immune response requires significant energy and therefore requires using resources that could otherwise be allocated to other physiological processes. Energetic trade-offs are likely when energy demands are high (e.g., during winter, pregnancy, or lactation). Melatonin appears to play an adaptive role in coordinating reproductive, immunologic, and energetic processes. C1 JOHNS HOPKINS UNIV, DEPT NEUROSCI, DIV REPROD BIOL, BALTIMORE, MD 21218 USA. JOHNS HOPKINS UNIV, DEPT POPULAT DYNAM, DIV REPROD BIOL, BALTIMORE, MD 21218 USA. NIA, GERONTOL RES CTR, BEHAV SCI LAB, NIH, BALTIMORE, MD 21224 USA. RP Demas, GE (reprint author), JOHNS HOPKINS UNIV, DEPT PSYCHOL, BEHAV NEUROENDOCRINOL GRP, DIV REPROD BIOL, BALTIMORE, MD 21218 USA. NR 35 TC 218 Z9 226 U1 4 U2 28 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regul. Integr. Comp. Physiol. PD NOV PY 1997 VL 273 IS 5 BP R1631 EP R1637 PG 7 WC Physiology SC Physiology GA YF569 UT WOS:A1997YF56900010 ER PT J AU Mandon, B Nielsen, S Kishore, BK Knepper, MA AF Mandon, B Nielsen, S Kishore, BK Knepper, MA TI Expression of syntaxins in rat kidney SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY LA English DT Article DE collecting duct; vesicle-targeting receptors; water channel; aquaporin; vasopressin ID REGULATED WATER CHANNEL; POLYMERASE CHAIN-REACTION; COLLECTING DUCT; PLASMA-MEMBRANE; INTERCALATED CELLS; H+-ATPASE; PROTEIN; VASOPRESSIN; LOCALIZATION; TRAFFICKING AB Previously, we demonstrated that a putative vesicle-targeting protein, syntaxin-4, is expressed in renal collecting duct principal cells and is localized to the apical plasma membrane, suggesting a role in targeting aquaporin-2-containing vesicles to the apical plasma membrane. To investigate whether other syntaxin isoforms are present in the renal collecting duct, we determined the intrarenal localization of syntaxin-2 and -3. Reverse transcription-polymerase chain reaction (RT-PCR) experiments using total RNA extracted from kidney and various organs revealed that both syntaxin-2 and -3 are expressed in kidney cortex and medulla. RT-PCR experiments using microdissected tubules and vascular structures from the kidney revealed that syntaxin-3 mRNA, but not syntaxin-2, is expressed in collecting duct cells. Syntaxin-3 mRNA aias also relatively abundant in the thick ascending limb of Henle's loop and in vasa recta. Syntaxin-2 mRNA was found chiefly in glomeruli. To investigate the localization of syntaxin-3 protein, a peptide-derived polyclonal antibody was raised in rabbits. In immunoblotting experiments, this antibody labeled a 37-kDa protein in inner medulla that was most abundant in plasma membrane-enriched subcellular fractions. Immunoperoxidase labeling of thin cryosections combined with immunogold electron microscopy showed that, in contrast to the labeling seen for syntaxin-4, syntaxin-3 labeling in medullary collecting duct was predominantly in the basolateral plasma membrane of intercalated cells. These results suggest the possibility that syntaxin-3 may be involved in selective targeting of acid-base transporters and/or in basolateral membrane remodeling in response to systemic acid-bass perturbations. C1 NHLBI, KIDNEY & ELECTROLYTE METAB LAB, NIH, BETHESDA, MD 20892 USA. AARHUS UNIV, INST ANAT, DEPT CELL BIOL, DK-8000 AARHUS, DENMARK. FU NHLBI NIH HHS [ZO1-HL-01282-KE] NR 46 TC 53 Z9 54 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1931-857X J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Physiol. PD NOV PY 1997 VL 273 IS 5 BP F718 EP F730 PG 13 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA YF558 UT WOS:A1997YF55800007 PM 9374835 ER PT J AU Klabunde, CN O'Malley, MS Kaluzny, AD AF Klabunde, CN O'Malley, MS Kaluzny, AD TI Physicians' reactions to change in recommendations for mammography screening SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE LA English DT Article DE mammography; screening; practice guidelines; health policy; primary care ID WOMEN AGED 40; NATIONAL-CANCER-INSTITUTE; PRIMARY-CARE PHYSICIANS; BREAST-CANCER; PRACTICE GUIDELINES; MEDICAL TECHNOLOGY; OLDER WOMEN; IMPACT; CONTROVERSY AB Introduction: In December 1993 the National Cancer Institute (NCI) decided to replace its mammography screening guidelines with a Statement of Evidence on Breast Cancer Screening. The Statement of Evidence represented a departure from the institute's previous policy of recommending routine mammography screening in women 40-49 and annual screening in women 50 and over. This study assesses knowledge of and attitudes toward the Statement of Evidence among primary care physicians. In addition, we explore the extent to which physicians changed their individual clinical policies on mammography screening in response to the Statement of Evidence. Methods: Between October 1994 and June 1995, 545 randomly selected North Carolina primary care physicians completed a mailed questionnaire (overall survey response rate = 42%). Results: Awareness of the Statement of Evidence was high (83%), but attitudes toward it were negative, with a majority of physicians stating that the change in policy was confusing to women and physicians. About 8% of physicians who were aware of the Statement of Evidence changed their practice accordingly. Most physicians reported recommending routine mammography screening in women 40-49 and annual screening in women 50 and over. A majority stated they believe scientific evidence supports these practices. Conclusions: When faced with a new policy in which guidelines are no longer provided and evidence supporting less use of an established technology is conveyed, physicians demonstrated disinclination to change. The impact of changes in recommendations on physician practice is an important consideration for those who develop and promote screening policies. C1 NCI, Appl Res Branch, Canc Prevent Fellowship Program, Div Canc Prevent & Control, Bethesda, MD 20892 USA. RP Klabunde, CN (reprint author), NCI, Appl Res Branch, Canc Prevent Fellowship Program, Div Canc Prevent & Control, Execut Plaza N Room 313,6130 Execut Blvd MSC 7344, Bethesda, MD 20892 USA. FU NCI NIH HHS [CA57726, CA58223] NR 41 TC 10 Z9 10 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0749-3797 J9 AM J PREV MED JI Am. J. Prev. Med. PD NOV-DEC PY 1997 VL 13 IS 6 BP 432 EP 438 PG 7 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA YL872 UT WOS:000071002300007 PM 9415788 ER PT J AU Robin, RW Chester, B Rasmussen, JK Jaranson, JM Goldman, D AF Robin, RW Chester, B Rasmussen, JK Jaranson, JM Goldman, D TI Prevalence and characteristics of trauma and posttraumatic stress disorder in a Southwestern American Indian community SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DIAGNOSTIC INTERVIEW; SCHIZOPHRENIA; SCHEDULE; LIFETIME; HEALTH; EVENTS; IMPACT AB Objective: High rates of violence and trauma in many American Indian communities have been reported. The authors investigated the relationship between both the frequency and type of traumatic events and the prevalence of posttraumatic stress disorder (PTSD) in a South-western American Indian tribe. Method: A structured psychiatric interview and the Traumatic Events Booklet were administered to a subset of 247 tribal members from an overall study population of 582. Subjects were recruited from the community on the basis of membership in pedigrees, and not by convenience. DSM-III-R diagnoses were assigned by consensus after the interviews were evaluated blindly by independent raters. Results: The prevalence of lifetime PTSD was 21.9% (N=54), and 81.4% of the subjects (N=201) had experienced at least one traumatic event apiece. The most predictive factor for lifetime PTSD among women was the experience of physical assault, and for men the most predictive factors were a history of combat and having experienced more than 10 traumatic events. Conclusions: In this South-western American Indian community, the prevalences of lifetime PTSD and of exposure to a traumatic event were higher than in the general U.S. population. However, the nearly 4:1 ratio of subjects who reported at least one traumatic event to those with PTSD diagnoses is similar to findings from studies of non-Indians. Individuals with a history of multiple traumatic events (66.0%, N=163) had a significantly higher risk of developing PTSD. Chronic and multiple trauma did not preclude the identification of acute and discrete traumatic events that resulted in PTSD. C1 NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20852. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 37 TC 70 Z9 71 U1 0 U2 0 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 NOV PY 1997 VL 154 IS 11 BP 1582 EP 1588 PG 7 WC Psychiatry SC Psychiatry GA YD365 UT WOS:A1997YD36500015 PM 9356568 ER PT J AU Maity, R Nair, SR Caspi, RR Nelson, LM AF Maity, R Nair, SR Caspi, RR Nelson, LM TI Post-thymectomy murine experimental autoimmune oophoritis is associated with reduced natural killer cell activity SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Article DE autoimmune oophoritis; IL-12; NK cell activity ID PREMATURE OVARIAN FAILURE; NK CELLS; IMMUNOGLOBULIN SECRETION; NEONATAL THYMECTOMY; IMMUNE-RESPONSES; MICE; LYMPHOCYTES; INTERFERON; EFFECTOR; OOCYTES AB PROBLEM: Natural killer (NK) cells can influence the immune response by secreting potent lymphokines. It has been suggested that NK cells have a suppressive action on B cells, and that impaired NK cell activity may play a role in some types of autoimmunity. NK cell abnormalities have been reported in women with premature ovarian failure. We therefore examined NK cell activity during the development of murine experimental autoimmune oophoritis, which serves as a model for autoimmune ovarian failure in women. METHOD OF STUDY: Neonatally thymectomized and sham-operated C57Bl/6 x A/J (B6A) mice were prepared and sacrificed at 4, 6, 8, and 10 weeks after surgery. Splenic NK cell activity was determined in groups of five or more mice by measuring the percent specific lysis of target YAC-1 lymphoma cells using a standard 4-hr chromium release cytotoxicity assay. The number of splenic NK cells in neonatally thymectomized and sham-operated animals was also compared using flow cytometry. In a subsequent experiment, interleukin 12 (IL-12; NK cell-stimulating factor) was administered to neonatal mice before neonatal thymectomy. RESULTS: Neonatally thymectomized mice with associated autoimmune oophoritis had a 75% reduction in the number of splenic NK cells, and 50% or greater reduction in splenic NK cell activity at 4, 6, and 8 weeks after surgery. IL-12 treatment before neonatal thymectomy maintained NK cell activity and was shown to ameliorate the associated autoimmune oophoritis. CONCLUSION: Murine post-thymectomy autoimmune oophoritis is associated with reduced NK cell number and impaired NK cell activity, and in these respects the model is similar to premature ovarian failure in women. Research to define the relationship between NK cell abnormalities and the mechanism of ovarian failure in this model might lend insight into the pathogenesis of premature ovarian failure in women. C1 NICHHD,SECT WOMENS HLTH,DEV ENDOCRINOL BRANCH,NIH,BETHESDA,MD 20892. NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 23 TC 9 Z9 9 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 8755-8920 J9 AM J REPROD IMMUNOL JI Am. J. Reprod. Immunol. PD NOV PY 1997 VL 38 IS 5 BP 360 EP 365 PG 6 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA YA213 UT WOS:A1997YA21300007 PM 9352028 ER PT J AU Rautalahti, M Virtamo, J Haukka, J Heinonen, OP Sundvall, J Albanes, D Huttunen, JK AF Rautalahti, M Virtamo, J Haukka, J Heinonen, OP Sundvall, J Albanes, D Huttunen, JK TI The effect of Alpha-Tocopherol and Beta-Carotene supplementation on COPD symptoms SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID OBSTRUCTIVE PULMONARY-DISEASE; CIGARETTE-SMOKE; VITAMIN-E; LUNG; ANTIOXIDANT; PLASMA; QUESTIONNAIRE; EPIDEMIOLOGY; DETERMINANTS; EMPHYSEMA AB The effects of alpha-tocopherol (50 mg/d) and beta-carotene (20 mg/d) supplementation on symptoms of chronic obstructive pulmonary disease were studied among the 29, 133 participants of the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study undertaken to investigate the effects of these two substances in the prevention of lung and other cancers. During the follow-up the supplementations did not affect the recurrence or incidence of chronic cough, phlegm, or dyspnea. The prevalence of chronic bronchitis and dyspnea at baseline was lower among those with high dietary intake of beta-carotene (OR = 0.78 and 0.67, respectively) or vitamin E (OR = 0.87 and 0.77) and high serum beta-carotene (OR = 0.59 and 0.62) and alpha-tocopherol (OR = 0.76 and 0.82). High intake and serum levels of retinol were associated with low prevalence of dyspnea (OR = 0.84 and 0.80, respectively) but not with chronic bronchitis. The results indicate no benefit from supplementation with alpha-tocopherol or beta-carotene on the symptoms of chronic obstructive pulmonary disorders but support the beneficial effect of dietary intake of fruits and vegetables rich in these compounds. C1 NCI,BETHESDA,MD 20892. RP Rautalahti, M (reprint author), NATL PUBL HLTH INST,MANNERHEIMINTIE 166,SF-00300 HELSINKI,FINLAND. RI Albanes, Demetrius/B-9749-2015; Haukka, Jari/G-1484-2014 OI Haukka, Jari/0000-0003-1450-6208 FU NCI NIH HHS [N01-CN-45165] NR 35 TC 79 Z9 81 U1 0 U2 2 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 NOV PY 1997 VL 156 IS 5 BP 1447 EP 1452 PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YF682 UT WOS:A1997YF68200014 PM 9372659 ER PT J AU Johnson, BE Chute, JP Rushin, J Williams, J Le, PT Venzon, D Richardson, GE AF Johnson, BE Chute, JP Rushin, J Williams, J Le, PT Venzon, D Richardson, GE TI A prospective study of patients with lung cancer and hyponatremia of malignancy SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID ATRIAL-NATRIURETIC-FACTOR; ANTIDIURETIC-HORMONE SECRETION; MILD HEART-FAILURE; TUMOR-CELL LINES; SODIUM; VASOPRESSIN; PEPTIDE; PLASMA; STAGE; GENE AB This study was undertaken to define the impact of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) on sodium homeostasis in patients with lung cancer. Patients had their serum and urine electrolytes and osmolality determined before and after a saline infusion of 500 ml. The plasma hormones, AVP, ANP, plasma renin activity (PRA), angiotensin II, and aldosterone were determined by radioimmunoassay every 15 min before, during and after the saline infusion. Fifty patients, 31 with small cell lung cancer and 19 with non-small cell lung cancer participated in this trial. All 11 patients (10 patients with small cell lung cancer and one patient with non-small cell lung cancer) who presented with hyponatremia had inappropriately elevated levels of AVP. Elevated plasma AVP levels were highly correlated with the presence of hyponatremia (p < 0.00001). Initial plasma ANP levels were not associated with hyponatremia (p = 0.73). Urinary sodium concentration increased during the saline infusion proportional to the initial plasma level of ANP (p = 0.0045). AVP appears to be elevated in nearly all patients with hyponatremia of malignancy. ANP plasma levels in patients with lung cancer are associated with the ability to excrete a sodium load but do not appear to downregulate renin, angiotensin II, and aldosterone production. C1 NATL NAVAL MED CTR, NCI, DIV CLIN SCI, DATA MANAGEMENT SECT, BETHESDA, MD 20889 USA. NATL NAVAL MED CTR, NCI, DEPT MED & PATHOL, BETHESDA, MD 20889 USA. RP Johnson, BE (reprint author), NATL NAVAL MED CTR, MED BRANCH, BLDG 8, ROOM 5101, BETHESDA, MD 20889 USA. RI Venzon, David/B-3078-2008 NR 35 TC 37 Z9 37 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 NOV PY 1997 VL 156 IS 5 BP 1669 EP 1678 PG 10 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YF682 UT WOS:A1997YF68200047 PM 9372692 ER PT J AU You, L Jakowlew, SB AF You, L Jakowlew, SB TI Identification of early growth response gene-1 (Egr-1) as a phorbol myristate acetate-induced gene in lung cancer cells by differential mRNA display SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID TRANSFORMING GROWTH-FACTOR-BETA-1; TRANSCRIPTION FACTORS; MESSENGER-RNAS; C-FOS; PROTEIN; JUN; AP-1; BETA; EXPRESSION; ONCOGENE AB Cellular regulatory genes including transcription factors may play an important role in the induction, maintenance, and progression of lung cancer, These regulatory genes are inducible by various mitogenic stimuli including phorbol myristate acetate (PMA). The differential mRNA display method was used to identify potential early response genes regulated by PMA in non-small cell lung cancer (NSCLC) cell lines, Using this technique, several cDNA fragments were found to be potentially differentially regulated by PMA in the squamous NSCLC cell line NCI-H157. One of these cDNA fragments of approximately 100 bp was determined to be differentially induced by at least 30-fold by PMA by northern blot analysis and to hybridize to a single 3.4 kb mRNA species, This cDNA fragment was cloned, sequenced, and identified to be identical to a portion of the 3'-untranslated region of the human early growth response gene-1 (Egr-1). Using Egr-1 cDNA as a probe, it was demonstrated that PMA induces Egr-1 mRNA expression in at least three other NSCLC cells as well. In addition, PMA caused a transient increase in expression of the Egr-1 transcript reaching a maximum level by 1 h before decreasing in NCI-H157 and three other types of NSCLC cells. Treatment of these NSCLC cells with TGF-beta(1) showed a transient increase in Egr-1 mRNA similar to PMA which also reached a maximum level after 1 h, Normal human bronchial epithelial (NHBE) cells also showed a rapid, transient increase in expression of Egr-1 mRNA after treatment with PMA, In contrast, treatment of NHBE cells with TGF-beta(1) showed that expression of Egr-1 mRNA increased by 1 h but reached a maximum level only after 6 h, These results indicate that both PMA and TGF-beta(1) can induce Egr-1 mRNA expression in NSCLC cells and NHBE cells; however, while PMA induces Egr-1 mRNA similarly in both cell types, TGF-beta(1) induces Egr-1 mRNA expression more rapidly and more transiently in NSCLC cells than in NHBE cells. Our results suggest that Egr-1 may play different roles in response to mitogens in normal and malignant lung cells. C1 NCI,MED BRANCH,DEPT CELL & CANC BIOL,ROCKVILLE,MD 20850. NR 34 TC 7 Z9 7 U1 0 U2 0 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 NOV PY 1997 VL 17 IS 5 BP 617 EP 624 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA YG287 UT WOS:A1997YG28700010 PM 9374113 ER PT J AU Courcoutsakis, NA Hill, SC Chow, CK Gralnick, H AF Courcoutsakis, NA Hill, SC Chow, CK Gralnick, H TI Breast hemangiomas in a patient with Kasabach-Merritt syndrome: Imaging findings SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BETHESDA,MD 20892. NR 7 TC 9 Z9 11 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 1997 VL 169 IS 5 BP 1397 EP 1399 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA YC823 UT WOS:A1997YC82300040 PM 9353467 ER PT J AU Morrell, CH Pearson, JD Brant, LJ AF Morrell, CH Pearson, JD Brant, LJ TI Linear transformations of linear mixed-effects models SO AMERICAN STATISTICIAN LA English DT Article DE hierarchical linear models; hierarchical ordering; random coefficient models; variable selection; well-formulated models ID POLYNOMIAL REGRESSION-MODELS AB A number of articles have discussed the way lower order polynomial and interaction terms should be handled in linear regression models. Only if all lower order terms are included in the model will the regression model be invariant with respect to coding transformations of the variables. If lower order terms are omitted, the regression model will not be well formulated. In this paper, we extend this work to examine the implications of the ordering of variables in the linear mixed-effects model. We demonstrate how linear transformations of the variables affect the model and tests of significance of fixed effects in the model. We show how the transformations modify the random effects in the model, as well as their covariance matrix and the value of the restricted log-likelihood. We suggest a variable selection strategy for the linear mixed-effects model. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP Morrell, CH (reprint author), LOYOLA COLL,DEPT MATH SCI,BALTIMORE,MD 21210, USA. NR 14 TC 73 Z9 74 U1 2 U2 7 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 SN 0003-1305 J9 AM STAT JI Am. Stat. PD NOV PY 1997 VL 51 IS 4 BP 338 EP 343 DI 10.2307/2685902 PG 6 WC Statistics & Probability SC Mathematics GA YH217 UT WOS:A1997YH21700008 ER PT J AU Qiao, YL Taylor, PR Yao, SX Erozan, YS Luo, XC Barrett, MJ Yan, QY Giffen, CA Huang, SQ Maher, MM Forman, MR Tockman, MS AF Qiao, YL Taylor, PR Yao, SX Erozan, YS Luo, XC Barrett, MJ Yan, QY Giffen, CA Huang, SQ Maher, MM Forman, MR Tockman, MS TI Risk factors and early detection of lung cancer in a cohort of Chinese tin miners SO ANNALS OF EPIDEMIOLOGY LA English DT Article DE lung cancer; radon; arsenic; tobacco; cohort; early detection; biologic specimen bank ID YUNNAN PROVINCE; SOUTHERN CHINA; TOBACCO USE; EXPOSURE; RADON; CIGARETTE; MARKERS; RATIO AB PURPOSE: To examine risk factors and establish a biologic specimen and data bank for the study of early markers of lung cancer. METHODS: We designed a dynamic cohort using an ongoing lung cancer screening program among radon-and arsenic-exposed tin miners in Yunnan China. Through the first four years of the study, 8,346 miners aged 40 years and older with over 10 years of occupational exposure have been enrolled, risk factors have been assessed, annual sputum and chest radiographs have been obtained, and numerous biologic specimens have been collected. RESULTS: A total of 243 new lung cancer cases have been identified through 1995. Radon and arsenic exposures are the predominant risk factors, but lung cancer risk is also associated with chronic bronchitis and silicosis, as well as a number of measures of exposure to tobacco smoke, including early age of first use, duration, and cumulative exposure. Tumor and sputum samples are being examined for early markers of lung cancer. CONCLUSION: A cohort of occupationally-exposed tin miners with an extensive biologic specimen repository has been successfully established to simultaneously study the etiology and early detection of lung cancer. Published by Elsevier Science Inc. C1 NCI,CANC PREVENT STUDIES BRANCH,NIH,BETHESDA,MD 20892. YUNNAN TIN CORP,LABOR PROTECT INST & GEN HOSP,GEJIU,PEOPLES R CHINA. JOHNS HOPKINS MED INST,DEPT ENVIRONM HLTH SCI,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT ONCOL,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT PATHOL,BALTIMORE,MD 21205. INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. RI Qiao, You-Lin/B-4139-2012 OI Qiao, You-Lin/0000-0001-6380-0871 FU NCI NIH HHS [N01-CN-25420] NR 28 TC 28 Z9 33 U1 0 U2 7 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1047-2797 J9 ANN EPIDEMIOL JI Ann. Epidemiol. PD NOV PY 1997 VL 7 IS 8 BP 533 EP 541 DI 10.1016/S1047-2797(97)00115-4 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YK238 UT WOS:A1997YK23800004 PM 9408549 ER PT J AU Kimm, SYS Barton, BA Berhane, K Ross, JW Payne, GH Schreiber, GB AF Kimm, SYS Barton, BA Berhane, K Ross, JW Payne, GH Schreiber, GB TI Self-esteem and adiposity in black and white girls: The NHLBI growth and health study SO ANNALS OF EPIDEMIOLOGY LA English DT Article DE adiposity; self-concept; self-esteem; race; childhood obesity ID CHILDHOOD OBESITY; WEIGHT; CHILDREN; PERSPECTIVE; ADOLESCENTS AB PURPOSE: Obesity is assumed to have a negative impact on self-esteem because of the associated social stigmatization in Western society. Studies of the psychological effect of obesity in children are inconclusive and limited, particularly pertaining to minority populations. Most studies have assessed global rather than domain-specific measures of self-esteem and hence, may have lacked specificity to detect impairment of certain aspects of self-esteem most closely associated with obesity. The purpose of this study is to examine the effect of adiposity and other environmental factors on measures of perceived competence and self-adequacy in 2205 black and white girls aged 9-10 years. METHODS: Domain specific measures of self-esteem were studied by race and degree of adiposity, using Harter's ''Self-Perception Profile for Children''. Three Harter scales deemed more relevant to obesity (social acceptance (SA), physical appearance (PA), and global self worth (GSW)) were selected for univariate and multivariate linear regression models to examine relationships between self-esteem level and adiposity (measured by the sum of triceps, subscapular, and suprailiac skinfolds (SSF)), race, pubertal maturation, and parental education. The relationship between adiposity and Harter scores was further examined with LOESS curves and also by comparing the mean scores of each quintile of SSF by race, as well as inter-quintile differences within race. RESULTS: Adiposity in general impacted negatively on the scores of all three selected Harter scales. There was also racial variation in the relationship between the scores and adiposity, with the magnitude of the effect somewhat less in black girls. White girls exhibited a significant inverse relationship between SSF and SA scores while, in striking contrast, there was no variation in scores iii black girls across all ranges of adiposity. Although there was a significant inverse relationship between adiposity and PA and GSW in both groups, the slope was steeper in white girls, particularly at higher ranges of SSF. Non linearity in the relationship between SSF and the scores was seen in SA and PA scales. CONCLUSIONS: The present study demonstrated a significant negative association between adiposity and the level of self-esteem in girls as young as 9 to 10 years. There were also intriguing racial differences in the selected domains of esteem. These results may help better understand cultural differences regarding the psychological impact of obesity and could be used to formulate appropriate strategies for public health policy. (C) 1997 Elsevier Science Inc. C1 MARYLAND MED RES INST,BALTIMORE,MD. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,NIH,BETHESDA,MD 20892. WESTAT CORP,ROCKVILLE,MD 20850. RP Kimm, SYS (reprint author), UNIV PITTSBURGH,SCH MED,DEPT FAMILY MED & CLIN EPIDEMIOL,M-200 SCAIFE HALL,PITTSBURGH,PA 15261, USA. OI Barton, Bruce/0000-0001-7878-8895 FU NHLBI NIH HHS [N0-HC-55023-26] NR 36 TC 44 Z9 46 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1047-2797 J9 ANN EPIDEMIOL JI Ann. Epidemiol. PD NOV PY 1997 VL 7 IS 8 BP 550 EP 560 DI 10.1016/S1047-2797(97)00124-5 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YK238 UT WOS:A1997YK23800006 PM 9408551 ER PT J AU Suarez, JI Metman, LV Reich, SG Dougherty, PM Hallett, M Lenz, FA AF Suarez, JI Metman, LV Reich, SG Dougherty, PM Hallett, M Lenz, FA TI Pallidotomy for hemiballismus: Efficacy and characteristics of neuronal activity SO ANNALS OF NEUROLOGY LA English DT Article ID MPTP-INDUCED PARKINSONISM; GLOBUS-PALLIDUS NEURONS; BASAL GANGLIA; POSTEROVENTRAL PALLIDOTOMY; MOVEMENT; DISEASE; OSCILLATIONS; DISORDERS; MONKEYS AB A patient with unremitting, medically intractable hemiballismus underwent a pallidotomy that abolished his involuntary movements. Firing rates of cells in the internal segment of the globus pallidus (GPi) recorded during this procedure were significantly lower than those observed during pallidotomy for Parkinson's disease, either ''on'' or ''off'' medication. Firing patterns in hemiballismus were characterized by low-frequency modulation of the firing rate. These results are consistent with the hyperkinetic model, which suggests that hemiballismus. results from decreased inhibition of the pallidal relay nucleus of the thalamus by the GPi. The efficacy of surgery in the case of hemiballismus demonstrates that pallidotomy can be an effective treatment for this condition and suggests that patterned neuronal activity in the GPi is important in the mechanism of hyperkinetic disorders. C1 JOHNS HOPKINS UNIV,DEPT NEUROL,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,DEPT NEUROSURG,BALTIMORE,MD 21218. NINCDS,EXPT THERAPEUT BRANCH,NIH,BETHESDA,MD 20892. NINCDS,HUMAN MOTOR CONTROL SECT,NIH,BETHESDA,MD 20892. OI Dougherty, Patrick/0000-0002-2177-2734 FU NINDS NIH HHS [P01 NS32386] NR 24 TC 80 Z9 80 U1 1 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD NOV PY 1997 VL 42 IS 5 BP 807 EP 811 DI 10.1002/ana.410420519 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA YE970 UT WOS:A1997YE97000018 PM 9392582 ER PT J AU Yu, BW Nguyen, D Anderson, S Allegra, CA AF Yu, BW Nguyen, D Anderson, S Allegra, CA TI Phosphorothioated antisense c-myc oligonucleotide inhibits the growth of human colon carcinoma cells SO ANTICANCER RESEARCH LA English DT Article DE colon; carcinoma; c-myc; antisense; differentiation ID HUMAN COLORECTAL-CARCINOMA; SODIUM-BUTYRATE; GENE-EXPRESSION; ONCOGENE EXPRESSION; RETINOBLASTOMA GENE; PROTEIN EXPRESSION; DOWN-REGULATION; MESSENGER-RNA; CANCER; DIFFERENTIATION AB Background: The functional significance of c-myc overexpression in human colon carcinoma is unclear. Materials and methods: Three human colon carcinoma cell lines, LS174T, SW1116 and SW48, were treated in vitro with phosphorothioate modified antisense oligonucleotides (ASO), complementary to the c-myc translation initiation site, or two control oligonucleotides. Growth was assayed by the methyl tetrazolium (MTT) assay and colony formation. C-myc, retinoblastoma (Rb), carcinoembryonic antigen (CEA), and alkaline phosphatase (AP) expression was assessed by immunoblotting. Results: The ASO specifically inhibited growth of all three human colon carcinoma cell lines. Further studies were conducted on LS174T because growth inhibition was associated with a more differentiated morphology. In LS174T cells, ASO caused a dose dependent decrease in c-myc and Rb protein expression, but an increase in CEA and RP expression Conclusions: The growth of human colon carcinoma cells is dependent on c-myc expression, and the inhibition of c-myc expression in LS174T is associated with a more differentiated phenotype. C1 NCI, NMOB, Natl Naval Med Ctr, Bethesda, MD 20889 USA. NHLBI, NIH, Bethesda, MD 20892 USA. RP Yu, BW (reprint author), Henry Ford Hosp, Div Hematol & Oncol, K13,2799 W Grand Blvd, Detroit, MI 48202 USA. NR 41 TC 4 Z9 5 U1 0 U2 0 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDNTIOU-KALAMOU RD KAPANDRITI, POB 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD NOV-DEC PY 1997 VL 17 IS 6D BP 4407 EP 4413 PG 7 WC Oncology SC Oncology GA YY890 UT WOS:000072197500027 PM 9494542 ER PT J AU Tendler, Y Ben-Hur, H Gurevich, P Berman, V Sandler, B Nyska, A Zion, H Zinder, O Zusman, I AF Tendler, Y Ben-Hur, H Gurevich, P Berman, V Sandler, B Nyska, A Zion, H Zinder, O Zusman, I TI Role of apoptosis, proliferating cell nuclear antigen and p53 protein in the immune response of rat colon cells to cancer and vaccination with anti-p53 polyclonal antibodies SO ANTICANCER RESEARCH LA English DT Article DE antibodies; anticancer; apoptosis; PCNA; proliferation; p53 protein ID TUMOR-SUPPRESSOR GENE; EXPRESSION; TISSUE; DEATH AB Background: Previously it was shown that rabbit anti-p53 antibodies can exert tumor-suppressive effects on chemically induced rat colon cancer (Cancer J, 10:116-120, 1997). This work examines the role of some components of the immune system in the response of the rat colon cells to treatment with a carcinogen and anti-p53 antibodies. Methods: The following groups of rats were studied: a) control non treated rats; b) tumor-free non vaccinated rats treated with a carcinogen; c) tumor-bearing non vaccinated rats; d) tumor-free vaccinated rats exposed to a carcinogen; e) tumor-bearing vaccinated rats. The manifestation of apoptosis, proliferating cell nuclear antigen (PCNA), mitotic index, T lymphocytes and p53 protein was compared between the different groups of rats. Results: The apoptotic index and the number of p53-positive cells and T lymphocytes were significantly higher in colon adenocarcinomas obtained from vaccinated rats than in unvaccinated rats. PCNA was lower in tumors from the vaccinated rats, whereas the proliferating cell index was not different between the both groups of rats. An inverse relationship was seen between apoptosis and most other parameters studied. The inverse correlation found between apoptosis and p53 protein in this study demonstrated that apoptosis acts as a p53-independent parameter in chemically induced rat colon cancer. Conclusions: our findings demonstrated that vaccination significantly activated apoptosis in both types of colon tissue, and induced synthesis of p53 protein in tumor tissue. Vaccination with anti-p53 polyclonal antibodies seemed to activate the immune system and to stimulate some of its cellular components responsible for tumor suppression. C1 Hebrew Univ Jerusalem, Koret Sch Vet Med, Lab Teratol & Expt Oncol, IL-76100 Rehovot, Israel. Rambam Med Ctr, Dept Clin Biochem, Haifa, Israel. Kaplan Hosp, Dept Obstet & Gynecol, IL-76100 Rehovot, Israel. NIH, Res Triangle Pk, NC USA. RP Zusman, I (reprint author), Hebrew Univ Jerusalem, Koret Sch Vet Med, Lab Teratol & Expt Oncol, POB 12, IL-76100 Rehovot, Israel. NR 28 TC 13 Z9 14 U1 1 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDNTIOU-KALAMOU RD KAPANDRITI, POB 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD NOV-DEC PY 1997 VL 17 IS 6D BP 4653 EP 4657 PG 5 WC Oncology SC Oncology GA YY890 UT WOS:000072197500069 PM 9494584 ER PT J AU Pommier, Y Pilon, AA Bajaj, K Mazumder, A Neamati, N AF Pommier, Y Pilon, AA Bajaj, K Mazumder, A Neamati, N TI HIV-1 integrase as a target for antiviral drugs SO ANTIVIRAL CHEMISTRY & CHEMOTHERAPY LA English DT Review DE integrase; chemotherapy; inhibitors; drug design; nucleotides; hydroxylated aromatics; AIDS ID HUMAN-IMMUNODEFICIENCY-VIRUS; IN-VITRO INTEGRATION; DNA-BINDING DOMAIN; MG2+-DEPENDENT 3'-PROCESSING ACTIVITY; NUCLEAR-LOCALIZATION SIGNAL; CARBOXYL-TERMINAL DOMAINS; ACID PHENETHYL ESTER; VIRAL LIFE-CYCLE; TYPE-1 INTEGRASE; RETROVIRAL INTEGRATION AB Retrovirus integration requires at least two viral components, one of the three retroviral enzymes, integrase, and cis-acting sequences at the ends of the retroviral DNA termini U3 and U5 ends of the long terminal repeats. Because the virus cannot replicate without integration into a host chromosome, integrase is a logical therapeutic target. Therapeutic inhibitors already exist for reverse transcriptase and protease, and attacking the virus on these sites together has already proven effective for combination therapy. Thus, the discovery of integrase inhibitors should provide an additional benefit. Screening and pharmacology of anti-integrase drugs is facilitated by the cloning and expression of recombinant retroviral integrases and their use in a series of in vitro assays that mimic integration in vivo. This review first describes the integration reactions in the retrovirus life cycle and the integrase protein. Then we provide a comprehensive review of the inhibitors identified to date. RP Pommier, Y (reprint author), NCI, MOL PHARMACOL LAB,DIV BASIC SCI,NIH,BLDG 37, ROOM 5C25, BETHESDA, MD 20892 USA. NR 180 TC 63 Z9 63 U1 0 U2 2 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 0956-3202 EI 2040-2066 J9 ANTIVIR CHEM CHEMOTH JI Antivir. Chem. Chemother. PD NOV PY 1997 VL 8 IS 6 BP 463 EP 483 PG 21 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Virology SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Virology GA YJ917 UT WOS:A1997YJ91700001 ER PT J AU Neamati, N Mazumder, A Sunder, S Owen, JM Schultz, RJ Pommier, Y AF Neamati, N Mazumder, A Sunder, S Owen, JM Schultz, RJ Pommier, Y TI 2-mercaptobenzenesulphonamides as novel inhibitors of human immunodeficiency virus type 1 integrase and replication SO ANTIVIRAL CHEMISTRY & CHEMOTHERAPY LA English DT Article DE HIV; integrase; inhibitors; sulphonamides ID NUCLEOCAPSID PROTEIN; HIV-1 INTEGRASE; ZINC FINGERS; ACID; AIDS; AGENTS AB An obligatory requirement in the retroviral life cycle is the integration of the viral dsDNA into the host chrome some, a process performed by viral integrase. The retroviral integrase is able to catalyse at least three discrete enzymatic steps. Two of these steps, 3' processing and DNA strand transfer, can be measured in an in vitro assay In the presence of a duplex oligonucleotide corresponding to the viral long terminal repeat, recombinant integrase and the divalent cations, Mg2+ or Mn2+. This assay provides an efficient means of testing integrase inhibitors. As part of our continuous effort in developing novel inhibitors we examined a series of 2-mercaptobenzenesulphonamides (MBSAs) for their inhibitory activity against human immunodeficiency virus type 1 (HIV-1) integrase. From the list of compounds tested in an assay specific for HIV-1 integrase, 26 compounds inhibited the 3' processing and strand transfer step with 50% inhibitory concentration (IC50) values below 25 mu M. All the thioether derivatives were inactive. These results were further compared with the ability of MBSAs to protect HIV-l-infected T4 lymphocyte CEM cells. Among 68 compounds tested, 27 exhibited antiviral activity in cell-based assays with therapeutic indices of 1-16. All the MBSAs with antiviral activity were also effective inhibitors of recombinant HIV-1 integrase. Several aromatic disulphides were also tested and found to exhibit moderate antiviral and anti-integrase activities. These data demonstrate that MBSAs can be developed as inhibitors of HIV-1 integrase with the potential for antiviral activity. C1 NCI,MOL PHARMACOL LAB,DIV BASIC SCI,BETHESDA,MD 20892. NCI,DRUG SYNTH & CHEM BRANCH,DEV THERAPEUT PROGRAM,DIV CANC TREATMENT DIAG & CTR,BETHESDA,MD 20892. NR 30 TC 54 Z9 54 U1 0 U2 4 PU INT MEDICAL PRESS PI LONDON PA 125 HIGH HOLBORN, LONDON, ENGLAND WC1V 6QA SN 0956-3202 J9 ANTIVIR CHEM CHEMOTH JI Antivir. Chem. Chemother. PD NOV PY 1997 VL 8 IS 6 BP 485 EP 495 PG 11 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Virology SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Virology GA YJ917 UT WOS:A1997YJ91700002 ER PT J AU Uchida, H Maeda, Y Mitsuya, H AF Uchida, H Maeda, Y Mitsuya, H TI HIV-1 protease does not play a critical role in the early stages of HIV-1 infection SO ANTIVIRAL RESEARCH LA English DT Article DE human immunodeficiency virus type 1; protease inhibitors; proviral DNA ID HUMAN-IMMUNODEFICIENCY-VIRUS; VIRAL PROTEASE; INHIBITOR; REPLICATION; PROTEINASE; INVITRO; DESIGN AB We asked whether human immunodeficiency virus type 1 (HIV-1) protease plays a major role in the early stages of infection (i.e. from viral entry to reverse transcription) by using various protease inhibitors (saquinavir, ritonavir, and KNI-272). When assessed in the two-day multinuclear activation of a galactosidase indicator (MAGI) assay, involving a single cycle of HIV-1 replication, all protease inhibitors failed to block infection of HeLa-CD4-LTR-beta-gal cells by HIV-1, while reverse transcriptase (RT) inhibitors (AZT and ddI) completely blocked the infection. Moreover, when HIV-1 proviral DNA synthesis was examined by polymerase chain reaction in HeLa-CD4-LTR-beta-gal cells exposed to HIV-1 and cultured in the presence of protease inhibitors, a significant amount of proviral DNA was detected, while no proviral DNA synthesis was detected when the cells were cultured in the presence of RT inhibitors. Protease inhibitors also failed to block chloramphenicol acetyltransferase (CAT) expression in HLCD4-CAT cells exposed to HIV-1, while RT inhibitors completely suppressed CAT expression. These results strongly suggest, contrary to a previous report by Nagy et al. (1994), that HIV-1 protease does not play a major role in the early stages of infection. (C) 1997 Elsevier Science B.V. C1 NCI, Expt Retrovirol Sect, Med Branch, NIH, Bethesda, MD 20892 USA. RP Mitsuya, H (reprint author), NCI, Expt Retrovirol Sect, Med Branch, NIH, Bethesda, MD 20892 USA. NR 23 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD NOV PY 1997 VL 36 IS 2 BP 107 EP 113 DI 10.1016/S0166-3542(97)00047-8 PG 7 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA YM646 UT WOS:000071085600005 PM 9443667 ER PT J AU Falls, JG Cherrington, NJ Clements, KM Philpot, RM Levi, PE Rose, RL Hodgson, E AF Falls, JG Cherrington, NJ Clements, KM Philpot, RM Levi, PE Rose, RL Hodgson, E TI Molecular cloning, sequencing, and expression in Escherichia coli of mouse flavin-containing monooxygenase 3 (FMO3): Comparison with the human isoform SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE flavin-containing monooxygenase 3; FMO3; FMO3 sequence; FMO3 expression ID ADULT HUMAN LIVER; FUNCTION AMINE OXIDASE; MULTIPLE FORMS; RABBIT LIVER; GUINEA-PIG; CATALYTIC PROPERTIES; LUNG; PURIFICATION; METABOLISM; MICROSOMES AB The sequence of mouse flavin-containing monooxygenase 3 (FMO3) was obtained from several clones isolated from a mouse liver cDNA library, The nucleotide sequence of mouse FMO3 was 2020 bases in length containing 37 bases in the 5' flanking region, 1602 in the coding region, and 381 in the 3' flanking region, The derived protein sequence consisted of 534 amino acids including the putative flavin adenine dinucleotide and NADP(+) pyrophosphate binding sites (characteristic of mammalian FMOs) starting at positions 9 and 191, respectively. The mouse FMO3 protein sequence was 79 and 82% identical to the human and rabbit FMO3 sequences, respectively, Mouse FMO3 was expressed in Escherichia coli and compared to E. coli expressed human FMO3. The FMO3 proteins migrated with the same mobility (similar to 58 kDa) as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. The expressed FMO3 enzymes (mouse and human forms) were sensitive to heat and reacted in a similar manner toward metal ions and detergent, Catalytic activities of mouse and human FMO3 were high toward the substrate methimazole; however, in the presence of trimethylamine and thioacetamide, FMO-dependent methimazole oxidation by both enzymes was reduced by greater than 85%. Other substrates which inhibited methimazole oxidation were thiourea and thiobenzamide and to a lesser degree N,N-dimethylaniline. When probed with mouse FMO3 cDNA, FMO3 transcripts were detected in hepatic mRNA samples from female mice, but not in samples from males. FMO3 was detected in mRNA samples from male and female mouse lung, but FMO3 message was not detected in mouse kidney sample from either gender, Results of immunoblotting confirmed the tissue-and gender-dependent expression of mouse FMO3. (C) 1997 Academic Press. C1 N CAROLINA STATE UNIV, DEPT ENTOMOL, RALEIGH, NC 27695 USA. NIEHS, LAB SIGNAL TRANSDUCT, RES TRIANGLE PK, NC 27709 USA. RP Falls, JG (reprint author), N CAROLINA STATE UNIV, DEPT TOXICOL, BOX 7633, RALEIGH, NC 27695 USA. FU NIEHS NIH HHS [ES00044] NR 56 TC 27 Z9 28 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD NOV 1 PY 1997 VL 347 IS 1 BP 9 EP 18 DI 10.1006/abbi.1997.0322 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA YE951 UT WOS:A1997YE95100002 PM 9344459 ER PT J AU Schecter, A Toniolo, P Dai, LC Thuy, LTB Wolff, MS AF Schecter, A Toniolo, P Dai, LC Thuy, LTB Wolff, MS TI Blood levels of DDT and breast cancer risk among women living in the North of Vietnam SO ARCHIVES OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY LA English DT Article ID HUMAN ADIPOSE-TISSUE; DIBENZOFURAN LEVELS; DIOXIN; PESTICIDES; RESIDUES; SERUM; SOUTH; MILK AB A positive association has been reported between elevated tissue organochlorines (p,p'-DDT/p,p'-DDE, PCBs, dioxins) and breast cancer in some case-control studies and occupational cohort studies. We previously reported high serum levels of p,p'-DDT and its metabolite p,p'-DDE in women living throughout Vietnam. We report here the results of a small hospital-based case-control study examining the association between blood levels of p,p'-DDT/p,p'-DDE and the risk of invasive breast cancer among residents of the north of Vietnam-an area where insecticides such as p,p'-DDT have been heavily used in the recent past. The study was conducted among patients admitted to a single hospital in the capital city of Hanoi in 1994. Study subjects were 21 women newly diagnosed with invasive adenocarcinoma of the breast, who served as cases, and 21 women of similar age with fibrocystic breast disease, who served as controls. No increase was evident in the relative risk of breast cancer with increasing tertiles of serum concentration of the compounds of interest, even after adjustment for major potential confounders, such as age at menarche, parity, history of lactation, and body weight. These results suggest that recent and past exposure to p,p'-DDT does not play an important role in the etiology of breast cancer among women living in a country with a tropical climate where insecticide use for mosquito control is common. C1 SUNY Hlth Sci Ctr, Dept Prevent Med, Binghamton, NY 13903 USA. NYU, Med Ctr, Inst Environm Med, New York, NY 10016 USA. Coll Med, Natl 10 80 Comm Invest Consequences Chem Used War, Hanoi, Vietnam. Mt Sinai Med Ctr, New York, NY 10029 USA. RP Schecter, A (reprint author), NIEHS, NIH, POB 12233,MD A3-02, Res Triangle Pk, NC 27709 USA. FU NIEHS NIH HHS [ES06928] NR 12 TC 63 Z9 66 U1 3 U2 11 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0090-4341 J9 ARCH ENVIRON CON TOX JI Arch. Environ. Contam. Toxicol. PD NOV PY 1997 VL 33 IS 4 BP 453 EP 456 PG 4 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA YN353 UT WOS:000071159400014 PM 9419265 ER PT J AU Solomon, DA Keller, MB Leon, AC Mueller, TI Shea, MT Warshaw, M Maser, JD Coryell, W Endicott, J AF Solomon, DA Keller, MB Leon, AC Mueller, TI Shea, MT Warshaw, M Maser, JD Coryell, W Endicott, J TI Recovery from major depression - A 10-year prospective follow-up across multiple episodes SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID AFFECTIVE-DISORDERS; RELIABILITY; CHRONICITY; TIME; RISK AB Background: Major depressive disorder is often marked by repeated episodes of depression. We describe recovery from major depession across multiple mood episodes in patients with unipolar major depression at intake and examine the association of sociodemographic and clinical variables with duration of illness. Methods: A cohort of 258 subjects treated for unipolar major depressive disorder was followed up prospectively for 10 years as part of the Collaborative Depression Study, a multicenter naturalistic study of the mood disorders. Diagnoses were made according to the Research Diagnostic Criteria, and the course of illness was assessed with the Longitudinal Interval Follow-up Evaluation. Survival analyses were used to calculate the duration of illness for the first 5 recurrent mood episodes after recovery from the index episode. Results: Diagnosis remained unipolar major depressive disorder for 235 subjects (91%). The median duration of illness was 22 weeks for the first recurrent mood episode, 20 weeks for the second, 21 weeks for the third, and 19 weeks for the fourth and fifth recurrent mood episodes; the 95% confidence intervals were highly consistent. From one episode to the next, the proportion of subjects who recovered by any one time point was similar. For subjects with 2 or more recoveries, the consistency of duration of illness from one recovery to the next was low to moderate. None of the sociodemographic or clinical variables consistently predicted duration of illness. Conclusion: In this sample of patients treated at tertiary care centers for major depressive disorder, the duration of recurrent mood episodes was relatively uniform. and averaged approximately 20 weeks. C1 BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. CORNELL UNIV,DEPT PSYCHIAT,ITHACA,NY 14853. NIMH,WASHINGTON,DC. UNIV IOWA,COLL MED,DEPT PSYCHIAT,IOWA CITY,IA 52242. NEW YORK STATE PSYCHIAT INST & HOSP,DEPT RES & TRAINING,NEW YORK,NY 10032. FU NIMH NIH HHS [R01 MH025478] NR 22 TC 134 Z9 135 U1 3 U2 4 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 NOV PY 1997 VL 54 IS 11 BP 1001 EP 1006 PG 6 WC Psychiatry SC Psychiatry GA YE748 UT WOS:A1997YE74800003 PM 9366656 ER PT J AU Cao, GH Prior, RL Cutler, RG Yu, BP AF Cao, GH Prior, RL Cutler, RG Yu, BP TI Effect of dietary restriction on serum antioxidant capacity in rats SO ARCHIVES OF GERONTOLOGY AND GERIATRICS LA English DT Article DE free radical; antioxidant capacity; dietary restriction; rats ID RADICAL ABSORBENCY CAPACITY; CHRONIC FOOD RESTRICTION; LIPID-PEROXIDATION; ENZYME-ACTIVITIES; OXIDATIVE STRESS; AGING RATS; AGE; LIVER; DAMAGE; ASSAY AB The effects of dietary restriction on serum antioxidant capacities were studied in male Fischer 344 rats. Dietary restriction was started at the age of 6 weeks and consisted of 60% of the mean daily food intake of the ad libitum fed controls. They were killed at 7 and 18 months of age. The antioxidant capacities of whole serum and the non-protein fraction of serum were assessed using the oxygen radical absorbance capacity (ORAC) assay with a peroxyl radical generator. Rats that consumed a diet restricted by 40% in calories had significantly lower ORAC activities in whole serum and the non-protein fraction of serum. The decreased serum ORAC activity is seemingly an organism's physiologically appropriate response to reduced oxidative stress through a down-regulation mechanism. (C) 1997 Elsevier Science Ireland Ltd. C1 UNIV CONNECTICUT,DEPT NUTR SCI,STORRS,CT 06269. NIA,GERONTOL RES CTR,NIH,BALTIMORE,MD 21224. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. RP Cao, GH (reprint author), TUFTS UNIV,USDA ARS,JEAN MAYER HUMAN NUTR RES CTR AGING,BOSTON,MA 02111, USA. NR 38 TC 19 Z9 19 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0167-4943 J9 ARCH GERONTOL GERIAT JI Arch. Gerontol. Geriatr. PD NOV-DEC PY 1997 VL 25 IS 3 BP 245 EP 253 DI 10.1016/S0167-4943(97)00014-9 PG 9 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA XZ004 UT WOS:A1997XZ00400003 PM 18653112 ER PT J AU Martin, DF Ferris, FL Parks, DJ Walton, RC Mellow, SD Gibbs, D Remaley, NA Ashton, P Davis, MD Chan, CC Nussenblatt, RB AF Martin, DF Ferris, FL Parks, DJ Walton, RC Mellow, SD Gibbs, D Remaley, NA Ashton, P Davis, MD Chan, CC Nussenblatt, RB TI Ganciclovir implant exchange - Timing, surgical procedure, and complications SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID SUSTAINED-RELEASE GANCICLOVIR; CYTOMEGALOVIRUS RETINITIS; THERAPY; AIDS AB Background: The ganciclovir implant is effective for the treatment of cytomegalovirus (CMV) retinitis. The device eventually runs out of drug, however, and must be replaced. We report our experience with exchanging ganciclovir implants during the course of a randomized clinical trial. Methods: During our study, patients with newly diagnosed peripheral CMV retinitis were treated with a ganciclovir implant. The implant was scheduled for exchange at 32 weeks. It was exchanged earlier if progression of CMV retinitis occurred. Patient examinations and standard fundus photography were performed at 2-week intervals after the exchange procedure. Results: Twenty-six exchange procedures were performed. Twenty-two eyes in 15 patients received a second implant and 4 eyes in 4 patients later received a third implant. Cytomegalovirus retinitis was rendered or maintained inactive in 22 of 23 cases with more than 1 month of follow-up after the second or third implants. Complications after the second implant procedure included transient vitreous hemorrhage in 5 eyes, postoperative inflammation in 1 eye, and retinal detachment in 1 eye. Median visual acuity returned to 20/25 by 28 days and to 20/20 by 42 days. Complications after the third implant procedure included dense vitreous hemorrhage in 3 of 4 eyes. Median survival time after a second implant procedure was 89 days. Conclusions: The initial ganciclovir implant exchange procedure is well tolerated with continued long-term control of CMV retinitis. Multiple reentries through the same wound mag be associated with an increased risk for vitreous hemorrhage. C1 NEI,NIH,BETHESDA,MD 20892. NEW ENGLAND EYE CTR,BOSTON,MA. UNIV WISCONSIN,DEPT OPHTHALMOL,MADISON,WI. RP Martin, DF (reprint author), EMORY UNIV,SCH MED,DEPT OPHTHALMOL,1365B CLIFTON RD NE,ATLANTA,GA 30322, USA. NR 19 TC 38 Z9 41 U1 1 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 NOV PY 1997 VL 115 IS 11 BP 1389 EP 1394 PG 6 WC Ophthalmology SC Ophthalmology GA YE633 UT WOS:A1997YE63300005 PM 9366668 ER PT J AU Deleyiannis, FWB Weymuller, EA Garcia, I Potosky, AL AF Deleyiannis, FWB Weymuller, EA Garcia, I Potosky, AL TI Geographic variation in the utilization of esophagoscopy and bronchoscopy in head and neck cancer SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article; Proceedings Paper CT Meeting of the American-Society-of-Head-and-Neck-Surgery CY MAY 11-12, 1997 CL SCOTTSDALE, AZ SP Amer Soc Head & Neck Surg ID EARLY ESOPHAGEAL CANCER; TRIPLE ENDOSCOPY; PRIMARY TUMORS; BREAST-CANCER; CARCINOMA; MEDICARE; TRACT; MALIGNANCIES; PANENDOSCOPY; REGRESSION AB Objective: To determine the extent to which esophagoscopy and bronchoscopy are being used in various regions of the United States in the initial examination of patients with head and neck cancer. Design: Population-based study derived from Medicare claims data and information from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program. Setting: Five SEER areas (San Francisco, Calif; Connecticut; Seattle, Wash; Iowa; and Detroit, Mich). Participants: The cohort included 1410 Medicare patients with squamous cell carcinoma of the oral cavity, oropharynx, hypopharynx, or larynx diagnosed between March 1, 1991, and December 31, 1993, in the 5 SEER areas. Main Outcome Measure: Rates of esophagoscopy and bronchoscopy according to SEER area. Results: The proportion of patients who underwent esophagoscopy ranged from 12.9% (San Francisco) to 39.8% (Detroit) for patients with local cancer and from 22.2% (San Francisco) to 59.7% (Detroit) for patients with regional cancer. The proportion of patients who underwent bronchoscopy ranged from 6.9% (San Francisco) to 32.6% (Detroit) for patients with local cancer and from 12.8% (San Francisco) to 50.7% (Detroit) for patients with regional cancer. After controlling for differences in age, sex, race, tumor site, tumor grade, comorbidity, and socioeconomic status, SEER area remained independently associated with esophagoscopy and bronchoscopy (both P<.001). Conclusions: There is substantial geographic variation in the use of esophagoscopy and bronchoscopy as part of the initial examination of patients diagnosed as having head and neck cancer that cannot be explained by differences in patient or tumor characteristics. This variation likely underscores uncertainty and disagreement about the Value of endoscopic screening for synchronous tumors. Additional research is required to determine whether routine endoscopic screening increases survival rates or improves quality of life. C1 NIDR,ORAL HLTH PROMOT RISK FACTORS & MOL EPIDEMIOL BRA,NIH,BETHESDA,MD 20892. NCI,APPL RES BRANCH,NIH,BETHESDA,MD 20892. RP Deleyiannis, FWB (reprint author), UNIV WASHINGTON,DEPT OTOLARYNGOL HEAD & NECK SURG,1959 NE PACIFIC ST,BOX 356515,SEATTLE,WA 98195, USA. FU NIDCD NIH HHS [DC00018] NR 49 TC 23 Z9 23 U1 2 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0886-4470 J9 ARCH OTOLARYNGOL JI Arch. Otolaryngol. Head Neck Surg. PD NOV PY 1997 VL 123 IS 11 BP 1203 EP 1210 PG 8 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA YF123 UT WOS:A1997YF12300008 PM 9366700 ER PT J AU Compton, CC Henson, DE AF Compton, CC Henson, DE TI Protocol for the examination of specimens removed from patients with carcinoma of the exocrine pancreas - A basis for checklists SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Review ID GIANT-CELL TUMOR; PAPILLARY-CYSTIC TUMOR; FACTORS INFLUENCING PROGNOSIS; SERUM ALPHA-FETOPROTEIN; MUCINOUS DUCTAL ECTASIA; LYMPH-NODE INVOLVEMENT; LONG-TERM SURVIVAL; ADENOSQUAMOUS CARCINOMA; DIFFERENTIAL-DIAGNOSIS; LATENT MALIGNANCY C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. NR 147 TC 24 Z9 26 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 NOV PY 1997 VL 121 IS 11 BP 1129 EP 1136 PG 8 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA YF312 UT WOS:A1997YF31200001 PM 9372738 ER PT J AU Kullo, IJ Schwartz, RS Pompili, VJ Tsutsui, M Milstien, S Fitzpatrick, LA Katusic, ZS OBrien, T AF Kullo, IJ Schwartz, RS Pompili, VJ Tsutsui, M Milstien, S Fitzpatrick, LA Katusic, ZS OBrien, T TI Expression and function of recombinant endothelial NO synthase in coronary artery smooth muscle cells SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article; Proceedings Paper CT 69th Annual Scientific Session of the American-Heart-Association CY NOV 09-16, 1996 CL NEW ORLEANS, LA SP Amer Heart Assoc, Hoechst Marion Roussel Inc, Kansas City DE nitric oxide; gene transfer; nitric oxide synthase; adenovirus; vascular smooth muscle cells ID NITRIC-OXIDE SYNTHASE; GENE-TRANSFER; CARDIOVASCULAR-DISEASE; ADENOVIRUS TYPE-5; ORGANIC NITRATES; RAT; RESTENOSIS; THERAPY; PROLIFERATION; VASODILATORS AB Smooth muscle cells (SMCs) play a key role in the pathogenesis of vascular diseases. The objectives of this study were to determine whether transfer of recombinant endothelial nitric oxide synthase (eNOS) gene to porcine coronary artery smooth muscle cell (CSMCs) would result in expression of a functional enzyme and to assess the effect of expression of eNOS on cell proliferation. CSMCs were transduced in vitro with adenoviral vectors encoding cDNA for eNOS (AdeNOS) and beta-galactosidase (Ad beta Gal). In contrast to Ad beta Gal- or sham-transduced cells, CSMCs transduced with AdeNOS stained positive with the NADPH-diaphorase stain, acquired calcium-dependent NOS activity (measured by the conversion of [H-3]L-arginine to [H-3]-citrulline), had increasing cyclic 3',5' cGMP levels with increasing concentrations of the vector, and produced increased amounts of nitrite. cGMP production by AdeNOS-transduced cells was augmented by increasing intracellular levels of the eNOS cofactor tetrahydrobiopterin. CSMCs transduced with AdeNOS showed diminished serum-stimulated DNA synthesis as measured by thymidine uptake. Cell proliferation was diminished in AdeNOS-transduced CSMCs as assessed by cell counts 3 and 6 days after serum stimulation of quiescent CSMCs. The present study demonstrates that adenovirus-mediated gene transfer of eNOS to CSMCs results in the expression of a functional enzyme whose activity can be augmented by increasing intracellular levels of tetrahydrobiopterin. Expression of recombinant eNOS in CSMCs results in inhibition of serum-stimulated DNA synthesis and cell proliferation. These findings imply that eNOS gene transfer to SMCs may be a unique mode of increasing local NO production in the arterial wall. C1 MAYO CLIN & MAYO FDN,DEPT ENDOCRINOL & METAB,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,DIV CARDIOVASC DIS,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,DEPT ANESTHESIOL & PHARMACOL,ROCHESTER,MN 55905. NIMH,CELL BIOL LAB,NIH,BETHESDA,MD 20892. RI O'Brien, Timothy/N-7112-2014 OI O'Brien, Timothy/0000-0001-9028-5481 FU NHLBI NIH HHS [HL-44116, HL-51736, HL-53532] NR 40 TC 47 Z9 49 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1079-5642 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD NOV PY 1997 VL 17 IS 11 BP 2405 EP 2412 PG 8 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA YL008 UT WOS:A1997YL00800013 PM 9409208 ER PT J AU Gray, RS Robbins, DC Wang, WY Yeh, JLL Fabsitz, RR Cowan, LD Welty, TK Lee, ET Krauss, RM Howard, BV AF Gray, RS Robbins, DC Wang, WY Yeh, JLL Fabsitz, RR Cowan, LD Welty, TK Lee, ET Krauss, RM Howard, BV TI Relation of LDL size to the insulin resistance syndrome and coronary heart disease in American Indians - The Strong Heart Study SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE American Indians; LDL size; coronary heart disease; diabetes mellitus; Strong Heart Study ID LOW-DENSITY LIPOPROTEINS; ARTERY DISEASE; PLASMA TRIGLYCERIDE; RISK-FACTORS; HETEROGENEITY; PHENOTYPES; POPULATION; WOMEN; MEN AB Small, dense LDL has been shown to be associated with the insulin resistance syndrome and coronary heart disease (CHD). We examined the distribution of LDL size and phenotype within a population-based sample of American Indians to determine the relationships with prevalent CHD and to examine associations with hyperinsulinemia and other components of the insulin resistance syndrome. Data were available for 4505 men and women between 45 and 74 years of age who are members of 13 American Indian communities in three geographic areas. Diabetes, CHD, and CHD risk factors were assessed by standardized techniques, and LDL size was measured by gradient gel electrophoresis. LDL size was smaller in men than in women and in individuals with diabetes than in those without diabetes. In multivariate analysis, LDL size was significantly related to several components of the insulin resistance syndrome, including triglycerides (inversely) and HDL cholesterol (positively). Although univariate relations were positive, LDL size was not significantly related to fasting insulin concentrations or body mass index in the multivariate model. LDL size also showed no relationship to apolipoprotein E phenotype. When LDL size was compared in individuals with and without CHD, no significant differences were observed, either in nondiabetic or diabetic individuals. We conclude that LDL size is most strongly related to lipoprotein components of the insulin resistance syndrome, especially plasma triglycerides. However, in this population with low LDL, it is not related to cardiovascular disease. C1 MEDLANT RES INST,WASHINGTON,DC 20010. UNIV OKLAHOMA,DEPT BIOSTAT & EPIDEMIOL,OKLAHOMA CITY,OK. CTR EPIDEMIOL RES,OKLAHOMA CITY,OK. NHLBI,BETHESDA,MD 20892. LAWRENCE BERKELEY LAB,BERKELEY,CA. FU NHLBI NIH HHS [U01-HL41642, U01HL41652, UL01HL41654] NR 24 TC 66 Z9 68 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1079-5642 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD NOV PY 1997 VL 17 IS 11 BP 2713 EP 2720 PG 8 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA YL008 UT WOS:A1997YL00800052 PM 9409247 ER PT J AU Hu, YH Cheng, L Hochleitner, BW Xu, QB AF Hu, YH Cheng, L Hochleitner, BW Xu, QB TI Activation of mitogen-activated protein kinases (ERK/JNK) and AP-1 transcription factor in rat carotid arteries after balloon injury SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE mitogen-activated protein kinase; restenosis; signal transduction; transcription factor AP-1; vascular injury ID MUSCLE CELL-PROLIFERATION; SIGNAL-TRANSDUCTION PATHWAY; C-JUN; MAP KINASE; CARDIAC MYOCYTES; DNA-SYNTHESIS; S6 KINASE; GROWTH; PHOSPHORYLATION; INHIBITION AB Smooth muscle cell proliferation is a key event in neointimal formation after balloon angioplasty. The molecular signals that mediate this process have yet to be identified. Mitogen-activated protein (MAP) kinases are thought to play a pivotal role in transmitting transmembrane signals required for cell proliferation in vitro. The present studies were designed to investigate whether the signal transduction pathways of MAP kinases were involved in the development of restenosis in the injured arteries. Rat carotid arteries were isolated at various lime points after balloon injury, and activities of MAP kinases, including extracellular signal-regulated kinases (ERK), and stress activated protein kinases (SAPK)/c-Jun N-terminal protein kinases (JNK), were determined in protein extracts of the vasculature using protein kinase assay and Western blot analysis. After balloon angioplasty, ERK2 and JNK1 activities in the vessel wall increased rapidly, reached a high level in 5 minutes and maintained for 1 hour. A sustained increase in ERK2 kinase activity was observed over the next 7 days in the arterial wall and 14 days in neointima after injury. In contrast, opposite and uninjured arteries did not show significant changes in these kinase activities. Concomitantly, Western blot analysis confirmed that the ERK2 kinase in the injured vessels was indeed activated or phosphorylated, showing a slowly migrating species of a 42-kDa protein containing phosphorylated tyrosine. Kinase activation is followed by an increase in c-fos and c-jun gene expression and enhanced activator protein 1 (AP-1) DNA-binding activity. Thus, balloon injury rapidly activates the MAP kinases in rat carotid arteries. These kinase activations may be crucial in mediating smooth muscle cell proliferation in response to vascular angioplasty. C1 AUSTRIAN ACAD SCI,INST BIOMED AGING RES,A-6020 INNSBRUCK,AUSTRIA. UNIV INNSBRUCK HOSP,DEPT SURG,A-6020 INNSBRUCK,AUSTRIA. NIA,CARDIOVASC SCI LAB,NIH,BALTIMORE,MD 21224. NR 51 TC 130 Z9 138 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1079-5642 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD NOV PY 1997 VL 17 IS 11 BP 2808 EP 2816 PG 9 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA YL008 UT WOS:A1997YL00800064 PM 9409259 ER PT J AU Lefevre, M Ginsberg, HN KrisEtherton, PM Elmer, PJ Stewart, PW Ershow, A Pearson, TA Roheim, PS Ramakrishnan, R Derr, J Gordon, DJ Reed, R AF Lefevre, M Ginsberg, HN KrisEtherton, PM Elmer, PJ Stewart, PW Ershow, A Pearson, TA Roheim, PS Ramakrishnan, R Derr, J Gordon, DJ Reed, R TI ApoE genotype does not predict lipid response to changes in dietary saturated fatty acids in a heterogeneous normolipidemic population SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE dietary saturated fat; step 1 diet; apoE genotype ID APOLIPOPROTEIN-E PHENOTYPE; DENSITY-LIPOPROTEIN CHOLESTEROL; PLASMA-CHOLESTEROL; SERUM-CHOLESTEROL; E POLYMORPHISM; INDIVIDUAL RESPONSIVENESS; DOSE-RESPONSE; MEN; WOMEN; HYPERCHOLESTEROLEMIA AB Recent studies have suggested that variations in apoE genotypes may influence the magnitude of plasma lipid changes in response to dietary interventions. We examined the ability of apoE genotype to predict plasma lipid response to reductions in percent of calories from total fat (TF) and saturated fat (SF) in a normolipidemic study population (n=103) heterogeneous with respect to age, gender, race, and menopausal status. Three diets, an average American diet (34.3% TF, 15.0% SF), an AHA Step 1 diet (28.6% TF, 9.0% SF), and a low saturated fat (Low-Sat) diet (25.3% TF, 6.1% SF) were each fed for a period of 8 weeks in a three-way crossover design. Cholesterol was kept constant at 275 mg/d; monounsaturated and polyunsaturated fat were kept constant at approximately 13% and 6.5% of calories, respectively. Fasting lipid levels were measured during each of the final 4 weeks of each diet period. Participants were grouped by apoE genotype: E2 (E2/2, E2/3, E2/4); E3 (E3/3); E4 (E3/4, E4/4). Relative to the average American diet, both the Step 1 and Low-Sat diets significantly reduced total cholesterol, LDL cholesterol, and HDL cholesterol in all three apoE genotype groups. No evidence of a significant diet by genotype interaction, however, could be identified for any of the measured lipid and lipoprotein end points. Additional analysis of the data within individual population subgroups (men and women, blacks and whites) likewise provided no evidence of a significant diet by genotype interaction. Thus, in a heterogeneous, normolipidemic study population, apoE genotype does not predict the magnitude of lipid response to reductions in dietary saturated fat. C1 COLUMBIA UNIV,COLL PHYS & SURG,DEPT MED,NEW YORK,NY. PENN STATE UNIV,DEPT NUTR,UNIVERSITY PK,PA 16802. UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. UNIV N CAROLINA,COLLABORATING STUDIES COORDINATING CTR,DEPT BIOSTAT,CHAPEL HILL,NC 27515. NHLBI,DIV HEART & VASC DIS,NIH,BETHESDA,MD 20892. MARY IMOGENE BASSETT HOSP,RES INST,COOPERSTOWN,NY 13326. LOUISIANA STATE UNIV,MED CTR,DEPT PHYSIOL,NEW ORLEANS,LA 70112. RP Lefevre, M (reprint author), PENNINGTON BIOMED RES CTR,6400 PERKINS RD,BATON ROUGE,LA 70808, USA. RI Lefevre, Michael/B-5030-2014 OI Lefevre, Michael/0000-0002-2046-3593 FU NHLBI NIH HHS [5-U01-HL49644, 5-U01-HL49648, 5-U01-HL49699] NR 53 TC 34 Z9 34 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1079-5642 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD NOV PY 1997 VL 17 IS 11 BP 2914 EP 2923 PG 10 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA YL008 UT WOS:A1997YL00800081 PM 9409276 ER PT J AU Tall, A Welch, C ApplebaumBowden, D Wassef, M AF Tall, A Welch, C ApplebaumBowden, D Wassef, M TI Interaction of diet and genes in atherogenesis report of an NHLBI working group SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE atherogenesis; diet; genes ID DENSITY-LIPOPROTEIN RECEPTOR; RECOMBINANT INBRED STRAINS; ESTER TRANSFER PROTEIN; SPONTANEOUSLY HYPERTENSIVE RAT; APOLIPOPROTEIN-E POLYMORPHISM; MULTIFACTORIAL MOUSE MODEL; QUANTITATIVE TRAIT LOCI; LEUCINE ZIPPER PROTEIN; HIGH-CHOLESTEROL DIETS; FATTY-ACIDS AB Recent advances in genetics and information emerging from the Human Genome Project make it feasible to examine the importance of dietary-genetic interactions in the development of atherosclerosis. In the opinion of the Working Group, three approaches are necessary to examine this concern. The first approach utilizes animal models to map and identify candidate genes involved in dietary responsiveness and atherogenesis. The second approach involves the evaluation of these genes in specific physiological processes involved in dietary responsiveness and atherogenesis. Finally, the third approach is to extend the studies performed in animal models to human populations using linkage or association studies. C1 NHLBI,NIH,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,SW MED SCH,DALLAS,TX 75235. UNIV TEXAS,CTR HLTH,CTR HUMAN NUTR,DALLAS,TX 75235. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. UNIV OTTAWA,INST HEART,OTTAWA,ON K1Y 4E9,CANADA. UNIV CALIF IRVINE,DEPT MOL BIOL & BIOCHEM,IRVINE,CA 92717. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC 27517. TUFTS UNIV,LIPID METAB LAB,BOSTON,MA 02111. DIV HEART & VASC DIS,CARDIOVASC HOMEOSTASIS & BIONUTR RES GRP,BETHESDA,MD 20892. DIV HEART & VASC DIS,ATHEROSCLEROSIS RES GRP,BETHESDA,MD 20892. RP Tall, A (reprint author), COLUMBIA UNIV COLL PHYS & SURG,DEPT MED,630 W 168TH ST,NEW YORK,NY 10032, USA. NR 73 TC 19 Z9 20 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1079-5642 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD NOV PY 1997 VL 17 IS 11 BP 3326 EP 3331 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA YL008 UT WOS:A1997YL00800134 PM 9409329 ER PT J AU Pillemer, SR Bradley, LA Crofford, LJ Moldofsky, H Chrousos, GP AF Pillemer, SR Bradley, LA Crofford, LJ Moldofsky, H Chrousos, GP TI The neuroscience and endocrinology of fibromyalgia SO ARTHRITIS AND RHEUMATISM LA English DT Editorial Material ID PITUITARY-ADRENAL AXIS; FUNCTIONAL HYPOTHALAMIC AMENORRHEA; SUSTAINED SLEEP-DEPRIVATION; CHRONIC FATIGUE SYNDROME; HUMAN BRAIN MEASURES; GROWTH-HORMONE; CIRCADIAN RHYTHMICITY; SEX-DIFFERENCES; CLINICAL PAIN; REM-SLEEP C1 UNIV ALABAMA,BIRMINGHAM,AL. UNIV MICHIGAN,ANN ARBOR,MI 48109. TORONTO WESTERN HOSP,TORONTO,ON M5T 2S8,CANADA. NICHHD,NIH,BETHESDA,MD 20892. RP Pillemer, SR (reprint author), NIAMSD,OFF DIRECTOR,NIH,BLDG 45,ROOM 5AS-37G,45 CTR DR,MSC 6500,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013; OI Bradley, Laurence/0000-0002-1206-2263; Moldofsky, Harvey/0000-0002-5234-8864 NR 68 TC 143 Z9 145 U1 2 U2 8 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD NOV PY 1997 VL 40 IS 11 BP 1928 EP 1939 DI 10.1002/art.1780401103 PG 12 WC Rheumatology SC Rheumatology GA YE639 UT WOS:A1997YE63900002 PM 9365080 ER PT J AU Rider, LG Feldman, BM Perez, MD Rennebohm, RM Lindsley, CB Zemel, LS Wallace, CA Ballinger, SH Bowyer, SL Reed, AM Passo, MH Katona, IM Miller, FW Lachenbruch, PA AF Rider, LG Feldman, BM Perez, MD Rennebohm, RM Lindsley, CB Zemel, LS Wallace, CA Ballinger, SH Bowyer, SL Reed, AM Passo, MH Katona, IM Miller, FW Lachenbruch, PA TI Development of validated disease activity and damage indices for the juvenile idiopathic inflammatory myopathies .1. Physician, parent, and patient global assessments SO ARTHRITIS AND RHEUMATISM LA English DT Article ID ARTHRITIS CLINICAL-TRIALS; SYSTEMIC LUPUS-ERYTHEMATOSUS; RHEUMATOID-ARTHRITIS; OUTCOME MEASURES; HEALTH-STATUS; DERMATOMYOSITIS; DISABILITY; CHILDREN; PAIN; INDEX AB Objective. To determine the reliability, content validity, and responsiveness of physician global assessments of disease activity and damage in the juvenite idiopathic inflammatory myopathies (IIM), and to investigate concordance among physician, parent, and patient global ratings. Methods. Sixteen pediatric rheumatologists rated 10 juvenile IIM paper patient cases far global disease activity and damage, and assessed the importance of 51 clinical and laboratory parameters in formulating their global assessments, Then, 117 juvenile IIM patients were enrolled in a protocol to examine the relationship between Likert and visual analog scale global assessments, their sensitivity to change, and the comparability of physician, parent, and patient global ratings. Results. Pediatric rheumatologists demonstrated excellent interrater reliability in their global assessments of juvenile IIM disease activity and damage (97.7% and 94.7% agreement among raters, respectively), and agreed on a core set of clinical parameters in formulating their judgments. Likert scale ratings correlated with those on a visual analog scale, and both were comparable in responsiveness (standardized response means -0.56 for disease activity, 0.02 [Likert] and 0.14 [visual analog] for damage, measured over 8 months). Parent global ratings of disease activity correlated with physician assessments, but were not colinear (Spearman's correlation [r] = 0.41-0.45). Patient global disease activity assessments correlated with those done by parents (r = 0.57-0.84) and physicians (r = 0.37-0.63), but demonstrated less responsiveness (standardized response means -0.21 and -0.12, respectively, over 8 months). Conclusion. Physician global assessments of juvenile IIM disease activity and damage demonstrated high interrater reliability and were shown to be comprehensive measures. Both physician and parent disease activity assessments should be considered valuable as quantitative measures for evaluating therapeutic responses in juvenile IIM patients. C1 NIAMSD,NIH,BETHESDA,MD 20892. UNIV TORONTO,HOSP SICK CHILDREN,TORONTO,ON M5G 1X8,CANADA. TEXAS CHILDRENS HOSP,BAYLOR COLL MED,HOUSTON,TX 77030. OHIO STATE UNIV,COLUMBUS CHILDRENS HOSP,COLUMBUS,OH 43210. UNIV KANSAS,KANSAS CITY,KS 66103. UNIV CONNECTICUT,CONNECTICUT CHILDRENS MED CTR,HARTFORD,CT 06112. UNIV WASHINGTON,CHILDRENS HOSP,SEATTLE,WA 98195. INDIANA UNIV,JAMES WHITCOMB RILEY HOSP CHILDREN,INDIANAPOLIS,IN 46204. UNIV N CAROLINA,CHAPEL HILL,NC. UNIV CINCINNATI,CHILDRENS HOSP,CINCINNATI,OH. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. US FDA,ROCKVILLE,MD 20857. RP Rider, LG (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV MONOCLONAL ANTIBODIES,BLDG 29B,ROOM 2G11,HFM-561,BETHESDA,MD 20892, USA. RI Feldman, Brian/A-8586-2011; OI Rider, Lisa/0000-0002-6912-2458 NR 42 TC 72 Z9 75 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD NOV PY 1997 VL 40 IS 11 BP 1976 EP 1983 DI 10.1002/art.1780401109 PG 8 WC Rheumatology SC Rheumatology GA YE639 UT WOS:A1997YE63900008 PM 9365086 ER PT J AU George, TM Cash, JM Farver, C Sneller, M vanDyke, CW Derus, CL Hoffman, GS AF George, TM Cash, JM Farver, C Sneller, M vanDyke, CW Derus, CL Hoffman, GS TI Mediastinal mass and hilar adenopathy - Rare thoracic manifestations of Wegener's granulomatosis SO ARTHRITIS AND RHEUMATISM LA English DT Article ID CLASSIFICATION AB Objective. To assess the frequency and characteristics of hilar and mediastinal involvement in patients with Wegener's granulomatosis (WG). Methods. A patient with WG presented with the unusual finding of a mediastinal mass, prompting a comprehensive review of 302 patient records from 2 WG registries to obtain evidence of hilar adenopathy or mediastinal masses. Clinic progress notes and findings of chest imaging studies (routine imaging and computed tomography) were reviewed for the presence of hilar lymphadenopathy, mediastinal masses, or mediastinal lymphadenopathy. All radiographs and surgical pathology specimens from these lesions were reviewed. Results. Six examples of mediastinal or hilar involvement (2.0%) were identified among 302 patients with WG. Three of these 6 patients had mediastinal masses. One patient with a mediastinal mass also had mediastinal lymphadenopathy. Two of the patients with mediastinal masses had lung parenchymal lesions. The remaining 3 patients had enlarged hilar lymph nodes in addition to pulmonary parenchymal lesions, All of the patients were treated with corticosteroids and cytotoxic drugs. Followup information was available on all patients. Two patients died. In the remaining 4 patients, the mediastinal mass or hilar lymphadenopathy decreased in size or resolved after 2 months of immunosuppressive therapy. Conclusion. In the past, hilar adenopathy and/or mediastinal mass have been considered unlikely features of WG, and their presence has prompted consideration of an alternative diagnosis, Although this caution remains valuable, the present retrospective review of data from 2 large WG registries illustrates that such findings may rarely be a part of the spectrum of WG chest disease, Because these findings are uncommon, they necessitate consideration of a primary or concurrent infection or malignancy in the diagnostic evaluation. C1 CLEVELAND CLIN FDN,CLEVELAND,OH 44195. NIAIID,NIH,BETHESDA,MD. DREYER MED GRP,AURORA,IL. NR 15 TC 31 Z9 33 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 NOV PY 1997 VL 40 IS 11 BP 1992 EP 1997 DI 10.1002/art.1780401111 PG 6 WC Rheumatology SC Rheumatology GA YE639 UT WOS:A1997YE63900010 PM 9365088 ER PT J AU Slavkin, HC AF Slavkin, HC TI Government research and development funding SO ASAIO JOURNAL LA English DT Article RP Slavkin, HC (reprint author), NIDR,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1058-2916 J9 ASAIO J JI Asaio J. PD NOV-DEC PY 1997 VL 43 IS 6 BP 880 EP 881 DI 10.1097/00002480-199711000-00004 PG 2 WC Engineering, Biomedical; Transplantation SC Engineering; Transplantation GA YF563 UT WOS:A1997YF56300004 PM 9386834 ER PT J AU Foti, G Kolobow, T Rossi, F Mandava, S Yamada, K Jones, M AF Foti, G Kolobow, T Rossi, F Mandava, S Yamada, K Jones, M TI Cardiopulmonary bypass through peripheral cannulation with percutaneous decompression of the left heart in a model of severe myocardial failure SO ASAIO JOURNAL LA English DT Article ID EXTRACORPOREAL MEMBRANE-OXYGENATION; POSTCARDIOTOMY CARDIOGENIC-SHOCK AB Prolonged closed chest cardiopulmonary bypass for severe total biventricular myocardial dysfunction requires invasive decompression of the left heart. The authors have developed an elongated helical coil that is permanently attached to the distal 8-10 cm of a flow directed Swan-Cant catheter. When properly positioned, the helical coil kept the pulmonary artery (PA) and the tricuspid valves open, and allowed closed chest retrograde decompression of the left heart. The authors have evaluated the merits of closed chest cardiopulmonary bypass with decompression of the left heart in this manner in four sheep subjected to 30 min of warm global myocardial ischemia, along with induced ventricular fibrillation. All sheep developed severe global myocardial failure, with no left ventricular (LV) ejection. The authors have shown that pulmonary blood flow during cardiopulmonary bypass was reversed from the left heart, across the lungs, and into the right heart. The wedge pressure never exceeded 12 mmHg at any time, attesting to good decompression during periods of total ventricular failure, during partial recovery with some LV ejection, and after good recovery of LV function, followed by weaning from bypass after 44, 67, and 78 h of such support. One sheep could not be weaned from bypass, even after 5 days of CPBP. Lung function in all sheep remained unimpaired throughout, and there was no wound bleeding. The authors conclude that in this model of total myocardial failure, and while on closed chest CPBP, at all times and with all degrees of myocardial dysfunction, excellent LV decompression with the helical coil catheter was attained. C1 NHLBI,PULM CRIT CARE MED BRANCH,NIH,BETHESDA,MD 20892. OSPED NUOVO,MONZA,MILANO,ITALY. INST ANESTESIA E RIANIMAZ,MILAN,ITALY. RI Foti, Giuseppe/K-8627-2016 NR 18 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1058-2916 J9 ASAIO J JI Asaio J. PD NOV-DEC PY 1997 VL 43 IS 6 BP 927 EP 931 DI 10.1097/00002480-199711000-00015 PG 5 WC Engineering, Biomedical; Transplantation SC Engineering; Transplantation GA YF563 UT WOS:A1997YF56300015 PM 9386845 ER PT J AU Wiebel, FJ Andersson, TB Casciano, DA Dickins, M Fischer, V Glatt, H Horbach, J Langenbach, RJ Luyten, W Turchi, G Vandewalle, A AF Wiebel, FJ Andersson, TB Casciano, DA Dickins, M Fischer, V Glatt, H Horbach, J Langenbach, RJ Luyten, W Turchi, G Vandewalle, A TI Genetically engineered cell lines: Characterisation and applications in toxicity testing SO ATLA-ALTERNATIVES TO LABORATORY ANIMALS LA English DT Editorial Material ID CHINESE-HAMSTER CELLS; CDNA-DIRECTED EXPRESSION; STABLE EXPRESSION; MAMMALIAN-CELLS; HUMAN-LIVER; METABOLIC-ACTIVATION; CATALYTIC ACTIVITIES; CYTOCHROME-P450 3A4; DRUG-METABOLISM; GENE C1 ASTRA HASSLE AB,DEPT METAB & PHARMACOKINET,S-43183 MOLNDAL,SWEDEN. NCTR,DIV GENET TOXICOL,JEFFERSON,AR 72079. GLAXO WELLCOME,BIOMET DEPT,WARE SG12 0DP,HERTS,ENGLAND. NOVARTIS PHARMACEUT CORP,DRUG METAB & PHARMACOKINET,E HANOVER,NJ 07936. DEUTSCH INST ERNAHRUNGSFORSCH,ABT ERNAHRUNGSTOXIKOL,D-14558 BERGHOLZ REHBRUCK,GERMANY. UNIV UTRECHT,RITOX,NL-3508 TD UTRECHT,NETHERLANDS. NIEHS,LAB CARCINOGENESIS MUTAGENESIS,RES TRIANGLE PK,NC 27709. JANSSEN PHARMACEUT,DEPT BIOCHEM PHARMACOL,B-2340 BEERSE,BELGIUM. UNIV PISA,DIPARTIMENTO SCI AMBIENTE & TERR,I-56100 PISA,ITALY. UNIV PARIS 07,INSERM,U246,F-75018 PARIS,FRANCE. RP Wiebel, FJ (reprint author), GSF MUNICH,NATL RES CTR ENVIRONM & HLTH,INST TOXICOL,D-85758 NEUHERBERG,GERMANY. NR 48 TC 18 Z9 18 U1 0 U2 0 PU FRAME PI NOTTINGHAM PA RUSSELL & BURCH HOUSE 96-98 NORTH SHERWOOD ST, NOTTINGHAM, NOTTS, ENGLAND NG1 4EE SN 0261-1929 J9 ATLA-ALTERN LAB ANIM JI ATLA-Altern. Lab. Anim. PD NOV-DEC PY 1997 VL 25 IS 6 BP 625 EP 639 PG 15 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YL235 UT WOS:A1997YL23500010 ER PT J AU Chiaradia, M Gulson, BL James, M Jameson, CW Johnson, D AF Chiaradia, M Gulson, BL James, M Jameson, CW Johnson, D TI Identification of secondary lead sources in the air of an urban environment SO ATMOSPHERIC ENVIRONMENT LA English DT Article DE Pb; urban air; gasoline; lead isotopes ID AIRBORNE LEAD; BLOOD LEAD; PETROL; STREET; DUST; SOIL; CONTAMINATION; PARTICLES; CHILDREN; CADMIUM AB High precision lead isotopic data have been measured from particulates deposited on filters from two suburbs of Sydney (NSW, Australia) and gasoline from two main brands to evaluate the source of lead in air following the phasing out of leaded gasoline in Sydney in 1986 and a 25% reduction of lead in leaded gasoline in 1994. These measures have resulted in a 75% reduction of lead in Sydney air nowadays. Despite these positive figures, our results indicate that gasoline still accounts for more than 90% of the lead in the atmosphere of this city. However, when compared with an earlier investigation carried out in the period 1979-1981, our data show that a background source with a Pb-206/Pb-204 isotopic ratio higher than petrol has become detectable. We have used a best fitting mathematical procedure to identify the isotopic ratio and percentage contribution of this source to the air. The values that we have obtained are similar to 18.2 and similar to 7%, respectively, for the Pb-206/Pb-204 ratio and the percentage contribution. Several local background sources are considered, including natural lead from soils, wood burning, coal burning in power stations and aircraft propellants. We also draw attention to the similarity of the background isotopic composition in Sydney air and isotopic ratios measured in snows of Antarctica. (C) 1997. Published by Elsevier Science Ltd. C1 CSIRO,EM,N RYDE,NSW 2113,AUSTRALIA. MACQUARIE UNIV,GRAD SCH ENVIRONM,SYDNEY,NSW 2109,AUSTRALIA. NATL INST ENVIRONM HLTH SCI,RES TRIANGLE PK,NC 27709. NEW S WALES ENVIRONM PROTECT AUTHOR,LIDCOMBE,NSW 2141,AUSTRALIA. NR 29 TC 51 Z9 57 U1 1 U2 7 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 1352-2310 J9 ATMOS ENVIRON JI Atmos. Environ. PD NOV PY 1997 VL 31 IS 21 BP 3511 EP 3521 DI 10.1016/S1352-2310(97)00218-5 PG 11 WC Environmental Sciences; Meteorology & Atmospheric Sciences SC Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences GA XV754 UT WOS:A1997XV75400003 ER PT J AU Lerman, C Caporaso, N Main, D Audrain, J Bowman, E Lockshin, B Shields, P AF Lerman, C Caporaso, N Main, D Audrain, J Bowman, E Lockshin, B Shields, P TI Association of dopamine transporter SLC6A3 and DRD2 receptor genes with risk of cigarette smoking. SO BEHAVIOR GENETICS LA English DT Meeting Abstract C1 Georgetown Univ, Med Ctr, Washington, DC 20007 USA. NCI, Rockville, MD 20892 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD NOV PY 1997 VL 27 IS 6 BP 598 EP 598 PG 1 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA YV287 UT WOS:000071808100070 ER PT J AU Furlanetto, RW Dey, BR Lopaczynski, W Nissley, SP AF Furlanetto, RW Dey, BR Lopaczynski, W Nissley, SP TI 14-3-3 proteins interact with the insulin-like growth factor receptor but not the insulin receptor SO BIOCHEMICAL JOURNAL LA English DT Article ID FACTOR-I RECEPTOR; 14-3-3-PROTEINS ASSOCIATE; RAF-1; ACTIVATION; MITOGENESIS; BINDING; DOMAINS; ISOFORM; MANNER; FORM AB We have used a yeast two-hybrid system to identify proteins which bind to the cytosolic portion of the type 1 insulin-like growth factor (IGF) receptor (IGFIR) but not the insulin receptor (IR). This analysis identified 14-3-3 beta and zeta proteins. 14-3-3 beta also binds to the IGFIR but not the IR in vitro and 14-3-3-IGFIR complexes are present in insect cells overexpressing the IGFIR cytoplasmic domain. 14-3-3 proteins are substrates of the IGFIR in the yeast system and in vitro. The interaction of 14-3-3 with the IGFIR requires receptor-kinase activity and maps to the C-terminus of the receptor, but does not depend on tyrosine residues in this or the juxtamembrane regions. Instead, the binding maps to serine residue 1283 and requires phosphorylation of this residue. 14-3-3 proteins are phosphoserine-binding proteins which have been shown to interact directly with components of the mitogenic and apoptotic signalling pathways, suggesting that they participate in growth regulation. Our findings suggest that 14-3-3 proteins may play a role in IGFIR signal transduction and may contribute to the differences in IGF and IR signalling capabilities. C1 NCI, METAB BRANCH, NIH, BETHESDA, MD 20892 USA. RP Furlanetto, RW (reprint author), UNIV ROCHESTER, SCH MED & DENT, DEPT PEDIAT, STRONG CHILDRENS RES CTR, ROCHESTER, NY 14642 USA. NR 35 TC 74 Z9 78 U1 0 U2 1 PU PORTLAND PRESS LTD PI LONDON PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD NOV 1 PY 1997 VL 327 BP 765 EP 771 PN 3 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF865 UT WOS:A1997YF86500019 PM 9581554 ER PT J AU Kurenova, EV Mason, JM AF Kurenova, EV Mason, JM TI Telomere functions. A review SO BIOCHEMISTRY-MOSCOW LA English DT Review DE telomere; Drosophila melanogaster; yeast; chromosomes; transcription; replication; nuclear architecture; silencing; chromosome stability; mitosis; meiosis; chromosome structure; telomerase; heterochromatin; position effect; Tetrahymena ID POSITION-EFFECT VARIEGATION; ORIGIN RECOGNITION COMPLEX; BROKEN CHROMOSOME ENDS; SALIVARY-GLAND NUCLEI; DNA-BINDING PROTEIN; SILENT MATING LOCI; SACCHAROMYCES-CEREVISIAE; DROSOPHILA-MELANOGASTER; TETRAHYMENA-TELOMERASE; FISSION YEAST AB Telomers are structurally and functionally complex. They consist of an array of simple DNA repeals at the extreme end of the chromosome, with a more complex array of repeats adjacent to it. A large number of proteins have been identified that bind to the telomeric DNA repeats or to the protein complexes that are-built at the chromosome end, Telomeres rend reform associations with each other. These associations have been implicated in the formation of nuclear domains that may be important for transcriptional regulation, for sister chromatid pairing at mitosis, and for homologous meiotic synapsis. Telomeric chromosome ends do not cause delays in cell cycle progression, nor are they subject to DNA repair as are broken chromosome ends. Telomeres also provide a separate mechanism for adding additional copies of the telomeric DNA to chromosome ends. This is needed to counterbalance the loss of DNA sequences from chromosome ends due to incomplete DNA replication. The components that participate in the latter mechanism and this process have been characterized in detail the other functions of telomeres are less well understood but are the subjects of active investigation. C1 NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA. RP Mason, JM (reprint author), NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA. NR 164 TC 24 Z9 24 U1 1 U2 3 PU PLENUM PUBL CORP PI NEW YORK PA CONSULTANTS BUREAU, 233 SPRING ST, NEW YORK, NY 10013 USA SN 0006-2979 J9 BIOCHEMISTRY-MOSCOW+ JI Biochem.-Moscow PD NOV PY 1997 VL 62 IS 11 BP 1242 EP 1253 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YV290 UT WOS:000071808400010 PM 9467848 ER PT J AU Darawshe, S Millar, DB Ahmed, SA Miles, EW Minton, AP AF Darawshe, S Millar, DB Ahmed, SA Miles, EW Minton, AP TI Dissociation equilibria of the tryptophan synthase alpha(2)beta(2) complex in saline buffer and guanidine isothiocyanate, as studied by sedimentation equilibrium SO BIOPHYSICAL CHEMISTRY LA English DT Article DE tryptophan synthase; dissociation equilibria; sedimentation equilibrium ID ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; SUBUNIT; ALPHA; BINDING AB The dissociation equilibria of Salmonella typhimurium tryptophan synthase alpha(2) beta(2) complex were studied via centrifugation of the complex to sedimentation equilibrium in neutral saline buffers containing 0 to 137 mM guanidine isothiocyanate (GuSCN). The resulting concentration gradients were analyzed in the context of an equilibrium model for sequential dissociation of two cu subunits from a stable beta(2) subunit. Under the conditions of these experiments, the first dissociation constant alone could be evaluated at GuSCN concentrations less than or equal to 100 mM, and the second dissociation constant alone could be evaluated at GuSCN = 137 mM. At intermediate GuSCN, both dissociation constants were sufficiently well defined to rule out the presence of a large equilibrium cooperative effect in the stepwise dissociation of the alpha subunits. Published by Elsevier Science B.V. C1 NIDDKD, Sect Phys Biochem, Biochem Pharmacol Lab, NIH, Bethesda, MD 20892 USA. NIDDKD, Sect Enzyme Struct & Funct, Biochem Pharmacol Lab, NIH, Bethesda, MD 20892 USA. RP Minton, AP (reprint author), NIDDKD, Sect Phys Biochem, Biochem Pharmacol Lab, NIH, Bldg 8,Room 226, Bethesda, MD 20892 USA. NR 18 TC 6 Z9 6 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0301-4622 J9 BIOPHYS CHEM JI Biophys. Chem. PD NOV PY 1997 VL 69 IS 1 BP 53 EP 62 DI 10.1016/S0301-4622(97)00078-1 PG 10 WC Biochemistry & Molecular Biology; Biophysics; Chemistry, Physical SC Biochemistry & Molecular Biology; Biophysics; Chemistry GA YN346 UT WOS:000071158700006 PM 9440208 ER PT J AU Xu, S Malinchik, S Gilroy, D Kraft, T Brenner, B Yu, LC AF Xu, S Malinchik, S Gilroy, D Kraft, T Brenner, B Yu, LC TI X-ray diffraction studies of cross-bridges weakly bound to actin in relaxed skinned fibers of rabbit psoas muscle SO BIOPHYSICAL JOURNAL LA English DT Article ID LOW IONIC-STRENGTH; MYOSIN HEADS; FORCE GENERATION; SKELETAL-MUSCLE; PARALLEL INHIBITION; RIGOR; STIFFNESS; CROSSBRIDGES; CALDESMON; FILAMENTS AB X-ray diffraction patterns were obtained from skinned rabbit psoas muscle under relaxing and rigor conditions over a wide range of ionic strengths (50-170 mM) and temperatures (1 degrees C-30 degrees C). For the first time, an intensification of the first actin-based layer line is observed in the relaxed muscle, The intensification, which increases with decreasing ionic strength at various temperatures, including 30 degrees C, parallels the formation of weakly attached cross-bridges in the relaxed muscle, However, the overall intensities of the actin-based layer lines are low, Furthermore, the level of diffuse scattering, presumably a measure of disorder among the cross-bridges, is little affected by changing ionic strength at a given temperature, The results suggest that the intensification of the first actin layer line is most likely due to the cross-bridges weakly bound to actin, and that the orientations of the weakly attached cross-bridges are hardly distinguishable from the detached cross-bridges. This suggests that the orientations of the weakly attached cross-bridges are not precisely defined with respect to the actin helix, i.e., nonstereospecific. Intensities of the myosin-based layer lines are only marginally affected by changing ionic strength, but markedly by temperature, The results could be explained if in a relaxed muscle the cross-bridges are distributed between a helically ordered and a disordered population with respect to myosin filament structure. Within the disordered population, some are weakly attached to actin and others are detached, The fraction of cross-bridges in the helically ordered assembly is primarily a function of temperature, while the distribution between the weakly attached and the detached within the disordered population is mainly affected by ionic strength, Some other notable features in the diffraction patterns include a approximate to 1% decrease in the pitch of the myosin helix as the temperature is raised from 4 degrees C to 20 degrees C. C1 NIAMS, NIH, BETHESDA, MD 20892 USA. HANNOVER MED SCH, D-3000 HANNOVER, GERMANY. NR 37 TC 31 Z9 31 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD NOV PY 1997 VL 73 IS 5 BP 2292 EP 2303 PG 12 WC Biophysics SC Biophysics GA YD848 UT WOS:A1997YD84800006 PM 9370426 ER PT J AU Malinchik, S Xu, S Yu, LC AF Malinchik, S Xu, S Yu, LC TI Temperature-induced structural changes in the myosin thick filament of skinned rabbit psoas muscle SO BIOPHYSICAL JOURNAL LA English DT Article ID X-RAY-DIFFRACTION; SKELETAL-MUSCLE; HEADS; PATTERN; MODEL; ACTIN AB By using synchrotron radiation and an imaging plate for recording diffraction patterns, we have obtained high-resolution x-ray patterns from relaxed rabbit psoas muscle at temperatures ranging from 1 degrees C to 30 degrees C. This allowed us to obtain intensity profiles of the first six myosin layer lines and apply a model-building approach for structural analysis. At temperatures 20 degrees C and higher, the layer lines are sharp with clearly defined maxima, Modeling based on the data obtained at 20 degrees C reveals that the average center of the cross-bridges is at 135 Angstrom from the center of the thick filament and both of the myosin heads appear to wrap around the backbone. At 10 degrees C and lower, the layer lines become very weak and diffuse scattering increases considerably. At 4 degrees C, the peak of the first layer line shifts toward the meridian from 0.0047 to 0.0038 Angstrom(-1) and decreases in intensity approximately by a factor of four compared to that at 20 degrees C, although the intensities of higher-order layer lines remain similar to 10-15% of the first layer line. Our modeling suggests that as the temperature is lowered from 20 degrees C to 4 degrees C the center of cross-bridges extends radially away from the center of the filament (135 Angstrom to 175 Angstrom). Furthermore, the fraction of helically ordered cross-bridges decreases at least by a factor of two, while the isotropic disorder (the temperature factor) remains approximately unchanged. Our results on the order/disordering effects of temperature are in general agreement with earlier results of Wray [Wray, J. 1987. Structure of relaxed myosin filaments in relation to nucleotide state in vertebrate skeletal muscle. J. Muscle Res. Cell Motil. 8:62a (Abstr.)] and Lowy et al. (Lowy, J., D. Popp, and A. A. Stewart. 1991. X-ray studies of order-disorder transitions in the myosin heads of skinned rabbit psoas muscles. Biophys. J. 60:812-824). and support Poulsen and Lowy's hypothesis of coexistence of ordered and disordered cross-bridge populations in muscle (Poulsen, F. R., and J. Lowy. 1983. Small angle scattering from myosin heads in relaxed and rigor frog skeletal muscle. Nature (Lend.). 303:146-152.). However, our results added new insights into the disordered population. Present modeling together with data analysis (Xu, S., S. Malinchik, Th. Kraft, B. Brenner, and L. C. Yu. 1997. X-ray diffraction studies of cross-bridges weakly bound to actin in relaxed skinned fibers of rabbit psoas muscle. Biophys. J. 73:000-000) indicate that in a relaxed muscle, cross-bridges are distributed in three populations: those that are ordered on the thick filament helix and those that are disordered; and within the disordered population, some cross-bridges are detached and some are weakly attached to actin. One critical conclusion of the present study is that the apparent order <-> disorder transition as a function of temperature is not due to an increase/decrease in thermal motion (temperature factor) for the entire population, but a redistribution of cross-bridges among the three populations, Changing the temperature leads to a change in the fraction of cross-bridges located on the helix, while changing the ionic strength at a given temperature affects the disordered population leading to a change in the relative fraction of cross-bridges detached from and weakly attached to actin, Since the redistribution is reversible, we suggest that there is an equilibrium among the three populations of cross-bridges. C1 NATL INST ARTHRITIS & MUSCULOSKELETAL & SKIN DIS, PHYS BIOL LAB, NIH, BETHESDA, MD 20892 USA. NR 21 TC 37 Z9 37 U1 1 U2 4 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD NOV PY 1997 VL 73 IS 5 BP 2304 EP 2312 PG 9 WC Biophysics SC Biophysics GA YD848 UT WOS:A1997YD84800007 PM 9370427 ER PT J AU Bezrukov, SM Vodyanoy, I AF Bezrukov, SM Vodyanoy, I TI Signal transduction across alamethicin ion channels in the presence of noise SO BIOPHYSICAL JOURNAL LA English DT Article ID STOCHASTIC RESONANCE; BISTABLE SYSTEMS; PHYSICAL LIMITS; MODEL; ENHANCEMENT; MEMBRANE; CRAYFISH; MECHANORECEPTORS; BEHAVIOR; STIMULI AB We have studied voltage-dependent ion channels of alamethicin reconstituted into an artificial planar lipid bilayer membrane from the point of view of electric signal transduction. Signal transduction properties of these channels are highly sensitive to the external electric noise. Specifically, addition of bandwidth-restricted ''white'' noise of 10-20 mV (r.m.s.) to a small sine wave input signal increases the output signal by similar to 20-40 dB conserving, and even slightly increasing, the signal-to-noise ratio at the system output. We have developed a small-signal adiabatic theory of stochastic resonance for a threshold-free system of voltage-dependent ion channels. This theory describes our main experimental findings giving good qualitative understanding of the underlying mechanism. It predicts the right value of the output signal-to-noise ratio and provides a reliable estimate for the noise intensity corresponding to its maximum. Our results suggest that the alamethicin channel in a lipid bilayer is a good model system for studies of mechanisms of primary electrical signal processing in biology showing an important feature of signal transduction improvement by a fluctuating environment. C1 ST PETERSBURG NUCL PHYS INST, GATCHINA 188350, RUSSIA. OFF NAVAL RES EUROPE, LONDON, ENGLAND. RP Bezrukov, SM (reprint author), NIH, DCRT, BLDG 5, ROOM 405, BETHESDA, MD 20892 USA. NR 50 TC 51 Z9 52 U1 0 U2 7 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD NOV PY 1997 VL 73 IS 5 BP 2456 EP 2464 PG 9 WC Biophysics SC Biophysics GA YD848 UT WOS:A1997YD84800019 PM 9370439 ER PT J AU Adachi, M Iwasa, KH AF Adachi, M Iwasa, KH TI Effect of diamide on force generation and axial stiffness of the cochlear outer hair cell SO BIOPHYSICAL JOURNAL LA English DT Article ID ELECTROKINETIC SHAPE CHANGES; GUINEA-PIG COCHLEA; MECHANICAL RESPONSES; MEMBRANE-PROTEINS; CORTICAL LATTICE; MOTILITY; ERYTHROCYTES; CAPACITANCE; INHIBITION; SPECTRIN AB We found that diamide, which affects spectrin, reduces the axial stiffness of the cochlear outer hair cell, the cylindrically shaped mechanoreceptor cell with a unique voltage-sensitive motility. This effect thus provides a means of examining the relationship between the stiffness and the motility of the cell. For measuring axial stiffness and force production, we used an experimental configuration in which an elastic probe was attached to the cell near the cuticular plate and the other end of the cell was held with a patch pipette in the whole-cell recording mode. Diamide at concentrations of up to 5 mM reduced the axial stiffness in a dose-dependent manner to 165 nN per unit strain from 502 nN for untreated cells. The isometric force elicited by voltage pulses under whole-cell voltage clamp was also reduced to 35 pN/mV from 105 pN/mV for untreated cells, Thus the isometric force was approximately proportional to the axial stiffness. Our observations suggest a series connection between the motor and cytoskeletal elements and can be explained by the area motor model previously proposed for the outer hair cell. C1 NATL INST DEAFNESS & OTHER COMMUN DISORDERS, BIOPHYS SECT, CELLULAR BIOL LAB, NIH, BETHESDA, MD 20892 USA. OI Iwasa, Kuni/0000-0002-9397-7704 NR 41 TC 26 Z9 27 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD NOV PY 1997 VL 73 IS 5 BP 2809 EP 2818 PG 10 WC Biophysics SC Biophysics GA YD848 UT WOS:A1997YD84800055 PM 9370475 ER PT J AU Wildt, DE Rall, WF Critser, JK Monfort, SL Seal, US AF Wildt, DE Rall, WF Critser, JK Monfort, SL Seal, US TI Genome resource banks SO BIOSCIENCE LA English DT Article ID CRYOPRESERVATION; CONSERVATION; SPERMATOZOA; SPERMATOGENESIS; INSEMINATION; OOCYTES; SHEEP C1 SMITHSONIAN INST, NATL ZOOL PK, CONSERVAT & RES CTR, REPROD PHYSIOL PROGRAM, FRONT ROYAL, VA 22630 USA. NIH, NATL CTR RES RESOURCES, EMBRYO CRYOPRESERVAT UNIT, BETHESDA, MD 20892 USA. METHODIST OUTPATIENT CTR N, ADV FERTIL INST, CRYOBIOL RES INST, INDIANAPOLIS, IN 46202 USA. IUCN, WORLD CONSERVAT UNION, SPECIES SURVIVAL COMMISS, CONSERVAT BREEDING SPECIALIST GRP, APPLE VALLEY, MN 55124 USA. RP Wildt, DE (reprint author), SMITHSONIAN INST, NATL ZOOL PK, CONSERVAT & RES CTR, NOAHS, FRONT ROYAL, VA 22630 USA. RI Rall, William/C-5104-2008 NR 54 TC 102 Z9 106 U1 2 U2 7 PU AMER INST BIOLOGICAL SCI PI WASHINGTON PA 1444 EYE ST, NW, STE 200, WASHINGTON, DC 20005 USA SN 0006-3568 J9 BIOSCIENCE JI Bioscience PD NOV PY 1997 VL 47 IS 10 BP 689 EP 698 DI 10.2307/1313209 PG 10 WC Biology SC Life Sciences & Biomedicine - Other Topics GA YC164 UT WOS:A1997YC16400017 ER PT J AU Han, LY Ma, WP Crouch, RJ AF Han, LY Ma, WP Crouch, RJ TI Ribonuclease H renaturation gel assay using a fluorescent-labeled substrate SO BIOTECHNIQUES LA English DT Article ID SODIUM DODECYL-SULFATE; ESCHERICHIA-COLI; RNASE-H; ELECTROPHORESIS; PROTEINS; ENZYMES AB Ribonucleases H (RNases H) are enzymes that specifically degrade the RNA of RNA-DNA hybrids. These enzymes are involved in DAN replication, reverse transcription (RT) and antisense oligodexoyribonucleotide-mediated arrest of translation. One of the most valuable tools for assaying RNase H activity is the renaturation gel assay with which such activities can be detected using purified protein preparations or crude extracts. Radioactive substrates [P-32-labeled poly(rA)-poly(dT) hybrid] are commonly used with exposure of the gel to X-ray film; this is possible at any time without disturbing the renaturation-degradation process. Here, we describe a method using fluorescent-labeled substrates. RNA-DNA substrates are synthesized by first transcribing DNA with T7 RNA polymerase using Bodipy(R)-TR-14-UTP and the four normal nucleoside triphosphates. The run-off transcript is annealed to a short oligomeric DNA complementary to the 3'-end of the transcript, and the DNA portion of the hybrid is formed by RT. This RNA-DNA is added to the polyacrylamide mixture before polymerization, and SDS-PAGE is performed as usual. After various periods of renaturation, the gel is scanned to detect fluorescent substrate using the red-excited laser of a fluorescence scanner. This fluorescence method has all of the advantages of using radio-labeled substrates and none of its disadvantages, and the sensitivities of the two methods are comparable. In addition, we show that the sensitivity of this procedure can be increased if damaging chemicals remaining in the gel after polymerization are eliminated by simultaneous electrophoresis of the RNase H and a protein with higher mobility. C1 NICHHD,BETHESDA,MD 20892. NR 13 TC 10 Z9 12 U1 2 U2 2 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD NOV PY 1997 VL 23 IS 5 BP 920 EP & PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YE032 UT WOS:A1997YE03200027 PM 9383560 ER PT J AU Fu, KL Lo Ten Foe, JR Joenje, H Rao, KW Liu, JM Walsh, CE AF Fu, KL Lo Ten Foe, JR Joenje, H Rao, KW Liu, JM Walsh, CE TI Functional correction of Fanconi anemia group A hematopoietic cells by retroviral gene transfer SO BLOOD LA English DT Article ID GROUP-C GENE; VECTOR; MUTATION; LINES; THERAPY; FACC AB Fanconi anemia (FA) is an autosomal recessive genetic disorder characterized by a variety of physical anomalies, hone marrow failure, and an increased risk for malignancy, FA cells exhibit chromosomal instability and are hypersensitive to DNA cross-linking agents such as mitomycin C (MMC). FA is a clinically heterogeneous disorder and can be functionally divided into at least five different complementation groups (A-E), We previously described the use of a retroviral vector expressing the FAC cDNA in the complementation of mutant hematopoietic cells from FA-C patients. This vector is currently being tested in a clinical trial of ex vivo hematopoietic progenitor cell transduction. The FA-A group accounts for over 65% of all FA cases, and the FAA cDNA was recently identified by both expression and positional cloning techniques. We report here the transduction and phenotypic correction of lymphoblastoid cell lines from four unrelated FA-A patients, using two amphotropic FAA retroviral vectors. Expression of the FAA transgene was adequate to normalize cell growth, cell-cycle kinetics, and chromosomal breakage in the presence of MMC. We then analyzed the effect of retroviral vector transduction an hematopoietic progenitor cell growth. After FAA transduction of mutant progenitor cells, either colony number or colony size increased in the presence of MMC. In addition, FAA but not FAC retroviral transduction markedly improved colony growth of progenitor cells derived from an unclassified FA patient. FAA retroviral vectors should be useful for both complementation studies and clinical trials of gene transduction. (C) 1997 by The American Society of Hematology. C1 UNIV N CAROLINA, GENE THERAPY CTR, CHAPEL HILL, NC 27599 USA. UNIV N CAROLINA, DEPT MED, CHAPEL HILL, NC 27599 USA. UNIV N CAROLINA, DEPT PATHOL, CHAPEL HILL, NC 27599 USA. UNIV N CAROLINA, DEPT PEDIAT, CHAPEL HILL, NC 27599 USA. FREE UNIV AMSTERDAM, DEPT HUMAN GENET, AMSTERDAM, NETHERLANDS. NHLBI, NIH, BETHESDA, MD 20892 USA. NR 29 TC 23 Z9 24 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 NOV 1 PY 1997 VL 90 IS 9 BP 3296 EP 3303 PG 8 WC Hematology SC Hematology GA YD108 UT WOS:A1997YD10800003 PM 9345011 ER PT J AU Oritani, K Kanakura, Y Aoyama, K Yokota, T Copeland, NG Gilbert, DJ Jenkins, NA Tomiyama, Y Matsuzawa, Y Kincade, PW AF Oritani, K Kanakura, Y Aoyama, K Yokota, T Copeland, NG Gilbert, DJ Jenkins, NA Tomiyama, Y Matsuzawa, Y Kincade, PW TI Matrix glycoprotein SC1/ECM2 augments B lymphopoiesis SO BLOOD LA English DT Article ID STROMAL CELL-LINES; EXTRACELLULAR-MATRIX; HEMATOPOIETIC MICROENVIRONMENT; CHROMOSOMAL LOCALIZATION; LYMPHO-HEMATOPOIESIS; MOLECULAR-CLONING; GROWTH; PROTEIN; CALCIUM; SPARC AB The extracellular matrix produced by stromal cells plays a critical role in lympho-hematopoiesis. It was recently discovered that matrix glycoprotein SC1/ECM2 is a component of that matrix and preliminary evidence suggested that it could contribute to the nurturing environment for B-lymphocyte precursors. A fusion protein prepared from the amino terminal portion of SC1/ECM2 and the constant region of human Ig preferentially bound to pre-B cells, Furthermore, the cloning efficiency of interleukin-7-dependent B cell precursors was increased in a dose-dependent manner by addition of this fusion protein, We now report the complete cDNA sequence for murine SC1/ECM2 and its localization to the central region of chromosome 5. A fusion protein prepared from the full length of SC1/EGM2 and Ig was found to recognize pre-a cells in a divalent cation dependent manner, and to augment mitogen-dependent proliferation of mature B cells, as well as the cloning of pre-B cells, but to have no influence on myeloid progenitor cells, Although SC1/ECM2 is normally a secreted protein, we show that it is also capable of augmenting lymphopoiesis when expressed as a transmembrane protein on fibroblasts. Although the C-terminal portion of SC1/ECM2 has sequence homology to osteonectin/ SPARC, the unique hi-terminal one fifth of the protein was sufficient to augment lymphocyte growth. (C) 1997 by The American Society of Hematology. C1 OSAKA UNIV,SCH MED,DEPT HEMATOL ONCOL,SUITA,OSAKA 565,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. RP Oritani, K (reprint author), OSAKA UNIV,SCH MED,DEPT INTERNAL MED 2,2-2 YAMADAOKA,SUITA,OSAKA 565,JAPAN. FU NIAID NIH HHS [AI-33085] NR 45 TC 22 Z9 23 U1 0 U2 2 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 NOV 1 PY 1997 VL 90 IS 9 BP 3404 EP 3413 PG 10 WC Hematology SC Hematology GA YD108 UT WOS:A1997YD10800015 PM 9345023 ER PT J AU Frankel, AE Hall, PD Burbage, C Vesely, J Willingham, M Bhalla, K Kreitman, RJ AF Frankel, AE Hall, PD Burbage, C Vesely, J Willingham, M Bhalla, K Kreitman, RJ TI Modulation of the apoptotic response of human myeloid leukemia cells to a diphtheria toxin granulocyte-macrophage colony-stimulating factor fusion protein SO BLOOD LA English DT Article ID ACUTE MYELOBLASTIC-LEUKEMIA; HUMAN GM-CSF; MULTIDRUG-RESISTANCE; BETA-SUBUNIT; EXPRESSION; RECEPTOR; LINE; IL-3; GROWTH; ESTABLISHMENT AB It has previously been shown that human granulocyte-macrophage colony-stimulating factor (GM-CSF) can he fused to a truncated diphtheria toxin (DT) to produce a recombinant fusion toxin that kills GM-CSF receptor-bearing cells. We now report that DT388-GM-CSF induces apoptosis and inhibition of colony formation in semisolid medium in receptor positive cells, and that the induction of apoptosis correlates with GM-CSF-receptor occupancy at low ligand concentrations. Also, the induction of apoptosis correlates with the inhibition of protein synthesis and is inversely related to the amount of intracellular antiapoptotic proteins (Bcl2 and Bc1X(L)). Nine myeloid leukemia cells lines and four nonmyeloid leukemia cell lines were incubated with 0.7 nmol/L of I-125-GM-CSF in the presence or absence of excess cold GM-CSF and bound label measured. High affinity receptor numbers varied from 0 to 291 molecules per cell. Cells were incubated with varying concentrations of recombinant fusion toxin for 48 hours and incorporation of H-3-leucine (protein synthesis), segmentation of nuclei after DAPI staining (apoptosis), and colony formation in 0.2% agarose (clonogenicity) were measured. DT388-CM-CSF at 4 x 10(-9) mol/L inhibited colony formation 1.5 to 3.0 logs for receptor positive cell lines. Protein synthesis and apoptosis IC(50)s varied among cell lines from greater than 4 x 10(-9) mol/L to 3 x 10(-13) mol/L. GM-CSF-receptor occupancy at 0.7 nmol/L GMCSF-ligand concentration correlated with the protein synthesis IC50. Similarly, the protein synthesis inhibition and apoptosis induction correlated well, except in cells overexpressing Bcl2 and BclX(L), in which 25- to 150-fold inhibition of apoptosis was observed. We conclude that DT388-GM-CSF can kill acute myeloid leukemia blasts but that apoptotic sensitivities will depend on the presence of at least 100 high affinity GM-CSF receptors/cell and the absence of overexpressed antiapopiotic proteins. (C) 1997 by The American Society of Hematology. C1 MED UNIV S CAROLINA, DEPT MED, CHARLESTON, SC 29425 USA. MED UNIV S CAROLINA, DEPT PATHOL, CHARLESTON, SC 29425 USA. MED UNIV S CAROLINA, DEPT PHARMACEUT SCI, CHARLESTON, SC 29425 USA. EMORY UNIV, SCH MED, DEPT MED, ATLANTA, GA 30322 USA. NCI, MOL BIOL LAB, NIH, BETHESDA, MD 20892 USA. NR 57 TC 43 Z9 43 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 NOV 1 PY 1997 VL 90 IS 9 BP 3654 EP 3661 PG 8 WC Hematology SC Hematology GA YD108 UT WOS:A1997YD10800042 PM 9345050 ER PT J AU Terpstra, W Rozemuller, H Breems, DA Rombouts, EJC Prins, A FitzGerald, DJP Kreitman, RJ Wielenga, JJ Ploemacher, RE Lowenberg, B Hagenbeek, A Martens, ACM AF Terpstra, W Rozemuller, H Breems, DA Rombouts, EJC Prins, A FitzGerald, DJP Kreitman, RJ Wielenga, JJ Ploemacher, RE Lowenberg, B Hagenbeek, A Martens, ACM TI Diphtheria toxin fused to granulocyte-macrophage colony-stimulating factor eliminates acute myeloid leukemia cells with the potential to initiate leukemia in immunodeficient mice, but spares normal hemopoietic stem cells SO BLOOD LA English DT Article ID GM-CSF RECEPTOR; INTERLEUKIN-6 FUSION PROTEIN; NONHEMATOPOIETIC TUMOR-CELLS; BINDING DOMAIN SUBSTITUTION; ACUTE MYELOCYTIC-LEUKEMIA; GENETIC CONSTRUCTION; FREQUENCY-ANALYSIS; SCID MICE; GROWTH; CLONING AB We studied the cell kill induced by granulocyte-macrophage colony-stimulating factor (GM-CSF) fused to Diphtheria Toxin (DT-GM-CSF) in acute myeloid leukemia (AML) samples and in populations of normal primitive hemopoietic progenitor cells. AML samples from three patients were incubated in vitro with 100 ng/mL DT-GM-CSF for 48 hours, and AML cell kill was determined in a proliferation assay, a clonogenic assay colony-forming unit-AML (CFU-AML) and a quantitative long-term bone marrow (BM) culture ie, the leukemic-cobblestone area forming cell assay (L-CAFC). To measure an effect on cells with int vivo leukemia initiating potential DT-GM-CSF exposed AML cells were transplanted into immunodeficient mice. In two out of three samples it was shown that all AML subsets, including those with long-term abilities in vivo (severe combined immunodeficient mice) and in vitro (L-CAFC assay) were reduced in number by DT-GM-CSF. Cell kill induced by DT-GM-CSF could be prevented by coincubation with an excess of GM-CSF, demonstrating that sensitivity to DT-GMCSF is specifically mediated by the GM-CSF receptor. Therefore, binding and internalization of GM-CSF probably occur in immature AML precursors of these two cases of AML, The third AML sample was not responsive to either GM-CSF or DT-GM-CSF. The number of committed progenitors of normal bone marrow (burst-forming unit-erythroid, colony-forming unit granulocyte-macrophage, and cobble stone area forming cell [CAFC] week 2) and also the number of cells with long-term repopulating ability, assayed as week 6 CAFC, were unchanged after exposure to DT-GM-CSF (100 ng/mL, 48 hours). These studies show that DT-GM-CSF may be used to eliminate myeloid leukemic cells with long-term potential in vitro and in immunodeficient mice, whereas normal hemopoietic stem cells are spared. (C) 1997 by The American Society of Hematology. C1 ERASMUS UNIV ROTTERDAM,INST HEMATOL,NL-3000 DR ROTTERDAM,NETHERLANDS. DR DANIEL DEN HOED CANC CTR,NL-3008 AE ROTTERDAM,NETHERLANDS. NATL CANC INST,DCBDC,MOL BIOL LAB,BETHESDA,MD. NR 38 TC 21 Z9 22 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 NOV 1 PY 1997 VL 90 IS 9 BP 3735 EP 3742 PG 8 WC Hematology SC Hematology GA YD108 UT WOS:A1997YD10800052 PM 9345060 ER PT J AU Hakim, FT Cepeda, R Kaimei, S Mackall, CL McAtee, N Zujewski, J Cowan, K Gress, RE AF Hakim, FT Cepeda, R Kaimei, S Mackall, CL McAtee, N Zujewski, J Cowan, K Gress, RE TI Constraints on CD4 recovery postchemotherapy in adults: Thymic insufficiency and apoptotic decline of expanded peripheral CD4 cells SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; HIV-INFECTED PERSONS; T-CELLS; INTENSIVE CHEMOTHERAPY; ISOFORM EXPRESSION; NAIVE-PHENOTYPE; RECONSTITUTION; REGENERATION; EXPANSION; AGE AB To examine the mechanisms of CD4 reconstitution in an adult population, lymphocyte repopulation was assessed following dose-intense chemotherapy in 25 breast cancer patients, ages 33 to 69 years. Chemotherapy resulted in a greater than 60% reduction in total CD4 T cells and, in particular, a greater than 90% loss of the CD45RA(+) CD4 cells. CD4 recovery was protracted, achieving less than 50% of pretreatment levels after 12 to 14 months, Two facets of the CD4 recovery were notable. First, generation of CD45RA(+) CD4 cells played only a minor role in the first year, suggesting that thymic production was not the main route of CD4 regeneration. Indeed, recovery of CD45RA(+) CD4 cell levels remained limited in half of the patients even after 2 years. Second, expansion of the mature peripheral CD4 cells (CD45RO(+)) remaining after chemotherapy was the main source of early CD4 repopulation, peaking at 3 to 6 months postchemotherapy. This expansion was limited in duration, however, and was followed by a secondary decline, such that the total CD45RO(+) CD4 levels at 9 to 12 months were lower than at 6 months. When stimulated by mitogens, an increased susceptibility to apoptosis was observed in post-chemotherapy CD4 cells as compared with those from normal donors. The elevated expression of markers such as HLA-DR during chemotherapy and for several months post-chemotherapy is consistent with the presence of an activated T-cell population. CD4 apoptotic frequency correlated with the frequency of HLA-DR expression on T cells, Thus, CD4 recovery is constrained in adults by a limited thymic regenerative capacity and by an increased susceptibility to apoptosis within the expanding peripheral CD4 population. C1 NCI,PEDIAT BRANCH,NIH,BETHESDA,MD 20892. RP Hakim, FT (reprint author), NCI,MED BRANCH,NIH,BLDG 10,ROOM 12N226,BETHESDA,MD 20892, USA. NR 31 TC 228 Z9 230 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 NOV 1 PY 1997 VL 90 IS 9 BP 3789 EP 3798 PG 10 WC Hematology SC Hematology GA YD108 UT WOS:A1997YD10800059 PM 9345067 ER PT J AU Fay, MP Freedman, LS AF Fay, MP Freedman, LS TI Meta-analyses of dietary fats and mammary neoplasms in rodent experiments SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE breast cancer; monounsaturated fats; n-3 fatty acids; n-6 fatty acids; saturated fats ID BREAST-CANCER RISK; OLIVE OIL; CONSUMPTION; TUMORIGENESIS; METAANALYSIS; CALORIES; TUMORS; FISH AB We review two meta-analyses of experiments on dietary fat and mammary tumor incidence in rodents, emphasizing a recent meta-analysis on the effects of different types of dietary fatty acids. This analysis shows that n-6 polyunsaturated fatty acids most strongly enhance mammary tumors in rodents, and saturated fats also enhance these tumors but less strongly. Further, the analysis shows that energy restriction protects against mammary tumors. We show that these results agree qualitatively with estimates of effects on human breast cancer derived from international correlations. C1 NCI, Biometry Branch, Div Canc Prevent & Control, Bethesda, MD 20892 USA. RP Fay, MP (reprint author), NCI, Biometry Branch, Div Canc Prevent & Control, Plaza N,Suite 344,6130 Execut Blvd MSC 7354, Bethesda, MD 20892 USA. EM m7f@helix.nih.gov RI Fay, Michael/A-2974-2008; OI Fay, Michael P./0000-0002-8643-9625 NR 38 TC 21 Z9 21 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD NOV-DEC PY 1997 VL 46 IS 2-3 BP 215 EP 223 DI 10.1023/A:1005927503865 PG 9 WC Oncology SC Oncology GA YU840 UT WOS:000071761300009 PM 9478276 ER PT J AU Heselmeyer, K duManoir, S Blegen, H Friberg, B Svensson, C Schrock, E Veldman, T Shah, K Auer, G Ried, T AF Heselmeyer, K duManoir, S Blegen, H Friberg, B Svensson, C Schrock, E Veldman, T Shah, K Auer, G Ried, T TI A recurrent pattern of chromosomal aberrations and immunophenotypic appearance defines anal squamous cell carcinomas SO BRITISH JOURNAL OF CANCER LA English DT Article DE anal carcinoma; chromosome aberration; immunophenotype; human papillomavirus; comparative genomic hybridization ID COMPARATIVE GENOMIC HYBRIDIZATION; HUMAN PAPILLOMAVIRUS INFECTION; CANCER; TUMORS; REVEALS; GENESIS; LOSSES; GAINS; P53 AB Squamous cell carcinomas of the anus are rare neoplasias that account for about 3% of large bowel tumours, infections with human papillomaviruses are frequently detected in these cancers, suggesting that pathogenic pathways in anal carcinomas and in carcinomas of the uterine cervix are similar, Little is known regarding recurrent chromosomal aberrations in this subgroup of squamous cell carcinomas. We have applied comparative genomic hybridization to identify chromosomal gains and losses in 23 cases of anal carcinomas, A non-random copy number increase of chromosomes 17 and 19, and chromosome arm 3q was observed. Consistent losses were mapped to chromosome arms 4p, 11q, 13q and 18q. A majority of the tumours were aneuploid, and most of them showed increased proliferative activity as determined by staining for Ki-67 antigen. p53 expression was low or undetectable, and expression of p21/WAF-1 was increased in most tumours, Sixteen cancers were satisfactorily tested for the presence of HPV by consensus L1-primer polymerase chain reaction; nine were HPV positive, of which eight were positive for HPV 16. C1 NATL HUMAN GENOME RES INST,NIH,BETHESDA,MD 20892. KAROLINSKA INST,DEPT TUMOR PATHOL,DIV CELL & MOL ANAL,S-17176 STOCKHOLM,SWEDEN. SODER SJUKHUSET,DEPT SURG,STOCKHOLM,SWEDEN. HUDDINGE HOSP,STOCKHOLM,SWEDEN. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21205. NR 21 TC 33 Z9 34 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD NOV PY 1997 VL 76 IS 10 BP 1271 EP 1278 DI 10.1038/bjc.1997.547 PG 8 WC Oncology SC Oncology GA YG082 UT WOS:A1997YG08200003 PM 9374370 ER PT J AU Karkera, JD Taymans, SE Turner, G Yoshikawa, T DeteraWadleigh, SD Wadleigh, RG AF Karkera, JD Taymans, SE Turner, G Yoshikawa, T DeteraWadleigh, SD Wadleigh, RG TI Deletion of a consensus oestrogen response element half-site in the glucocorticoid receptor of human multiple myeloma SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article DE glucocorticoid resistance; PCR-SSCP; deletion; exon 9 alpha; 3' untranslated region ID MESSENGER-RNA; POLYMORPHISMS; REGION; CELLS; GENE AB We have carried out molecular scanning of the glucocorticoid receptor (GR) of the glucocorticoid resistant multiple myeloma cell line U266. An amplified fragment from the 3' untranslated region displayed an aberrant migration by PCR-single-stranded conformational polymorphism (PCR-SSCP) analysis. The mutant allele had a deletion of an 8 base pair sequence containing a half-site of an oestrogen response element. This motif was found conserved in rat GR. This same allele lacked four as in an upstream region with 18 consecutive As in the normal allele. These mutations may affect mRNA stability or alter interactions with regulatory factors. C1 VET AFFAIRS MED CTR,MED ONCOL SECT,WASHINGTON,DC 20422. NIMH,CLIN NEUROGENET BRANCH,UNIT GENE MAPPING & EXPRESS,NIH,BETHESDA,MD 20892. NR 12 TC 8 Z9 8 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD NOV PY 1997 VL 99 IS 2 BP 372 EP 374 DI 10.1046/j.1365-2141.1997.4123227.x PG 3 WC Hematology SC Hematology GA YG535 UT WOS:A1997YG53500024 PM 9375757 ER PT J AU Wilson, CA Bekele, G Nicolson, M Ravussin, E Pratley, RE AF Wilson, CA Bekele, G Nicolson, M Ravussin, E Pratley, RE TI Relationship of the white blood cell count to body fat: role of leptin SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article DE haemopoiesis; leptin; body fat; humans; white blood cell count ID LEUKOCYTE COUNT; RISK-FACTORS; HEMATOPOIESIS; RECEPTOR; WEIGHT; OBESE AB The white blood cell (WBC) count is correlated to the amount of body fat in humans, but the mechanism for this association is unknown, Leptin, a 16 kD protein produced in adipocytes, circulates in humans in direct proportion to the amount and percentage of body fat. Recent evidence suggests that leptin and the leptin receptor are part of a novel pathway which stimulates haemopoiesis. This study was designed to test whether fasting plasma leptin concentrations contribute to the relationship between the WBC count and body fat. 117 Pima Indians with a wide range in body composition were studied. The WBC count was positively correlated with percentage of body fat (r = 0.44, P = 0.0001) and fasting plasma leptin concentration (r = 0.38. P = 0.0001). In multiple regression analyses, age, gender and percent body fat were significant independent determinants of the WBC count. After controlling for age and gender, percent body fat accounted for 23% of the variance in the WBC count (partial r = 0.48, P = 0.0001). In similar models which also included plasma leptin concentration, percent body fat remained significantly related to the WBC count, but only accounted for 7% of its variance (partial r = 0.27, P = 0.003). Based on these results, and the demonstration that leptin directly effects the stimulation of proliferation of haemopoietic stem cells in vitro, we hypothesize that the relation of the WBC count to percent body fat may be mediated, in part, through the effect of leptin. C1 NIDDK,CLIN DIABET & NUTR SECT,PHOENIX EPIDEMIOL & CLIN RES BRANCH,NIH,PHOENIX,AZ 85016. INDIAN HLTH SERV,PHOENIX INDIAN MED CTR,DEPT INTERNAL MED,PHOENIX,AZ. AMGEN INC,THOUSAND OAKS,CA 91320. CARL T HAYDEN VET AFFAIRS MED CTR,PHOENIX,AZ. NR 15 TC 39 Z9 42 U1 2 U2 3 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD NOV PY 1997 VL 99 IS 2 BP 447 EP 451 DI 10.1046/j.1365-2141.1997.3873201.x PG 5 WC Hematology SC Hematology GA YG535 UT WOS:A1997YG53500038 PM 9375771 ER PT J AU Liu, YF Cortopassi, G Goedert, JJ Rabkin, CS AF Liu, YF Cortopassi, G Goedert, JJ Rabkin, CS TI Frequency of Bcl-2 rearrangements in peripheral blood of HIV-infected individuals SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Letter DE lymphoma; HIV infection; Bcl-2 rearrangements C1 UNIV CALIF DAVIS,DEPT MOL BIOSCI,DAVIS,CA 95616. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP Liu, YF (reprint author), UNIV CALIF BERKELEY,SCH PUBL HLTH,140 WARREN HALL,BERKELEY,CA 94720, USA. NR 4 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD NOV PY 1997 VL 99 IS 2 BP 465 EP 466 PG 2 WC Hematology SC Hematology GA YG535 UT WOS:A1997YG53500042 PM 9375775 ER PT J AU Peoples, RW White, G Lovinger, DM Weight, FF AF Peoples, RW White, G Lovinger, DM Weight, FF TI Ethanol inhibition of N-methyl-D-aspartate-activated current in mouse hippocampal neurones: whole-cell patch-clamp analysis SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE NMDA; ethanol; hippocampus; glycine; Mg2+; Zn2+; ketamine; polyamine; proton; oxidation-reduction ID HETEROMERIC NMDA RECEPTORS; CEREBELLAR GRANULE CELLS; VOLTAGE-DEPENDENT BLOCK; XENOPUS OOCYTES; NEUROTRANSMITTER RELEASE; INDUCED NORADRENALINE; H-3 NOREPINEPHRINE; CORTICAL-NEURONS; SINGLE-CHANNEL; ION CURRENT AB 1 The action of ethanol on N-methyl-D-aspartate (NMDA)-activated ion current was studied in mouse hippocampal neurones in culture using whole-cell patch-clamp recording. 2 Ethanol inhibited NMDA-activated current in a voltage-independent manner, and did not alter the reversal potential of NMDA-activated current. 3 Concentration-response analysis of NMDA-and glycine-activated current revealed that ethanol decreased the maximal response to both agonists without affecting their EC50 values. 4 The polyamine spermine (1 mu M) increased amplitude of NMDA-activated current but did not alter the percentage inhibition of ethanol. 5 Compared to an extracellular pH of 7.0, pH 6.0 decreased and pH 8.0 increased the amplitude of NMDA-activated current, but these changes in pH did not significantly alter the percentage inhibition by ethanol. 6 The sulphydryl reducing agent dithiothreitol (2 mM) increased the amplitude of NMDA-activated current, but did not affect the percentage inhibition by ethanol. 7 Mg2+ (10, 100, 500 mu M), Zn2+ (5, 20 mu M) or ketamine (2, 10 mu M) decreased the amplitude of NMDA-activated current, but did not affect the percentage inhibition by ethanol. 8 The observations are consistent with ethanol inhibiting the function of NMDA receptors by a noncompetitive mechanism that does not involve several modulatory sites on the NMDA receptor-ionophore complex. RP Peoples, RW (reprint author), NIAAA,MOL & CELLULAR BIOL LAB,NIH,12501 WASHINGTON AVE,ROCKVILLE,MD 20852, USA. NR 58 TC 70 Z9 71 U1 1 U2 6 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD NOV PY 1997 VL 122 IS 6 BP 1035 EP 1042 DI 10.1038/sj.bjp.0701483 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YG220 UT WOS:A1997YG22000010 PM 9401766 ER PT J AU Chen, R Cohen, LG Hallett, M AF Chen, R Cohen, LG Hallett, M TI Role of the ipsilateral motor cortex in voluntary movement SO CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES LA English DT Article; Proceedings Paper CT 31st Meeting of the Canadian-Congress-of-Neurological-Sciences CY JUN 27, 1996 CL ONTARIO, CANADA SP Canadian Congress Neurol Sci ID TRANSCRANIAL MAGNETIC STIMULATION; LEFT-HEMISPHERE DAMAGE; CEREBRAL BLOOD-FLOW; CORTICAL POTENTIALS; FINGER MOVEMENTS; FUNCTIONAL REORGANIZATION; NEURAL REPRESENTATIONS; MIRROR MOVEMENTS; ARM MOVEMENTS; RECOVERY AB The ipsilateral primary motor cortex (Mi) plays a role in voluntary movement. In our studies, we used repetitive transcranial magnetic stimulation (rTMS) to study the effects of transient disruption of the ipsilateral M1 on the performance of finger sequences in right-handed normal subjects. Stimulation of the M1 ipsilateral to the movement induced timing errors in both simple and complex sequences performed with either hand, but with complex sequences, the effects were more pronounced with the left-sided stimulation. Recent studies in both animals and humans have confirmed the traditional view that ipsilateral projections from M1 to the upper limb are mainly directed to truncal and proximal muscles, with little evidence for direct connections to distal muscles. The ipsilateral motor pathway appears to be an important mechanism for functional recovery after focal brain injury during infancy, but its role in functional recovery for older children and adults has not yet been clearly demonstrated. There is increasing evidence from studies using different methodologies such as rTMS, functional imaging and movement-related cortical potentials, that M1 is involved in ipsilateral hand movements, with greater involvement in more complex tasks and the left hemisphere playing a greater role than the right. RP Chen, R (reprint author), NINCDS,HUMAN CORT PHYSIOL UNIT,HUMAN MOTOR CONTROL SECT,MED NEUROL BRANCH,NIH,BLDG 10,BETHESDA,MD 20892, USA. RI Chen, Robert/B-3899-2009 OI Chen, Robert/0000-0002-8371-8629 NR 74 TC 89 Z9 89 U1 0 U2 3 PU CANADIAN J NEUROL SCI INC PI CALGARY PA PO BOX 4220, STATION C EDITORIAL & SUBSCRIPTION SERV, CALGARY AB T2T 5N1, CANADA SN 0317-1671 J9 CAN J NEUROL SCI JI Can. J. Neurol. Sci. PD NOV PY 1997 VL 24 IS 4 BP 284 EP 291 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA YK745 UT WOS:A1997YK74500004 PM 9398974 ER PT J AU Burke, HB Henson, DE AF Burke, HB Henson, DE TI Histologic grade as a prognostic factor in breast carcinoma SO CANCER LA English DT Editorial Material C1 NCI,DIV CANC PREVENT,NIH,BETHESDA,MD 20892. NEW YORK MED COLL,DEPT MED,VALHALLA,NY 10595. NR 11 TC 13 Z9 14 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 NOV 1 PY 1997 VL 80 IS 9 BP 1703 EP 1705 DI 10.1002/(SICI)1097-0142(19971101)80:9<1703::AID-CNCR1>3.0.CO;2-F PG 3 WC Oncology SC Oncology GA YC306 UT WOS:A1997YC30600001 PM 9351537 ER PT J AU Wingo, PA Landis, S Ries, LAG AF Wingo, PA Landis, S Ries, LAG TI An adjustment to the 1997 estimate for new prostate cancer cases SO CANCER LA English DT Article; Proceedings Paper CT American-Cancer-Society Workshop on Review of Current Data Impacting Early Detection Guidelines for Prostate Cancer CY MAR 10-11, 1997 CL PHOENIX, AZ SP Amer Canc Soc C1 NCI,DIV CANC PREVENT & CONTROL,CANC CONTROL RES PROGRAM,BETHESDA,MD 20892. RP Wingo, PA (reprint author), AMER CANC SOC,DEPT EPIDEMIOL & SURVEILLANCE RES,ATLANTA,GA 30329, USA. NR 8 TC 20 Z9 20 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 NOV 1 PY 1997 VL 80 IS 9 BP 1810 EP 1813 DI 10.1002/(SICI)1097-0142(19971101)80:9<1810::AID-CNCR19>3.0.CO;2-8 PG 4 WC Oncology SC Oncology GA YC306 UT WOS:A1997YC30600018 PM 9351553 ER PT J AU Smart, CR AF Smart, CR TI The results of prostate carcinoma screening in the US as reflected in the surveillance, epidemiology, and end results program SO CANCER LA English DT Article; Proceedings Paper CT American-Cancer-Society Workshop on Review of Current Data Impacting Early Detection Guidelines for Prostate Cancer CY MAR 10-11, 1997 CL PHOENIX, AZ SP Amer Canc Soc DE prostate carcinoma; screening; prostate specific antigen; surveillance; epidemiology; and End Results Program; grade; significant ID DIGITAL RECTAL EXAMINATION; CANCER-DETECTION-PROJECT; ANTIGEN; MEN AB BACKGROUND. The rapid escalation in the incidence of prostate carcinoma between the years 1988 and 1992 has been attributed to prostate specific antigen screening. There have been concerns regarding the possible diagnosis and treatment of insignificant tumors in the absence of randomized, controlled trial evidence of a decrease in mortality. Descriptive studies suggest that serial screening decreases the detection of advanced disease. In November 1996, the National Center for Health Statistics recorded a decrease in prostate carcinoma mortality. METHODS. The basis of this analysis is 208,234 prostate carcinoma cases diagnosed between 1973 and 1993 in population-based Surveillance, Epidemiology, and End Results registries. The general staging system was used rather than that of the American Joint Committee on Cancer to permit observation of long term trends. Grade incorporating Gleason scores was used as an indication of the significance of the prostate carcinoma. Age-adjusted survival rates were used to separate prostate carcinoma deaths from deaths due to other causes. RESULTS. The increase in the incidence of prostate carcinoma has been greater than for any other malignancy. The increase was largely in Grade 2 significant tumors and not in Grade 1 (15%) insignificant tumors. There was a decrease in the detection of advanced disease. After the peak incidence in 1992, a progressive decrease to near baseline levels occurred. Approximately 38% of all deaths were from prostate carcinoma. Deaths from other causes increased with age. When corrected for death from other causes, men age > 69 years had a greater rate of death from prostate carcinoma than men age 50-69 years. Approximately 61% of all deaths from prostate carcinoma occurred within 5 years of diagnosis and 88% within 10 years. The 10-year survival rate for patients treated by radical prostatectomy was 100%, 78% for patients treated by radiation, and 33% for patients treated with other (noncomparable modalities). CONCLUSIONS. The indirect evidence suggested that prostate carcinoma screening of men ages >50 years decreased the incidence of distant disease, which influences the mortality rate. (C) 1997 American Cancer Society. C1 NCI,EARLY DETECT BRANCH,BETHESDA,MD 20892. NR 13 TC 77 Z9 78 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 NOV 1 PY 1997 VL 80 IS 9 BP 1835 EP 1844 DI 10.1002/(SICI)1097-0142(19971101)80:9<1835::AID-CNCR23>3.0.CO;2-5 PG 10 WC Oncology SC Oncology GA YC306 UT WOS:A1997YC30600022 PM 9351557 ER PT J AU Brawley, OW AF Brawley, OW TI Prostate carcinoma incidence and patient mortality - The effects of screening and early detection SO CANCER LA English DT Article; Proceedings Paper CT American-Cancer-Society Workshop on Review of Current Data Impacting Early Detection Guidelines for Prostate Cancer CY MAR 10-11, 1997 CL PHOENIX, AZ SP Amer Canc Soc DE prostate carcinoma; incidence; mortality; early detection; screening; SEER ID CANCER; SURVIVAL; ADENOCARCINOMA; TRENDS AB BACKGROUND. Screening for and the aggressive treatment of prostate carcinoma are controversial, but they are nevertheless being practiced in the U.S. Current clinical studies of the effectiveness of screening will take years to complete. Meanwhile, screening for prostate carcinoma is already having an effect on society. METHODS. National and regional trends in prostate carcinoma incidence and data on patient mortality and survival from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute are described in this article. SEER is a population-based cancer data base comprised of nine discrete areas. Fundamental principles of screening are used in this article to explain the impact that prostate carcinoma screening has had in the U.S. RESULTS. According to the data in the SEER registries, overall prostate carcinoma incidence rates increased at a far greater pace than prostate carcinoma mortality rates during the period 1973-1994. During that period, there was a shift in stage at diagnosis characterized by an increase in local and regional disease, and a decline in distant disease at diagnosis. Overall 5-year survival rates for prostate carcinoma patients also increased. The increase in incidence rates, the shift in stage at diagnosis, and the increase in survival rates are all evidence of increasing early detection. However, these changes are consistent with lead-time bias, length bias, a decline in mortality, and ail three could have occurred. In the geographic SEER registries, the prostate carcinoma incidence rates vary markedly. These variations in incidence rates are due to regional variations in practice patterns and screening efforts. On the other hand, the SEER registries have comparable mortality rates. This is evidence of both lead-time bias and length bias. CONCLUSIONS. Substantial regional variations in incidence were found, but regional mortality rates were similar. This is evidence that screening and early detection efforts are resulting in the diagnosis of prostate carcinoma in some men who do not need therapy; thus, prostate carcinoma screening can lead to unnecessary treatment for such men. Furthermore, epidemiologic data do not demonstrate that screening is decreasing mortality. The benefits of screening and early detection, although theoretically possible, are yet unproven, whereas the risks and harms of screening and resultant treatment are definite. (C) 1997 American Cancer Society. RP Brawley, OW (reprint author), NCI,OFF SPECIAL POPULAT RES,7550 WISCONSIN AVE,312 FED BLDG,MSC 9010,BETHESDA,MD 20895, USA. NR 22 TC 101 Z9 102 U1 2 U2 2 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 NOV 1 PY 1997 VL 80 IS 9 BP 1857 EP 1863 DI 10.1002/(SICI)1097-0142(19971101)80:9<1857::AID-CNCR26>3.0.CO;2-3 PG 7 WC Oncology SC Oncology GA YC306 UT WOS:A1997YC30600025 PM 9351560 ER PT J AU Goldstein, AM Yuen, J Tucker, MA AF Goldstein, AM Yuen, J Tucker, MA TI Second cancers after medulloblastoma: population-based results from the United States and Sweden SO CANCER CAUSES & CONTROL LA English DT Article DE medulloblastoma; radiation; second cancers; survival; Sweden; United States ID CELL CARCINOMA SYNDROME; CENTRAL-NERVOUS-SYSTEM; CHILDHOOD-CANCER; HODGKINS-DISEASE; TURCOTS-SYNDROME; THYROID-CANCER; BREAST-CANCER; 2ND NEOPLASMS; BRAIN-TUMORS; CHILDREN AB Medulloblastoma, one of the most common central nervous system (CNS) tumors in children, requires aggressive multimodality therapy including surgery, radiation therapy, and occasionally chemotherapy. Given its intensive treatment regimen and improved survival during the past 20 years, it is likely that a cohort of survivors will result who may incur consequences of therapy, including a second cancer. We used population-based data from the United States and Sweden to estimate risks of second neoplasms in patients with histologically confirmed medulloblastoma (n = 1,262). Overall, there was a 5.4-fold excess of second neoplasms (95 percent confidence interval = 3.3-8.4) based on 20 observed and 3.7 expected cancers. The second cancers occurred eight to 432 months after initial diagnosis (median, 73 months) with significantly elevated ratios for all intervals examined except for less than one year after initial diagnosis. Significantly elevated risks were seen for cancers of the salivary glands, cervix uteri, brain and CNS, thyroid gland, and acute lymphoblastic leukemia. Of the 15 second cancers with treatment data, seven occurred in the radiation field or within areas of scatter while two others may have been radiation-related. Although based on small numbers of second cancers, the results suggest that as survival increases, some patients with medulloblastoma will have an increased risk of a second cancer, particularly a radiation-related cancer. Thus, as survival improves, late-occurring consequences of diagnosis and treatment will need to be carefully assessed. Identification of patients hypersensitive to radiation therapy, such as those with Gorlin Syndrome, should also be attempted in order to reduce the sequelae from intensive radiation exposure. C1 UNIV UPPSALA HOSP,DEPT CANC EPIDEMIOL,UPPSALA,SWEDEN. RP Goldstein, AM (reprint author), NCI,GENET EPIDEMIOL BRANCH,DIV CANC EPIDEMIOL & GENET,EXECUT PLAZA N,ROOM 439,6130 EXECUT BLVD,BETHESDA,MD 20892, USA. RI Tucker, Margaret/B-4297-2015 NR 36 TC 52 Z9 54 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD NOV PY 1997 VL 8 IS 6 BP 865 EP 871 DI 10.1023/A:1018464328836 PG 7 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA YF740 UT WOS:A1997YF74000007 PM 9427429 ER PT J AU Swanson, CA Brown, CC Sinha, R Kulldorff, M Brownson, RC Alavanja, MCR AF Swanson, CA Brown, CC Sinha, R Kulldorff, M Brownson, RC Alavanja, MCR TI Dietary fats and lung cancer risk among women: The Missouri Women's Health Study (United States) SO CANCER CAUSES & CONTROL LA English DT Article DE diet; fat intake; lung cancer; meat consumption; women; United States ID BREAST-CANCER; CHOLESTEROL; SMOKING; ASSOCIATION; SURROGATE; HAWAII; DESIGN; MEN AB In a population-based case-control study of women in Missouri (United States), most of whom were smokers, we obtained information on adult diet to evaluate the effects of dietary fats in relation to lung cancer risk. All newly diagnosed, primary lung cancer cases among women 35 to 84 years of age reported to the Missouri Cancer Registry from 1 January 1993 to 31 January 1994 were invited to participate, as were population-based controls. The analysis focused on interviews obtained from 624 controls and 587 cases. In-person interviews were obtained from 99.0 percent of controls and 60.6 percent of cases. Age and energy-adjusted relative risks suggested a direct relation between risk of lung cancer and intake of dietary fats (e.g., total fat, saturated fat) and frequency of meat consumption. After adjusting for confounders, dietary fats were no longer associated with risk, but the adverse effect of frequent consumption of meat persisted. Risk was elevated about 90 percent (95 percent confidence interval = 1.2-3.0) among women in the highest quintile of red meat intake compared with those in the lowest quintile. Risk estimates associated with red meat consumption, however, were dependent on interview status; the effect was restricted to cases whose dietary information was provided by proxy. In summary, after adjusting for potential confounders and removing data obtained from proxy respondents, dietary fats and consumption of red meat were not associated with lung cancer risk among women in Missouri. C1 NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,BETHESDA,MD 20892. ST LOUIS UNIV,HLTH SCI CTR,SCH PUBL HLTH,ST LOUIS,MO 63103. RP Swanson, CA (reprint author), NCI,NUTR EPIDEMIOL BRANCH,EPIDEMIOL & BIOSTAT PROGRAM,DCEG,NCI,EXECUT PLAZA N,SUITE 443,BETHESDA,MD 20892, USA. RI Kulldorff, Martin/H-4282-2011; Sinha, Rashmi/G-7446-2015; OI Sinha, Rashmi/0000-0002-2466-7462; Kulldorff, Martin/0000-0002-5284-2993 NR 31 TC 33 Z9 33 U1 2 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD NOV PY 1997 VL 8 IS 6 BP 883 EP 893 DI 10.1023/A:1018468429744 PG 11 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA YF740 UT WOS:A1997YF74000009 PM 9427431 ER PT J AU Chang, S Hulka, BS Baird, DD Ingle, JN Newman, B Graham, ML Qaqish, B Donohue, JH Melton, LJ AF Chang, S Hulka, BS Baird, DD Ingle, JN Newman, B Graham, ML Qaqish, B Donohue, JH Melton, LJ TI Breast cancer survival and the timing of tumor removal during the menstrual cycle SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID PREMENOPAUSAL WOMEN; SURGERY; PROGNOSIS; PHASE; DISEASE; PATIENT AB In a retrospective cohort study of 262 premenopausal breast cancer patients treated at the Mayo Clinic between 1965 and 1985, we investigated whether survival was associated with the timing of tumor removal during the menstrual cycle, Participants were women less than or equal to 50 years old who had not used exogenous hormones, been pregnant, been lactating, or given birth within 6 months of diagnosis, The menstrual cycle day at surgery was used to assign women to group 1 (cycle days 0-7), group 2 (cycle days 8-15), or group 3 (after cycle day 15), Cox proportional hazards analysis adjusting for age at diagnosis, stage, tumor size, grade, and node involvement showed a nonsignificantly worse survival for group 2 than for group 3 [hazard ratio (KR), 1.41; 95% confidence interval (CI), 0.89-2.23], Stratification revealed that the association between survival and timing of tumor removal during the menstrual cycle was slightly stronger among patients with stage II disease (adjusted HR, 1.56; 95% CI, 0.92-2.63), The association was the same among patients with stage II disease and node involvement (adjusted HR, 1.57; 95% CI, 0.82-3.03), Prospective studies using hormone measurements to define menstrual cycle status more accurately than the reported day of the menstrual cycle could provide further insight about the postulated association. C1 Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Publ Hlth, Dept Biostat, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Med, Div Hematol Oncol, Chapel Hill, NC 27599 USA. NIEHS, Dept Epidemiol, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. Mayo Clin & Mayo Fdn, Div Med Oncol, Rochester, MN 55905 USA. Mayo Clin & Mayo Fdn, Dept Surg, Rochester, MN 55905 USA. Mayo Clin & Mayo Fdn, Dept Hlth Sci Res, Rochester, MN 55905 USA. RP Chang, S (reprint author), Univ Texas, MD Anderson Canc Ctr, Dept Epidemiol, Box 189,1515 Holcombe Blvd, Houston, TX 77030 USA. EM schang@notes.mdacc.tmc.edu OI Baird, Donna/0000-0002-5544-2653 FU NCI NIH HHS [5-T32-CA 09330] NR 31 TC 5 Z9 5 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD NOV PY 1997 VL 6 IS 11 BP 881 EP 886 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA YW298 UT WOS:000071918400003 PM 9367060 ER PT J AU Longnecker, MP Newcomb, PA Mittendorf, R Greenberg, ER Willett, WC AF Longnecker, MP Newcomb, PA Mittendorf, R Greenberg, ER Willett, WC TI Intake of carrots, spinach, and supplements containing vitamin A in relation to risk of breast cancer SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID FOOD FREQUENCY QUESTIONNAIRE; BETA-CAROTENE; VEGETABLES; DIET; CONSUMPTION; FRUIT; PREVENTION AB Intake of fruits, vegetables, vitamin A, and related compounds are associated with a decreased risk of breast cancer in some studies, but additional data are needed. To estimate intake of beta-carotene and vitamin A, the authors included nine questions on food and supplement use in a population-based case-control study of breast cancer risk conducted in Maine, Massachusetts, New Hampshire, and Wisconsin in 1988-1991, Multivariate-adjusted models were fit to data for 3543 cases and 9406 controls, Eating carrots or spinach more than twice weekly, compared with no intake, was associated with an odds ratio of 0.56 (95% confidence interval 0.34-0.91), Estimated intake of preformed vitamin A from all evaluated foods and supplements showed no trend or monotonic decrease in risk across categories of intake, These data do not allow us to distinguish among several potential explanations for the protective association observed between intake of carrots and spinach and risk of breast cancer, The findings are, however, consistent with a diet rich in these foods having a modest protective effect. C1 NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Chicago, Pritzker Sch Med, Dept Obstet & Gynecol, Chicago, IL 60637 USA. Dartmouth Hitchcock Med Ctr, Norris Cotton Canc Ctr, Lebanon, NH 03756 USA. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Channing Lab, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. RP Longnecker, MP (reprint author), NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. OI Longnecker, Matthew/0000-0001-6073-5322 FU NCI NIH HHS [CA 47305, CA 47147] NR 36 TC 38 Z9 38 U1 2 U2 7 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD NOV PY 1997 VL 6 IS 11 BP 887 EP 892 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA YW298 UT WOS:000071918400004 PM 9367061 ER PT J AU Qiao, YL Tockman, MS Li, L Erozan, YS Yao, SX Barrett, MJ Zhou, WH Giffen, CA Luo, XC Taylor, PR AF Qiao, YL Tockman, MS Li, L Erozan, YS Yao, SX Barrett, MJ Zhou, WH Giffen, CA Luo, XC Taylor, PR TI A case-cohort study of an early biomarker of lung cancer in a screening cohort of Yunnan tin miners in China SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID SQUAMOUS-CELL CARCINOMA; 2ND PRIMARY TUMORS; MONOCLONAL-ANTIBODIES; SPUTUM CELLS; ISOTRETINOIN; PREVENTION; ANTIGEN; HEAD; NECK AB We initiated the present study to evaluate the accuracy of a new epithelial biomarker of early lung cancer, We tested the hypothesis that expression of a tumor-associated antigen by exfoliated sputum epithelial cells has greater accuracy (sensitivity and specificity) for the detection of preclinical, localized lung cancer than do routine clinical detection methods, Monoclonal antibody (MAb) 703D4 recognizes heterogeneous nuclear ribonuclear protein (hnRNP) A2/B1, We compared the accuracy of hnRNP up-regulation with cytology and radiographic screening for lung cancer detection in miners who were highly exposed to tobacco smoke, radon, and arsenic in southwestern China, The results showed that MAb 703D4 detection of hnRNP expression by sputum epithelial cells had greater accuracy for the detection of lung cancer than did routine screening methods, particularly for early (localized) disease, Among 57 cases and 76 noncases at the first screening, overall MAb detection of hnRNP was more sensitive (74 versus 21% for cytology and 42% for chest x-ray) but had lower specificity (70 versus 100% for cytology and 90% for chest x-ray) than standard methods, Recognizing hnRNP up-regulation resulted in detection of approximately one-third more early cases than did the combination of X-ray and cytology. Detection of hnRNP A2/B1 expression appears to be a good initial screening test for lung carcinogenesis, as it identified 74% of those who developed subsequent clinical lung cancer, Future studies might separate individuals with high lung cancer risk by MAb detection, confirming the positives with markers having greater specificity (e.g., clinical studies that become positive later in the morphological progression). C1 NCI, Canc Prevent Studies Branch, NIH, Bethesda, MD 20892 USA. Johns Hopkins Med Inst, Dept Environm Hlth Sci, Baltimore, MD 20205 USA. Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 20205 USA. Yunnan Tin Corp, Labor Protect Inst & Gen Hosp, Gejiu, Yunnan, Peoples R China. Informat Management Serv Inc, Silver Spring, MD 20910 USA. RP Tockman, MS (reprint author), H Lee Moffit Canc Ctr & Res Inst, Mol Screening Program, 12902 Magnolia Dr, Tampa, FL 33612 USA. RI Qiao, You-Lin/B-4139-2012 OI Qiao, You-Lin/0000-0001-6380-0871 FU NCI NIH HHS [N01-CN-25] NR 27 TC 28 Z9 36 U1 0 U2 5 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD NOV PY 1997 VL 6 IS 11 BP 893 EP 900 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA YW298 UT WOS:000071918400005 PM 9367062 ER PT J AU Hung, HC Chuang, J Chien, YC Chern, HD Chiang, CP Kuo, YS Hildesheim, A Chen, CJ AF Hung, HC Chuang, J Chien, YC Chern, HD Chiang, CP Kuo, YS Hildesheim, A Chen, CJ TI Genetic polymorphisms of CYP2E1, GSTM1, and GSTT1; Environmental factors and risk of oral cancer SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID HUMAN CYTOCHROME-P450IIE1 GENE; FRAGMENT-LENGTH-POLYMORPHISM; S-TRANSFERASE GENES; LUNG-CANCER; GLUTATHIONE TRANSFERASE; HEPATOCELLULAR-CARCINOMA; BLADDER-CANCER; NECK-CANCER; HUMAN HEAD; SUSCEPTIBILITY AB Both genetic and environmental factors are involved in the development of cancer; some phase I and II enzymes involved in the metabolism of carcinogens are polymorphic in genotypes, This case-control study focused on the interactions between oral cancer risk factors and genetic polymorphisms of cytochrome P-450 (CYP) 2E1 and glutathione S-transferase (GST) M1 and GSTT1, A total of 41 male oral cancer cases was recruited from National Taiwan University Hospital, and 123 healthy controls frequency-matched on ethnicity, sex, and age were recruited from residents living in Taipei City and Taipei County. History of cigarette smoking, alcohol drinking, and betel quid chewing was obtained through a standardized questionnaire interview, and genotypes of CYP2E1, GSTM1, and GSTT1 were determined by PCR, Cigarette smoking, alcohol drinking, and betel quid chewing were significantly associated with the risk of oral cancer in a dose-response relationship, All betel quid chewers smoked cigarettes in both the case and control groups, In the multiple logistic regression analysis, those who had null genotypes of GSTM1 and/or GSTT1 had an increased oral cancer risk compared with those who had non-null genotypes of both GSTM1 and GSTT1, showing a multivariate-adjusted odds ratio (OR) of 4.6 with a 95% confidence interval (CI) of 0.9-23.7 (P = 0.08), The CYP2E1 c1/c2 and c2/c2 genotypes were associated with a significantly increased oral cancer risk compared with the c1/c1 genotype among those who did not chew betel quid (OR, 4.7; 95% CI, 1.1-20.2), but not among betel quid chewers, Habitual alcohol drinking was associated with a significantly increased oral cancer risk, showing an OR of 3.0 (95% CI, 1.1-8.8), These results implied that there are gene-gene and gene-environment interactions in the development of oral cancer. C1 Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Epidemiol, Taipei 10018, Taiwan. Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Publ Hlth, Taipei 10018, Taiwan. Natl Taiwan Univ, Coll Med, Grad Inst Pharmaceut Sci, Taipei 10018, Taiwan. Natl Taiwan Univ, Coll Med, Sch Dent, Taipei 10018, Taiwan. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Chen, CJ (reprint author), Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Epidemiol, No 1 Jen Ai Rd,Sect 1, Taipei 10018, Taiwan. RI Chen, Chien-Jen/C-6976-2008; OI Chiang, Chun-Pin/0000-0002-6190-7162 NR 31 TC 134 Z9 141 U1 0 U2 5 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD NOV PY 1997 VL 6 IS 11 BP 901 EP 905 PG 5 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA YW298 UT WOS:000071918400006 PM 9367063 ER PT J AU Stierum, RH Hageman, GJ van Herwijnen, MHM van der Veer, MSE Kleinjans, JCS AF Stierum, RH Hageman, GJ van Herwijnen, MHM van der Veer, MSE Kleinjans, JCS TI Age-related negative associations between parameters of cytogenetic damage and ex vivo (+/-)-anti-benzo(a)pyrene diolepoxide-induced unscheduled DNA synthesis in smoking humans SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID PERIPHERAL-BLOOD LYMPHOCYTES; SISTER-CHROMATID EXCHANGES; REPAIR SYNTHESIS; HUMAN-FIBROBLASTS; IN-VITRO; ADDUCT; IRRADIATION; LEUKOCYTES; POPULATION; EXCISION AB Chemical or physical modification of DNA may cause an increase in genomic mutations or other genetic alterations, which may ultimately result in the onset of cancer, To avoid these deleterious effects of DNA damage, humans possess DNA repair mechanisms, Decreased DNA repair, induced ex vivo by UV light or ionizing radiation in human peripheral blood lymphocytes (PBLs), has been associated with aging, The aim of this study was to investigate whether repair of DNA damage, after ex vivo exposure of PBLs obtained from smokers (rt = 20) to (+/-)-anti-benzo(alpha)pyrene diolepoxide [(+/-)-anti-BPDE], which is a mixture of reactive metabolites from the environmental carcinogen benzo(alpha)pyrene, is also associated with age, Furthermore, age-related associations between ex vivo (+/-)-anti-BPDE-induced DNA repair and the frequency of endogenous cytogenetic damage (sister chromatid exchange frequencies and micronuclei frequencies) in PBLs were evaluated, A statistically significant negative association was observed between ex vivo (+/-)-anti-BPDE-induced unscheduled DNA synthesis and age of the donors, Also, parameters of endogenous lymphocytic cytogenetic damage were negatively associated with ex vivo (+/-)-anti-BPDE-induced unscheduled DNA synthesis and positively associated with age in this population, It is concluded that, with increasing age, a decrease in lymphocytic excision repair capacity may be responsible for increased lymphocytic DNA damage in smokers. C1 Univ Limburg, Dept Hlth Risk Anal & Toxicol, NL-6200 MD Maastricht, Netherlands. RP Stierum, RH (reprint author), NIA, Gerontol Res Ctr, Mol Genet Lab, NIH, Box 01,4940 Eastern Ave, Baltimore, MD 21224 USA. EM stierumr@grc.nia.nih.gov RI Hageman, Geja/B-5298-2013; Kleinjans, Jos/E-7241-2015 NR 30 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD NOV PY 1997 VL 6 IS 11 BP 943 EP 948 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA YW298 UT WOS:000071918400011 PM 9367068 ER PT J AU Bennett, WP von Brevern, MC Zhu, SM Bartsch, H Muehlbauer, KR Hollstein, MC AF Bennett, WP von Brevern, MC Zhu, SM Bartsch, H Muehlbauer, KR Hollstein, MC TI p53 mutations in esophageal tumors from a high incidence area of China in relation to patient diet and smoking history SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID LUNG-CANCER; CLINICAL IMPLICATIONS; SUPPRESSOR GENE; URANIUM MINERS; HOTSPOT; EPIDEMIOLOGY; PATHOGENESIS; CARCINOMAS; ETIOLOGY AB Esophageal tumors from 29 patients residing in Guangzhou, China were examined for mutations in exons 5-8 of the p53 tumor suppressor gene and for p53 protein accumulation in tumor cell nuclei, Anamnestic data for each patient, which included information on family history of cancer, tobacco smoking, drinking of alcoholic beverages, and dietary habits such as consumption of pickled vegetables, were recorded, Screening of DNA from tumor cells microdissected from biopsies was performed by PCR amplification of p53 gene exons 5-8, denaturing gradient gel electrophoresis analysis, and DNA sequencing, Mutations were identified in 20 of 29 tumors (69%), All tumors harboring a missense mutation in the p53 gene also showed nuclear accumulation of the tumor suppressor protein by immunohistochemistry. The most common p53 mutations in these tumors were guanine to adenine (G --> A) transitions (10 of 20 tumors; 50%). We did not find multiple mutations at codon 176, in contrast to Lung et al, in their recent study of esophageal cancer patients from Guangzhou (M. L. Lung et at, Cancer Epidemiol. Biomark. Prev., 5: 277-284, 1996). The mutation prevalence was high both in smokers (13 mutations in 20 smokers; 65%) and in nonsmokers (7 of 9 tumors with mutations; 78%), an observation that differs from that of studies in European and North American patients, which demonstrate a much higher prevalence of p53 mutations in smokers than in nonsmokers (reviewed in R. Montesano et at., Int. J. Cancer Predict. Oncol., 69: 225-235, 1996.). Our findings in this pilot study of tumor suppressor gene mutations in patients from Guangzhou support a large body of epidemiological observations pointing to dietary mutagenic carcinogens peculiar to populations in China at high risk of esophageal cancer. C1 Deutsch Krebsforschungszentrum, German Canc Res Ctr, D-69120 Heidelberg, Germany. Sun Yat Sen Univ Med Sci, Guangzhou, Peoples R China. NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA. RP Hollstein, MC (reprint author), Deutsch Krebsforschungszentrum, German Canc Res Ctr, Neuenheimer Feld 280, D-69120 Heidelberg, Germany. EM m.hollstein@dkfz-heidelberg.de NR 27 TC 16 Z9 17 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD NOV PY 1997 VL 6 IS 11 BP 963 EP 966 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA YW298 UT WOS:000071918400014 PM 9367071 ER PT J AU Seth, P Katayose, D Li, ZW Kim, M Wersto, R Craig, C Shanmugam, N Ohri, E Mudahar, B Rakkar, ANS Kodali, P Cowan, K AF Seth, P Katayose, D Li, ZW Kim, M Wersto, R Craig, C Shanmugam, N Ohri, E Mudahar, B Rakkar, ANS Kodali, P Cowan, K TI A recombinant adenovirus expressing wild type p53 induces apoptosis in drug-resistant human breast cancer cells: A gene therapy approach for drug-resistant cancers SO CANCER GENE THERAPY LA English DT Article DE adenovirus; drug resistance; bone marrow purging; gene therapy; breast cancer ID MULTIDRUG-RESISTANCE; TUMOR SUPPRESSION; MEDIATED TRANSFER; LUNG-CANCER; PROTEIN; CHEMOTHERAPY; ENHANCEMENT; INHIBITOR; SEQUENCES; CYCLE AB The cytotoxicity of a recombinant adenovirus expressing the wild type tumor suppressor gene p53 (AdWTp53) was studied in two human breast cancer MCF-7 sublines selected for resistance to adriamycin (MCF-Adr) and mitoxantrone (MCF-Mito). Although the levels of wild type p53 protein following infection with AdWTp53 are comparable in all cell lines, the two drug-resistant MCF-7 sublines were 300- and 18-fold more sensitive to killing by AdWTp53 compared with the drug-sensitive parental MCF-7 cell lines. In each cell line, AdWTp53 infection led to cell cycle arrest, and reduction of Cdk2 and cyclin B1-Cdc2 activity. Nucleosomal DNA fragmentation analysis (as a function of apoptosis) following AdWTp53 infection revealed that, while the parental MCF-7 cells failed to undergo apoptosis, both drug-resistant cell lines showed distinct DNA laddering. In MCF-Adr cells, a combination treatment of AdWTp53 and adriamycin was much more toxic than either of the reagents used individually. Finally, exposure of a mixed population of MCF-Adr and CD34(+) cells to AdWTp53 selectively prevented MCF-Adr cell colony formation, while there was no inhibition of CFU-GM colony formation from CD34(+) cells. These findings suggest that some drug-resistant human breast cancers may be effectively treated with adenovirus expressing wild type p53. C1 NCI,PATHOL BRANCH,NIH,BETHESDA,MD 20892. RP Seth, P (reprint author), NCI,MED BREAST CANC SECT,MED BRANCH,NIH,BLDG 10,ROOM 12 N 226,BETHESDA,MD 20892, USA. NR 30 TC 38 Z9 42 U1 1 U2 1 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0929-1903 J9 CANCER GENE THER JI Cancer Gene Ther. PD NOV-DEC PY 1997 VL 4 IS 6 BP 383 EP 390 PG 8 WC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Research & Experimental Medicine GA YH924 UT WOS:A1997YH92400007 PM 9408609 ER PT J AU Wickham, TJ Haskard, D Segal, D Kovesdi, I AF Wickham, TJ Haskard, D Segal, D Kovesdi, I TI Targeting endothelium for gene therapy via receptors up-regulated during angiogenesis and inflammation SO CANCER IMMUNOLOGY IMMUNOTHERAPY LA English DT Article; Proceedings Paper CT 5th World Conference on Bispecific Antibodies CY JUN 25-28, 1997 CL VOLENDAM, NETHERLANDS SP EFIS DE gene therapy; receptors; angiogenesis; inflammation ID ADENOVIRUS; DELIVERY; TROPISM AB Endothelial cells are an attractive target for gene therapy because they are intimately involved in disease processes associated with inflammation and angiogenesis and because endothelial cells are readily accessible to gene therapy vectors via the circulation. Furthermore, specific receptors are up-regulated during angiogenesis or during inflammation. Therefore it should be possible to target the specific populations of endothelial cells involved in each of these disease processes. We have utilized two bispecific antibodies to target entry of an adenovirus vector into endothelial cells expressing a receptor up-regulated during angiogenesis (alpha(v) integrins) and a receptor up-regulated during inflammation (E-selectin). Both bispecific antibodies contain the anti-FLAG M2 mAb, which binds to a FLAG epitope genetically incorporated into the penton base protein of the vector, AdFLAG. The anti-alpha(v)-integrin x anti-FLAG bsAb was able to direct binding and entry of AdFLAG into endothelial cells via alpha(v) integrins. Likewise, the anti-E-selectin x anti-FLAG bsAb was able to direct binding and entry of AdFLAG into tumor-necrosis-factor(TNF)-activated endothelial cells via E-selectin. Endothelial cells not activated with TNF were not efficiently transduced by the AdFLAG/E-selectin bsAb complex. These results demonstrate that bispecific antibodies can be successfully used to target adenovirus to endothelially expressed receptors that are up-regulated during angiogenesis or inflammation. C1 ROYAL POSTGRAD MED SCH,DEPT MED,HAMMERSMITH HOSP,LONDON W12 0NN,ENGLAND. NCI,BETHESDA,MD 20892. RP Wickham, TJ (reprint author), GENVEC INC,12111 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 13 TC 45 Z9 45 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-7004 J9 CANCER IMMUNOL IMMUN JI Cancer Immunol. Immunother. PD NOV-DEC PY 1997 VL 45 IS 3-4 BP 149 EP 151 DI 10.1007/s002620050419 PG 3 WC Oncology; Immunology SC Oncology; Immunology GA YK485 UT WOS:A1997YK48500008 PM 9435860 ER PT J AU Dunn, SE Kari, FW French, J Leininger, JR Travlos, G Wilson, R Barrett, JC AF Dunn, SE Kari, FW French, J Leininger, JR Travlos, G Wilson, R Barrett, JC TI Dietary restriction reduces insulin-like growth factor I levels, which modulates apoptosis, cell proliferation, and tumor progression in p53-deficient mice SO CANCER RESEARCH LA English DT Article ID BLADDER-CANCER; TRANSGENIC MICE; RECEPTOR; TUMORIGENESIS; INHIBITION; TAMOXIFEN; CALORIE; SERUM; GENE; VIVO AB Diet contributes to over one-third of cancer deaths in the Western world, yet the factors in the diet that influence cancer are not elucidated, A reduction in caloric intake dramatically slows cancer progression in rodents, and this may be a major contribution to dietary effects on cancer, Insulin-like growth factor I (IGF-I) is lowered during dietary restriction (DR) in both humans and rats, Because IGF-I modulates cell proliferation, apoptosis, and tumorigenesis, the mechanisms behind the protective effects of DR may depend on the reduction of this multifaceted growth factor, To test this hypothesis, IGF-I was restored during DR to ascertain if lowering of IGF-I was central to slowing bladder cancer progression during DR. Heterozygous p53-deficient mice received a bladder carcinogen, p-cresidine, to induce preneoplasia, After confirmation of bladder urothelial preneoplasia, the mice were divided into three groups: (a) ad libitum; (b) 20% DR; and (c) 20% DR plus IGF-I (IGF-I/DR). Serum IGF-I was lowered 24% by DR but was completely restored in the IGF-I/DR-treated mice using recombinant IGF-I administered via osmotic minipumps, Although tumor progression was decreased by DR, restoration of IGF-I serum levels in DR-treated mice increased the stage of the cancers, Furthermore, IGF-I modulated tumor progression independent of changes in body weight, Rates of apoptosis in the preneoplastic lesions were 10 times higher in DR-treated mice compared to those in IGF/DR- and ad libitum-treated mice, Administration of IGF-I to DR-treated mice also stimulated cell proliferation 6-fold in hyperplastic foci, In conclusion, DR lowered IGF-I levels, thereby favoring apoptosis over cell proliferation and ultimately slowing tumor progression, This is the first mechanistic study demonstrating that IGF-I supplementation abrogates the protective effect of DR on neoplastic progression. C1 NIEHS,MOL CARCINOGENESIS LAB,NIH,RES TRIANGLE PK,NC 27709. NIEHS,LAB ENVIRONM CARCINOGENESIS & MUTAGENESIS,NIH,RES TRIANGLE PK,NC 27709. NIEHS,LAB EXPT PATHOL,NIH,RES TRIANGLE PK,NC 27709. NR 38 TC 323 Z9 331 U1 0 U2 9 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 NOV 1 PY 1997 VL 57 IS 21 BP 4667 EP 4672 PG 6 WC Oncology SC Oncology GA YD358 UT WOS:A1997YD35800002 PM 9354418 ER PT J AU Zhuang, ZP Vortmeyer, AO Pack, S Huang, S Pham, TA Wang, CY Park, WS Agarwal, SK Debelenko, LV Kester, M Guru, SC Manickam, P Olufemi, SE Yu, F Heppner, C Crabtree, JS Skarulis, MC Venzon, DJ EmmertBuck, MR Spiegel, AM Chandrasekharappa, SC Collins, FS Burns, AL Marx, SJ Jensen, RT Liotta, LA Lubensky, IA AF Zhuang, ZP Vortmeyer, AO Pack, S Huang, S Pham, TA Wang, CY Park, WS Agarwal, SK Debelenko, LV Kester, M Guru, SC Manickam, P Olufemi, SE Yu, F Heppner, C Crabtree, JS Skarulis, MC Venzon, DJ EmmertBuck, MR Spiegel, AM Chandrasekharappa, SC Collins, FS Burns, AL Marx, SJ Jensen, RT Liotta, LA Lubensky, IA TI Somatic mutations of the MEN1 tumor suppressor gene in sporadic gastrinomas and insulinomas SO CANCER RESEARCH LA English DT Article ID ENDOCRINE NEOPLASIA TYPE-1; ZOLLINGER-ELLISON SYNDROME; RENAL-CARCINOMA; MULTIPLE; SENSITIVITY; METHYLATION; DNA AB Gastrinomas and insulinomas are frequent in multiple endocrine neoplasia type 1 (MEN1), The MEN1 tumor suppressor gene was recently identified. To elucidate the etiological role of the MEN1 gene in sporadic enteropancreatic endocrine tumorigenesis, we analyzed tumors (28 gastrinomas and 12 insulinomas) from 40 patients for MEN1 gene mutations and allelic deletions. One copy of the MEN1 gene was found to be deleted in 25 of 27 (93%) sporadic gastrinomas and in 6 of 12 (50%) sporadic insulinomas. MEN1 gene mutations were identified in 9 of 27 (33%) sporadic gastrinomas and 2 of 12 (17%) insulinomas and were not seen in corresponding germ-line DNA sequence, A specific MEN1 mutation was detected in one gastrinoma and in the corresponding germ-line DNA of a patient who had no family history of MEN1. Somatic MEN1 gene mutations and deletions play a critical role in the tumorigenesis of sporadic gastrinomas and may also contribute to the development of a subgroup of insulinomas. C1 NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. NIDDKD,METAB DIS BRANCH,NIH,BETHESDA,MD 20892. NIDDKD,LAB GENE TRANSFER,NATL HUMAN GENOME RES INST,NIH,BETHESDA,MD 20892. NIDDKD,DIGEST DIS BRANCH,NIH,BETHESDA,MD 20892. NIDDKD,DIABET BRANCH,NIH,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,NIH,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008; Pack, Svetlana/C-2020-2014; Agarwal, Sunita/D-1428-2016 OI Agarwal, Sunita/0000-0002-7557-3191 NR 27 TC 219 Z9 224 U1 0 U2 2 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 NOV 1 PY 1997 VL 57 IS 21 BP 4682 EP 4686 PG 5 WC Oncology SC Oncology GA YD358 UT WOS:A1997YD35800005 PM 9354421 ER PT J AU Gronberg, H Xu, JF Smith, JR Carpten, JD Isaacs, SD Freije, D Bova, GS Walsh, PC Collins, FS Trent, JM Meyers, DA Isaacs, WB AF Gronberg, H Xu, JF Smith, JR Carpten, JD Isaacs, SD Freije, D Bova, GS Walsh, PC Collins, FS Trent, JM Meyers, DA Isaacs, WB TI Early age at diagnosis in families providing evidence of linkage to the hereditary prostate cancer locus (HPC1) on chromosome 1 SO CANCER RESEARCH LA English DT Article ID BREAST-CANCER; INHERITANCE AB In a recent study of 91 families having at least three first degree relatives with prostate cancer, we reported the localization of a major susceptibility locus for prostate cancer (HPC1) to chromosome 1 [band q24; J. R. Smith et al., Science (Washington DC), 274: 1371-1373, 1996]. There was significant evidence for locus heterogeneity, with an estimate of 34% of the families being linked to this locus, In this report, we investigate the importance of age at diagnosis of prostate cancer and number of affected individuals within a family as variables in the linkage analysis of an expanded set of markers on 1q24, Under two different models for the prostate cancer locus, we find that the evidence for linkage to HPC1 is provided primarily by large (five or more members affected) families with an early average age at diagnosis, Specifically, for 40 North American families with an average age at diagnosis <65 years, the multipoint lod score is 3.96, whereas for 39 families with an older average age at diagnosis, this value is -0.84, Assuming heterogeneity, the proportion of families linked is 66% for the 14 families with the earliest average ages at diagnoses, but it decreases to 7% for the families with the latest ages at diagnoses, A similar age effect is observed in 12 Swedish pedigrees analyzed, To test the hypotheses generated by these analyses, we examined an additional group of 13 newly identified prostate cancer families, Overall, these families provided additional evidence for linkage to this region (nonparametric linkage Z = 1.91; P = 0.04 at marker D1S1660), contributed primarily by the families in this group with early age at diagnosis [nonparametric linkage Z = 2.50 (P = 0.01) at D1S422], These results are consistent with the existence of a locus in this region that predisposes men to develop early-onset prostate cancer. C1 JOHNS HOPKINS UNIV,JAMES BUCHANAN BRADY UROL INST,SCH MED,BALTIMORE,MD 21287. UMEA UNIV,DEPT ONCOL,S-90185 UMEA,SWEDEN. UNIV MARYLAND,SCH MED,CTR GENET ASTHMA & COMPLEX DIS,BALTIMORE,MD 21201. NIH,NATL HUMAN GENOME RES INST,BETHESDA,MD 20892. RI Smith, Jeff/C-3484-2012 FU NCI NIH HHS [CA58236] NR 14 TC 74 Z9 76 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 NOV 1 PY 1997 VL 57 IS 21 BP 4707 EP 4709 PG 3 WC Oncology SC Oncology GA YD358 UT WOS:A1997YD35800010 PM 9354426 ER PT J AU Risinger, JI Hayes, AK Berchuck, A Barrett, JC AF Risinger, JI Hayes, AK Berchuck, A Barrett, JC TI PTEN/MMAC1 mutations in endometrial cancers SO CANCER RESEARCH LA English DT Article ID MICROSATELLITE INSTABILITY; REPLICATION ERRORS; BETA RECEPTOR; CHROMOSOME-10; CARCINOMA; COLON AB Endometrial carcinomas represent the most common gynecological cancer in the United States, yet the molecular genetic events that underlie the development of these tumors remain obscure, Chromosome 10 is implicated in the pathogenesis of endometrial carcinoma based on loss of heterozygosity (LOH), comparative genomic hybridization, and cytogenetics, Recently, a potential tumor suppressor gene, PTEN/MMAC1, with homology to dual-specificity phosphatases and to the cytoskeletal proteins tensin and auxillin was identified on chromosome 10. This gene is mutated in several types of advanced tumors that display frequent LOH on chromosome 10, most notably glioblastomas. Additionally, germ-line mutations of PTEN/MMAC1 are responsible for several familial neoplastic disorders, including Cowden disease and Bannayan-Zonana syndrome, Because this locus is included in the region of LOH in many endometrial carcinomas, we examined 70 endometrial carcinomas for alterations in PTEN/MMAC1. Somatic mutations were detected in 24 cases (34%) including 21 cases that resulted in premature truncation of the protein, 2 tumors with missense alterations in the conserved phosphatase domain, and 1 tumor with a large insertion, These data indicate that PTEN/MMAC1 is more commonly mutated than any other known gene in endometrial cancers. C1 NIEHS,MOL CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,DURHAM,NC 27710. NR 17 TC 426 Z9 453 U1 0 U2 4 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 NOV 1 PY 1997 VL 57 IS 21 BP 4736 EP 4738 PG 3 WC Oncology SC Oncology GA YD358 UT WOS:A1997YD35800017 PM 9354433 ER PT J AU Peters, JM Cattley, RC Gonzalez, FJ AF Peters, JM Cattley, RC Gonzalez, FJ TI Role of PPAR alpha in the mechanism of action of the nongenotoxic carcinogen and peroxisome proliferator Wy-14,643 SO CARCINOGENESIS LA English DT Article ID <4-CHLORO-6-(2,3-XYLIDINO)-2-PYRIMIDINYLTHIO>ACETIC ACID WY-14,643; ACTIVATED RECEPTOR; CLOFIBRIC ACID; DNA-SYNTHESIS; HEPATOCELLULAR CARCINOMAS; FATTY-ACIDS; LIVER; RATS; MICE; DEHYDROEPIANDROSTERONE AB Chronic administration of peroxisome proliferators to mice and rats results in hepatomegaly and ultimately carcinogenesis. The mechanism underlying the carcinogenic effect of nongenotoxic peroxisome proliferators is not well understood, To determine whether nongenotoxic carcinogenesis is receptor mediated, we evaluated the effect of the proto-typical peroxisome proliferator Wy-14,643 on replicative DNA synthesis and carcinogenesis in the PPAR alpha-null mouse line, Male mice (F-4, Sv/129 ter) of both genotypes (+/+) and (-/-) were fed either a control diet or one containing 0.1% Wy-14,643 for either 1 week, 5 weeks, or Il months, Wild-type mice fed the Wy-14,643 diet for 1 or 5 weeks showed increased hepatic labeling by bromodeoxyuridine (BrDU) compared to untreated controls, In contrast, there was no increase in hepatic BrDU labeling index in (-/-) mice fed the Wy-14,643 diet for the same time periods compared to controls, After 11 months, 100% of the (+/+) mice fed the Wy-14,643 diet had multiple hepatocellular neoplasms, including adenomas and carcinomas, while the (-/-) mice fed the Wy-14,643 diet were unaffected, This work demonstrates that the effects of Wy-14,643 on replicative DNA synthesis and hepatocarcinogenesis are mediated by PPAR alpha. C1 CHEM IND INST TOXICOL,RES TRIANGLE PK,NC 27709. RP Peters, JM (reprint author), NCI,LAB METAB,NIH,BETHESDA,MD 20892, USA. RI Peters, Jeffrey/D-8847-2011 NR 20 TC 357 Z9 365 U1 1 U2 7 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD NOV PY 1997 VL 18 IS 11 BP 2029 EP 2033 DI 10.1093/carcin/18.11.2029 PG 5 WC Oncology SC Oncology GA YG756 UT WOS:A1997YG75600001 PM 9395198 ER PT J AU Witschi, H Espiritu, I Maronpot, RR Pinkerton, KE Jones, AD AF Witschi, H Espiritu, I Maronpot, RR Pinkerton, KE Jones, AD TI The carcinogenic potential of the gas phase of environmental tobacco smoke SO CARCINOGENESIS LA English DT Article ID ARTERIOSCLEROTIC PLAQUE DEVELOPMENT; SIDESTREAM CIGARETTE-SMOKE; STRAIN A/J MICE; LUNG-CANCER; MOUSE LUNG; CELL-KINETICS; INHALATION; EXPOSURE; LIVER; INHIBITION AB Female strain A/J mice were exposed to unfiltered or HEPA-filtered environmental tobacco smoke (ETS), Total suspended particulates (TSP) in the full smoke exposure chamber was 78.5 mg/m(3) and in the filtered smoke chamber 0.1 mg/m(3); nicotine concentrations in the full and filtered smoke chamber were 13.4 and 3.1 mg/m(3), respectively. Animals exposed to filtered ETS (6 h a day, 5 days a week) and killed after 5 months had a higher lung tumor incidence and multiplicity than controls maintained in filtered air, although the differences were not statistically significant, Animals exposed to filtered and full ETS and allowed to recover in air for 4, months had an average of 1.2 +/- 0.3 tumors per lung and 1.3 +/- 0.3 tumors per lung, respectively, Air exposed control animals had an average tumor multiplicity 0.5 +/- 0.1 tumors per lung. Increased immunstaining for CYP 1A1 was not evident in the lung of animals exposed to filtered smoke. Based on the chamber concentrations of selected nitrosamines and polycyclic aromatic hydrocarbons, the possible maximum uptakes by the mice of NNK, NNN and benzo[a]pyrene during the 5 months exposure period were three to six orders of magnitude below doses reported in the literature to produce 1 lung tumor in strain A/J mice, It was concluded that the gas phase of ETS is as carcinogenic as is full ETS, The carcinogenicity of the gas phase may be due to some as yet unidentified, yet highly potent carcinogens or by placing a substantial, possibly free radical-mediated oxidative stress on the lung. C1 SCH VET MED,DEPT MOL BIOSCI,RES TRIANGLE PK,NC. NIEHS,RES TRIANGLE PK,NC 27709. RP Witschi, H (reprint author), UNIV CALIF DAVIS,INST TOXICOL & ENVIRONM HLTH,DAVIS,CA 95616, USA. RI Jones, Arthur/C-2670-2013 OI Jones, Arthur/0000-0002-7408-6690 FU NIEHS NIH HHS [ES-05707] NR 66 TC 108 Z9 111 U1 0 U2 8 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD NOV PY 1997 VL 18 IS 11 BP 2035 EP 2042 DI 10.1093/carcin/18.11.2035 PG 8 WC Oncology SC Oncology GA YG756 UT WOS:A1997YG75600002 PM 9395199 ER PT J AU Karam, WG Ghanayem, BI AF Karam, WG Ghanayem, BI TI Induction of replicative DNA synthesis and PPAR alpha-dependent gene transcription by Wy-14 643 in primary rat hepatocyte and non-parenchymal cell co-cultures SO CARCINOGENESIS LA English DT Article; Proceedings Paper CT 36th Annual Meeting of the Society-of-Toxicology CY MAR 09-13, 1997 CL CINCINNATI, OH SP Soc Toxicol ID ACID-BINDING PROTEIN; PEROXISOME PROLIFERATORS; KUPFFER CELLS; CLOFIBRIC ACID; ACTIVATED RECEPTOR; LIVER; 8-HYDROXYDEOXYGUANOSINE; HEPATOCARCINOGENS; CARCINOGENESIS; NAFENOPIN AB Peroxisome proliferators (PP) are known hepatocarcinogens in rats and mice. We have investigated the ability of Wyeth-14 643 (Wy), a PP and potent rodent carcinogen, to induce replicative DNA synthesis and to modulate the levels of peroxisome proliferator activated receptor-alpha (PPAR alpha) transcriptionally-dependent genes in primary rat hepatocyte (HPC) cultures and hepatocyte/non-parenchymal cell (HPC/NPC) co-cultures maintained on Matrigel, Four days after plating, cells were treated with Wy and replicative DNA synthesis was quantitated using [H-3]thymidine incorporation and specific mRNA transcript levels were determined by reverse-transcriptase polymerase chain reaction (RT-PCR). An increase in HPC replicative DNA synthesis was detected at 48 h in both Wy-treated HPC and HPC/NPC co-cultures relative to controls, This increase was approximately 3- and 6-fold in HPC and HPC/NPC cultures respectively, and was Wy concentration-dependent, The levels of PPAR alpha-transcriptionally dependent genes [cytochrome P4504A1, acyl-CoA oxidase (AOxase), and liver-fatty acid binding protein (L-FABP)] transcripts were determined as indicators of PPAR alpha activation, These transcripts increased dose-dependently at 48 h in HPC/NPC cultures up to 10 mu M Wy, Similarly, RT-PCR product levels were also increased in HPC cultures with 10 mu M Wy at 48 h, In conclusion, we have investigated the transcription of PPAR alpha-dependent genes and HPC replicative DNA synthesis by Wy in HPC/NPC co-cultures. Results of this work are clearly more reflective of the known in vivo effects of PP and suggest that HPC/NPC cocultures are more appropriate than HPC cultures for such studies, The effect of PP on human HPC/NPC co-cultures is currently being investigated in our laboratory in an attempt to assess human risks to these chemicals more directly. C1 NIEHS,LAB PHARMACOL & CHEM,NIH,RES TRIANGLE PK,NC 27709. NR 36 TC 24 Z9 24 U1 1 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD NOV PY 1997 VL 18 IS 11 BP 2077 EP 2083 DI 10.1093/carcin/18.11.2077 PG 7 WC Oncology SC Oncology GA YG756 UT WOS:A1997YG75600008 PM 9395205 ER PT J AU Zheng, Y Kramer, PM Olson, G Lubet, A Steele, VE Kelloff, GJ Pereira, MA AF Zheng, Y Kramer, PM Olson, G Lubet, A Steele, VE Kelloff, GJ Pereira, MA TI Prevention by retinoids of azoxymethane-induced tumors and aberrant crypt foci and their modulation of cell proliferation in the colon of rats SO CARCINOGENESIS LA English DT Article ID CANCER CHEMOPREVENTIVE AGENTS; ACUTE PROMYELOCYTIC LEUKEMIA; F344 RATS; DIFFERENTIATION THERAPY; FAMILIAL POLYPOSIS; C-FOS; ACID; GROWTH; N-(4-HYDROXYPHENYL)RETINAMIDE; INHIBITION AB Retinoids are proposed chemopreventive agents that inhibit cell proliferation and induce differentiation. Their ability to prevent azoxymethane (AOM)-induced aberrant crypt foci (ACF) and tumors and to modulate cell proliferation was investigated in the colon of male F344 rats, Thirteen retinoids were evaluated for prevention of ACF and two of them, 9-cis-retinoic acid (RA) and 4-(hydroxyphenyl)retinamide (4-HPR), were also evaluated for prevention of colon cancer, The retinoids were administered continuously in the diet starting 1 week prior to the first of two weekly 15 mg/kg i.p. injections of AOM and for a total of either 5 or 36 weeks in order to evaluate their effect on colonic ACF and tumors, At a concentration of 1 mmol/kg diet, 2-(carboxyphenyl)retinamide caused the greatest reduction (57.7 %) in the yield of ACF, 9-cis-RA was toxic at 1 mmol/kg so that it was evaluated at 0.1 mmol/kg, resulting in a 41.6% reduction in ACF, The ability of the retinoids to reduce the proliferating cell nuclear antigen (PCNA) labeling index in ACF and in non-involved crypts correlated with their ability to prevent ACF. Both 9-cis-RA (0.1 and 0.2 mmol/kg diet) and 4-HPR (1 and 2 mmol/kg diet) were highly effective in decreasing the yield of AOM-induced colon tumors, In summary, retinoids were demonstrated to reduce cell proliferation and to prevent ACF and tumors in the colon, suggesting promise as preventive agents for colon cancer. C1 PATHOL ASSOCIATES INT, W CHESTER, OH 45069 USA. NCI, CHEMOPREVENT LAB, DIV CANC CHEMOPREVENT & CONTROL, BETHESDA, MD 20892 USA. RP Zheng, Y (reprint author), MED COLL OHIO, DEPT PATHOL, TOLEDO, OH 43614 USA. FU NCI NIH HHS [N01-CN-55175] NR 43 TC 48 Z9 49 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD NOV PY 1997 VL 18 IS 11 BP 2119 EP 2125 DI 10.1093/carcin/18.11.2119 PG 7 WC Oncology SC Oncology GA YG756 UT WOS:A1997YG75600014 PM 9395211 ER PT J AU Chomarat, P Sipowicz, MA Diwan, BA Fornwald, LW Awasthi, YC Anver, MR Rice, JM Anderson, LM Wild, CP AF Chomarat, P Sipowicz, MA Diwan, BA Fornwald, LW Awasthi, YC Anver, MR Rice, JM Anderson, LM Wild, CP TI Distinct time courses of increase in cytochromes P450 1A2, 2A5 and glutathione S-transferases during the progressive hepatitis associated with Helicobacter hepaticus SO CARCINOGENESIS LA English DT Article ID CHRONIC ACTIVE HEPATITIS; OXIDATIVE DNA-DAMAGE; MESSENGER-RNA STABILIZATION; TRANSGENIC MOUSE MODEL; HEPATOCELLULAR-CARCINOMA; COUMARIN 7-HYDROXYLASE; METABOLIZING-ENZYMES; FULMINANT-HEPATITIS; DRUG-METABOLISM; HUMAN-LIVER AB Mice naturally infected by Helicobacter hepaticus develop a chronic active hepatitis leading to hepatocellular carcinoma, This mouse model of liver cancer was used to examine the impact of bacterial infection on the hepatic expression and activity of enzymes involved in carcinogen bioactivation (phase I enzymes) and detoxification (phase II enzymes), No major differences in total cytochrome P450 (CYP) content were found between control and infected mice during the course of the study. The most striking modulations of individual isoenzymes were the increases in immunohistochemical staining observed for CYP1A and CYP2A5 in relation to increasing age and liver lesions. The increase in CYP2A5 in mice aged over 12 months was confirmed by the observed increases in coumarin 7-hydroxylation (CYP2A5 substrate) in vitro and CYP2A5 mRNA levels by Northern blot analysis, Immunoblotting confirmed the specific induction of CYP1A2 in infected mice 12 and 18 months of age, Perfusion of liver with nitroblue tetrazolium, an indicator for superoxide formation, demonstrated that in livers of infected mice, hepatocytes often co-expressed CYP2A5 and formazan deposition, Concerning phase II enzymes, an enhancement of glutathione S-transferase (GST) activities, related to the disease process, was observed in infected mice, An age-specific increase of GST pi and A4.4 (early stage of disease) and GST YaYa (>9 months) expression was also demonstrated by immunohistochemical staining, In contrast, catalase and glutathione-peroxidase activities, as well as reduced glutathione content were decreased in the early stages of disease (3-9 months) in infected mice compared to age-matched control mice, Overall, these results suggest that alterations in CYP and GST expression may contribute to the aetiology of tumour incidence due to H.hepaticus infection via production of reactive oxygen species. C1 INT AGCY RES CANC,UNIT ENVIRONM CARCINOGENESIS,F-69372 LYON 08,FRANCE. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. SAIC FREDERICK,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. INT AGCY RES CANC,UNIT CARCINOGEN IDENTIFICAT & EVALUAT,F-69372 LYON,FRANCE. UNIV LEEDS,RES SCH MED,MOL EPIDEMIOL UNIT,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND. FU NIEHS NIH HHS [1-P01 ES06052] NR 65 TC 32 Z9 33 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD NOV PY 1997 VL 18 IS 11 BP 2179 EP 2190 DI 10.1093/carcin/18.11.2179 PG 12 WC Oncology SC Oncology GA YG756 UT WOS:A1997YG75600022 PM 9395219 ER PT J AU SantoniRugiu, E Silverman, JA AF SantoniRugiu, E Silverman, JA TI Functional characterization of the rat mdr1b encoded P-glycoprotein: not all inducing agents are substrates SO CARCINOGENESIS LA English DT Article ID MULTIDRUG-RESISTANCE GENE; HEAT-SHOCK; METABOLIC-ACTIVATION; HEPATOCYTE CULTURES; CARCINOMA CELLS; MOUSE MDR1; EXPRESSION; LIVER; INDUCTION; PROMOTER AB The multidrug resistance (mdr) genes encode P-glycoproteins, integral membrane proteins which function as drug efflux transporters, Exposure of animals in vivo and cells in vitro to a variety of xenobiotics leads to increased mdr1 gene expression and higher levels of P-glycoprotein. This response may protect cells from the cytotoxic effects of these compounds, In this investigation we functionally expressed the rat mdr1b gene in NIH 3T3 cells and assessed the ability of the encoded P-glycoprotein to protect these cells from the cytotoxicity of xenobiotics known to induce mdr1b expression, In long-term colony survival assays, stably expressed mdr1b conferred resistance to cytotoxic drugs such as colchicine, vinblastine and doxorubicin, but not to 5-fluorouracil nor to the carcinogens aflatoxin B-1 and N-hydroxy-acetylaminofluorene, The mdr reversal agent verapamil restored cytotoxicity of colchicine, doxorubicin, actinomycin D, vinblastine and taxol, but had no effect on the sensitivity of these cells to 5-fluorouracil, aflatoxin B-1 or N-hydroxy-acetylaminofluorene. In a competitive transport assay, verapamil and, to a lesser extent, colchicine blocked the increased efflux of the fluorescent dye rhodamine 123 from mdr1b-transfected cells, whereas aflatoxin B-1 did not compete for this export, These data demonstrate that expression of the rat mdr1b encoded P-glycoprotein can protect cells from a diverse group of compounds previously identified to be mdr substrates, however, other effective inducers of mdr expression, such as aflatoxin B-1 and N-hydroxy-acetylaminoffuorene, remain potent cytotoxins despite high levels of P-glycoprotein. The fact that compounds which are not themselves substrates can induce P-glycoprotein expression may have implications for pharmacokinetic interactions and chemotherapy. C1 NCI,DIV BASIC SCI,EXPT CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 56 TC 19 Z9 19 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD NOV PY 1997 VL 18 IS 11 BP 2255 EP 2263 DI 10.1093/carcin/18.11.2255 PG 9 WC Oncology SC Oncology GA YG756 UT WOS:A1997YG75600032 PM 9395229 ER PT J AU Davenport, RW AF Davenport, RW TI Functional guidance components and their cellular distribution in retinotectal co-cultures SO CELL AND TISSUE RESEARCH LA English DT Article DE retinotectal co-culture; growth cones; time-lapse photography; topographic projection repulsion ID CHICK OPTIC TECTUM; RECEPTOR TYROSINE KINASES; GROWTH CONES; AXON GUIDANCE; RETINAL AXONS; IN-VITRO; FILOPODIAL CONTACTS; TIME-LAPSE; COLLAPSE; INVITRO AB Recent advances in the study of the developmental processes that direct afferent axons toward their final destinations are beginning to elucidate the cellular and molecular bases for the early development of retinotectal topography. The present review focuses on two guidance components (repulsive and adhesive) and their cellular localization as revealed by a newly established retinotectal co-culture system. These co-cultures enable general outgrowth patterns to be examined when retinal ganglion cell (RGC) axons attempt to traverse cells dissociated from their target nuclei. Additionally, the recording of RGC growth cone responses to single living target cells allows a cellular localization of guidance components that is not possible by other methods. This co-culture system, therefore, complements the repertoire of cell-culture techniques used to investigate the sequence of cellular events that underlie the establishment of retinotopic development. With this new approach, time-lapse micrographs were collected when RGC growth cones from temporal or nasal regions of embryonic chick retinae encountered individual cells dissociated from optic tecta. Temporal RGC growth cones collapsed and retracted with a high probability from neuronal cells dissociated from posterior tecta, indicating that repellent components were enriched on posterior target neurons. The response to non-neuronal cells revealed a separate effect on axonal outgrowth that was less dependent upon the particular region of retina or tectum from which the cells originated: most RGC axons adhered to the edge of non-neuronal cells, without retracting. Together, the localization of repellent and adhesive components suggests a sequence of events that occurs during the early stages of tectal innervation and that results in the rudiments of retinotopic projection, and furthermore, it raises a number of experimentally approachable questions concerning the functional expression of several guidance components. RP Davenport, RW (reprint author), NICHHD,DEV NEUROBIOL LAB,NIH,MSC 4480,BLDG 49,RM 5A38,BETHESDA,MD 20892, USA. NR 54 TC 5 Z9 5 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0302-766X J9 CELL TISSUE RES JI Cell Tissue Res. PD NOV PY 1997 VL 290 IS 2 BP 201 EP 208 DI 10.1007/s004410050924 PG 8 WC Cell Biology SC Cell Biology GA YA698 UT WOS:A1997YA69800005 PM 9321681 ER PT J AU Izraeli, S ColaizzoAnas, T Bertness, VL Mani, K Aplan, PD Kirsch, IR AF Izraeli, S ColaizzoAnas, T Bertness, VL Mani, K Aplan, PD Kirsch, IR TI Expression of the SIL gene is correlated with growth induction and cellular proliferation SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID IMMEDIATE-EARLY GENE; ACUTE LYMPHOBLASTIC-LEUKEMIA; PRIMARY RESPONSE GENES; C-MYC; MOUSE FIBROBLASTS; CYCLE PROGRESSION; 3T3 CELLS; G1 PHASE; PRODUCT; SCL AB The SIL gene was discovered at the site of a cancer-associated interstitial deletion in which its promoter assumed the regulation of a second gene, SCL. The human SIL gene encodes a 1287-amino acid cytosolic protein that has been found to be highly conserved in the mouse. SIL is expressed in proliferating cells and is down-regulated when cellular proliferation ceases because of serum starvation, contact inhibition, or induction of terminal differentiation. SIL is induced within 1 h of stimulation by 20% serum in growth-arrested 3T3 cells. This induction is independent of protein synthesis because ''superinduction'' is observed in the presence of the protein synthesis inhibitor cyclohexamide. Thus, SIL is an immediate-early gene. Upon release from serum starvation of 3T3 fibroblasts SIL mRNA and protein levels display a biphasic pattern during the first cell cycle. In contrast, in exponentially growing EL4 lymphoblasts, SIL mRNA is stable throughout the cell cycle, whereas SIL protein accumulates into G(2) phase and then falls precipitously at the completion of the cell cycle. This pattern of cell cycle expression suggests that SIL may play an important role in cellular growth and proliferation. C1 NCI,DEPT GENET,MED BRANCH,DIV CLIN SCI,BETHESDA,MD 20889. ROSWELL PK CANC INST,DEPT PEDIAT,BUFFALO,NY. ROSWELL PK CANC INST,DEPT MOL MED,BUFFALO,NY. RI Aplan, Peter/K-9064-2016 NR 52 TC 41 Z9 42 U1 1 U2 2 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 NOV PY 1997 VL 8 IS 11 BP 1171 EP 1179 PG 9 WC Cell Biology SC Cell Biology GA YF162 UT WOS:A1997YF16200004 PM 9372240 ER PT J AU McNairy, SA AF McNairy, SA TI Message from the director SO CELLULAR AND MOLECULAR BIOLOGY LA English DT Editorial Material RP McNairy, SA (reprint author), NIH,NATL CTR RES RESOURCES,RES INFRASTRUC & RES CTR MINOR INST PROGRAM,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CELLULAR & MOLECULAR BIOLOGY PI NOISY-LE-GRAND PA PROF R WEGMANN RESIDENCE HAUSSMANN 1 AVENUE DU PAVE NEUF, 93160 NOISY-LE-GRAND, FRANCE SN 0145-5680 J9 CELL MOL BIOL JI Cell. Mol. Biol. PD NOV PY 1997 VL 43 IS 7 BP R5 EP R7 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA YK970 UT WOS:A1997YK97000002 ER PT J AU Barlow, T Ding, JM Vouros, P Dipple, A AF Barlow, T Ding, JM Vouros, P Dipple, A TI Investigation of hydrolytic deamination of 1-(-hydroxy-1-phenylethyl)adenosine SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID OXIDE; DNA; 1-POSITION; ADENOSINE; PRODUCTS; ADDUCTS; PURINES AB The ring nitrogen of adenosine reacts at both the alpha-(benzylic) and beta-carbons of styrene oxide to form 1-substituted products. The 1-(2-hydroxy-1-phenylethyl)adenosines formed by oxirane ring opening at the alpha-position are prone to an unusually facile hydrolytic deamination. By conducting hydrolysis reactions in [O-18]water and analyzing the reaction products by electrospray mass spectrometry, we find that deamination occurs by direct attack of water at the beta-position of the adenine ring system with displacement of the exocyclic amino group. C1 NORTHEASTERN UNIV,BARNETT INST,DEPT CHEM,BOSTON,MA 02115. RP Barlow, T (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [IR01CA69390-01] NR 16 TC 27 Z9 28 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD NOV PY 1997 VL 10 IS 11 BP 1247 EP 1249 DI 10.1021/tx970091m PG 3 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA YH252 UT WOS:A1997YH25200007 PM 9403177 ER PT J AU Mawhorter, S Temeck, B Chang, R Pass, H Nash, T AF Mawhorter, S Temeck, B Chang, R Pass, H Nash, T TI Nonsurgical therapy for pulmonary hydatid cyst disease SO CHEST LA English DT Article DE albendazole; cyst; Echinococcus granulosus; hydatid; percutaneous; pulmonary ID PERCUTANEOUS ASPIRATION; ALBENDAZOLE; INJECTION; LIVER AB Therapeutic and diagnostic aspiration of Echinococcus granulosus liver cysts, but not pulmonary cysts, are increasingly being pet-formed. Documented herein is the utility of percutaneous drainage and of albendazole treatment in a patient with a large recurrent, isolated, pulmonary echinococcal cyst for whom traditional therapy would have resulted in severe morbidity. Therapeutic options and possible complications are discussed. C1 NCI,SURG BRANCH,BETHESDA,MD 20892. NIH,CTR CLIN,DEPT RADIOL,BETHESDA,MD 20892. RP Mawhorter, S (reprint author), NIAID,DEPT INFECT DIS S32,PARASIT DIS LAB,9500 EUCLID AVE,CLEVELAND,OH 44195, USA. NR 18 TC 33 Z9 34 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD NOV PY 1997 VL 112 IS 5 BP 1432 EP 1436 DI 10.1378/chest.112.5.1432 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YF052 UT WOS:A1997YF05200043 PM 9367489 ER PT J AU Sternberg, KJ Lamb, ME Hershkowitz, I Yudilevitch, L Orbach, Y Esplin, PW Hovav, M AF Sternberg, KJ Lamb, ME Hershkowitz, I Yudilevitch, L Orbach, Y Esplin, PW Hovav, M TI Effects of introductory style on children's abilities to describe experiences of sexual abuse SO CHILD ABUSE & NEGLECT LA English DT Article DE forensic interviews; open-ended invitations; sexual abuse; disclosure ID INVESTIGATIVE UTTERANCE TYPES; DISCLOSURE; WITNESSES AB Objective: The goal of this study was to evaluate the relative effectiveness of two rapport-building techniques for eliciting information from children who made allegations of sexual abuse. Method: Fourteen interviewers conducted 51 investigations of child sexual abuse with children ranging from 4.5 to 12.9 years of age. In 25 of the investigations, interviewers used a script including many open-ended utterances to establish rapport, whereas in 26 of the investigations the same interviewers used a rapport-building script involving many direct questions. Both rapport-building scripts took about 7 minutes to complete. All children were asked the same open-ended question to initiate the substantive phase of the interview. Results: Children who had been trained in the open-ended condition provided 2 1/2 times as many details and words in response to the first substantive utterance as did children in the direct introduction condition. Children in the open-ended condition continued to respond more informatively to open-ended utterances in the later (unscripted) portion of the interview. Two-thirds of the children mentioned the core details of the incident in their responses to the first substantive utterance and a further 20% mentioned core details more vaguely. Conclusions: These results demonstrate that children respond more informatively to an open-ended invitation when they have previously been trained to answer such questions rather than more focused questions. These results demonstrate the sensitivity of children to the goals and expectations of forensic interviewers. Structured interview protocols also increase the amount of information provided by young interviewees. (C) 1997 Elsevier Science Ltd. C1 UNIV HAIFA, IL-31999 HAIFA, ISRAEL. ISRAELI MINIST LABOR & SOCIAL AFFAIRS, JERUSALEM, ISRAEL. RP Sternberg, KJ (reprint author), NICHHD, SECT SOCIAL & EMOT DEV, 9190 ROCKVILLE PIKE, BETHESDA, MD 20814 USA. NR 29 TC 115 Z9 116 U1 3 U2 9 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PD NOV PY 1997 VL 21 IS 11 BP 1133 EP 1146 DI 10.1016/S0145-2134(97)00071-9 PG 14 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA YF049 UT WOS:A1997YF04900010 PM 9422833 ER PT J AU Jenkins, NA Woollatt, E Crawford, J Gilbert, DJ Baldwin, ME Sutherland, GR Copeland, NG Achen, MG AF Jenkins, NA Woollatt, E Crawford, J Gilbert, DJ Baldwin, ME Sutherland, GR Copeland, NG Achen, MG TI Mapping of the gene for vascular endothelial growth factor-D in mouse and man to the X chromosome SO CHROMOSOME RESEARCH LA English DT Article ID GENOME; FAMILY C1 ROYAL MELBOURNE HOSP,LUDWIG INST CANC RES,MELBOURNE,VIC 3050,AUSTRALIA. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. WOMENS & CHILDRENS HOSP,CTR GENET MED,ADELAIDE,SA 5006,AUSTRALIA. RI Sutherland, Grant/D-2606-2012; Crawford, Joanna /F-9135-2013 OI Crawford, Joanna /0000-0003-0786-6889 NR 12 TC 19 Z9 20 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0967-3849 J9 CHROMOSOME RES JI Chromosome Res. PD NOV PY 1997 VL 5 IS 7 BP 502 EP 505 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA YK139 UT WOS:A1997YK13900012 PM 9421270 ER PT J AU London, B Trudeau, MC Newton, KP Beyer, AK Copeland, NG Gilbert, DJ Jenkins, NA Satler, CA Robertson, GA AF London, B Trudeau, MC Newton, KP Beyer, AK Copeland, NG Gilbert, DJ Jenkins, NA Satler, CA Robertson, GA TI Two isoforms of the mouse ether-a-go-go-related gene coassemble to form channels with properties similar to the rapidly activating component of the cardiac delayed rectifier K+ current SO CIRCULATION RESEARCH LA English DT Article DE K+ channel; coassembly; long-QT syndrome; rapidly activating component of delayed rectifier K+ current; HERG ID LONG QT SYNDROME; HUMAN INWARD RECTIFIER; POTASSIUM-CHANNEL; 2 COMPONENTS; MISSENSE MUTATION; XENOPUS-OOCYTES; MOLECULAR-BASIS; BETA-SUBUNIT; HERG; INACTIVATION AB HERG, the human ether-a-go-go-related gene, encodes a K+-selective channel with properties similar to the rapidly activating component of the delayed rectifier K+ current (I-Kr). Mutations of HERG cause the autosomal-dominant long-QT syndrome (LQTS), presumably by disrupting the normal function of I-Kr. The current produced by HERG is not identical to I-Kr, however, and the mechanism by which HERG mutations cause LQTS remains uncertain. To better define the role of Erg in the heart, we cloned Merg1 from mouse genomic and cardiac cDNA libraries. Merg1 has 16 exons and maps to mouse chromosome 5 in an area syntenic to human chromosome 7q, the map locus of HERG. We isolated three cardiac isoforms of Merg1: Merg1a is homologous to HERG and is expressed in heart, brain, and testes, Merg1a' lacks the first 59 amino acids of Merg1a and is not expressed abundantly, and Merg1b has a markedly shorter divergent N-terminal cytoplasmic domain and is expressed specifically in the heart. The Merg1 isoforms, like HERG, produce inwardly rectifying E-4031-sensitive currents when heterologously expressed in Xenopus oocytes. Merg1a and HERG produce currents with slow deactivation kinetics, whereas Merg1a' and Merg1b currents deactivate more rapidly. Merg1b coassembles with Merg1a to form channels with deactivation kinetics that are more rapid than those of Merg1a or HERG and nearly identical to I-Kr. In addition, a homologue of Merg1b is present in human cardiac and smooth muscle. Thus, we have identified a novel N-terminal Erg isoform that is expressed specifically in the heart, has rapid deactivation kinetics, and coassembles with the longer isoform in Xenopus oocytes. This N-terminal Erg isoform may determine the properties of I-Kr and contribute to the pathogenesis of LQTS. C1 UNIV WISCONSIN,SCH MED,DEPT PHYSIOL,MADISON,WI 53706. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD. PFIZER INC,DIV CENT RES,GROTON,CT 06340. RP London, B (reprint author), UNIV PITTSBURGH,MED CTR,DIV CARDIOL,BST 1744,200 LOTHROP ST,PITTSBURGH,PA 15213, USA. FU NHLBI NIH HHS [R01 HL-55793, K08 HL-02843] NR 53 TC 203 Z9 209 U1 2 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD NOV PY 1997 VL 81 IS 5 BP 870 EP 878 PG 9 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA YD713 UT WOS:A1997YD71300028 PM 9351462 ER PT J AU Wu, YG Palad, AJ Wasilenko, WJ Blackmore, PF Pincus, WA Schechter, GL Spoonster, JR Kohn, EC Somers, KD AF Wu, YG Palad, AJ Wasilenko, WJ Blackmore, PF Pincus, WA Schechter, GL Spoonster, JR Kohn, EC Somers, KD TI Inhibition of head and neck squamous cell carcinoma growth and invasion by the calcium influx inhibitor carboxyamido-triazole SO CLINICAL CANCER RESEARCH LA English DT Article ID SIGNAL-TRANSDUCTION; IV COLLAGENASE; CANCER; EXPRESSION; LINES; ANGIOGENESIS; L651582; CAI AB Local invasion and lymph node metastasis are correlated with a decreased overall survival in head and neck cancer patients and warrant new strategies to intervene in the metastatic cascade. One approach is to focus on the intracellular signaling pathways underlying the metastatic process. A common regulatory point in several signal transduction pathways is intracellular calcium homeostasis. We assessed the effect of a novel calcium influx inhibitor, carboxyamido-triazole (CAI), on the growth and invasive phenotype of cell lines derived from head and neck squamous cell carcinoma (HNSCC). CAI inhibited the growth of FaDu and EVSCC17M cells in a dose-dependent (IC50, 13-15 mu M) and reversible manner. CAI also caused a generalized attenuation of receptor-mediated calcium elevation to several calcium mobilization agonists, including epidermal growth factor and bradykinin. The effects of CAI on the invasive phenotype of HNSCC cell lines were assessed by a chemoinvasion assay. HNSCC cell lines exhibited a range of invasive potential as measured by the capacity of tumor cells to penetrate a reconstituted basement membrane of Matrigel. HNSCCs were classified as highly invasive (EVSCC14M and EVSCC17M) or weakly invasive (EVSCC18, EVSCC19M, UMSCC10A, and FaDu). Treatment of HNSCC cell lines with 10 mu M CAI for 24 h reduced invasion 2-14-fold in a dose-dependent manner. HNSCCs also exhibited different motilities as measured by a chemotaxis assay. EVSCC14M and EVSCC17M were highly motile, whereas EVSCC18, EVSCC19M, UMSCC10A, and FaDu were less motile, CAI reduced the migration of all cell lines. Conditioned medium from HNSCC cell lines was analyzed by zymography for production of M-r 72,000 type IV collagenase [matrix metalloproteinase (MMP)-2] and M-r 92,000 type IV collagenase (MMP-9). All HNSCC cell lines secreted MMP-2 and/or MMP-9 into conditioned medium. Treatment of cells with 10 mu M CAI for 24 h resulted in a reduction of both MMP-2 and MMP-9 production. The results demonstrate that CAI blocks cellular proliferation, migration, chemoinvasion, and MMP production by HNSCC in vitro and identify calcium-dependent signaling as a new target for inhibition of the malignant phenotype of HNSCC. C1 EASTERN VIRGINIA MED SCH,DEPT MICROBIOL & IMMUNOL,NORFOLK,VA 23507. EASTERN VIRGINIA MED SCH,DEPT PHARMACOL,NORFOLK,VA 23507. EASTERN VIRGINIA MED SCH,DEPT OTOLARYNGOL HEAD & NECK SURG,NORFOLK,VA 23507. EASTERN VIRGINIA MED SCH,HEAD & NECK TUMOR BIOL PROGRAM,NORFOLK,VA 23507. NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. NR 30 TC 32 Z9 32 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 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD NOV PY 1997 VL 3 IS 11 BP 1915 EP 1921 PG 7 WC Oncology SC Oncology GA YE927 UT WOS:A1997YE92700002 PM 9815580 ER PT J AU Panza, JA AF Panza, JA TI Endothelial dysfunction in essential hypertension SO CLINICAL CARDIOLOGY LA English DT Article DE acetylcholine; angiotensin-converting enzyme inhibitor; endothelial function; hypertension; nitric oxide ID DEPENDENT VASCULAR RELAXATION; NITRIC-OXIDE; CORONARY-ARTERIES; SUPEROXIDE-DISMUTASE; RELAXING FACTOR; SMOOTH-MUSCLE; L-ARGININE; VASODILATION; ACETYLCHOLINE; ATHEROSCLEROSIS AB In the last decade, significant advances have occurred in our understanding of the presence and nature of endothelial dysfunction in a number of cardiovascular conditions, including hypertension. Endothelium-derived nitric oxide (NO) is recognized as an important mediator of endothelium-dependent vascular relaxation, and a defect in the endothelium-derived NO system-possibly decreased synthesis and/or release of NO by endothelial cells-is now known to cause the abnormal response to acetylcholine in hypertensive vessels and to account at least in part for the increased vascular resistance observed in hypertension. Extensive research by our laboratory and others to determine the nature of the defect in the NO system has found that the defect is not related to decreased availability of L-arginine, the NO precursor, or to a defect at the muscarinic receptor level or a specific G protein-dependent intracellular signal-transduction pathway; nor is it related to extracellular inactivation of NO by superoxide anion. These findings have contributed to our understanding of endothelial dysfunction in essential hypertension and have pointed out distinctions between the mechanisms leading to this vascular abnormality in hypertensive and hypercholesterolemic patients. While the exact nature of the NO system defect in hypertension is still to be clarified, the vasoconstrictive and proatherogenic effects of endothelial dysfunction probably contribute to the cardiovascular complications associated with elevated blood pressure. Continued research targeted at the identification of the precise mechanism(s) responsible for endothelial dysfunction in hypertension may lead to the development of novel therapeutic strategies to reduce the vascular complications associated with the hypertensive process. C1 NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA. RP Panza, JA (reprint author), NHLBI, Cardiol Branch, NIH, Bldg 10,Room 7B15,10 Ctr Dr,MSC-1650, Bethesda, MD 20892 USA. NR 47 TC 62 Z9 63 U1 0 U2 1 PU CLINICAL CARDIOLOGY PUBL CO PI MAHWAH PA PO BOX 832, MAHWAH, NJ 07430-0832 USA SN 0160-9289 J9 CLIN CARDIOL JI Clin. Cardiol. PD NOV PY 1997 VL 20 IS 11 SU 2 BP 26 EP 33 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YM171 UT WOS:000071036900006 ER PT J AU Potapova, O Haghighi, A Bost, F McKay, R Dean, N Gjerset, R Mercola, D AF Potapova, O Haghighi, A Bost, F McKay, R Dean, N Gjerset, R Mercola, D TI Inhibition of the JNK pathway by antisense oligonucleotides sensitizes human tumor cells to cisplatin. SO CLINICAL CHEMISTRY LA English DT Meeting Abstract C1 NIA,NIH,BALTIMORE,MD 21224. SANDY KIMMEL CANC CTR,SAN DIEGO,CA. ISIS PHARMACEUT,CARLSBAD,CA 92008. UCSD,CTR MOL GENET,LA JOLLA,CA. NR 0 TC 0 Z9 0 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 NOV PY 1997 VL 43 IS 11 BP 53 EP 53 PG 1 WC Medical Laboratory Technology SC Medical Laboratory Technology GA YE072 UT WOS:A1997YE07200092 ER PT J AU Gottesman, II Moldin, SO AF Gottesman, II Moldin, SO TI Schizophrenia genetics at the millennium: cautious optimism SO CLINICAL GENETICS LA English DT Article; Proceedings Paper CT 3rd Symposium on From Phenotype to Gene in Common Disorders CY MAY 29-31, 1997 CL OSLO, NORWAY SP Sig K Thoresen Fdn, Norwegian Acad Sci & Lett DE epigenetic; linkage; multifactorial disease; QTL; susceptibility genes ID SUSCEPTIBILITY GENES; COMPLEX TRAITS; LINKAGE; GENOME; LOCUS; PERSPECTIVES; EPIDEMIOLOGY; INDICATORS; REGION; MODELS AB As the new millennium approaches, research into the genetic aspects of schizophrenia has already made an impressive start toward an integrated model which is discovering roles for genetic agents, environmental agents and experiences, and chance factors. The best model follows that proposed for understanding such complex diseases as coronary artery disease and diabetes. Genetic information has come from both genetic epidemiology and molecular genetics. Evidence for gene regions on 6p and 8p gives the strongest support for harboring schizophrenia susceptibility genes, based on international collaborative studies that "generally" replicate one another; evidence for regions on 3p, 5q, 9p, 20p, and 22q, while less compelling, will encourage focused work. Determining the steps between the regions and the phenotype will challenge the next generation of scientists. C1 Univ Virginia, Charlottesville, VA 22903 USA. NIMH, Bethesda, MD 20892 USA. RP Gottesman, II (reprint author), Univ Virginia, Gilmer Hall, Charlottesville, VA 22903 USA. RI G, I/D-8042-2011 NR 32 TC 17 Z9 17 U1 1 U2 2 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 NOV PY 1997 VL 52 IS 5 BP 404 EP 407 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA YX077 UT WOS:000072004100021 PM 9520134 ER PT J AU Ajmani, RS AF Ajmani, RS TI Hypertension and hemorheology SO CLINICAL HEMORHEOLOGY AND MICROCIRCULATION LA English DT Review ID RED-CELL DEFORMABILITY; LEFT-VENTRICULAR HYPERTROPHY; NA+-LI+ COUNTERTRANSPORT; WHOLE-BLOOD VISCOSITY; ARTERIAL-HYPERTENSION; ERYTHROCYTE DEFORMABILITY; CARDIAC-HYPERTROPHY; PLATELET-FUNCTION; RISK FACTOR; RHEOLOGICAL DETERMINANTS AB Hemorheological disturbances in hypertension are the outcome of changes in red cell characteristics, their interaction in the presence of fibrinogen, and the magnitude and distribution of flow forces. Hemorheological alteration coupled with changes in biochemical variables and vessel characteristics in hypertension may affect the hemodynamic profile, which could possibly contribute to the development of hemorrhagic disorders. The complex pathophysiology of hypertension also depends upon the life style, presence of other risk factors, emotional/psychological stress, age and the genetic constitution of an individual. This review article summarizes the hemorheological changes in hypertension and their probable role in the deterioration of blood flow. C1 NIA, NIH, Gerontol Res Ctr, Cellular & Mol Biol Lab, Baltimore, MD 21224 USA. RP Ajmani, RS (reprint author), NIA, NIH, Gerontol Res Ctr, Cellular & Mol Biol Lab, Room 4-B-12,4940 Eastern Ave, Baltimore, MD 21224 USA. EM ranjeet@helix.nih.gov NR 157 TC 37 Z9 41 U1 1 U2 4 PU IOS PRESS PI AMSTERDAM PA VAN DIEMENSTRAAT 94, 1013 CN AMSTERDAM, NETHERLANDS SN 1386-0291 J9 CLIN HEMORHEOL MICRO JI Clin. Hemorheol. Microcirc. PD NOV-DEC PY 1997 VL 17 IS 6 BP 397 EP 420 PG 24 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA ZB430 UT WOS:000072471700002 PM 9502525 ER PT J AU Abugo, OO Peddada, RR Kelly, JF Roth, GS Rifkind, JM AF Abugo, OO Peddada, RR Kelly, JF Roth, GS Rifkind, JM TI Effect of cholesterol content in diet on capillary flow of rat erythrocytes. Part I: Geometric and flow characteristics SO CLINICAL HEMORHEOLOGY AND MICROCIRCULATION LA English DT Article DE erythrocytes; deformability; high cholesterol diet; capillary flow; cell geometry; mechanical properties ID RED-CELL MEMBRANES; PERMEABILITY AB Four different groups of male Fisher rats were placed on one of the following diets for a period of one month: normal (control) diet, high cholesterol (HC) diet, high saturated fat (HF) diet and low fat (LF) diet. Subsequently, blood samples were drawn and washed in phosphate buffered saline (PBS), and the red cells were resuspended in the same buffer. These samples were introduced into a polycarbonate capillary flow system and their how characteristics observed. In addition, the mean cell volumes (MCV) in isotonic PBS and the maximum swollen cell volume (MCVmax) in hypotonic PBS were determined using a Coulter counter. From these, the mean surface area (MSA) and the excess surface area (ESA) were calculated. It was found that rats on a high cholesterol diet develop erythrocyte geometric characteristics which should contribute to improved capillary flow, namely, a decreased mean cell volume and an increased excess surface area. Nevertheless, in these rats a decreased capillary flow was observed as indicated by an increase in mean cell transit time, MCTT, and an appreciable drop in the number of cells per second passing through the capillary flow system. The flow and geometric properties of the high saturated fat and low fat fed rats did not differ significantly from those of the control group. C1 NIA, Cellular & Mol Biol Lab, Ctr Gerontol Res, Baltimore, MD 21224 USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. RP Rifkind, JM (reprint author), NIA, Cellular & Mol Biol Lab, Ctr Gerontol Res, 4940 Eastern Ave, Baltimore, MD 21224 USA. NR 19 TC 5 Z9 5 U1 0 U2 0 PU IOS PRESS PI AMSTERDAM PA VAN DIEMENSTRAAT 94, 1013 CN AMSTERDAM, NETHERLANDS SN 1386-0291 J9 CLIN HEMORHEOL MICRO JI Clin. Hemorheol. Microcirc. PD NOV-DEC PY 1997 VL 17 IS 6 BP 437 EP 443 PG 7 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA ZB430 UT WOS:000072471700005 PM 9502528 ER PT J AU Peddada, RR Abugo, OO Kelly, JF Roth, GS Rifkind, JM AF Peddada, RR Abugo, OO Kelly, JF Roth, GS Rifkind, JM TI Effect of cholesterol content in diet on capillary flow of rat erythrocytes. Part II: Mechanical properties SO CLINICAL HEMORHEOLOGY AND MICROCIRCULATION LA English DT Article DE erythrocyte; deformability; high cholesterol diet; capillary flow; apparent viscosity; Fahraeus effect; intrinsic viscosity; membrane shear modulus of elasticity ID BLOOD-CELLS AB Erythrocytes from male Fisher 344 rats on a high cholesterol diet (HC) exhibited a decreased ability to flow through capillaries when compared with those on a normal diet (control), a phenomenon which could not be explained by changes in geometric characteristics [1]. To explain these results, changes in capillary-dependent rheological characteristics and intrinsic mechanical properties of red blood cells (RBC) due to diet were calculated. The hematocrit deficit in the capillary with respect to the reservoir was greater in the high cholesterol diet fed rats than in the control ones. This was attributed to an overall decrease in red cell deformability which, in turn, was related to an increase in the membrane shear viscosity, the cytoplasmic viscosity, the membrane shear modulus of elasticity, and the membrane bending rigidity. By an independent calculation, we determined that the shear modulus of elasticity increased with a high cholesterol diet. The changes in both the capillary hematocrit deficit and the shear modulus of elasticity with a high cholesterol diet were found to be statistically significant (p less than or equal to 0.05). C1 NIA, Mol & Cellular Biol Lab, Ctr Gerontol Res, Baltimore, MD 21224 USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. RP Rifkind, JM (reprint author), NIA, Mol & Cellular Biol Lab, Ctr Gerontol Res, 4940 Eastern Ave, Baltimore, MD 21224 USA. NR 16 TC 7 Z9 7 U1 0 U2 1 PU IOS PRESS PI AMSTERDAM PA VAN DIEMENSTRAAT 94, 1013 CN AMSTERDAM, NETHERLANDS SN 1386-0291 J9 CLIN HEMORHEOL MICRO JI Clin. Hemorheol. Microcirc. PD NOV-DEC PY 1997 VL 17 IS 6 BP 445 EP 457 PG 13 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA ZB430 UT WOS:000072471700006 PM 9502529 ER PT J AU Arns, PA Adedoyin, A DiBisceglie, AM Waggoner, JG Hoofnagle, JH Wilkinson, GR Branch, RA AF Arns, PA Adedoyin, A DiBisceglie, AM Waggoner, JG Hoofnagle, JH Wilkinson, GR Branch, RA TI Mephenytoin disposition and serum bile acids as indices of hepatic function in chronic viral hepatitis SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Article ID CONTROLLED TRIAL; LIVER-DISEASE; METABOLISM; CIRRHOSIS; HYDROXYLATION; POLYMORPHISM; INTERFERON; POPULATION; CLEARANCE; HUMANS AB Background and objectives: The effect of chronic viral hepatitis on Liver function may vary from none to hepatic failure. Changes in function are usually the result of impaired hepatocyte function or altered vascular now and architecture. Conventional liver function tests usually cannot distinguish contributions from these mechanisms or indicate degree of hepatic metabolic dysfunction. An alternative approach is to measure the hepatic metabolism of a highly extracted compound whose oral clearance and systemic bioavailability are dependent on both hepatocyte function and degree of portosystemic shunt. Methods: The stereoselective metabolism of racemic mephenytoin (100 mg oral dose) was investigated in 35 patients with chronic viral hepatitis and compared with 153 healthy subjects. The mephenytoin R/S enantiomeric ratio and cumulative excretion of the 4'-hydroxymephenytoin metabolite in a 0- to 8-hour urine sample were used in addition to serum bile acid levels and pathologic examination of biopsy specimens to assess the severity of hepatic dysfunction and portosystemic shunting. Results: The patients as a group excreted less 4'-hydroxymephenytoin and had a smaller R/S enantiomeric ratio of mephenytoin. The two measures were discriminatory between the patient groups classified by either serum cholylglycine level or pathologic examination of biopsy specimens. Combination of the two measures of mephenytoin metabolism allowed the patients to be classified into three groups: normal hepatocyte function without portosystemic shunt, normal hepatocyte function with portosystemic shunt, and low hepatocyte function with or without portosystemic shunt. Conclusion: This study has shown the potential usefulness of mephenytoin metabolism as a sensitive indicator of hepatic pathologic condition with an ability to discriminate between contributory alternative mechanisms. C1 UNIV PITTSBURGH,MED CTR,CTR CLIN PHARMACOL,PITTSBURGH,PA 15213. VANDERBILT UNIV,SCH MED,DEPT PHARMACOL,NASHVILLE,TN 37212. UNIV PITTSBURGH,DEPT PHARMACEUT SCI,PITTSBURGH,PA 15213. NIDDKD,LIVER DIS SECT,NIH,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM31304] NR 24 TC 15 Z9 16 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 NOV PY 1997 VL 62 IS 5 BP 527 EP 537 DI 10.1016/S0009-9236(97)90048-5 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YH965 UT WOS:A1997YH96500007 PM 9390109 ER PT J AU Post, RM Denicoff, KD Leverich, GS Frye, MA AF Post, RM Denicoff, KD Leverich, GS Frye, MA TI Drug-induced switching in bipolar disorder - Epidemiology and therapeutic implications SO CNS DRUGS LA English DT Article ID TRANSCRANIAL MAGNETIC STIMULATION; ANTIDEPRESSANTS CAUSE MANIA; CYCLING AFFECTIVE-DISORDER; HIGH-DOSE THYROXINE; AFFECTIVE-ILLNESS; TRICYCLIC ANTIDEPRESSANTS; RESISTANT DEPRESSION; CONTINGENT TOLERANCE; LITHIUM-CARBONATE; CARBAMAZEPINE AB The use of antidepressants in patients with unipolar depression is associated with a negligible rate of switching into mania. In contrast, in patients with bipolar disorder, even those treated concomitantly with a mood stabiliser, such switching appears to represent a greater problem. Preliminary evidence from some controlled studies suggests that antidepressants may double the incidence of a switch, from some 25% in patients receiving placebo to 50% in these receiving tricyclic antidepressants. Other series in patients with rapid cycling bipolar disorder suggest an even higher switch rate; however, only about one-third of the observed switches are likely to be attributable to the antidepressant (i.e. unrelated to the natural course of illness). In addition to these phenomena, cycle acceleration has been observed consistently in a subgroup of patients with bipolar disorder who are receiving maintenance treatment with tricyclic antidepressants, and this has been verified by periods of discontinuation and reintroduction of the drug. Cycle acceleration appears to occur in approximately one-fifth of patients with refractory bipolar illness. Given these potential liabilities, it is unclear as to what is the most judicious treatment algorithm to follow for the bipolar patient with depression that is breaking through treatment with a mood stabiliser. In the absence of adequate studies, our own algorithm is to use antidepressants judiciously in nonrapid cycling patients, but to relatively avoid them in rapid and ultra-rapid cyclers. Instead, we prefer to use adjunctively a second mood stabiliser prior to the introduction of a unimodal antidepressant. Systematic controlled clinical trials are eagerly awaited, comparing not only the acute antidepressant efficacy of the newer antidepressants, but their liability in causing a switch or cycle induction when introduced into long term prophylaxis. With the advent of a series of new potential mood stabilising agents, direct comparison of the addition of a second mood stabiliser with that of a unimodal antidepressant will help establish the comparative risk:benefit ratios of these differential approaches. It is also hoped that clinical and biological markers of differential antidepressant responsivity will ultimately be identified and help to refine the process of choosing the best antidepressant modality for depression breaking through prophylaxis with mood stabilisers in patients with bipolar disorder. RP Post, RM (reprint author), NIMH,BIOL PSYCHIAT BRANCH,NIH,BLDG 10,ROOM 3N212,10 CTR DR,MSC 1272,BETHESDA,MD 20892, USA. NR 80 TC 34 Z9 34 U1 1 U2 5 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PD NOV PY 1997 VL 8 IS 5 BP 352 EP 365 DI 10.2165/00023210-199708050-00002 PG 14 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA YF895 UT WOS:A1997YF89500002 ER PT J AU Thomas, DG Mark, SD AF Thomas, DG Mark, SD TI Max_r: an optimal method for the selection of subsets of foods for the measurement of specific nutrient exposures SO COMPUTER METHODS AND PROGRAMS IN BIOMEDICINE LA English DT Article DE diet; nutrition; optimal food selection; questionnaires ID DIET AB Max_r, a new method of food subset selection for the measurement of specific nutrient exposures, is programmed. Frequently, epidemiologic questionnaires are designed to measure several individual level exposures, including exposure to one or more nutrients. Although most nutrients are contained in a large number of foods, constraints on questionnaire size allow inclusion of only a subset of these. When nutrient exposure as measured in a subset of foods will be used to estimate the effect of the nutrient on disease risk with a logistic regression model, max_r is the optimal method of choosing the subset. Various aspects of the program are illustrated with a numerical example measuring dietary protein intake. The executable version of this Fortran program for IBM compatible PCs requires 3Mb of memory. It is available (along with complete documentation, test data and output) via e-mail from thomasd@epndce.nci.nih.gov or upon submission of a diskette formatted for MS-DOS. (C) 1997 Elsevier Science Ireland Ltd. RP Thomas, DG (reprint author), NCI,EPN 403,BETHESDA,MD 20892, USA. NR 5 TC 6 Z9 6 U1 1 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0169-2607 J9 COMPUT METH PROG BIO JI Comput. Meth. Programs Biomed. PD NOV PY 1997 VL 54 IS 3 BP 151 EP 156 DI 10.1016/S0169-2607(97)00023-0 PG 6 WC Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Engineering, Biomedical; Medical Informatics SC Computer Science; Engineering; Medical Informatics GA YH139 UT WOS:A1997YH13900002 PM 9421661 ER PT J AU Newlin, DB AF Newlin, DB TI Heroin addiction: Theory, research, and treatment, vol 2, The addict, the treatment process, and social control, vol 3, Treatment advances and AIDS - Platt,JJ SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review RP Newlin, DB (reprint author), NIDA,ADDICT RES CTR,CLIN NEUROGENET SECT,NIH,POB 5180,BALTIMORE,MD 21224, USA. NR 4 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 1997 VL 42 IS 11 BP 988 EP 990 PG 3 WC Psychology, Multidisciplinary SC Psychology GA YD708 UT WOS:A1997YD70800009 ER PT J AU Muntaner, C AF Muntaner, C TI Untitled SO CONTEMPORARY SOCIOLOGY-A JOURNAL OF REVIEWS LA English DT Letter C1 NIMH,BETHESDA,MD 20892. RP Muntaner, C (reprint author), W VIRGINIA UNIV,MORGANTOWN,WV 26506, USA. RI Muntaner, C/A-5043-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOCIOLOGICAL ASSOC PI WASHINGTON PA 1722 N ST NW, WASHINGTON, DC 20036-2981 SN 0094-3061 J9 CONTEMP SOCIOL JI Contemp. Sociol.-J. Rev. PD NOV PY 1997 VL 26 IS 6 BP 788 EP 788 PG 1 WC Sociology SC Sociology GA YH966 UT WOS:A1997YH96600087 ER PT J AU Whitcomb, RF French, FE Tully, JG Carle, P Henegar, R Hackett, KJ Gasparich, GE Williamson, DL AF Whitcomb, RF French, FE Tully, JG Carle, P Henegar, R Hackett, KJ Gasparich, GE Williamson, DL TI Spiroplasma species, groups, and subgroups from north American Tabanidae SO CURRENT MICROBIOLOGY LA English DT Article ID CLASS MOLLICUTES; SP-NOV; LAMPYRIDAE; COLEOPTERA; DIPTERA; CLASSIFICATION; DEFORMATION AB Twenty-one triply cloned spiroplasma strains from the United States east of the Rocky Mountains, all isolated from tabanid (Diptera:Tabanidae) flies or serologically related to strains from tabanids, were compared reciprocally by spiroplasma deformation (DF) and metabolism inhibition (MI) serological. tests. Many of the strains were also tested against 28 antisera representing known spiroplasma groups, subgroups, and putative groups isolated from nontabanid hosts. Relationships among strains were indicated by reciprocal cross-reactivity in both DF and MI tests. The strains were found to represent 11 recognized spiroplasma groups or subgroups. On the basis of serological, biochemical, and genomic data, strain BARC 1901 from Tabanus lineola appeared to represent a previously unrecognized candidate group. Strain BARC 2649, also from T. lineola, also appeared to represent a new group, but its morphology, arginine utilization, and some one-way serological crossing patterns suggested that it may be distantly related to group VIII spiroplasmas. Morphological, serological, and genomic data were used to place tabanid spiroplasma strains into three informal clusters. These are (i) groups IV (strain B31) and XXXI (strain HYOS-1); (ii) the three existing subgroups and a new candidate subgroup of group Vm represented by strain BARC 1357 plus ungrouped strain BARC 2649; and (iii) 14 strains, including EC-1 and TATS-1 (group XIV); strains TN-1 and TAAS-2 (group XVIII); strains TG-1, TASS-1, and BARC 4689 (group XXIII), strains TALS-2 (group XXVII), strain TABS-2 (group XXXII), and strains TAUS-1 and TABS-1 (group XXXIII) and ungrouped but closely related strains BARC 1901, BARC 2264 and BARC 2555. Analysis of tabanids from other geographic regions probably will substantially increase the number of known spiroplasma groups from this insect family. C1 GEORGIA SO UNIV,DEPT BIOL,STATESBORO,GA 30460. NIAID,FREDERICK CANC RES FACIL,MYCOPLASMA SERV,MOL MICROBIOL LAB,FREDERICK,MD 21702. INST NATL RECH AGRON,BIOL CELLULAIRE & MOL LAB,F-33883 VILLENAVE DORNON,FRANCE. USDA,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705. SUNY STONY BROOK,DEPT ANAT SCI,STONY BROOK,NY 11794. RP Whitcomb, RF (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,VEGETABLE LAB,HH3,RANGE 2,BLDG 010,BELTSVILLE,MD 20705, USA. NR 44 TC 13 Z9 15 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0343-8651 J9 CURR MICROBIOL JI Curr. Microbiol. PD NOV PY 1997 VL 35 IS 5 BP 287 EP 293 DI 10.1007/s002849900256 PG 7 WC Microbiology SC Microbiology GA YC102 UT WOS:A1997YC10200008 ER PT J AU Knezevic, V De Santo, R Schughart, K Huffstadt, U Chiang, C Mahon, KA Mackem, S AF Knezevic, V De Santo, R Schughart, K Huffstadt, U Chiang, C Mahon, KA Mackem, S TI Hoxd-12 differentially affects preaxial and postaxial chondrogenic branches in the limb and regulates Sonic hedgehog in a positive feedback loop SO DEVELOPMENT LA English DT Article DE Hoxd-12; limb development; Sonic hedgehog; luxate mutants; luxoid mutants; extra-toes; chondrogenesis ID GENE-EXPRESSION; POLARIZING ACTIVITY; HOMEOTIC TRANSFORMATIONS; SEQUENCE RECOGNITION; ECTOPIC EXPRESSION; PATTERN-FORMATION; AXIAL SKELETON; RETINOIC ACID; MUTANT MICE; HOX GENES AB `Several 5' members of the Herd cluster are expressed in nested posterior-distal domains of the limb bud suggesting a role in regulating anteroposterior pattern of skeletal elements, While loss-of-function mutants have demonstrated a regulatory role for these genes in the developing limb, extensive functional overlaps between various different Hox genes has hampered elucidation of the roles played by individual members, In particular, the function of Hoxd-12 in the limb remains obscure, Using a gain-of-function approach, we find that Hoxd-12 misexpression in transgenic mice produces apparent transformations of anterior digits to posterior morphology and digit duplications, while associated tibial hemimelia and other changes indicate that formation/growth of certain skeletal elements is selectively inhibited, If the digital arch represents an anterior bending of the main limb axis, then the results are all reconcilable with a model in which Hoxd-12 promotes formation of postaxial chondrogenic condensations branching from this main axis (including the anteriormost digit) and selectively antagonizes formation of 'true' preaxial condensations that branch from this main axis (such as the tibia), Hoxd-12 misexpression can also induce ectopic Sonic hedgehog (Shh) expression, resulting in mirror-image polydactyly in the limb, Misexpression of Hoxd-12 in other lateral plate derivatives (sternum, pelvis) likewise phenocopies several luxoid/luxate class mouse mutants that all share ectopic Shh signalling. This suggests that feedback activation of Shh expression may be a major function of Hoxd-12, Hoxd-12 can bind to and transactivate the Shh promoter in vitro, Furthermore, expression of either exogenous Hoxd-11 or Hoxd-12 in cultured limb bud cells, together with FGF, induces expression of the endogenous Shh gene, Together these results suggest that certain 5' Herd genes directly amplify the posterior Shh polarizing signal in a reinforcing positive feedback loop during limb bud outgrowth. C1 NCI, Pathol Lab, Bethesda, MD 20892 USA. NICHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD 20892 USA. GSF, Natl Res Ctr Environm & Hlth, Inst Mammalian Genet, D-85764 Neuherberg, Germany. RP Mackem, S (reprint author), NCI, Pathol Lab, Bethesda, MD 20892 USA. NR 62 TC 104 Z9 105 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD NOV PY 1997 VL 124 IS 22 BP 4523 EP 4536 PG 14 WC Developmental Biology SC Developmental Biology GA YM889 UT WOS:000071111800011 PM 9409670 ER PT J AU Dix, DJ Allen, JW Collins, BW Poorman-Allen, P Mori, C Blizard, DR Brown, PR Goulding, EH Strong, BD Eddy, EM AF Dix, DJ Allen, JW Collins, BW Poorman-Allen, P Mori, C Blizard, DR Brown, PR Goulding, EH Strong, BD Eddy, EM TI HSP70-2 is required for desynapsis of synaptonemal complexes during meiotic prophase in juvenile and adult mouse spermatocytes SO DEVELOPMENT LA English DT Article DE heat shock protein; HSP70; meiosis; spermatogenesis; synaptonemal complex; mouse ID DEVELOPMENTALLY-REGULATED EXPRESSION; RAD51 RECOMBINATION PROTEIN; HEAT-SHOCK PROTEINS; DNA MISMATCH REPAIR; SPERMATOGENIC CELLS; CDC2 PROTEIN; GERM-CELL; NUCLEOTIDE-SEQUENCE; FIBROUS SHEATH; GENE FAMILY AB Spermatogenic cells synthesize a unique 70-kDa heat shock protein (HSP70-2) during prophase of meiosis I, and targeted disruption of the Hsp 70-2 gene has shown that this protein is required for spermatogenic cell differentiation in adult mice, HSP70-2 is associated with synaptonemal complexes formed between paired homologous chromosomes during meiotic prephase, The present study focuses on the nearly synchronous first wave of spermatogenesis in 12- to 28-day old juvenile mice to determine more precisely when HSP70-2 is required and what meiotic processes are affected by its absence. Spermatogenesis in homozygous mutant mice (Hsp70-2(-/-)) proceeded normally until day 15 when increasing numbers of pachytene spermatocytes became apoptotic and differentiation of cells beyond the pachytene stage began to falter, Synaptonemal complexes assembled in Hsp 70-2(-/-) mice and spermatocytes developed through the final pachytene substage, However, synaptonemal complexes failed to desynapse and normal diplotene spermatocytes were not observed, Metaphase spermatocytes were not seen in tissue sections from testes of Hsp70-2(-/-) mice, and expression of mRNAs and antigens characteristic of late pachytene spermatocytes (e.g., cyclin Al) and development of spermatids did not occur. Thus, HSP70-2 is required for synaptonemal complex desynapsis, and its absence severely impairs the transition of spermatogenic cells through the late meiotic stages and results in apoptosis beginning with the first wave of germ cell development in juvenile mice. C1 US EPA, Reprod Toxicol Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA. US EPA, Div Environm Carcinogenesis, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA. Glaxo Wellcome Inc, Div Med Safety Evaluat, Res Triangle Pk, NC 27709 USA. Kyoto Univ, Fac Med, Dept Anat & Dev Biol, Kyoto 60601, Japan. NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Dix, DJ (reprint author), US EPA, Reprod Toxicol Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA. NR 54 TC 161 Z9 170 U1 0 U2 6 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD NOV PY 1997 VL 124 IS 22 BP 4595 EP 4603 PG 9 WC Developmental Biology SC Developmental Biology GA YM889 UT WOS:000071111800017 PM 9409676 ER PT J AU Ershler, WB Harman, SM Keller, ET AF Ershler, WB Harman, SM Keller, ET TI Immunologic aspects of osteoporosis SO DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY LA English DT Review DE osteoporosis; aging; interleukin-6; osteoclast; estrogen ID GROWTH-HORMONE GH; OSTEOBLAST-LIKE CELLS; SOLUBLE INTERLEUKIN-6 RECEPTOR; ESTROGEN REPLACEMENT THERAPY; BONE-MINERAL DENSITY; FACTOR-I LEVELS; SPINAL OSTEOPOROSIS; PARATHYROID-HORMONE; BIOAVAILABLE TESTOSTERONE; ELDERLY MEN AB Osteoporosis is a major cause of morbidity in older people, There are a large number of risk factors for the development of osteoporosis, However, these risk factors eventually must mediate their effects through modulation of bone remodeling, A variety of compounds including hormones and mutrients modulate bone remodeling, In addition to these well-characterized substances, the immune system plays a role in bone remodeling through pro-inflammatory cytokines, Specifically, interleukin-1 (IL-1), IL-11, interferon-g are known to influence osteoclasts and osteoblasts. Recently, the cytokine IL-6 has joined ranks with these cytokines as a bone reactive agent, IL-6 has been shown to increase with age and menopause, Additionally, murine models suggest that IL-6 plays a central role in bone resorption, Finally, in vitro studies demonstrate that IL-6 induces osteoclast activity, In this review, we will discuss the pathogenesis of osteoporosis in the context of aging and IL-6. (C) 1997 Elsevier Science Ltd. All rights reserved. C1 NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. Eastern Virginia Med Sch, Glennan Ctr Geriatr & Gerontol, Norfolk, VA 23501 USA. RP Ershler, WB (reprint author), NIA, Gerontol Res Ctr, NIH, Box 9,4940 Eastern Ave, Baltimore, MD 21224 USA. RI Keller, Evan/M-1446-2016 OI Keller, Evan/0000-0002-7592-7535 FU NIA NIH HHS [AG11970] NR 125 TC 45 Z9 47 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0145-305X J9 DEV COMP IMMUNOL JI Dev. Comp. Immunol. PD NOV-DEC PY 1997 VL 21 IS 6 BP 487 EP 499 DI 10.1016/S0145-305X(97)00029-3 PG 13 WC Immunology; Zoology SC Immunology; Zoology GA YQ833 UT WOS:000071427700005 PM 9463782 ER PT J AU Silver, K Walston, J Chung, WK Yao, F Parikh, VV Andersen, R Cheskin, LJ Elahi, D Muller, D Leibel, RL Shuldiner, AR AF Silver, K Walston, J Chung, WK Yao, F Parikh, VV Andersen, R Cheskin, LJ Elahi, D Muller, D Leibel, RL Shuldiner, AR TI The Gln(223)Arg and Lys(656)Asn polymorphisms in the human leptin receptor do not associate with traits related to obesity SO DIABETES LA English DT Article ID MUTATION; GENE; MICE C1 JOHNS HOPKINS UNIV,SCH MED,DIV ENDOCRINOL & METAB,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,DIV GERIATR MED & GERONTOL,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,DIV GASTROENTEROL,BALTIMORE,MD. NIA,LAB CLIN PHYSIOL,NIH,BALTIMORE,MD 21224. ROCKEFELLER UNIV,HUMAN BEHAV & METAB LAB,NEW YORK,NY 10021. FU NCRR NIH HHS [3M01-RR02719-11S3]; NIDDK NIH HHS [1F32DK09340-01, F32DK09241-01] NR 10 TC 39 Z9 42 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD NOV PY 1997 VL 46 IS 11 BP 1898 EP 1900 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YC480 UT WOS:A1997YC48000033 PM 9356043 ER PT J AU Charles, MA Eschwege, E Bennett, PH AF Charles, MA Eschwege, E Bennett, PH TI Non-insulin-dependent diabetes mellitus in populations at risk: the Pima Indians SO DIABETES & METABOLISM LA French DT Article; Proceedings Paper CT Symposium on Non-Insulin-Dependent Diabetes Mellitus in 1997 - Causes and Perspectives CY JAN 17, 1997 CL PARIS, FRANCE DE diabetes; Pima Indians; obesity ID CARDIOVASCULAR-DISEASE; RESISTANCE SYNDROME; OBESITY; NIDDM; PREVALENCE; PLASMA; WOMEN AB Pima Indians have the highest prevalence of non-insulin-dependent diabetes mellitus reported in the world. reaching 70% in the 55-64 year age-group. Although obesity is also quite prevalent in this population, it cannot in itself be held responsible for the high frequency of the disease. Profound changes in the way of life of the Pima Indians during the past century have been associated with the emergence of diabetes. A genetic susceptibility in this population probably explains why diabetes became an ''epidemic''. Compared to Caucasians with similar degrees of obesity and glucose tolerance, Pima Indians are insulin-resistant. This characteristic, which is a strong predictor of diabetes, seems to be genetically determined in this population, and an active search for the gene(s) involved has started. Surprisingly, for an insulin-resistant population, cardiovascular mortality is low in Pima Indians. An understanding of the similarities and differences between diabetic Caucasians and Pima Indians is one means of advancing our knowledge of non-insulin-dependent diabetes mellitus and insulin resistance. C1 NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,PHOENIX,AZ. RP Charles, MA (reprint author), INSERM,U21,16 AV PAUL VAILLANT COUTURIER,F-94807 VILLEJUIF,FRANCE. NR 29 TC 2 Z9 2 U1 0 U2 3 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0338-1684 J9 DIABETES METAB JI Diabetes Metab. PD NOV PY 1997 VL 23 SU 4 BP 6 EP 9 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YH508 UT WOS:A1997YH50800002 PM 9463026 ER PT J AU Lee, SH Wang, W Yajima, S Jose, PA Mouradian, MM AF Lee, SH Wang, W Yajima, S Jose, PA Mouradian, MM TI Tissue-specific promoter usage in the D-1A dopamine receptor gene in brain and kidney SO DNA AND CELL BIOLOGY LA English DT Article ID PROXIMAL CONVOLUTED TUBULE; K+-ATPASE ACTIVITY; MOLECULAR-CLONING; TRANSCRIPTIONAL ACTIVATORS; ADENYLATE-CYCLASE; EXPRESSION; D1; RAT; REGION; DNA AB The D-1A dopamine receptor gene consists of a short, noncoding exon 1 separated from a longer coding exon 2 by a small intron, Recently, we found that in addition to its original TATA-less promoter located upstream of exon 1, the human D-1A dopamine receptor gene is transcribed in neural cells from a second strong promoter located In its intron, In the present study, we addressed the possibility that these two promoters are used for the tissue-specific regulation of the D-1A gene in neuronal and renal cells, Reverse transcription polymerase chain reaction revealed that D-1A transcripts in the kidneys of humans and rats lack exon 1, Transient transfection analysis of these two promoters in D-1A-expressing cells indicated that the upstream promoter has no detectable activity in the opossum kidney (OK) cell line, in contrast to its strong activity in two neuronal cell lines, SK-N-MC and NS20Y, On the other hand, the D-1A intron promoter showed transcriptional activity both in OK cells and in neuronal cells, The activator sequence AR1, which enhances transcription from the upstream promoter in SK-N-MC and NS20Y cells, could not activate this promoter in OK cells, In addition, no protein binding to AR1 could be detected by gel mobility shift assay using nuclear extracts from either OK cells or from rat kidney tissue, These findings indicate that the differential expression of short and long D-1A transcripts is due, at least in part, to the tissue-specific expression of the activator protein binding to AR1 driving transcription from the upstream promoter, Absence of this activator protein accounts for the nonfunctional D-1A upstream promoter in the kidney. C1 NINCDS,ETB,GENET PHARMACOL UNIT,NIH,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20007. OI Mouradian, M. Maral/0000-0002-9937-412X NR 45 TC 13 Z9 15 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD NOV PY 1997 VL 16 IS 11 BP 1267 EP 1275 DI 10.1089/dna.1997.16.1267 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA YK481 UT WOS:A1997YK48100002 PM 9406999 ER PT J AU Neamati, N Sunder, S Pommier, Y AF Neamati, N Sunder, S Pommier, Y TI Design and discovery of HIV-1 integrase inhibitors SO DRUG DISCOVERY TODAY LA English DT Review ID VIRUS TYPE-1 INTEGRASE; IN-VITRO INTEGRATION; CATALYTIC DOMAIN; MONOCLONAL-ANTIBODIES; PROTEIN; DNA; ANALOGS AB The rapid emergence of human immunodeficiency virus (HIV) strains resistant to available drugs implies that effective treatment modalities will require the use of a combination of drugs targeting different sites of the HIV life cycle. Integrase is emerging as a novel target for intervention by chemotherapeutics. As part of a program to develop novel antiviral agents, we have studied a large number of compounds with activity against HIV-1 replication in the National Cancer Institute (NCI) Antiviral Drug Program. In this review, we present a comprehensive review of all such inhibitors reported to date. RP Neamati, N (reprint author), NATL CANC INST,DIV BASIC SCI,MOL PHARMACOL LAB,BLDG 37,ROOM 5C25,BETHESDA,MD 20892, USA. NR 57 TC 61 Z9 61 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 1359-6446 J9 DRUG DISCOV TODAY JI Drug Discov. Today PD NOV PY 1997 VL 2 IS 11 BP 487 EP 498 DI 10.1016/S1359-6446(97)01105-7 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YD837 UT WOS:A1997YD83700007 ER PT J AU Nunez, PL Srinivasan, R Westdorp, AF Wijesinghe, RS Tucker, DM Silberstein, RB Cadusch, PJ AF Nunez, PL Srinivasan, R Westdorp, AF Wijesinghe, RS Tucker, DM Silberstein, RB Cadusch, PJ TI EEG coherency .1. Statistics, reference electrode, volume conduction, Laplacians, cortical imaging, and interpretation at multiple scales SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE coherence; spline-Laplacian; cortical image ID ARTIFACTUALLY HIGH COHERENCES; CURRENT-DENSITY; SPLINE-LAPLACIAN; SURFACE LAPLACIANS; MODEL; RESOLUTION; COMPUTATION; PROPAGATION; DEPENDENCE; DERIVATION AB Several methodological issues which impact experimental design and physiological interpretations in EEG coherence studies are considered, including reference electrode and volume conduction contributions to erroneous coherence estimates. A new measure, 'reduced coherency', is introduced as the difference between measured coherency and the coherency expected from uncorrelated neocortical sources, based on simulations and analytic-statistical studies with a volume conductor model. The concept of reduced coherency is shown to be in semi-quantitative agreement with experimental EEG data. The impact of volume conduction on statistical confidence intervals for coherence estimates is discussed. Conventional reference, average reference, bipolar, Laplacian, and cortical image coherencies are shown to be partly independent measures of neocortical dynamic function at different spatial scales, due to each method's unique spatial filtering of intracranial source activity. (C) 1997 Elsevier Science Ireland Ltd. C1 ELECT GEODES INC,EUGENE,OR. UNIV OREGON,DEPT PSYCHOL,EUGENE,OR 97403. NIAAA,NIH,WASHINGTON,DC. BRAIN SCI INST,MELBOURNE,VIC,AUSTRALIA. SWINBURNE UNIV TECHNOL,SCH BIOPHYS & ELECT ENGN,MELBOURNE,VIC,AUSTRALIA. LOUISIANA STATE UNIV,SCH MED,DEPT NEUROL,NEW ORLEANS,LA 70112. RP Nunez, PL (reprint author), TULANE UNIV,DEPT BIOMED ENGN,BRAIN PHYS GRP,NEW ORLEANS,LA 70118, USA. NR 71 TC 641 Z9 648 U1 3 U2 45 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD NOV PY 1997 VL 103 IS 5 BP 499 EP 515 DI 10.1016/S0013-4694(97)00066-7 PG 17 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA YK624 UT WOS:A1997YK62400001 PM 9402881 ER PT J AU Issaq, HJ AF Issaq, HJ TI Capillary electrophoresis of natural products SO ELECTROPHORESIS LA English DT Review DE natural products; capillary electrophoresis; micellar electrokinetic capillary chromatography; Chinese herbal preparations; alkaloids; toxins; illicit drugs ID MICELLAR ELECTROKINETIC CHROMATOGRAPHY; INDUCED FLUORESCENCE DETECTION; FLAVONOID-O-GLYCOSIDES; ZONE ELECTROPHORESIS; MASS-SPECTROMETRY; BORATE COMPLEXATION; TAXUS-BREVIFOLIA; SEPARATION; ALKALOIDS; TAXOL AB Capillary-electrophoresis (CE) and micellar electrokinetic chromatography were used for the separation of widely different compounds from natural materials including antibiotics, humic substances, flavonoids isoflavonoids, illicit drugs, coumarins, alkaloids, steroids. Chinese herbal preparations, nicotine, caffeine, amphetamines, toxins such as aflatoxins B-1, B-2, G(1), G(2), mycotoxins, heptapeptide toxins and others, ephedrine compounds, mineral elements, and natural compounds in biological samples. A discussion of sample extraction and clean-up and the advantages of using CE is also presented. C1 NCI, Chem Synth & Anal Lab, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. RP Issaq, HJ (reprint author), NCI, Chem Synth & Anal Lab, SAIC Frederick, Frederick Canc Res & Dev Ctr, POB B, Frederick, MD 21702 USA. NR 72 TC 61 Z9 65 U1 1 U2 10 PU WILEY-V C H VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD NOV PY 1997 VL 18 IS 12-13 BP 2438 EP 2452 DI 10.1002/elps.1150181234 PG 15 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA YN538 UT WOS:000071178600033 PM 9456058 ER PT J AU Couse, JF Lindzey, J Grandien, K Gustafsson, JA Korach, KS AF Couse, JF Lindzey, J Grandien, K Gustafsson, JA Korach, KS TI Tissue distribution and quantitative analysis of estrogen receptor-alpha (ER alpha) and estrogen receptor-beta (ER beta) messenger ribonucleic acid in the wild-type and ER alpha-knockout mouse SO ENDOCRINOLOGY LA English DT Article ID TARGETED DISRUPTION; TRANSGENIC MICE; GENE; TRANSCRIPTION; MECHANISMS; PHENOTYPES; BINDING AB Until recently, only a single type of estrogen receptor (ER) was thought to exist and mediate the genomic effects of the hormone 17 beta-estradiol in mammalian tissues. However, the cloning of a gene encoding a second type of ER, termed ERP, from the mouse, rat, and human has prompted a reevaluation of the estrogen signaling system. Based on in vitro studies, the ERP protein binds estradiol with an affinity similar to that of the classical ER (now referred to as ER alpha) and is able to mediate the effects of estradiol in transfected mammalian cell lines. Essential to further investigations of the possible physiological roles of ERP, and its possible interactions with ER alpha, are data on the tissue distribution of the two ER types. Herein, we have described the optimization and use of an RNase protection assay able to detect and distinguish messenger RNA (mRNA) transcripts from both the ER alpha and ER beta genes in the mouse. Because this assay is directly quantitative, a comparison of the levels of expression within various tissues was possible. In addition, the effect of disruption of the ER alpha gene on the expression of the ERP gene was also investigated using the ER alpha-knockout (ERKO) mouse. Transcripts encoding ER alpha were detected in all the wild-type tissues assayed from both sexes. In the female reproductive tract, the highest expression of ER beta mRNA was observed in the ovary and showed great variation among individual animals; detectable levels were observed in the uterus and oviduct, whereas mammary tissue was negative. In the male reproductive tract, significant expression of ERP was seen in the prostate and epididymis, whereas the testes were negative. In other tissues of both sexes, the hypothalamus and lung were clearly positive for both ER alpha and ER beta mRNA. The ERKO mice demonstrated slightly reduced levels of ER beta mRNA in the ovary, prostate, and epididymis. These data, in combination with the several described phenotypes in both sexes of the ERKO mouse, suggest that the biological functions of the ER beta protein may be dependent on the presence of ER alpha in certain cell types and tissues. Further characterization of the physiological phenotypes in the ERKO mice may elucidate possible ER beta specific actions. C1 NIEHS,RECEPTOR BIOL SECT,REPROD & DEV TOXICOL LAB,NIH,RES TRIANGLE PK,NC 27709. KAROLINSKA INST,NOVUM,DEPT MED NUTR,S-14186 HUDDINGE,SWEDEN. OI Korach, Kenneth/0000-0002-7765-418X NR 31 TC 677 Z9 693 U1 2 U2 17 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1997 VL 138 IS 11 BP 4613 EP 4621 DI 10.1210/en.138.11.4613 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YB479 UT WOS:A1997YB47900014 PM 9348186 ER PT J AU Smith, MA Kim, SY VanOers, HJJ Levine, S AF Smith, MA Kim, SY VanOers, HJJ Levine, S TI Maternal deprivation and stress induce immediate early genes in the infant rat brain SO ENDOCRINOLOGY LA English DT Article ID PITUITARY-ADRENAL AXIS; HYPOTHALAMIC PARAVENTRICULAR NUCLEUS; CORTICOTROPIN-RELEASING HORMONE; RECEPTOR MESSENGER-RNA; NEONATAL RAT; EXPRESSION; GLUCOCORTICOIDS; ACTIVATION; SYSTEM; BASAL AB The hypothalamic-pituitary-adrenal (HPA) axis is normally quiescent during the stress-hyporesponsive period (SHRP) from day 4-14 in infant rats. However, maternal deprivation (DEP) can disinhibit the HPA axis, thus enabling neonatal rats to respond to mild stressors. In an effort to understand how DEP may alter HPA axis sensitivity, we used in situ hybridization to measure changes in the expression of stress-responsive genes in the brains of neonatal rats. Despite the minimal HPA axis response in nondeprived rats during the SHRP (postnatal day 12), the mild stress of a saline injection significantly increased messenger RNA levels of two immediate-early genes (IEGs), c-fos and NGFI-B, in the hypothalamic paraventricular nucleus (PVN) and in the cerebral cortex. Following 24 h of DEP, the induction of IEGs in response to stress was greatly potentiated in the PVN of P12 neonates. In contrast, DEP attenuated the effects of stress on IEG induction in rats that had matured beyond the SHRP (P20). Surprisingly, DEP decreased basal levels of CRH messenger RNA in the PVN at P12 and P20. Thus the SHRP most accurately refers to HPA axis insensitivity to stress because the brain itself readily responds to stress as evidenced by the induction of IEGs. C1 NIMH, BIOL PSYCHIAT BRANCH, BETHESDA, MD 20892 USA. UNIV DELAWARE, DEPT PSYCHOL, NEWARK, DE 19716 USA. NR 28 TC 108 Z9 110 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1997 VL 138 IS 11 BP 4622 EP 4628 DI 10.1210/en.138.11.4622 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YB479 UT WOS:A1997YB47900015 PM 9348187 ER PT J AU Farsetti, A Lazar, J Phyillaier, M Lippoldt, R Pontecorvi, A Nikodem, VM AF Farsetti, A Lazar, J Phyillaier, M Lippoldt, R Pontecorvi, A Nikodem, VM TI Active repression by thyroid hormone receptor splicing variant alpha 2 requires specific regulatory elements in the context of native triiodothyronine-regulated gene promoters SO ENDOCRINOLOGY LA English DT Article ID DOMINANT-NEGATIVE ACTIVITY; LIGAND-BINDING DOMAIN; RESPONSE ELEMENT; TRANSCRIPTIONAL REPRESSION; MOLECULAR-BASIS; RETINOIC ACID; TARGET GENES; DNA-BINDING; BETA; PROTEIN AB Structural requirements for the inhibitory action of thyroid hormone receptor splicing variant alpha 2 (TR alpha 2) on T-3/TR beta 1-mediated transactivation were investigated in native promoters of two T-3-regulated genes: the brain-specific myelin basic protein (MBP) and the housekeeping malic enzyme (ME). T-3/TR beta 1 transactivation of MBP256-chloramphenicol acetyl transferase (CAT) and ME315-CAT constructs was inhibited and unaffected by TR alpha 2, respectively. In electrophoretic mobility shift assays, TR alpha 2 bound MBP-thyroid response element (TRE) as a monomer but failed to interact with ME-TRE. Mutations of ME-TRE allowed TR alpha 2 binding but not inhibition of T-3/TR beta 1-mediated transactivation. In the context of the MBP promoter, replacement of MBP-TRE with ME-TRE or exchange of MBP TATA-like box with the ME CC-rich region spanning the transcription start site abolished TR alpha 2 dominant negative action. Simultaneous introduction of both MBP-TRE and MBP TATA-like box in the context of ME promoter, however, triggered TR alpha 2 inhibition of T-3/TR beta 1 transactivation, indicating that these regulatory elements are necessary, but not individually sufficient, to mediate TR alpha 2 dominant negative activity. Functional studies at low TR alpha 2/TR beta 1 ratios revealed that binding to TRE facilitates TR alpha 2 dominant negative action while prevention of DNA interaction by altering TR alpha 2 P-box structure preserved. TR alpha 2 inhibitory effect, although with lower potency. In conclusion, the results suggest that, in native promoters of T-3-regulated genes, a dual molecular mechanism, with DNA-binding dependent and DNA-binding independent components, underlies TR alpha 2 dominant negative activity. C1 NIDDKD, NIH, GENET & BIOCHEM BRANCH, BETHESDA, MD 20892 USA. UNIV CATTOLICA SACRO CUORE, INST MED PATHOL, I-00168 ROME, ITALY. CNR, INST EXPT MED, I-00168 ROME, ITALY. NR 41 TC 12 Z9 12 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1997 VL 138 IS 11 BP 4705 EP 4712 DI 10.1210/en.138.11.4705 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YB479 UT WOS:A1997YB47900025 PM 9348197 ER PT J AU Ghizzoni, L Mastorakos, G Vottero, A Barreca, A Furlini, M Cesarone, A Ferrari, B Chrousos, GP Bernasconi, S AF Ghizzoni, L Mastorakos, G Vottero, A Barreca, A Furlini, M Cesarone, A Ferrari, B Chrousos, GP Bernasconi, S TI Corticotropin-releasing hormone (CRH) inhibits steroid biosynthesis by cultured human granulosa-lutein cells in a CRH and interleukin-1 receptor-mediated fashion SO ENDOCRINOLOGY LA English DT Article; Proceedings Paper CT 10th Congress of the International-Society-for-Endocrinology CY JUN 12-15, 1996 CL SAN FRANCISCO, CA SP Int Soc Endocrinol ID RAT LEYDIG-CELLS; OVARIAN-FUNCTION; BETA-ENDORPHIN; SECRETION; SYSTEM; ANTAGONIST; STRESS; LOCALIZATION; EXPRESSION; ARTHRITIS AB The presence of immunoreactive CRH was recently demonstrated in human ovaries. CRH immunoreactivity was localized by immunohistochemistry in the cytoplasm of thecal cells surrounding the ovarian follicles, in luteinized cells of the stroma, and in large granulosa derived luteinized cells of developing corpora lutea. Also, CRH and its receptors were identified in Leydig cells of the testis where CRH was shown to inhibit testosterone biosynthesis. To examine the role of CRH in the ovary, we studied its effect on estradiol (E-2) and progesterone (P-4) release by human granulosa cells obtained from women undergoing in vitro fertilization for male factor infertility or uni-or bilateral tubal impatency. In all subjects, superovulation was induced by treatment ui th gonadotropins. The effects of graded doses of ovine CRH (10(-11)-10(-6) mol/liter) were evaluated in the conditioned medium obtained after 24 h incubation of the cells. All CRH concentrations employed except for the lowest one (10(-11) mol/liter) caused a significant decrease of media E-2 and P-4 levels. Maximal inhibition for both E-2 and P-4 production was obtained by 10(-6) mol/liter CRH concentration, which decreased hormone production by 39% and 34%, respectively. The alpha-helical CRH9-41 antagonist at 10(-6) and 10(-7) mol/liter blocked the suppressive effect of 10(-9) mol liter CRH on both E-2 and P-4 secretion, while it had no effect when added to the culture media without CRH. Since interleukin (IL-1)-1 mediates certain actions of CRH on leukocytes, we examined whether the CRH effect on ovarian steroidogenesis was IL-1-mediated. Interleukin-1 receptor antagonist at 10(-7) and 10(-6) mol/liter blocked the inhibitory effects of CRH on E-2 and P-4 secretion, while it had no effect in the absence of CRH. In conclusion, CRH exerts a CRH-and IL-1 receptor-mediated inhibitory effect on ovarian steroidogenesis and might be actively involved in the still enigmatic processes of follicular atresia and luteolysis. C1 UNIV PARMA, DEPT OBSTET & GYNECOL, I-43100 PARMA, ITALY. UNIV GENOA, DEPT ENDOCRINOL & METAB, I-16132 GENOA, ITALY. UNIV ATHENS, SCH MED, EVGENIDION HOSP, ENDOCRINE UNIT, ATHENS 11528, GREECE. NICHHD, NIH, BETHESDA, MD 20892 USA. UNIV MODENA, DEPT PEDIAT, I-41100 MODENA, ITALY. RP Ghizzoni, L (reprint author), UNIV PARMA, DEPT PEDIAT, VIA GRAMSCI 14, I-43100 PARMA, ITALY. NR 43 TC 47 Z9 49 U1 0 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1997 VL 138 IS 11 BP 4806 EP 4811 DI 10.1210/en.138.11.4806 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YB479 UT WOS:A1997YB47900037 PM 9348209 ER PT J AU Sciacchitano, S Taylor, SI AF Sciacchitano, S Taylor, SI TI Cloning, tissue expression, and chromosomal localization of the mouse IRS-3 gene SO ENDOCRINOLOGY LA English DT Article ID INSULIN-RECEPTOR SUBSTRATE-1; PHOSPHATIDYLINOSITOL 3-KINASE; SIGNALING SYSTEM; SH3 DOMAIN; PROTEIN; TRANSLOCATION; STIMULATION; RAS; PHOSPHORYLATION; KINASE AB Insulin receptor substrate (IRS) proteins are key regulators of basic functions such as cellular growth and metabolism. They provide an interface between multiple receptors and a complex network of intracellular signaling molecules. Two members of this family (IRS-1 and IRS-2) have been identified previously. In this investigation, we analyzed a mouse expressed sequence tag clone that proved to be a new member of the IRS family. Sequence analysis of this clone and comparison with the sequences deposited in GenBank demonstrates this protein may be the murine homolog of rat IRS-3, recently purified and cloned from rat adipocytes. Accordingly, we have named our protein mouse IRS-3. The expressed sequence tag clone contains the complete coding sequence of 1485 bp, encoding a protein of 495 amino acids. Sequence alignment with the other members of the IRS family shows that this protein contains pleckstrin homology and phosphotyrosine-binding domains that are highly conserved. In addition, there is conservation of many tyrosine phosphorylation motifs responsible for interactions with downstream signaling molecules containing SH2 domains. The murine IRS-3 messenger RNA (2.4 kilobases in length) is expressed in many tissues, with highest levels in liver and lung. Mouse IRS-3 is highly expressed in the first part of the embryonic life, when IRS-1 messenger RNA is barely detectable. Unlike the genes encoding IRS-1 and IRS-2, the IRS-3 gene contains an intror (344 bp in length) in the region between the pleckstrin homology and the phosphotyrosine-binding domains. Fluorescent in situ hybridization localized the mouse IRS-3 gene on the telomeric region of chromosome 5G2. Cloning of the murine IRS-3 gene will make it possible to apply genetic approaches to elucidate the physiological role of this new member of the IRS family of proteins. C1 NIDDKD, DIABET BRANCH, NIH, BETHESDA, MD 20892 USA. NR 34 TC 65 Z9 67 U1 0 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1997 VL 138 IS 11 BP 4931 EP 4940 DI 10.1210/en.138.11.4931 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YB479 UT WOS:A1997YB47900052 PM 9348224 ER PT J AU Song, WC Qian, YM Sun, XJ Negishi, M AF Song, WC Qian, YM Sun, XJ Negishi, M TI Cellular localization and regulation of expression of testicular estrogen sulfotransferase SO ENDOCRINOLOGY LA English DT Article ID HUMAN CHORIONIC-GONADOTROPIN; RAT LEYDIG-CELLS; MOLECULAR-CLONING; CYTOSOLIC SULFOTRANSFERASES; STEROID SULFOTRANSFERASES; ENVIRONMENTAL ESTROGENS; EPITHELIAL-CELLS; TESTIS; LIVER; MICE AB Estrogen sulfotransferase (EST) is a cytosolic enzyme that catalyzes the specific sulfonation of estrogens at the 3-hydroxyl position using 3'-phosphoadenosine-5'-phosphosulfate as an activated sulfate donor. Sulfated estrogens no longer bind to the estrogen receptor and are, therefore, hormonally inactive. Although liver has been considered a primary site for steroid sulfotransferase activities, we previously have cloned the mouse EST complementary DNA and found the enzyme to be expressed abundantly in the testis of normal mice. In this study we show by reverse transcription-PCR that EST is also expressed in the testes of rat and man, suggesting that testicular expression of EST may be a common phenomenon among different species. Using a purified polyclonal antibody raised against the bacterially expressed mouse EST protein, we demonstrate by immunohistochemistry that EST is localized selectively to the androgen-producing Leydig cells within the mouse testis. Additionally, we show that Legdig cell expression of EST is under the control of the pituitary hormone LH and is regulated differentially during development. In contrast to the high level of expression in mature intact animals, EST is not present in Leydig cells of hypophysectomized mice or in Leydig cells of fetal and prepubertal (day 5 or 17) mouse testes. Administration of hCG to hypophysectomized mice restored the testicular expression of EST. Together, these results suggest that testicular expression of EST may play an important role in male reproduction, conceivably by modulating the activity of locally synthesized estrogen in the testis of a sexually mature animal. C1 NIEHS, REPROD & DEV TOXICOL LAB, RES TRIANGLE PK, NC 27709 USA. RP Song, WC (reprint author), UNIV PENN, SCH MED, CTR EXPT THERAPEUT, 905 STELLAR CHANCE LABS, 422 CURIE BLVD, PHILADELPHIA, PA 19104 USA. NR 45 TC 44 Z9 44 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1997 VL 138 IS 11 BP 5006 EP 5012 DI 10.1210/en.138.11.5006 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YB479 UT WOS:A1997YB47900060 PM 9348232 ER PT J AU Oakley, RH Webster, JC Sar, M Parker, R Cidlowski, JA AF Oakley, RH Webster, JC Sar, M Parker, R Cidlowski, JA TI Expression and subcellular distribution of the beta-isoform of the human glucocorticoid receptor SO ENDOCRINOLOGY LA English DT Article ID METALLOPROTEASE SYNTHESIS; NUCLEAR-LOCALIZATION; STEROID-RECEPTORS; BINDING DOMAIN; DNA-BINDING; CELL-CYCLE; HORMONE; INVITRO; RESISTANCE; ANTIBODIES AB Alternative splicing of the human glucocorticoid receptor (hGR) primary transcript produces two highly homologous protein isoforms, termed hGR alpha and hGR beta, that differ at their carboxy-termini. In contrast to the well characterized hGR alpha isoform, which modulates gene expression in a hormone-dependent fashion, the biological significance of hGR beta has only recently begun to emerge. We and others have shown that the hGR beta messenger RNA transcript is widely expressed in human tissues and that the hGR beta protein functions as a dominant negative inhibitor of hGR alpha in transfected cells. Unfortunately, these initial studies did not determine whether the hGR beta protein was made in vivo. Such analyses are hindered because available anti-hGR antibodies cannot discriminate between the similarly sized hGR alpha anti hGR beta proteins. Therefore, to investigate the expression of the hGR beta protein, we have produced an antipeptide, hGR beta-specific antibody termed BShGR. This antibody was made against the unique 15-amino acid peptide at the carboxy-terminus of hGR beta and recognizes both the native and denatured conformations of hGR beta, but does not cross-react with hGR alpha. Using BShGR on Western blots and in immunoprecipitation experiments, we detected the hGR beta protein in a variety of human cell lines and tissues. Immunocytochemistry was then performed with BShGR on HeLa S-3 and CEM-C7 cells and on tissue sections prepared from lung, thymus, and liver to assess the cellular and subcellular distribution of hGR beta. In all immunopositive cells, hGR beta was found in the nucleus independent of glucocorticoid treatment. Within tissues, the hGR beta protein was expressed most abundantly in the epithelial cells lining the terminal bronchiole of the lung, forming the outer layer of Hassall's corpuscle in the thymus, and lining the bile duct in the liver. As a potential in vivo inhibitor of hGR alpha activity, expression of heap may be an important factor regulating target cell responsiveness to glucocorticoids. C1 NIEHS, LAB SIGNAL TRANSDUCT, NIH, RES TRIANGLE PK, NC 27709 USA. UNIV ALABAMA, DEPT OBSTET & GYNECOL, BIRMINGHAM, AL 35233 USA. NR 48 TC 139 Z9 146 U1 0 U2 7 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1997 VL 138 IS 11 BP 5028 EP 5038 DI 10.1210/en.138.11.5028 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YB479 UT WOS:A1997YB47900063 PM 9348235 ER PT J AU Longnecker, MP Sandler, DP Haile, RW Sandler, RS AF Longnecker, MP Sandler, DP Haile, RW Sandler, RS TI Phenolphthalein-containing laxative use in relation to adenomatous colorectal polyps in three studies SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE adenomatous; case-control studies; cathartics; colorectal neoplasms; pharmacoepidemiology; phenolphthaleins; polyps ID CANCER; RISK; EPIDEMIOLOGY; QUESTIONNAIRE; ALCOHOL; SMOKING; DIET AB Phenolphthalein, the active ingredient in many laxatives, was recently found to be a carcinogen in animal models. Human data suggest a laxative-colon cancer association, but few data specifically address the effects of phenolthalein-containing laxatives. We examined use of phenolphtalein-containing laxatives in relation to occurrence of adenomatous colorectal polyps in data from three case-control studies. The study conducted in Los Angeles, California (1991-1993), and the two studies conducted in North Carolina (1988-1990 and 1992-1995) altogether included 866 cases and 1,066 controls. The prevalence of using phenolphthaein-containing laxatives at least once a week in the recent past, however, was less than 5% among these subjects. The multivariate-adjusted odds ratios associated with recent use of phenolphthalein-containing laxatives once a week or more were 1.8 [95% confidence interval (CI), 0.5-6.2] in Los Angeles, 1.0 (CI, 0.4-2.2) in North Carolina (1988-1990), and 1.1 (CI, 0.2-5.7) in North Carolina (1992-1995). For use of other types of laxatives, the corresponding odds ratios were 1.3 (CI, 0.9-1.9) in Los Angeles, 1.0 (CI, 0.5-1.7) in North Carolina (1988-1990), and 0.9 (CI, 0.4-1.8) in North Carolina (1992-1995). Although the low prevalence of frequent use made for relatively wide confidence intervals, overall these data suggest that use of phenolphthalein-containing laxatives does not increase risk of adenomatous colorectal polyps. C1 NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA. Univ N Carolina, Ctr Gastrointestinal Biol & Dis, Div digest Dis & Nutr, Chapel Hill, NC 27599 USA. RP Longnecker, MP (reprint author), NIEHS, Epidemiol Branch, POB 12233,MD a3-05, Res Triangle Pk, NC 27709 USA. OI Longnecker, Matthew/0000-0001-6073-5322; Sandler, Dale/0000-0002-6776-0018 FU NCI NIH HHS [CA66635, CA44684] NR 18 TC 10 Z9 10 U1 2 U2 2 PU US DEPT HEALTH HUMAN SERVICES PUBLIC HEALTH SERVICE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SERVICES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD NOV PY 1997 VL 105 IS 11 BP 1210 EP 1212 DI 10.1289/ehp.971051210 PG 3 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA ZE642 UT WOS:000072815000014 PM 9370521 ER PT J AU Wilcox, AJ AF Wilcox, AJ TI From the shy trial defense: A leak, or red herring? SO EPIDEMIOLOGY LA English DT Editorial Material RP Wilcox, AJ (reprint author), NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709, USA. OI Wilcox, Allen/0000-0002-3376-1311 NR 1 TC 3 Z9 3 U1 0 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD NOV PY 1997 VL 8 IS 6 BP 684 EP 685 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YB072 UT WOS:A1997YB07200017 PM 9345671 ER PT J AU Campeau, L Knatterud, G Hunninghake, B Domanski, M AF Campeau, L Knatterud, G Hunninghake, B Domanski, M TI Optimizing cholesterol lowering therapy: contribution of the post coronary artery bypass graft trial SO EUROPEAN HEART JOURNAL LA English DT Editorial Material ID PRAVASTATIN C1 MARYLAND MED RES INST,BALTIMORE,MD. UNIV MINNESOTA,MINNEAPOLIS,MN. NHLBI,BETHESDA,MD 20892. RP Campeau, L (reprint author), MONTREAL HEART INST,MONTREAL,PQ H1T 1C8,CANADA. NR 12 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0195-668X J9 EUR HEART J JI Eur. Heart J. PD NOV PY 1997 VL 18 IS 11 BP 1683 EP 1685 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YG236 UT WOS:A1997YG23600001 PM 9402435 ER PT J AU Shepherd, J Cobbe, SM Lorimer, AR McKillop, JH Ford, I Packard, CJ Macfarlane, PW Isles, C Oliver, MF Lever, AF Brown, BW Ledingham, JGG Pocock, SJ Rifkind, BM Vallance, BD Lorimer, AR Ballantyne, D Anderson, L Duncan, D Kean, S Lawrence, A McGrath, J Montgomery, V Norrie, J Percy, M Pomphrey, E Whitehouse, A Cameron, P Parker, P Porteous, F Fletcher, L Kilday, C Shoat, D Latif, S Kennedy, J Bell, M Birrell, R Mellies, M Mayers, J Campbell, W AF Shepherd, J Cobbe, SM Lorimer, AR McKillop, JH Ford, I Packard, CJ Macfarlane, PW Isles, C Oliver, MF Lever, AF Brown, BW Ledingham, JGG Pocock, SJ Rifkind, BM Vallance, BD Lorimer, AR Ballantyne, D Anderson, L Duncan, D Kean, S Lawrence, A McGrath, J Montgomery, V Norrie, J Percy, M Pomphrey, E Whitehouse, A Cameron, P Parker, P Porteous, F Fletcher, L Kilday, C Shoat, D Latif, S Kennedy, J Bell, M Birrell, R Mellies, M Mayers, J Campbell, W TI Compliance and adverse event withdrawal: their impact on the west of Scotland Coronary Prevention Study SO EUROPEAN HEART JOURNAL LA English DT Article DE primary prevention; compliance; withdrawals; on-treatment analysis; coronary heart disease; all cause mortality; pravastatin ID CLINICAL-TRIALS; HEART-DISEASE; HYPERCHOLESTEROLEMIA; CHOLESTEROL; MEN AB Aims To assess the additional benefit gained from high compliance in the West of Scotland Coronary Prevention Study and to examine cases where withdrawal from trial medication was due to an adverse event. Methods The incidence of definite coronary heart disease or non-fatal myocardial infarction, cardiovascular mortality, definite or suspect coronary heart disease death or non-fatal myocardial infarction, the need for coronary revascularization procedures, all-cause mortality and incident cancers were measured in the entire cohort and compared with the high compliance group. The adverse events associated with withdrawal were coded by body system. Results In subjects with compliance greater than or equal to 75%, treatment with pravastatin resulted in a 38% risk reduction for definite coronary heart disease death or non-fatal myocardial infarction and for cardiovascular mortality, a 46% reduction in risk or coronary revascularization and a 32% risk reduction (P = 0.015) for all-cause mortality. Conclusions The analysis of the effect of pravastatin in the subgroup of high compliers to randomized medication demonstrated a substantial increase in the estimated risk reductions in comparison with that achieved in the intention-to-treat analysis. This result has significant implications for the motivation of high compliance among patients and for the assessment of the cost-effectiveness of treatment. C1 UNIV GLASGOW, ROBERTSON CTR BIOSTAT, GLASGOW G12 8QQ, LANARK, SCOTLAND. GLASGOW ROYAL INFIRM, GLASGOW G4 0SF, LANARK, SCOTLAND. DUMFRIES & GALLOWAY DIST GEN HOSP, DEPT MED, DUMFRIES, SCOTLAND. NATL HEART & LUNG INST, LONDON, ENGLAND. UNIV GLASGOW, WESTERN INFIRM, DEPT MED & THERAPEUT, GLASGOW G11 6NT, LANARK, SCOTLAND. STANFORD UNIV, STANFORD, CA 94305 USA. JOHN RADCLIFFE HOSP, NUFFIELD DEPT CLIN MED, OXFORD OX3 9DU, ENGLAND. UNIV LONDON LONDON SCH HYG & TROP MED, LONDON WC1E 7HT, ENGLAND. NHLBI, NIH, BETHESDA, MD 20892 USA. HAIRMYRES HOSP, DEPT CARDIOL, E KILBRIDE, LANARK, SCOTLAND. VICTORIA INFIRM, DEPT CARDIOL, GLASGOW G42 9TY, LANARK, SCOTLAND. NR 17 TC 56 Z9 57 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0195-668X EI 1522-9645 J9 EUR HEART J JI Eur. Heart J. PD NOV PY 1997 VL 18 IS 11 BP 1718 EP 1724 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YG236 UT WOS:A1997YG23600011 ER PT J AU Edler, D Blomgren, H Allegra, CJ Johnston, PG Lagerstedt, U Magnusson, I Ragnhammar, P AF Edler, D Blomgren, H Allegra, CJ Johnston, PG Lagerstedt, U Magnusson, I Ragnhammar, P TI Immunohistochemical determination of thymidylate synthase in colorectal cancer - methodological studies SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE thymidylate synthase; colorectal cancer; immunohistochemical determination; heterogeneity; enzyme activity; Dukes' stage ID MONOCLONAL-ANTIBODY; ADJUVANT THERAPY; RECTAL-CANCER; QUANTITATION; EXPRESSION; CARCINOMA; FLUOROURACIL; TUMORS; TRIAL; GENE AB With the aid of specific monoclonal antibodies, an immunohistochemical technique has recently been developed for the detection of intratumoral thymidylate synthase (TS), This technique can be applied to paraffin-embedded material suitable for retrospective studies. In order to examine this technique further, the TS enzyme activity of lysates from frozen-stored colorectal cancer (CRC) specimens were compared with their immunohistochemical TS staining intensity (arbitrarily graded from 0 to 3). A statistically significant correlation between these two methods on a total of 25 tumour specimens (P < 0.001) was observed. The staining intensity in different areas of 48 paraffin-embedded CRCs was examined. Sixty-seven per cent of the tumours were homogeneously stained (either grades 0-1 or 2-3), 33% showed a heterogeneity in TS staining. Increased TS expression correlated with more advanced Dukes' stage (P < 0.001). It is concluded that TS immunostaining intensity reflects TS enzyme activity in colorectal tumours and is well suited for paraffin-embedded material. The TS immunostaining pattern is heterogeneous in up to one-third of the tumours. (C) 1997 Elsevier Science Ltd. C1 South Hosp, Dept Surg, S-11823 Stockholm, Sweden. Karolinska Hosp, Dept Gen Oncol, S-10401 Stockholm, Sweden. NCI, Bethesda, MD 20892 USA. Queens Univ Belfast, Dept Oncol, Belfast BT7 1NN, Antrim, North Ireland. South Hosp, Dept Pathol, Stockholm, Sweden. RP Edler, D (reprint author), South Hosp, Dept Surg, S-11823 Stockholm, Sweden. NR 17 TC 47 Z9 50 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1997 VL 33 IS 13 BP 2278 EP 2281 DI 10.1016/S0959-8049(97)00306-7 PG 4 WC Oncology SC Oncology GA YR887 UT WOS:000071541400032 PM 9470819 ER PT J AU Van Laer, L Van Camp, G van Zuijlen, D Green, ED Verstreken, M Schatteman, I Van de Heyning, P Balemans, W Coucke, P Greinwald, JH Smith, RJH Huizing, E Willems, P AF Van Laer, L Van Camp, G van Zuijlen, D Green, ED Verstreken, M Schatteman, I Van de Heyning, P Balemans, W Coucke, P Greinwald, JH Smith, RJH Huizing, E Willems, P TI Refined mapping of a gene for autosomal dominant progressive sensorineural hearing loss (DFNA5) to a 2-cM region, and exclusion of a candidate gene that is expressed in the cochlea SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE sensorineural progressive hearing loss; DFNA5; chromosome 7p15; refinement; candidate gene CG1 ID HUMAN GENOME; CPG ISLANDS; IMPAIRMENT; FAMILY; DEAFNESS; EAR; DNA AB A gene for an autosomal dominant form of progressive sensorineural hearing loss (DFNA5) was previously assigned by us to a 15-cM region on chromosome 7p15. In this study, the DFNA5 candidate region was refined to less than 2 cM, and completely cloned in a YAC contig. The HOXA1 gene located in 7p15 was considered to be a good candidate gene for DFNA5 as it harbours mutations leading to developmental defects of the inner ear in mice. However, the refinement of the candidate region of DFNA5 excludes the HOXA1 gene as a candidate for DFNA5. We cloned a novel candidate gene (CG1, candidate gene 1), which is expressed in human fetal cochlea, from the DFNA5 candidate region. The complete cDNA sequence of CG1, encoding a 423 amino acid protein of unknown function, was determined. Mutation analysis of the CG1 gene in DFNA5 patients, however, could not reveal a disease-causing mutation. C1 Univ Instelling Antwerp, Dept Med Genet, B-2610 Antwerp, Belgium. Univ Utrecht Hosp, Dept Otorhinolaryngol, Utrecht, Netherlands. Natl Human Genome Res Inst, NIH, Bethesda, MD USA. Univ Antwerp Hosp, Dept Otorhinolaryngol, Antwerp, Belgium. Univ Iowa Hosp & Clin, Dept Otorhinolaryngol, Iowa City, IA 52242 USA. RP Van Camp, G (reprint author), Univ Instelling Antwerp, Dept Med Genet, Univ Plein 1, B-2610 Antwerp, Belgium. RI Van Camp, Guy/F-3386-2013 OI Van Camp, Guy/0000-0001-5105-9000 NR 32 TC 14 Z9 15 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PD NOV-DEC PY 1997 VL 5 IS 6 BP 397 EP 405 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA YQ578 UT WOS:000071401900009 PM 9450185 ER PT J AU Suess, PE Newlin, DB Porges, SW AF Suess, PE Newlin, DB Porges, SW TI Motivation, sustained attention, and autonomic regulation in school-age boys exposed in utero to opiates and alcohol SO EXPERIMENTAL AND CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID PRENATAL EXPOSURE; CHILDREN BORN; METHADONE; INFANCY AB The effects of incentive on sustained attention and autonomic regulation among boys exposed in utero to opiates were studied. Respiratory sinus arrhythmia (RSA), an indicator of autonomic regulation, was quantified during sustained attention in 3 groups of 7- to 12-year-old boys. RSA is a component of heart rate Variability controlled by cortical influences and affected by changes in demand for attention. The Gordon Diagnostic System-Distractibility Task was performed with and without monetary reward. A cartoon task and a video game were used as measures of interest. Although opiate-exposed boys did not differ in performance as a function of incentive or interest, they had a tendency to perform more poorly overall across tasks. Alcohol exposure rather than opiate exposure covaried with autonomic regulation, with greater RSA decreases being associated with more alcohol exposure. Post hoc analyses revealed that the alcohol-and opiate-exposed boys responded with these hyperreactive RSA changes along with poorer performance. C1 UNIV MARYLAND,DEPT HUMAN DEV,INST CHILD STUDY,COLLEGE PK,MD 20742. NIDA,INTRAMURAL RES PROGRAM,LEXINGTON,KY. NR 27 TC 26 Z9 26 U1 1 U2 2 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 1064-1297 J9 EXP CLIN PSYCHOPHARM JI Exp. Clin. Psychopharmacol. PD NOV PY 1997 VL 5 IS 4 BP 375 EP 387 PG 13 WC Psychology, Biological; Psychology, Clinical; Pharmacology & Pharmacy; Psychiatry SC Psychology; Pharmacology & Pharmacy; Psychiatry GA YF357 UT WOS:A1997YF35700006 PM 9386964 ER PT J AU Ralston, E McLaren, RS Horowitz, JA AF Ralston, E McLaren, RS Horowitz, JA TI Nuclear domains in skeletal myotubes: The localization of transferrin receptor mRNA is independent of its half-life and restricted by binding to ribosomes SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID SUBUNIT MESSENGER-RNA; ACETYLCHOLINE-RECEPTOR; MUSCLE-CELLS; ENDOPLASMIC-RETICULUM; INSITU HYBRIDIZATION; SINGLE NUCLEUS; EXPRESSION; ACTIN; TRANSCRIPTS; PROTEIN AB The retention of mRNAs near the nuclei that synthesize them may be an important feature of the organization of multinucleated skeletal myotubes. Here, we assess the possible role of two factors in this localization. First, we examine the role of mRNA half-life, by studying the distribution of the mRNA for the transferrin receptor (TfR), whose half-life can be manipulated in culture by changing the availability of iron. In situ hybridization of myotubes of the mouse muscle cell line C2 shows that TfR mRNA is concentrated in the core of the myotubes. Its distribution around the nuclei is often asymmetric and its concentration changes abruptly. Stable transcripts display the same asymmetric localization as unstable ones, suggesting that half-life does not determine subcellular localization of TfR mRNA. Differential effects of the protein synthesis inhibitors puromycin and cycloheximide suggest that the mRNA is retained in position by its association with ribosomes. We then examine the distribution of the rough endoplasmic reticulum (RER) and find it to be broader than the distribution of TfR mRNA. In contrast to TfR mRNA, the mRNA for a secreted immunoglobulin kappa light chain has a more uniform distribution. Taken together, the results suggest that TfR mRNA may associate with RER subdomains by specific targeting. (C) 1997 Academic Press. C1 USDA,CTR BIOL EVALUAT & RES,DIV HEMATOL PROD,BETHESDA,MD 20892. RP Ralston, E (reprint author), NINCDS,NEUROBIOL LAB,NIH,BLDG 36,RM 2A-21,BETHESDA,MD 20892, USA. NR 41 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD NOV 1 PY 1997 VL 236 IS 2 BP 453 EP 462 DI 10.1006/excr.1997.3753 PG 10 WC Oncology; Cell Biology SC Oncology; Cell Biology GA YG887 UT WOS:A1997YG88700012 PM 9367630 ER PT J AU Shim, K Picking, WL Kutty, RK Thomas, CF Wiggert, BN Stark, WS AF Shim, K Picking, WL Kutty, RK Thomas, CF Wiggert, BN Stark, WS TI Control of Drosophila Retinoid and Fatty Acid Binding Glycoprotein expression by retinoids and retinoic acid: Northern, western and immunocytochemical analyses SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE Drosophila Retinoid and Fatty Acid Binding Glycoprotein (RFABG); vitamin A; transcription; northern analysis; retinoic acid; western blots; immunocytochemistry ID COMPOUND EYE; CAROTENOID REPLACEMENT; RECEPTOR SUPERFAMILY; ELECTRON-MICROSCOPY; GLYCOSYLATION SITE; PIGMENT-EPITHELIUM; OUTER RHABDOMERES; VITAMIN-A; MELANOGASTER; GENE AB In Drosophila, thorough retinoid deprivation is possible, optimizing investigation of the effects of vitamin A metabolites and retinoic acid on the visual system. Retinoids had been found to control transcription and translation of Drosophila's opsin gene. To follow this line of inquiry, we examined the effect of retinoids on the translation and transcription of a Drosophila Retinoid and Fatty Acid Binding Glycoprotein. Western blots showed that this protein is high in retinoid replete flies and low in deprived flies. Flies grown on media capable of activating the opsin gene's transcription and which contain alternate transcription activators including retinoic acid yielded extracts containing significant amounts of Retinoid and Fatty Acid Binding Glycoprotein. Immunocytochemistry confirmed its absence in deprived flies and its presence in flies reared or replaced on these diverse media containing retinoids or general nutrients. Immunocytochemistry localized Retinoid and Fatty Acid Binding Glycoprotein to the Semper (cone) cells and the intraommatidial matrix (the interphotoreceptor matrix of the ommatidium). Positive staining of Semper cells in mutants of the opsin gene and a mutant lacking receptors suggests that Retinoid and Fatty Acid Binding Glycoprotein does not depend on presence of opsin and that it is not synthesized in receptor cells respectively. Northern blots demonstrated greatly diminished mRNA for Retinoid and Fatty Acid Binding Glycoprotein in flies grown on deprivation food relative to flies grown on normal food. Although the synthesis of Retinoid and Fatty Acid Binding Glycoprotein does not require chromophore precursors as does that of opsin, the control of Retinoid and Fatty Acid Binding Glycoprotein and opsin transcription by retinoids including retinoic acid might very well be the same. Our results suggest that Retinoid and Fatty Acid Binding Glycoprotein may be involved in retinoid transport. Also, Semper cells may be analogous to vertebrate retinal pigment epithelium in retinoid metabolism and/or delivery. (C) 1997 Academic Press Limited. C1 ST LOUIS UNIV, DEPT BIOL, ST LOUIS, MO 63103 USA. NEI, RETINAL CELL & MOL BIOL LAB, NIH, BETHESDA, MD 20892 USA. UNIV WISCONSIN, INTEGRATED MICROSCOPY RESOURCE, MADISON, WI 53706 USA. FU NCRR NIH HHS [DRR-570]; NEI NIH HHS [EY07192] NR 57 TC 10 Z9 10 U1 0 U2 1 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD NOV PY 1997 VL 65 IS 5 BP 717 EP 727 DI 10.1006/exer.1997.0383 PG 11 WC Ophthalmology SC Ophthalmology GA YG571 UT WOS:A1997YG57100014 PM 9367652 ER PT J AU Shefer, VI Talan, MI AF Shefer, VI Talan, MI TI The effect of exercise training in a cold environment on thermoregulation in adult and aged C57BL/6J mice SO EXPERIMENTAL GERONTOLOGY LA English DT Article DE heat production; heat loss; body temperature; cold tolerance; cold acclimation ID BROWN ADIPOSE-TISSUE; NONSHIVERING THERMOGENESIS; RATS; EXPOSURE; ACCLIMATION; EXPRESSION; TOLERANCE AB We studied the effect of exercise training in cold environment (six weeks of daily, one-hour runs on a treadmill at ambient temperature of 6 +/- 1 degrees C at 60-65% of VO2max) on cold-induced metabolic heat production, heat loss, and cold tolerance in adult and aged C57BL/6J male mice. In adult mice, exercise training in cold environment resulted in greater cold-induced heat production and cold tolerance without changes in heat loss, similar to the effects of daily cold exposure without exercise. In aged mice, daily cold exposures did not affect cold tolerance and cold-induced heat production, but exercise training in the cold resulted in greater cold-induced heat production and cold tolerance. Heat loss in aged mice increased similarly after both repeated cold exposures and exercise training in the cold. Therefore, mechanisms of effect of exercise training on cold tolerance are different in adult and aged animals. Exercise training in cold environment does not affect cold-induced heat production and cold tolerance in adult mice, but improves them in aged animals. Published by Elsevier Science Inc. C1 NIA,GERONTOL RES CTR,BEHAV SCI LAB,NIH,BALTIMORE,MD 21224. NR 28 TC 6 Z9 6 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD NOV-DEC PY 1997 VL 32 IS 6 BP 695 EP 705 DI 10.1016/S0531-5565(97)00085-5 PG 11 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA YJ452 UT WOS:A1997YJ45200008 PM 9785095 ER PT J AU Spangler, EL Hengemihle, J Blank, G Speer, DL Brzozowski, S Patel, N Ingram, DK AF Spangler, EL Hengemihle, J Blank, G Speer, DL Brzozowski, S Patel, N Ingram, DK TI An assessment of behavioral aging in the Mongolian gerbil SO EXPERIMENTAL GERONTOLOGY LA English DT Article DE animal model; epilepsy; motor skills; learning; memory ID BUTYL-ALPHA-PHENYLNITRONE AB Male Mongolian gerbils (Meriones unguiculatus) 14-54 months old (n = 77) were evaluated in a battery of psychomotor (open field, locomotor, and runwheel activity, rotorod performance) and learning (one-way active avoidance in a straight runway and in 14-unit T-maze performance) tests. Body weight and seizure activity were also monitored. According to Linear regression analysis, runwheel activity decreased with age; and the number of errors in the 14-unit T-maze increased as a function of age (ps < 0.05). None of the other behavioral measures or body weight were significantly correlated with age. This gerbil strain (Tumblebrook Farms; West Brookfield, MA) tended to be very prone to seizures with 64% of the gerbils experiencing at least one seizure while being tested. Seizures tended to occur when the gerbil was exposed to a novel situation (e.g., initial weighing, placement on the rotorod). An age-related decline in some aspects of psychomotor and learning performance was observed, suggesting the gerbil as an additional mammalian model of aging. The high incidence of seizure activity presented a complicating and confounding variable to the interpretation of the results of the behavioral tests used in the present study. Interventions to control seizure activity (e.g., systematic, controlled breeding; adaptation to apparati) in this model will likely increase its viability as a mammalian model of aging. Published by Elsevier Science he. C1 TOWSON STATE UNIV,DEPT PSYCHOL,TOWSON,MD 21252. RP Spangler, EL (reprint author), NIA,GERONTOL RES CTR,MOL PHYSIOL & GENET SECT,NATHAN W SHOCK LABS,NIH,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 13 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 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD NOV-DEC PY 1997 VL 32 IS 6 BP 707 EP 717 DI 10.1016/S0531-5565(97)00055-7 PG 11 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA YJ452 UT WOS:A1997YJ45200009 PM 9785096 ER PT J AU Westling, J Yowell, CA Majer, P Erickson, JW Dame, JB Dunn, BM AF Westling, J Yowell, CA Majer, P Erickson, JW Dame, JB Dunn, BM TI Plasmodium falciparum, P-vivax, and P-malariae: A comparison of the active site properties of plasmepsins cloned and expressed from three different species of the malaria parasite SO EXPERIMENTAL PARASITOLOGY LA English DT Article DE plasmepsin (EC3.4.23.38); aspartic endopeptidase; oligopeptide substrates; chromogenic assay; inhibition constants; malaria; protozoan; Plasmodium spp. ID HEMOGLOBIN DEGRADATION; ASPARTIC PROTEINASE; CYSTEINE PROTEINASE; SPECIFICITY; PATHWAY; INHIBITION; ORGANELLE; CLEAVAGE; SEQUENCE; KINETICS AB Aspartic endopeptidases (plasmepsins) have been implicated in the degradation of hemoglobin in the erythrocytic stage of infection by Plasmodium falciparum. To develop new targets for drug development, these enzymes have been isolated and cioned, expressed, and studied structurally and enzymatically. This study expands this approach to two other species of the malarial parasite, P. vivax and P. malariae. Expression of cloned genes from these species, utilizing methodology similar to that employed in the original reports on the enzymes from P. falciparum, has provided active enzymes for analysis by kinetic methods. We describe here studies of three enzymes, plasmepsin II from P. falciparum, and one plasmepsin from both P. vivax and P. malariae, utilizing oligopeptide substrates and low-molecular-weight inhibitors. These analyses provide new information on the properties of distinct regions of the active site cleft; such data can suggest strategies for drug design to inhibit these critical enzymes of the parasite. (C) 1997 Academic Press. C1 UNIV FLORIDA, COLL VET MED, DEPT PATHOBIOL, GAINESVILLE, FL 32610 USA. NCI, SAIC, STRUCT BIOCHEM PROGRAM, FREDERICK, MD 21702 USA. RP Westling, J (reprint author), UNIV FLORIDA, COLL MED, DEPT BIOCHEM & MOL BIOL, BOX 100245, GAINESVILLE, FL 32610 USA. FU NIAID NIH HHS [AI39211] NR 25 TC 40 Z9 40 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4894 J9 EXP PARASITOL JI Exp. Parasitol. PD NOV PY 1997 VL 87 IS 3 BP 185 EP 193 DI 10.1006/expr.1997.4225 PG 9 WC Parasitology SC Parasitology GA YG265 UT WOS:A1997YG26500003 PM 9371083 ER PT J AU Lin, MCM Li, JJ Wang, EJ Princler, GL Kauffman, FC Kung, HF AF Lin, MCM Li, JJ Wang, EJ Princler, GL Kauffman, FC Kung, HF TI Ethanol down-regulates the transcription of microsomal triglyceride transfer protein gene SO FASEB JOURNAL LA English DT Article DE MTP; gene expression; HepG2; rats ID MODERATE ALCOHOL-CONSUMPTION; B-CONTAINING LIPOPROTEINS; CORONARY HEART-DISEASE; APOLIPOPROTEIN-B; HEPG2 CELLS; SECRETION; ABETALIPOPROTEINEMIA; EXPRESSION; RISK; MEN AB Microsomal triglyceride transfer protein (MTP) plays a central role in the assembly and secretion of apoB-containing lipoproteins. In this study, we investigated the effect of ethanol on the expression of the large subunit of MTP in a human liver hepatoma cell line, the HepG2 cells, Exposure of HepG2 cells to low concentrations of ethanol reduced MTP mRNA levels in a concentration-and time-dependent manner, The level of MTP mRNA decreased significantly (P < 0.05, -26% relative to pretreatment control) when the concentration of ethanol in the culture medium was 50 ppm (0.005%, v/v), Maximal suppression (-50%) was observed at 100 ppm ethanol; the MTP mRNA levels remained at 50% of control when the ethanol concentration was raised to 10,000 ppm, Furthermore, a 10-day ethanol treatment caused a significant 50% decrease in the MTP activity and apoB secretion rate in HepG2 cells. To investigate the molecular mechanisms underlying this phenomenon, we examined the effect of ethanol on the promoter activity of the MTP gene. Transient transfection analysis of human MTP promoter-driven luciferase gene expression showed that ethanol down-regulates MTP promoter activity in a manner parallel to that observed for mRNA levels, Deletion analysis suggested that the MTP promoter sequence contains a negative ethanol response element -612 to -142 bp upstream of the transcription start site, To evaluate the in vivo relevance of the effect of ethanol on MTP mRNA levels, rats were given a single oral dose of ethanol, with hepatic and intestinal MTP mRNA measured 3 h after dosing, Rats receiving 1 or 3 g/kg of ethanol exhibited substantially lower hepatic and intestinal MTP mRNA levels, Taken together, these results strongly suggest that ethanol can modulate the secretion of apoB-containing lipoproteins by down-regulating the expression of MTP large subunit, primarily through inhibiting the transcription of the MTP gene. C1 NCI,FREDERICK CANC RES & DEV CTR,LAB BIOCHEM PHYSIOL,NIH,FREDERICK,MD 21702. RUTGERS STATE UNIV,DEPT PHARMACOL & TOXICOL,PISCATAWAY,NJ 08855. RP Lin, MCM (reprint author), UNIV MED & DENT NEW JERSEY,SCH OSTEOPATH MED,DEPT CELL BIOL,STRATFORD,NJ 08084, USA. NR 35 TC 29 Z9 29 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD NOV PY 1997 VL 11 IS 13 BP 1145 EP 1152 PG 8 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA YE983 UT WOS:A1997YE98300012 PM 9367349 ER PT J AU Wang, RYH Grandinetti, T Shih, JWK Weiss, SH Haley, CLD Hayes, MM Lo, SC AF Wang, RYH Grandinetti, T Shih, JWK Weiss, SH Haley, CLD Hayes, MM Lo, SC TI Mycoplasma genitalium infection and host antibody immune response in patients infected by HIV, patients attending STD clinics and in healthy blood donors SO FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY LA English DT Article DE Mycoplasma genitalium; lipid-associated membrane protein (LAMP); antibody; AIDS ID SEROLOGICAL CROSS-REACTIONS; PNEUMONIAE; ASSOCIATION; ONCOGENESIS; PARASITISM; PENETRANS; TRACT AB Prevalence of Mycoplasma genitalium in humans is still not clear. We have developed a sensitive and specific serological assay for M. genitalium using lipid-associated membrane proteins (LAMPs) as antigens. Antibodies to LAMPs from M. genitalium showed little cross-reactivity to LAMPs from antigenically similar M. pneumoniae. For validity testing, urines from 104 patients were tested by PCR for M. genitalium. All 15 PCR+ patients had M. genitalium-LAMPs antibodies. Moreover, none of 64 antibody-negative patients were PCR+. Serological study of 1800 patients of various diseased groups and healthy blood donors showed M. genitalium was primarily a sexually transmitted microbe that infected patients with AIDS (44.0%), intravenous drugs users with or without HIV infection (42.5%), and also HIV- patients attending STD clinics (42.6%). Only 5.5% HIV- healthy blood donors and 1.3% HIV+ hemophiliacs tested positive. M. genitalium has been associated with acute non-gonococcal urethritis in male patients. However, many sexually active men and women appear to be chronically infected or colonized by the microbe without apparent clinical symptoms and may continue to transmit the organism through sexual contacts. C1 ARMED FORCES INST PATHOL,DEPT INFECT & PARASIT DIS PATHOL,AMER REGISTRY PATHOL,WASHINGTON,DC 20306. AMER RED CROSS,NATL CAPITAL CHAPTER,WASHINGTON,DC 20006. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT PREVENT MED & COMMUNITY HLTH,NEWARK,NJ 07103. NR 33 TC 35 Z9 38 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0928-8244 J9 FEMS IMMUNOL MED MIC JI FEMS Immunol. Med. Microbiol. PD NOV PY 1997 VL 19 IS 3 BP 237 EP 245 DI 10.1016/S0928-8244(97)00089-8 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA YK218 UT WOS:A1997YK21800007 PM 9453394 ER PT J AU Miller, MS McCarver, DG Bell, DA Eaton, DL Goldstein, JA AF Miller, MS McCarver, DG Bell, DA Eaton, DL Goldstein, JA TI Genetic polymorphisms in human drug metabolic enzymes SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Editorial Material ID GLUTATHIONE-S-TRANSFERASE; TRANS-STILBENE OXIDE; HUMAN-LIVER ALCOHOL; HUMAN MONONUCLEAR LEUKOCYTES; LUNG-CANCER PATIENTS; GSTM1 NULL GENOTYPE; POLYMERASE CHAIN-REACTION; SQUAMOUS-CELL CARCINOMA; HEPATITIS-B CARRIERS; DNA ADDUCT LEVELS AB Results obtained from both epidemiologic studies and experimental animal model systems have shown a wide range of phenotypic variation in the ability of individuals to metabolize drugs and environmental chemicals. Several studies have noted correlations between specific metabolic phenotypes and the incidence of disease, suggesting that certain allelic forms of drug metabolic enzymes can render the individual either more sensitive or resistant to the toxic or therapeutic effects of exogenous drugs and chemicals, While some of this variation can be attributed to different environmental exposures, it has become clear that genetic factors also play an important role in determining the response of the individual organism to exogenous agents. Recent advances in molecular biological techniques have begun to allow scientists to correlate observed phenotypic differences with the actual differences in genetic sequence at the gene level. This has allowed a correlation between gene structure and function, thus providing a mechanistic basis to explain the interaction between genetic background and individual response to environmental exposures. Results presented at this symposium discussed how genetic polymorphisms for both Phase I and Phase II metabolic enzymes in the human population modulate the response to environmental toxicants. (C) 1997 Society of Toxicology. C1 WAYNE STATE UNIV,CHILDRENS HOSP MICHIGAN,DEPT PEDIAT,DETROIT,MI 48201. WAYNE STATE UNIV,CHILDRENS HOSP MICHIGAN,DEPT PHARMACOL,DETROIT,MI 48201. NIEHS,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709. NIEHS,HUMAN METAB SECT,LAB PHARMACOL & CHEM,RES TRIANGLE PK,NC 27709. UNIV WASHINGTON,DEPT ENVIRONM HLTH,CTR ECOGENET & ENVIRONM HLTH,SEATTLE,WA 98105. RP Miller, MS (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,CTR COMPREHENS CANC,DEPT CANC BIOL,300 S HAWTHORNE RD,WINSTON SALEM,NC 27157, USA. NR 135 TC 57 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 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD NOV PY 1997 VL 40 IS 1 BP 1 EP 14 DI 10.1006/faat.1997.2382 PG 14 WC Toxicology SC Toxicology GA YK776 UT WOS:A1997YK77600001 PM 9398483 ER PT J AU Chapin, RE Harris, MW Davis, BJ Ward, SM Wilson, RE Mauney, MA Lockhart, AC Smialowicz, RJ Moser, VC Burka, LT Collins, BJ Haskins, EA Allen, JD Judd, L Purdie, WA Harris, HL Lee, CA Corniffe, GM AF Chapin, RE Harris, MW Davis, BJ Ward, SM Wilson, RE Mauney, MA Lockhart, AC Smialowicz, RJ Moser, VC Burka, LT Collins, BJ Haskins, EA Allen, JD Judd, L Purdie, WA Harris, HL Lee, CA Corniffe, GM TI The effects of perinatal/juvenile methoxychlor exposure on adult rat nervous, immune, and reproductive system function SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID DECIDUAL CELL RESPONSE; OBSERVATIONAL BATTERY; SPERM COUNTS; FEMALE RATS; MICE; IMMUNOTOXICITY; ESTROGEN; METABOLITES; SENSITIVITY; PROSTATE AB In order to address data gaps identified by the NAS report Pesticides in the Diets of Infants and Children, a study was performed using methoxychlor (MXC). Female rats were gavaged with MXC at 0, 5, 50, or 150 mg/kg/day for the week before and the week after birth, whereupon the pups were directly dosed with MXC from postnatal day (pnd) 7. Some dams were killed pnd7 and milli and plasma were assayed for MXC and metabolites. For one cohort of juveniles, treatment stopped at pnd21; a modified functional observational battery was used to assess neurobehavioral changes. Other cohorts of juveniles were dosed until pnd42 and evaluated for changes to the immune system and for reproductive toxicity. Dose-dependent amounts of MXC and metabolites were present in milk and plasma of darns and pups. The high dose of MXC reduced litter size by approximate to 17%. Ano-genital distance was unchanged, although vaginal opening was accelerated in all treated groups, and male prepuce separation was delayed at the middle and high doses by 8 and 34 days, respectively. In the neurobehavioral evaluation, high-dose males were more excitable, but other changes were inconsistent and insubstantial. A decrease in the antibody plaque-forming cell response was seen in males only. Adult estrous cyclicity was disrupted at 50 and 150MXC, doses which also showed reduced rates of pregnancy and delivery. Uterine weights (corrected for pregnancy) were reduced in all treated pregnant females. High-dose males impregnated fewer untreated females; epididymal sperm count and testis weight were reduced at the high, or top two, doses, respectively. All groups of treated females showed uterine dysplasias and less mammary alveolar development; estrous levels of follicle stimulating hormone were lower in all treated groups, and estrus progesterone levels were lower at 50 and 150 MXC, attributed to fewer corpora lutea secondary to ovulation defects. These data collectively show that the primary adult effects of early exposure to MXC are reproductive, show that 5 mg/kg/day is not a NO(A)EL in rats with this exposure paradigm (based on changes in day of vaginal opening, pubertal ovary weights, adult uterine and seminal vesicle weights, and female hormone data) and imply that the sites of action are both central and peripheral. (C) 1997 Society of Toxicology. C1 NIEHS, LAB EXPT PATHOL, RES TRIANGLE PK, NC 27709 USA. NIEHS, CHEM GRP, RES TRIANGLE PK, NC 27709 USA. ANALYT SCI INC, DURHAM, NC 27713 USA. US EPA, NATL HLTH & ENVIRONM EFFECTS LAB, EXPT TOXICOL DIV, RES TRIANGLE PK, NC 27711 USA. US EPA, NATL HLTH & ENVIRONM EFFECTS LAB, DIV NEUROTOXICOL, RES TRIANGLE PK, NC 27711 USA. RP Chapin, RE (reprint author), NIEHS, REPROD TOXICOL GRP, NATL TOXICOL PROGRAM, MD B3-05, POB 12233, RES TRIANGLE PK, NC 27709 USA. OI Chapin, Robert/0000-0002-5997-1261 FU NIEHS NIH HHS [N01-ES-15307, N01-ES-25332] NR 64 TC 188 Z9 195 U1 2 U2 5 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD NOV PY 1997 VL 40 IS 1 BP 138 EP 157 DI 10.1006/faat.1997.2381 PG 20 WC Toxicology SC Toxicology GA YK776 UT WOS:A1997YK77600014 PM 9398496 ER PT J AU Lau, DTY Everhart, J Kleiner, DE Park, Y Vergalla, J Schmid, P Hoofnagle, JH AF Lau, DTY Everhart, J Kleiner, DE Park, Y Vergalla, J Schmid, P Hoofnagle, JH TI Long-term follow-up of patients with chronic hepatitis B treated with interferon alfa SO GASTROENTEROLOGY LA English DT Article ID HUMAN ALPHA-INTERFERON; CONTROLLED TRIAL; VIRAL-HEPATITIS; VIRUS-INFECTION; THERAPY; PERSISTENCE; SURVIVAL; LIVER; DNA AB Background & Aims: Therapy with interferon alfa (IFN-alpha) leads to remission of disease in one third of patients with chronic hepatitis B. The aim of this study was to better define the long-term prognosis of this outcome. Methods: One hundred three patients with chronic hepatitis B who underwent IFN-alpha therapy in three clinical trials between 1984 and 1991 were followed up for serological status, biochemical evidence of liver disease, and liver complications or mortality through 1994. Results: Among 103 patients, 31 (30%) responded to therapy with loss of hepatitis B e antigen and viral DNA from serum. Responders were more likely than nonresponders to be women, black, and to have more severe liver disease including cirrhosis (P < 0.05). Up to 11 years (mean, 6.2 years) after therapy, a higher percentage of responders than nonresponders were still negative for hepatitis B e antigen (94% vs. 40%; P < 0.001) and hepatitis 3 surface antigen (71% vs 8.3%; P < 0.001). Overall, the rate of liver-related complications and death did not differ by IFN-a response, but with adjustment for cirrhosis, nonresponders had higher rates of liver-related complications and mortality (hazard ratio, 13.7; 95% confidence interval, 3.0-63.5). Conclusions: The response to IFN-alpha therapy in chronic hepatitis B is usually a sustained improvement in disease markers and, when cirrhosis is considered, patient outcome. C1 NIDDK,DIV DIGEST DIS & NUTR,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NIH,CTR CLIN,BETHESDA,MD 20892. NATL INST GENET,LOS ANGELES,CA. RP Lau, DTY (reprint author), NIDDK,LIVER DIS SECT,DIGEST DIS BRANCH,NIH,ROOM 9B16,BLDG 10,10 CTR DR,BETHESDA,MD 20892, USA. OI Kleiner, David/0000-0003-3442-4453 NR 26 TC 220 Z9 230 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD NOV PY 1997 VL 113 IS 5 BP 1660 EP 1667 DI 10.1053/gast.1997.v113.pm9352870 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YC790 UT WOS:A1997YC79000035 PM 9352870 ER PT J AU Dickson, RC Everhart, JE Lake, JR Wei, YL Seaberg, EC Wiesner, RH Zetterman, RK Pruett, TL Ishitani, MB Hoofnagle, JH Detre, KM Demetris, AJ Lombardero, M Seaberg, E Lawlor, S Fitzgerald, S Haber, J Swanson, GL Wiesner, R Krom, R Porayko, MK Schwerman, L Groettum, C Shaw, B Taylor, K Ascher, N Lake, J BremerKamp, C Everhart, J Shores, S Broccoli, A Hausman, G Shepard, B Carrol, N McGory, R Stevenson, WC McCullough, C Caldwell, S AF Dickson, RC Everhart, JE Lake, JR Wei, YL Seaberg, EC Wiesner, RH Zetterman, RK Pruett, TL Ishitani, MB Hoofnagle, JH Detre, KM Demetris, AJ Lombardero, M Seaberg, E Lawlor, S Fitzgerald, S Haber, J Swanson, GL Wiesner, R Krom, R Porayko, MK Schwerman, L Groettum, C Shaw, B Taylor, K Ascher, N Lake, J BremerKamp, C Everhart, J Shores, S Broccoli, A Hausman, G Shepard, B Carrol, N McGory, R Stevenson, WC McCullough, C Caldwell, S TI Transmission of hepatitis B by transplantation of livers from donors positive for antibody to hepatitis B core antigen SO GASTROENTEROLOGY LA English DT Article ID SURFACE-ANTIGEN; VIRUS-DNA; POSTTRANSFUSION HEPATITIS; INFECTION; BLOOD; TRANSFUSION; PERSISTENCE; RECIPIENTS; RECURRENCE; AUSTRALIA AB Background & Aims: Organ donors are a potential source of transmissible disease after transplantation. The aim of this study was to evaluate the risk of acquiring hepatitis B among transplantation recipients of livers from donors without serum hepatitis B surface antigen (HBsAg) but with antibody to hepatitis B core antigen (anti-HBc). Methods: The transplantation experience of four centers between 1989 and 1994 was reviewed. Recipients of livers from 674 donors were considered informative for hepatitis B virus transmission. Results: Hepatitis B developed in 18 of 23 recipients of livers from anti-HBc-positive donors (78%) compared with only 3 of 651 recipients of anti-HBc-negative donor livers (0.5%) (P < 0.0001). HBsAg persisted in all recipients with donor-related hepatitis B. Liver histology showed chronic hepatitis of moderate severity in 2 of 13 recipients at 1 year and 5 of 8 recipients between 1.6 and 4.5 years from transplantation. Liver transplantation from an anti-HBc-positive donor was associated with decreased 4-year survival (adjusted mortality hazard ratio of 2.4; 95% confidence interval, 1.4-4.0). Conclusions: De novo posttransplantation hepatitis B infection occurs at a high rate in recipients of donors with anti-HBc. Transmission of hepatitis B through transplantation suggests that the virus may persist in the liver despite serological resolution of infection. C1 UNIV VIRGINIA,HLTH SCI CTR,CHARLOTTESVILLE,VA 22903. NIDDK,DIV DIGEST DIS & NUTR,BETHESDA,MD. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT SURG,SAN FRANCISCO,CA 94143. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT EPIDEMIOL,PITTSBURGH,PA 15260. MAYO CLIN & MAYO FDN,DEPT MED,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,DEPT SURG,ROCHESTER,MN 55905. UNIV NEBRASKA,MED CTR,DEPT MED,OMAHA,NE 68105. UNIV NEBRASKA,MED CTR,DEPT SURG,OMAHA,NE 68105. FU NIDDK NIH HHS [N01-DK-0-2251, N01-DK-0-2252, N01-DK-0-2253] NR 33 TC 269 Z9 279 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD NOV PY 1997 VL 113 IS 5 BP 1668 EP 1674 DI 10.1053/gast.1997.v113.pm9352871 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YC790 UT WOS:A1997YC79000036 PM 9352871 ER PT J AU Liang, TJ Koziel, MJ AF Liang, TJ Koziel, MJ TI Circling back to gene vaccines - Reply SO GASTROENTEROLOGY LA English DT Letter C1 BETH ISRAEL DEACONESS MED CTR,DIV INFECT DIS,BOSTON,MA. RP Liang, TJ (reprint author), NIH,LIVER DIS SECT,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD NOV PY 1997 VL 113 IS 5 BP 1813 EP 1814 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YC790 UT WOS:A1997YC79000060 ER PT J AU Choi, C Cho, SH Horikawa, I Berchuck, A Wang, N Cedrone, E Jhung, SW Lee, JB Kerr, J ChenevixTrench, G Kim, SY Barrett, JC Koi, M AF Choi, C Cho, SH Horikawa, I Berchuck, A Wang, N Cedrone, E Jhung, SW Lee, JB Kerr, J ChenevixTrench, G Kim, SY Barrett, JC Koi, M TI Loss of heterozygosity at chromosome segment Xq25-26.1 in advanced human ovarian carcinomas SO GENES CHROMOSOMES & CANCER LA English DT Article ID DINUCLEOTIDE REPEAT POLYMORPHISMS; X-CHROMOSOME; FREQUENT LOSS; LINKAGE MAP; CELL-LINES; LOW-GRADE; CANCER; GENE; LOCUS; ALLELOTYPE AB To determine whether a tumor suppressor gene of importance to epithelial ovarian cancer resides on the X chromosome, we examined loss of heterozygosity (LOH) in 123 epithelial ovarian cancer cases. In 54 such cases, we examined LOH at 26 loci on the human X chromosome. In eight cases, we examined LOH in 14 loci and in 61 cases we examined LOH in 13 loci. Matched DNA samples from tumors and corresponding normal tissues were analyzed by polymerase chain reaction (PCR) amplification of microsatellite markers. Frequent losses were found in epithelial carcinomas at the Xq25-26.1 region, including DXS1206 (34.5% loss in informative cases), DXS1047 (27.7%), HPRT (24.1%), and DXS1062 (33.3%). The minimum overlapping region of LOH was approximately 5 megabases (Mb), flanked by DXS1206 (Xq25) and HPRT (Xq26.1). The methylation status of the remaining allele of the androgen receptor gene in the tumors exhibiting LOH at the Xq25-26.1 region suggested that the loss was exclusively in the inactive X chromosome. We next determined whether a significant relationship exists between Xq LOH and other parameters, including histologic grade and/or clinical stage of the tumors and LOH at TP53. The Xq LOH had a significant association with grade 2 to 3 tumors at stages II to IV. Sixteen of 18 cases that showed Xq LOH revealed LOH at the TP53 locus, and 45% of tumors exhibiting LOH at TP53 showed Xq LOH. These results suggest that there may be a tumor suppressor gene or genes which escape inactivation of the X chromosome at Xq25-26.1, and that the loss of the gene(s) at Xq25-26.1 is frequently accompanied by loss of the TP53 or loss of another gene on chromosome 17. These losses may contribute to the progression from a well-differentiated to a more poorly differentiated state or to metastatic aggressiveness. 1997 Wiley-Liss, Inc.dagger. C1 NIEHS,MOL CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. DUKE UNIV,SCH MED,DEPT OBSTET & GYNECOL,DURHAM,NC. UNIV ROCHESTER,SCH MED & DENT,DEPT PEDIAT,ROCHESTER,NY 14642. CHONNAM NATL UNIV,SCH MED,DEPT PATHOL,KWANGJU 501190,SOUTH KOREA. SEOUL NATL UNIV,SCH MED,DEPT FORENS MED,SEOUL,SOUTH KOREA. QUEENSLAND INST MED RES,BRISBANE,QLD 4006,AUSTRALIA. N CAROLINA STATE UNIV,DEPT STAT,RALEIGH,NC 27695. RI Koi, Minoru/C-3489-2012; Koi, Minoru/G-9197-2014 NR 48 TC 45 Z9 46 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD NOV PY 1997 VL 20 IS 3 BP 234 EP 242 PG 9 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA YE519 UT WOS:A1997YE51900003 PM 9365830 ER PT J AU Schwartzberg, PL Xing, LP Hoffmann, O Lowell, CA Garrett, L Boyce, BF Varmus, HE AF Schwartzberg, PL Xing, LP Hoffmann, O Lowell, CA Garrett, L Boyce, BF Varmus, HE TI Rescue of osteoclast function by transgenic expression of kinase-deficient Src in src-/- mutant mice SO GENES & DEVELOPMENT LA English DT Article DE Src; tyrosine kinase; transgenic mice ID FOCAL ADHESION KINASE; MEDIATED SIGNAL-TRANSDUCTION; C-SRC; TYROSINE KINASE; SUBCELLULAR-LOCALIZATION; INDEPENDENT FUNCTION; BONE-RESORPTION; CELL-ADHESION; SH3 DOMAIN; PHOSPHORYLATION AB The Src tyrosine kinase has been implicated in a wide variety of signal transduction pathways, yet despite the nearly ubiquitous expression of c-src, src-/-mice show only one major phenotype-osteopetrosis caused by an intrinsic defect in osteoclasts, the cells responsible for resorbing bone. To explore further the role of Src both in osteoclasts and other cell types, we have generated transgenic mice that express the wild-type and phosphatase (TRAP), a gene that is expressed highly in osteoclasts. We demonstrate here that expression of a wild-type transgene in only a limited number of tissues can fully rescue the src-l-phenotype. Surprisingly, expression of kinase-defective alleles of c-src also reduces osteopetrosis in src-/-animals and partially rescues a defect in cytoskeletal organization observed in src-l-osteoclasts. These results suggest that there are essential kinase-independent functions for Src in vivo. Biochemical examination of osteoclasts from these mice suggest that Src may function in part by recruiting or activating other tyrosine kinases. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV VIENNA,DEPT PHARMACOL & TOXICOL,VIENNA,AUSTRIA. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. NIH,NATL HUMAN GENOME RES INST,BETHESDA,MD 20892. RP Schwartzberg, PL (reprint author), UNIV TEXAS,HLTH SCI CTR,NATL CANC INST,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAMS NIH HHS [AR 43510, R01 AR043510]; NIDDK NIH HHS [DK 45229] NR 45 TC 229 Z9 231 U1 0 U2 1 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 NOV 1 PY 1997 VL 11 IS 21 BP 2835 EP 2844 DI 10.1101/gad.11.21.2835 PG 10 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA YF583 UT WOS:A1997YF58300008 PM 9353253 ER PT J AU Holbeck, SL Strathern, JN AF Holbeck, SL Strathern, JN TI A role for REV3 in mutagenesis during double-strand break repair in Saccharomyces cerevisiae SO GENETICS LA English DT Article ID DNA-POLYMERASE; ADAPTIVE MUTATION; POINT MUTATIONS; EXCISION-REPAIR; YEAST; GENE; RECOMBINATION; SELECTION; MUTANTS; CELLS AB Recombinational repair of double-strand breaks (DSBs), traditionally believed to be an error-free DNA repair pathway, was recently shown to increase the frequency of mutations in a nearby interval. The reversion rate of trp1 alleles (either nonsense or frameshift mutations) near an HO-endonuclease cleavage site is increased at least 100-fold among cells that have experienced an HO-mediated DSB. We report here that in strains deleted for rev3 this DSB-associated reversion of a nonsense mutation was greatly decreased. Thus REV3, which encodes a subunit of the translesion DNA polymerase zeta, was responsible for the majority of these base substitution errors near a DSB. However, rev3 strains showed no decrease in HO-stimulated recombination, implying that another DNA polymerase also functioned in recombinational repair of a DSB. Reversion of trp1 frameshift alleles near a DSB was not reduced in rev3 strains, indicating that another polymerase could act during DSB repair to make these frameshift errors. Analysis of spontaneous reversion in haploid strains suggested that Rev3p had a greater role in making point mutations than in frameshift mutations. C1 NCI,FREDERICK CANC RES & DEV CTR,LAB EUKARYOT GENE EXPRESS,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 45 TC 156 Z9 157 U1 0 U2 5 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD NOV PY 1997 VL 147 IS 3 BP 1017 EP 1024 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA YF035 UT WOS:A1997YF03500007 PM 9383049 ER PT J AU Pruitt, KD AF Pruitt, KD TI WebWise: Navigating the human genome project SO GENOME RESEARCH LA English DT Article ID SEQUENCE RP Pruitt, KD (reprint author), NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,NIH,BETHESDA,MD 20894, USA. NR 5 TC 7 Z9 7 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 1054-9803 J9 GENOME RES JI Genome Res. PD NOV PY 1997 VL 7 IS 11 BP 1038 EP 1039 PG 2 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA YH823 UT WOS:A1997YH82300002 PM 9371738 ER PT J AU Marra, MA Kucaba, TA Dietrich, NL Green, ED Brownstein, B Wilson, RK McDonald, KM Hillier, LW McPherson, JD Waterston, RH AF Marra, MA Kucaba, TA Dietrich, NL Green, ED Brownstein, B Wilson, RK McDonald, KM Hillier, LW McPherson, JD Waterston, RH TI High throughput fingerprint analysis of large-insert clones SO GENOME RESEARCH LA English DT Article ID COSMID CLONES; PHYSICAL MAP; C-ELEGANS; GENOME; SEQUENCE; CHROMOSOMES AB As part of the Human Genome Project, the Washington University Genome Sequencing Center has commenced systematic sequencing of human chromsome 7. To organize and supply the effort, we have undertaken the construction of sequence-ready physical maps for defined chromosomal intervals. Map construction is a serial process composed of three main activities. First, candidate STS-positive large-insert PAC and BAC clones are identified. Next, these candidate clones are subjected to fingerprint analysis. Finally, the fingerprint data are used to assemble sequence-ready maps. The fingerprinting method we have devised is key to the success of the overall approach. We present here the details of the method and show that the fingerprints are of sufficient quality to permit the construction of megabase-size contigs in defined regions of the human genome. We anticipate that the high throughput and precision characteristic of our fingerprinting method will make it of general utility. C1 NATL HUMAN GENOME RES INST,NIH,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,CTR GENET MED,ST LOUIS,MO 63108. RP Marra, MA (reprint author), WASHINGTON UNIV,SCH MED,GENOME SEQUENCING CTR,ST LOUIS,MO 63108, USA. RI Marra, Marco/B-5987-2008 FU NHGRI NIH HHS [1P50HG01458, 5P01HG00956, P01 HG000956] NR 16 TC 298 Z9 305 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 1054-9803 J9 GENOME RES JI Genome Res. PD NOV PY 1997 VL 7 IS 11 BP 1072 EP 1084 PG 13 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA YH823 UT WOS:A1997YH82300007 PM 9371743 ER PT J AU Tada, Y Horio, Y Takumi, T Terayama, M Tsuji, L Copeland, NG Jenkins, NA Kurachi, Y AF Tada, Y Horio, Y Takumi, T Terayama, M Tsuji, L Copeland, NG Jenkins, NA Kurachi, Y TI Assignment of the glial inwardly rectifying potassium channel K-AB-2/Kir4.1 (Kcnj10) gene to the distal region of mouse chromosome 1 SO GENOMICS LA English DT Article ID RECTIFIER C1 OSAKA UNIV,FAC MED,DEPT PHARMACOL 2,SUITA,OSAKA 565,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. NR 7 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD NOV 1 PY 1997 VL 45 IS 3 BP 629 EP 630 DI 10.1006/geno.1997.4957 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA YF973 UT WOS:A1997YF97300019 PM 9367690 ER PT J AU Lindsay, CK Sinha, CC Thorgeirsson, UP AF Lindsay, CK Sinha, CC Thorgeirsson, UP TI Morphological study of vascular dissemination in a metastatic hepatocellular carcinoma model in the monkey SO HEPATOLOGY LA English DT Article ID TUMOR ANGIOGENESIS; CANCER; CARCINOGENESIS; PATIENT; GROWTH AB In this report we describe a metastatic monkey hepatocellular carcinoma (HCC) model in which intravascular metastatic development is clearly evident, The tumor-bearing livers contained intravenous tumor thrombi at different stages of progression within the small branches of the portal vein. These ranged from mural tumor thrombi lined with CD31-positive endothelial cells to tumor thrombi that had completely occluded the vascular lumen, Intravenous tumor expansion was frequently accompanied by the appearance of CD31-positive microvessels within the tumor thrombi and fibrous perivascular thickening, giving rise to isolated tumor nodules within the portal areas, Intravascular expansion of disseminating HCC was also evident within small branches of the pulmonary arteries in the lungs, These findings indicate that metastases of HCC can become established while still at an intravascular stage, suggesting that the direct interaction between tumor cells and parenchymal cells predicted from experimental rodent metastasis models is not a prerequisite for the metastatic development of these tumors. C1 NCI,TUMOR BIOL & CARCINOGENESIS SECT,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,DIV BASIC SCI,BETHESDA,MD 20892. FU NCI NIH HHS [N01-CP-40510] NR 34 TC 14 Z9 17 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD NOV PY 1997 VL 26 IS 5 BP 1209 EP 1215 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YE989 UT WOS:A1997YE98900020 PM 9362364 ER PT J AU Kresina, TF AF Kresina, TF TI Liver and biliary disease research supported by the National Institutes of Health SO HEPATOLOGY LA English DT Article RP Kresina, TF (reprint author), NIDDK,DIV DIGEST DIS & NUTR,NIH,ROOM 6AN-12A,BLDG 45,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD NOV PY 1997 VL 26 IS 5 BP 1355 EP 1360 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YE989 UT WOS:A1997YE98900040 PM 9362384 ER PT J AU Hoofnagle, JH Everhart, J AF Hoofnagle, JH Everhart, J TI Dose-finding study of interferon alfa-n3 in hepatitis C SO HEPATOLOGY LA English DT Letter RP Hoofnagle, JH (reprint author), NIDDKD,DIV DIGEST DIS & NUTR,NIH,BETHESDA,MD 20892, USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD NOV PY 1997 VL 26 IS 5 BP 1366 EP 1367 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YE989 UT WOS:A1997YE98900043 PM 9362387 ER PT J AU Zhao, H Neamati, N Pommier, Y Burke, TR AF Zhao, H Neamati, N Pommier, Y Burke, TR TI Design and synthesis of photoactivatable coumarin-containing HIV-1 integrase inhibitors SO HETEROCYCLES LA English DT Article AB Three dimeric coumarin analogues (1-3) were prepared, each containing the photoactivatable benzophenone moiety. These compounds exhibited low micromolar IC50 values against HIV-1 integrase mediated 3'-processing and strand transfer, and may represent useful probes for elucidating enzyme-inhibitor interactions. C1 NCI,MOL PHARMACOL LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892. RP Zhao, H (reprint author), NCI,MED CHEM LAB,DIV BASIC SCI,NIH,BLDG 37,ROOM 5C06,BETHESDA,MD 20892, USA. RI Burke, Terrence/N-2601-2014 NR 14 TC 12 Z9 13 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0385-5414 J9 HETEROCYCLES JI Heterocycles PD NOV 1 PY 1997 VL 45 IS 11 BP 2277 EP 2282 PG 6 WC Chemistry, Organic SC Chemistry GA YK546 UT WOS:A1997YK54600023 ER PT J AU Parenti, AR Rugge, M Shiao, YH Ruol, A Ancona, E Bozzola, L Ninfo, V AF Parenti, AR Rugge, M Shiao, YH Ruol, A Ancona, E Bozzola, L Ninfo, V TI bcl-2 and p53 immunophenotypes in pre-invasive, early and advanced oesophageal squamous cancer SO HISTOPATHOLOGY LA English DT Article DE apoptosis; bcl-2; p53; oesophageal cancer; oesophageal carcinogenesis; multistep carcinogenesis ID PROTEIN EXPRESSION; BREAST-CANCER; CARCINOMAS; APOPTOSIS; PATHOGENESIS; CARCINOGENESIS; SURVIVAL; ADENOMAS; TUMORS; CELLS AB Aims: An inverse correlation between bcl-2 and p53 expression has been reported in several types of epithelial tumour. The role of bcl-2 and p53 in the development of oesophageal squamous carcinoma has yet to be established. The expression of bcl-2 and p53 proteins has been evaluated in the multistage oesophageal tumorigenesis, which progresses from normal mucosa to dysplasia (squamous intraepithelial lesion, SIL), to invasive early and advanced oesophageal squamous cancer, Methods and Results: Sixty-four cases of squamous oesophageal cancer, coexisting with SIL in IS cases, were immunohistochemically analysed for ang overexpression of bcl-2 and p53 proteins, Any association of bcl-2 and p53 protein expression with patient survival was also analysed. We observed bcl-2 expression that decreased significantly during the progression of oesophageal carcinogenesis, A decreasing frequency in the expression of bcl-2 in advanced oesophageal squamous cancer coincided with frequent p53 overexpression, bcl-2 expression was correlated with patient survival by univariate analysis, The association disappeared after adjusting for tumour stage, p53 overexpression showed no association with patient survival by either univariate or multivariate analysis. Conclusions: The down-regulation of bcl-2 and upregulation of p53 in advanced oesophageal squamous cancer suggest that bcl-2 and p53 proteins may interact in the progression of oesophageal squamous cancer. C1 UNIV PADUA,DEPT PATHOL,IST ANAT PATOL,ULSS ALTA PADOVANA,I-35121 PADUA,ITALY. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,DBS,NIH,FREDERICK,MD 21702. UNIV PADUA,IST CHIRURG GEN 2,I-35100 PADUA,ITALY. OSPED VICENZA,SERV ANAT PATOL,VICENZA,ITALY. RI Rugge, Massimo/K-7525-2016 NR 33 TC 24 Z9 25 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0309-0167 J9 HISTOPATHOLOGY JI Histopathology PD NOV PY 1997 VL 31 IS 5 BP 430 EP 435 DI 10.1046/j.1365-2559.1997.2970888.x PG 6 WC Cell Biology; Pathology SC Cell Biology; Pathology GA YH489 UT WOS:A1997YH48900006 PM 9416483 ER PT J AU Manickam, P Guru, SC Debelenko, LV Agarwal, SK Olufemi, SE Weisemann, JM Boguski, MS Crabtree, JS Wang, YP Roe, BA Lubensky, IA Zhuang, ZP Kester, MB Burns, AL Spiegel, AM Marx, SJ Liotta, LA EmmertBuck, MR Collins, FS Chandrasekharappa, SC AF Manickam, P Guru, SC Debelenko, LV Agarwal, SK Olufemi, SE Weisemann, JM Boguski, MS Crabtree, JS Wang, YP Roe, BA Lubensky, IA Zhuang, ZP Kester, MB Burns, AL Spiegel, AM Marx, SJ Liotta, LA EmmertBuck, MR Collins, FS Chandrasekharappa, SC TI Eighteen new polymorphic markers in the multiple endocrine neoplasia type 1 (MEN1) region SO HUMAN GENETICS LA English DT Article ID PARATHYROID TUMORS; CHROMOSOME 11Q13; GENETIC-LINKAGE; INTEGRATED MAP; LOCALIZATION; FAMILY AB Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder in which affected individuals develop tumors primarily in the parathyroids, anterior pituitary, endocrine pancreas, and duodenum. The locus fur MEN1 is tightly linked to the marker PYGM on chromosome 11q13, and linkage analysis has previously placed the MEN1 gene within a 2-Mb Interval flanked by markers D11S1883 and D11S449. Loss of heterozygosity (LOH) studies in MEN1 and sporadic tumors have helped narrow the location of the gene to a 600-kb interval between PYGM and D11S449. Eighteen new polymerase chain reaction (PCR)-based polymorphic markers were generated for the MEN1 region, with ten mapping to the PYGM-D11S449 interval. These new markers, along with 14 previously known polymorphic markers, were precisely mapped on a 2.8-Mb (D11S480-D11S913) high-density clone contig-based, physical map generated for the MEN1 region. C1 NATL HUMAN GENOME RES INST,LAB GENE TRANSFER,NIH,BETHESDA,MD 20892. NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. NIDDKD,METAB DIS BRANCH,NIH,BETHESDA,MD 20892. UNIV OKLAHOMA,DEPT CHEM & BIOCHEM,NORMAN,OK 73019. NIH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BETHESDA,MD 20894. RI Agarwal, Sunita/D-1428-2016 OI Agarwal, Sunita/0000-0002-7557-3191 FU NHGRI NIH HHS [HG00313] NR 29 TC 48 Z9 48 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD NOV PY 1997 VL 101 IS 1 BP 102 EP 108 DI 10.1007/s004390050595 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA YC020 UT WOS:A1997YC02000021 PM 9385379 ER PT J AU Sidney, J del Guercio, MF Southwood, S Hermanson, G Maewal, A Appella, E Sette, A AF Sidney, J del Guercio, MF Southwood, S Hermanson, G Maewal, A Appella, E Sette, A TI The HLA-A*0207 peptide binding repertoire is limited to a subset of the A*0201 repertoire SO HUMAN IMMUNOLOGY LA English DT Article ID CLASS-I ALLELES; HLA-A2 SUBTYPES; CELL-LINE; MOLECULES; ANTIGENS; MOTIFS; POLYMORPHISM; EVOLUTIONARY; PURIFICATION; DEFINITION AB Quantitative A*0207 peptide binding assays have been developed utilizing HLA transfected cells and affinity purified molecules. By using a panel of single substitution analog peptides, it was demonstrated that A*0207 binds peptides with main anchor specificity at position 2 and the C-terminus similar to A*0201. Previous data indicating that A*0207 (bur not A*0201) also requires the presence of D or P in position 3 of its peptide ligands was confirmed by the analysis of additional single substituted analogs. Finally, by analyzing the A*0201 and A*0207 binding capacities of panels of unrelated synthetic peptides, it was found that 8/15 (53.3%) A*0201 binders with D or P in position 3 bound A*0207, while only 5/72 (6.9%) A*0201 binders without D or P in position 3 also bound A*0207, Together, these data indicate that although A*0207 may be included amongst A2 supertype alleles, its peptide binding repertoire is largely limited to a subset of that bound by A*0201. (C) American Society for Histocompatibility and Immunogenetics, 1997. Published by Elsevier Science Inc. C1 Cytel Corp, San Diego, CA 92121 USA. NCI, NIH, Bethesda, MD 20892 USA. RP Sette, A (reprint author), Cytel Corp, 3525 John Hopkins Court, San Diego, CA 92121 USA. FU NIAID NIH HHS [N01-AI-45241] NR 26 TC 20 Z9 22 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD NOV PY 1997 VL 58 IS 1 BP 12 EP 20 DI 10.1016/S0198-8859(97)00206-1 PG 9 WC Immunology SC Immunology GA YN918 UT WOS:000071221800002 PM 9438205 ER PT J AU Haider, AW Chen, L Larson, MG Evans, JC Chen, MH Levy, D AF Haider, AW Chen, L Larson, MG Evans, JC Chen, MH Levy, D TI Antecedent hypertension confers increased risk for adverse outcomes after initial myocardial infarction SO HYPERTENSION LA English DT Article; Proceedings Paper CT 68th Annual Scientific Sessions of the American-Heart-Association CY NOV 13-16, 1995 CL ANAHEIM, CA SP Amer Heart Assoc, Brazilian Natl Res Council, Sao Paolo, CNR DE myocardial infarction; Framingham Heart Study; prognosis; epidemiology ID CORONARY HEART-DISEASE; DIASTOLIC BLOOD-PRESSURE; CIGARETTE-SMOKING; SERUM-CHOLESTEROL; PROGNOSIS; FRAMINGHAM; MORTALITY; SURVIVAL; HISTORY; MEN AB Several studies have examined the association of blood pressure (BP) after myocardial infarction (MI) with a risk for adverse outcome; however, few studies have investigated prognosis after MI as a function of BP before MI. Our goal was to examine the relation of antecedent hypertension to risk of adverse outcomes after initial MI. From 1967 to 1990, 404 subjects followed at the Framingham Heart Study developed an initial MI. These subjects were classified on the basis of preinfarction BP into normotensive (BP<140/90 mm Hg and not receiving antihypertensive treatment; n=118), stage I-untreated hypertension (BP 140 to 159/90 to 99 mm Hg; n=89), and stage II to TV or treated hypertension (BP greater than or equal to 160/100 mm Kg or treated hypertension; n=197). Cox models were used to adjust for age, sex, smoking, glucose intolerance, total cholesterol, and prior cardiovascular disease. Antecedent hypertension was related to risk of adverse outcome after MI. Compared with normotensive individuals, stage II to IV hypertensives were at increased risk for reinfarction (hazard ratio [HR], 2.20; 95% confidence interval [CI], 1.20 to 4.04). A similar but nonsignificant association was seen in stage I hypertensives (PFR, 1.91; 95% CI, 0.97 to 3.77). Stage II to IV hypertensives were at increased risk for all-cause mortality compared with normotensive persons (HR, 1.35; 95% CI, 1.07 to 1.98). Thus, even after MI, a history of antecedent hypertension remains predictive of adverse outcome. These findings are consistent with beneficial effects of BP control in primary and secondary prevention settings. Effective BP control may both reduce the risk for an initial MI and improve outcome in the event that an MI occurs. C1 FRAMING HEART STUDY, NHLBI, FRAMINGHAM, MA 01701 USA. NHLBI, BETHESDA, MD 20892 USA. BOSTON UNIV, SCH MED, PREVENT MED & EPIDEMIOL SECT, BOSTON, MA 02118 USA. BETH ISRAEL DEACONESS MED CTR, DIV CARDIOL, BOSTON, MA USA. BETH ISRAEL DEACONESS MED CTR, DIV CLIN EPIDEMIOL, BOSTON, MA USA. FU NHLBI NIH HHS [N01-HC-38038] NR 35 TC 30 Z9 30 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD NOV PY 1997 VL 30 IS 5 BP 1020 EP 1024 PG 5 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YE990 UT WOS:A1997YE99000003 PM 9369249 ER PT J AU Post, WS Larson, MG Myers, RH Galderisi, M Levy, D AF Post, WS Larson, MG Myers, RH Galderisi, M Levy, D TI Heritability of left ventricular mass - The Framingham Heart Study SO HYPERTENSION LA English DT Article DE hypertrophy, left ventricular; genetics; epidemiology; echocardiography ID CONVERTING-ENZYME GENE; HYPERTROPHY; ASSOCIATION; PREVALENCE; GEOMETRY; DISEASE; IMPACT; TWINS AB Left ventricular hypertrophy is associated with an increased risk for cardiovascular disease. The known determinants of left ventricular hypertrophy only partially explain its variability. The purpose of this study was to estimate heritability of left ventricular mass. The study sample included adults in the original Framingham Heart Study and the Framingham Offspring Study who were not receiving antihypertensive medications and who were free of coronary heart disease, congestive heart failure, diabetes mellitus, renal insufficiency, valvular heart disease, and severe left ventricular hypertrophy. Intraclass correlations for left ventricular mass among first-degree relatives, second-degree relatives, and unrelated spouse pairs were calculated to determine the contribution of heredity to the variability in left ventricular mass. After adjustments for age, height, weight, and systolic blood pressure, the intraclass correlations between first-degree relatives were .15 (parent child, P<.001) to .16 (siblings, P<.001), between second-degree relatives the correlation was .06 (P=NS), and between spouses it was .05 (P=NS). The estimated heritability of adjusted left ventricular mass was between .24 and .32. The proportion of the variance in sex-specific left ventricular mass explained by age, height, weight, and systolic blood pressure was .26 in men and .34 in women. On the basis of intraclass correlations for left ventricular mass, incorporation of adjusted left ventricular mass of a parent or sibling would increase the explained variance by an additional .02 to .03. Heredity ex plains a small, but discernible proportion of the variance in left ventricular mass. Studies are currently under way to identify genetic markers that predict an individual's predisposition to left ventricular hypertrophy. This knowledge may lead to advances in the prevention of left ventricular hypertrophy, which is strongly associated with cardiovascular morbidity and mortality. C1 NHLBI, FRAMINGHAM HEART STUDY, FRAMINGHAM, MA 01701 USA. BETH ISRAEL HOSP, DIV CARDIOL, BOSTON, MA 02215 USA. BOSTON UNIV, SCH MED, DEPT NEUROL, BOSTON, MA 02215 USA. BOSTON UNIV, SCH MED, DIV EPIDEMIOL & PREVENT MED, BOSTON, MA 02215 USA. NHLBI, BETHESDA, MD 20892 USA. JOHNS HOPKINS UNIV HOSP, DIV CARDIOL, BALTIMORE, MD 21287 USA. UNIV NAPLES, I-80138 NAPLES, ITALY. OI Galderisi, Maurizio/0000-0003-0311-9069 NR 21 TC 138 Z9 141 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD NOV PY 1997 VL 30 IS 5 BP 1025 EP 1028 PG 4 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YE990 UT WOS:A1997YE99000004 PM 9369250 ER PT J AU DOro, U Vacchio, MS Weissman, AM Ashwell, JD AF DOro, U Vacchio, MS Weissman, AM Ashwell, JD TI Activation of the Lck tyrosine kinase targets cell surface T cell antigen receptors for lysosomal degradation SO IMMUNITY LA English DT Article ID DI-LEUCINE MOTIF; SIGNAL TRANSDUCTION; PROTEIN-KINASE; MONOCLONAL-ANTIBODY; MUTATIONAL ANALYSIS; DOWN-REGULATION; TCR EXPRESSION; COMPLEX; PHOSPHORYLATION; THYMOCYTES AB The mechanism by which TCR expression is regulated was explored by expressing a constitutively active form of the tyrosine kinase Lck (Lck(505F)) in T cells. Expression of Lck(505F) down-regulated TCR levels, an effect that was even more pronounced in CD45(-) T cells, in which the activity of this tyrosine kinase is further enhanced. Cells expressing Lck(505F) synthesized all TCR subunits, but lysosomal degradation of assembled receptors was enhanced. TCRs were rapidly internalized and degraded after removal of a tyrosine kinase inhibitor that had permitted cell surface expression. Finally, TCR levels on thymocytes were increased by an Lck inhibitor, and activation- but not phorbol ester-induced internalization of TCRs on Jurkat cells was prevented by inhibition or loss of Lck. These studies identify a regulated nonreceptor tyrosine kinase-mediated pathway for targeting cell surface receptors for lysosomal degradation. C1 NCI,LAB IMMUNE CELL BIOL,NIH,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL PROD,IMMUNOL LAB,BETHESDA,MD 20852. NR 51 TC 104 Z9 104 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD NOV PY 1997 VL 7 IS 5 BP 619 EP 628 DI 10.1016/S1074-7613(00)80383-0 PG 10 WC Immunology SC Immunology GA YH554 UT WOS:A1997YH55400005 PM 9390686 ER PT J AU Nakajima, H Liu, XW WynshawBoris, A Rosenthal, LA Imada, K Finbloom, DS Hennighausen, L Leonard, WJ AF Nakajima, H Liu, XW WynshawBoris, A Rosenthal, LA Imada, K Finbloom, DS Hennighausen, L Leonard, WJ TI An indirect effect of Stat5a in IL-2-induced proliferation: A critical role for Stat5a in IL-2-mediated IL-2 receptor alpha chain induction SO IMMUNITY LA English DT Article ID DEFECTIVE LYMPHOID DEVELOPMENT; DNA-BINDING ACTIVITY; MAMMARY-GLAND FACTOR; MICE LACKING JAK3; GAMMA-CHAIN; BETA-CHAIN; GENE-EXPRESSION; T-CELLS; INTERLEUKIN-2-DEFICIENT MICE; TARGETED DISRUPTION AB Stat5a was identified as a prolactin-induced transcription factor but also is activated by other cytokines, including interleukin-2 (IL-2) and IL-7. We have now analyzed the immune system of Stat5a-deficient mice. Stat5a(-/-) splenocytes exhibited defective IL-2-induced expression of the IL-2 receptor alpha chain (IL-2R alpha), a protein that together with IL-2R beta and the common cytokine receptor gamma chain (gamma(c)) mediates high-affinity IL-2 binding. Correspondingly, Stat5a(-/-) splenocytes exhibited markedly decreased proliferation to IL-2, although maximal proliferation was still achieved at IL-2 concentrations high enough to titrate intermediate-affinity IL-2R beta/gamma(c) receptors. Thus, defective Stat5a expression results in diminished proliferation by an indirect mechanism, resulting from defective receptor expression. Correspondingly, we show that Stat5a is essential for maximal responsiveness to antigenic stimuli in vivo, underscoring the physiological importance of IL-2-induced IL-2R alpha expression. C1 NHLBI,LAB MOL IMMUNOL,NIHON UNIV,BETHESDA,MD 20892. NIDDKD,BIOCHEM & METAB LAB,NIH,BETHESDA,MD 20892. NATL HUMAN GENOME RES INST,LAB GENET DIS RES,NIH,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,BETHESDA,MD 20892. RI Rosenthal, Louis/A-8868-2008 NR 64 TC 210 Z9 211 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD NOV PY 1997 VL 7 IS 5 BP 691 EP 701 DI 10.1016/S1074-7613(00)80389-1 PG 11 WC Immunology SC Immunology GA YH554 UT WOS:A1997YH55400011 PM 9390692 ER PT J AU Gu, XX Sun, JZ Jin, SJ Barenkamp, SJ Lim, DJ Robbins, JB Battey, J AF Gu, XX Sun, JZ Jin, SJ Barenkamp, SJ Lim, DJ Robbins, JB Battey, J TI Detoxified lipooligosaccharide from nontypeable Haemophilus influenzae conjugated to proteins confers protection against otitis media in chinchillas SO INFECTION AND IMMUNITY LA English DT Article ID NONTYPABLE HEMOPHILUS-INFLUENZAE; OUTER-MEMBRANE PROTEIN; EAR FLUID ANTIBODY; IMMUNE-RESPONSE; BACTERICIDAL ANTIBODY; BIOLOGIC ACTIVITY; SERUM; CHILDREN; MODEL; IMMUNIZATION AB Detoxified-lipooligosaccharide (dLOS)-protein conjugates from nontypeable Haemophilus influenzae (NTHi) elicited a significant rise of anti-LOS antibodies with bactericidal activity in rabbits (X.-X. Gu, C.-M. Tsai, T. Ueyama, S. J, Barenkamp, J. B. Bobbins, and D. J. Lim, Infect. Immun. 64:4047-4053, 1996), In this study, we evaluated whether vaccination with the conjugates would protect against NTHi otitis media in chinchillas. Fifty-eight chinchillas received three subcutaneous or intramuscular injections of dLOS-conjugated tetanus toroid, dLOS-conjugated high-molecular-weight proteins from NTHi, or saline (control) in Freund's adjuvant and then were challenged by intrabullar inoculation with 140 CFU of NTHi. All vaccinated animals responded with elevated serum titers of anti-LOS antibody, and 49% (19 of 39) demonstrated bactericidal activity against the homologous strain. Otitis media with culture-positive NTHi effusions developed in all 19 controls and 56% (22 of 39) of the vaccinated animals during a period of 21 days (P < 0.001). Bacterial counts of the middle ear effusions were lower in the vaccine groups than in the controls (P < 0.01). The incidences of infection in the unchallenged ear or inner ear were 26 or 28% in the vaccine groups and 53 or 58% in the controls (P < 0.05). The signs of infection observed by otoscopy were less severe in the vaccine groups than in the controls. There was no significant difference between the two vaccine groups. These data indicate that active immunization with LOS-based conjugates reduces the incidence of NTHi-induced otitis media. C1 ST LOUIS UNIV,SCH MED,DEPT PEDIAT,ST LOUIS,MO 63104. NICHHD,BETHESDA,MD 20892. RP Gu, XX (reprint author), NIDCD,IMMUNOL LAB,NIH,5 RES COURT,ROCKVILLE,MD 20850, USA. OI Barenkamp, Stephen/0000-0002-3054-8910 NR 42 TC 33 Z9 34 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD NOV PY 1997 VL 65 IS 11 BP 4488 EP 4493 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YD176 UT WOS:A1997YD17600018 PM 9353024 ER PT J AU Benfield, TL Lundgren, B Levine, SJ Kronborg, G Shelhamer, JH Lundgren, JD AF Benfield, TL Lundgren, B Levine, SJ Kronborg, G Shelhamer, JH Lundgren, JD TI The major surface glycoprotein of Pneumocystis carinii induces release and gene expression of interleukin-8 and tumor necrosis factor alpha in monocytes SO INFECTION AND IMMUNITY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; CULTURED LUNG-CELLS; ALVEOLAR MACROPHAGES; PROTEIN-1 NAP-1; PNEUMONIA; AIDS; ATTACHMENT; ANTIGENS; INFLAMMATION; FIBRONECTIN AB Recent studies suggest that interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) may play a central role in host defense and pathogenesis during Pneumocystis carinii pneumonia. In order to investigate whether the major surface antigen (MSG) of human P. carinii is capable of eliciting the release of IL-8 and TNF-alpha, human monocytes were cultured in the presence of purified MSG. MSG-stimulated cells released significant amounts of IL-8 within 4 h, and at 20 h, cells stimulated with MSG released 45.5 +/- 9.3 ng of IL-8/ml versus 3.7 +/- 1.1 ng/ml for control cultures (P = 0.01). In a similar fashion, MSG elicited release of TNF-alpha. Initial increases were also seen at 4 h, and at 20 h, TNF-alpha levels reached 6.4 +/- 1.1 ng/ml, compared to 0.08 +/- 0.01 ng/ml for control cultures (P < 0.01). A concentration-dependent increase in IL-8 and TNF-alpha secretion was observed at 20 h with 0.2 to 5 mu g of MSG/ml (P < 0.01). Secretion of IL-8 and TNF-alpha from MSG-stimulated monocytes at 20 h was inhibited by 60 and 86%, respectively, after coincubation with soluble yeast mannan (P = 0.01). With an RNase protection assay, increases in steady-state mRNA levels for IL-8 and TNF-alpha were detectable at 4 h. These data show that recognition of MSG by monocytes involves a mannose-mediated mechanism and results in the release of the proinflammatory cytokines IL-8 and TNF-alpha. C1 UNIV COPENHAGEN,HVIDOVRE HOSP,DEPT CLIN MICROBIOL,DK-2650 HVIDOVRE,DENMARK. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RP Benfield, TL (reprint author), UNIV COPENHAGEN,HVIDOVRE HOSP,DEPT INFECT DIS 144,DK-2650 HVIDOVRE,DENMARK. RI Kronborg, Gitte/E-4757-2010; OI Lundgren, Jens/0000-0001-8901-7850 NR 43 TC 14 Z9 19 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD NOV PY 1997 VL 65 IS 11 BP 4790 EP 4794 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YD176 UT WOS:A1997YD17600060 PM 9353066 ER PT J AU Luyten, FP AF Luyten, FP TI Cartilage-derived morphogenetic protein-1 SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY LA English DT Article ID FACTOR-BETA SUPERFAMILY; GROWTH/DIFFERENTIATION FACTOR-5; MEMBER AB A new morphogenic secreted protein has been identified with direct evidence for its involvement in skeletal development and joint morphogenesis. Cartilage-derived morphogenetic protein-1 (Cdmp1) and its mouse homologue growth/differentiation factor 5 (Gdf5) mere discovered independently using a degenerate PCR screen for bone morphogenetic protein-like genes. Cdmp1/Gdf5 belongs to the TGF-beta superfamily, a large group of signaling molecules that are secreted as biologically active dimers with a carboxyl-terminal domain containing seven highly conserved cysteines. Its temporal and spatial expression pattern is mostly restricted to the developing appendicular skeleton. Genetic studies revealed that effective null mutations in the gene are associated with short limbs, brachypodism (bp) in mice and acromesomelic chondrodysplasia in humans. Recombinantly expressed protein initiates and promotes chondrogenesis and to a limited extent osteogenesis in vitro and in vivo. This makes this polypeptide a potential therapeutic agent in the regeneration of skeletal tissues. (C) 1997 Elsevier Science Ltd. All rights reserved. C1 NIDR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA. RP Luyten, FP (reprint author), NIDR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA. NR 10 TC 55 Z9 61 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 1357-2725 J9 INT J BIOCHEM CELL B JI Int J. Biochem. Cell Biol. PD NOV PY 1997 VL 29 IS 11 BP 1241 EP 1244 DI 10.1016/S1357-2725(97)00025-3 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA YQ307 UT WOS:000071372200005 PM 9451821 ER PT J AU Becker, KG Lee, IJ Nagle, JW Canning, RD Gado, AM Torres, R Polymeropoulos, MH Massa, PT Biddison, WE Drew, PD AF Becker, KG Lee, IJ Nagle, JW Canning, RD Gado, AM Torres, R Polymeropoulos, MH Massa, PT Biddison, WE Drew, PD TI C2H2-171: A novel human cDNA representing a developmentally regulated POZ domain/zinc finger protein preferentially expressed in brain SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE zinc finger; transcription factor; neurodevelopment ID ZINC-FINGER; ENCODING GENE; CELL LYMPHOMA; WILMS-TUMOR; DROSOPHILA; KRUPPEL; ABNORMALITIES; SEGMENTATION; DIAGNOSIS; TRAMTRACK AB We describe a novel human zinc finger cNDA, C2H2-171. This cDNA represents an mRNA which encodes a protein of 484 amino acids and a calculated molecular weight of 54 kD. Four zinc fingerlike domains are found in the C-terminal end of the protein. At the N-terminus, C2H2-171 contains a POZ/tramtrack-like domain similar to that found in the tumor associated zinc finger proteins LAZ-3/BCL-6 and PLZ-F. as well as in non-zinc finger proteins. C2H2-171 RNA is preferentially expressed in the brain, and increases during the course of murine development, with maximal expression in the adult. C2H2-171 RNA is differentially expressed in bl ain regions, with the highest level of expression in the cerebellum. C2H2-171 RNA was expressed at high levels in primary cerebellar granule cell neurons compared to astrocytes. The gene encoding C2H2-171 is highly conserved in vertebrates, and maps to the terminus of human chromosome 1 (1q44-ter). This chromosomal location is associated with a number of cytogenetic aberrations including those involving brain developmental anomalies and tumorigenesis. These data suggest that C2H2-171 may play an important role in vertebrate brain development and function. (C) 1997 ISDN. Published by Elsevier Science Ltd. C1 NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA. NIAAA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA. NIH, Natl Ctr Human Genome Res, Gene Mapping Unit, Lab Genet Dis Res, Bethesda, MD 20892 USA. SUNY Hlth Sci Ctr, Dept Immunol & Microbiol, Syracuse, NY 13210 USA. SUNY Hlth Sci Ctr, Dept Neurol, Syracuse, NY 13210 USA. RP Drew, PD (reprint author), NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA. OI Becker, Kevin/0000-0002-6794-6656 NR 45 TC 14 Z9 15 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD NOV PY 1997 VL 15 IS 7 BP 891 EP 899 DI 10.1016/S0736-5748(97)00034-8 PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA ZD905 UT WOS:000072736200007 PM 9568537 ER PT J AU Watson, NC Di, YM Orr, MS Fornari, FA Randolph, JK Magnet, KJ Jain, PT Gewirtz, DA AF Watson, NC Di, YM Orr, MS Fornari, FA Randolph, JK Magnet, KJ Jain, PT Gewirtz, DA TI Influence of ionizing radiation on proliferation, c-myc expression and the induction of apoptotic cell death in two breast tumour cell lines differing in p53 status SO INTERNATIONAL JOURNAL OF RADIATION BIOLOGY LA English DT Article ID WILD-TYPE P53; DNA-DAMAGING AGENTS; CANCER CELLS; GROWTH ARREST; EPITHELIAL-CELLS; SUPPRESSOR GENE; LEUKEMIC-CELLS; LYMPHOMA-CELLS; G(1) ARREST; MCF-7 CELLS AB Purpose: To determine the capacity of ionizing radiation to inhibit proliferation, to suppress c-myc expression and to induce apoptotic cell death in the p53 wild-type MCF-7 cell line and the p53 mutated MDA-MB231 cell line. Materials and methods: Growth inhibition and cell killing were determined by cell number and trypan blue exclusion. Apoptosis was assessed through cell morphology and fluorescent end-labelling. c-myc expression was monitored by Northern blotting. Results: Inhibition of cell proliferation by ionizing radiation was similar in both cell lines. MDA-MB231 cells accumulated in G(2) while MCF-7 cells accumulated in both the G(1) and G(2) phases of the cell cycle after irradiation. There was no evidence of apoptosis in either cell line. In MCF-7 cells, growth inhibition correlated closely with an early dose-dependent suppression of c-myc expression; in MDA-MB231 cells, there was no correspondence between growth inhibition and a transient, dose-independent reduction in c-nye message. Conclusions: These findings suggest that in the absence of classical apoptotic cell death, radiosensitivity is not predictably related to the p53 status of the cell. While both p53 and c-myc may be linked to the DNA damage response pathway, neither p53 nor c-myr are essential for growth arrest in response to ionizing radiation. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED PHARMACOL & TOXICOL,RICHMOND,VA 23298. NCI,NIH,BETHESDA,MD 20892. FU NCI NIH HHS [CA55815] NR 85 TC 30 Z9 34 U1 1 U2 4 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0955-3002 J9 INT J RADIAT BIOL JI Int. J. Radiat. Biol. PD NOV PY 1997 VL 72 IS 5 BP 547 EP 559 PG 13 WC Biology; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA YE587 UT WOS:A1997YE58700008 PM 9374435 ER PT J AU Jaffer, FA Wen, H Jezzard, P Balaban, RS Wolff, SD AF Jaffer, FA Wen, H Jezzard, P Balaban, RS Wolff, SD TI Centric ordering is superior to gradient moment nulling for motion artifact reduction in EPI SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE MRI; flow; echo-planar imaging; motion artifact; artifact; phase-encoding ID ECHO-PLANAR; SENSITIVITY; IMAGES; HEART AB Echo-planar imaging [EPI] is sensitive to motion despite its rapid data acquisition rate. Compared with traditional imaging techniques, it is more sensitive to motion or now in the phase-encode direction, which can cause image artifacts such as ghosting, misregistration, and loss of spatial resolution. Consequently, EPI of dynamic structures (eg, the cardiovascular system) could benefit from methods that eliminate these artifacts. In this paper, two methods of artifact reduction for motion in the phase-encode direction are evaluated. First, the k-space trajectory is evaluated by comparing centric with top-down ordered sequences. Next, velocity gradient moment nulling (GMN) of the phase-encode direction is evaluated for each trajectory. Computer simulations and experiments in now phantoms and rabbits in vivo show that uncompensated centric ordering produces the highest image quality. This is probably due to a shorter readout duration, which reduces T2* relaxation losses and off-resonance effects, and to the Linear geometry of phantoms and vessels, which can obscure centric blurring artifacts. C1 NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA. RP Wolff, SD (reprint author), NHLBI, Cardiac Energet Lab, NIH, Bldg 10,Room B1D-161,MSC-1061, Bethesda, MD 20892 USA. RI Balaban, Robert/A-7459-2009; Wen, Han/G-3081-2010; OI Balaban, Robert/0000-0003-4086-0948; Wen, Han/0000-0001-6844-2997; Jaffer, Farouc/0000-0001-7980-384X; Jezzard, Peter/0000-0001-7912-2251 FU NCRR NIH HHS [RR-02050] NR 23 TC 4 Z9 4 U1 0 U2 1 PU SOC MAGNETIC RESONANCE IMAGING PI EASTON PA 1991 NORTHAMPTON ST, EASTON, PA 18042-3189 USA SN 1053-1807 J9 JMRI-J MAGN RESON IM JI JMRI-J. Magn. Reson. Imaging PD NOV-DEC PY 1997 VL 7 IS 6 BP 1122 EP 1131 DI 10.1002/jmri.1880070627 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 102UU UT WOS:000074944300024 PM 9400858 ER PT J AU Rida, W Fast, P Hoff, R Fleming, T AF Rida, W Fast, P Hoff, R Fleming, T TI Intermediate-size trials for the evaluation of HIV vaccine candidates: A workshop summary SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE AIDS vaccines; clinical trials; randomized controlled trials AB There has been considerable debate over what evidence from preclinical and clinical studies is required to advance an HIV vaccine candidate to phase III efficacy testing. Given this situation, conduct of intermediate-size trials is proposed as a method for assessing the plausibility that a vaccine candidate would prevent chronic HIV infection. Designed to observe 45 incident infections in the control group, these preliminary efficacy trials could rule out candidates with low or no efficacy while advancing those candidates with some evidence of protection to definitive trials. In addition, these trials could provide clues about correlates of immunity. A threefold or greater difference in the postvaccination geometric mean titer of neutralizing antibody can be readily detected between infected and uninfected vaccinees. Differences in CD8(+) cytotoxic T lymphocytes, however, are more difficult to detect. Intermediate-size trials could also discern a 0.5 log10 or greater difference in plasma HIV-1 RNA levels between infected vaccinees and infected controls. Such differences in viral load might suggest disease amelioration or reduction in infectiousness. Given the large variability in CD4 count and its relatively modest average decline in the year after infection, a slower decline in CD4 count among infected vaccinees would not be detectable. With limited resources, intermediate-size trials could contribute significantly to HIV vaccine development. C1 UNIV WASHINGTON,DEPT BIOSTAT,SEATTLE,WA 98195. RP Rida, W (reprint author), NIAID,DIV AIDS,BIOSTAT RES BRANCH,SOLAR BLDG,2A02,BETHESDA,MD 20892, USA. NR 9 TC 41 Z9 41 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD NOV 1 PY 1997 VL 16 IS 3 BP 195 EP 203 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YH657 UT WOS:A1997YH65700009 PM 9390572 ER PT J AU Chefer, SI Talan, MI Engel, BT AF Chefer, SI Talan, MI Engel, BT TI Central neural correlates of learned heart rate control during exercise: central command demystified SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE monkeys; nonhuman primates; central nervous system; operant conditioning; tachycardia of exercise ID CARDIOVASCULAR-RESPONSES AB To identify the brain areas involved in central command, four monkeys were trained to attenuate the tachycardia of exercise while different brain sites affecting heart rate (HR) were simultaneously stimulated electrically. Among 24 brain sites located mostly in the limbic structures, we have identified four types of control systems that mediate cardiovascular and motor behavior during exercise. One system increases HR equivalently during both exercise and operantly controlled HR, whereas another increases HR during both tasks and abolishes operant HR control. In the third system, the effect of brain stimulation on HR is attenuated during exercise and during exercise with operantly controlled HR. The fourth system increases HR in both tasks, but its effect is significantly attenuated during operant HR control. We believe that this last system, which includes the mediodorsal nucleus, nucleus ventralis anterior, and cingulate cortex, plays a significant role in central command. C1 NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,NIH,BALTIMORE,MD 21224. NR 14 TC 8 Z9 8 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD NOV PY 1997 VL 83 IS 5 BP 1448 EP 1453 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA YE867 UT WOS:A1997YE86700006 PM 9375304 ER PT J AU Freeman, BD Quezado, Z Zeni, F Natanson, C Danner, RL Banks, S Quezado, M Fitz, Y Bacher, J Eichacker, PQ AF Freeman, BD Quezado, Z Zeni, F Natanson, C Danner, RL Banks, S Quezado, M Fitz, Y Bacher, J Eichacker, PQ TI rG-CSF reduces endotoxemia and improves survival during E-coli pneumonia SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Thoracic-Society CY MAY, 1995 CL BOSTON, MA SP Amer Thorac Soc DE neutrophil; endotoxin; recombinant granulocyte colony-stimulating factor; sepsis; septic shock; Escherichia coli ID COLONY-STIMULATING FACTOR; TUMOR-NECROSIS-FACTOR; ACUTE LUNG INJURY; HUMAN SEPTIC SHOCK; CANINE MODEL; GUINEA-PIGS; GRANULOCYTE; LIPOPOLYSACCHARIDE; SEPSIS; RATS AB We investigated the effects of recombinant granulocyte colony-stimulating factor (rG-CSF) during canine bacterial pneumonia. Beagles with chronic tracheostomies received daily subcutaneous rG-CSF (5 mu g/kg body wt) or placebo for 14 days, beginning 9 days before intrabronchial inoculation with E. coli. Animals received antibiotics and fluid support; a subset received humidified oxygen (fractional inspired O-2 0.40). Compared with controls, rG-CSF increased circulating neutrophil counts (57.4 vs. 11.0 x 10(3)/mm(3), day 1 after infection; P = 0.0001), decreased plasma endotoxin (7.5 vs. 1.1 EU/ml at 8 h; P < 0.01) and serum tumor necrosis factor-alpha (3,402 vs. 729 pg/ml at 2 h; P = 0.01) levels, and prolonged survival (relative risk of death = 0.45, 95% confidence interval 0.21-0.97; P = 0.038). Also, rG-CSF attenuated sepsis-associated myocardial dysfunction (P < 0.001). rG-CSF had no effect on pulmonary function or on blood and lung bacteria counts (all P = not significant). Other animals challenged with endotoxin (4 mg/kg iv) after similar treatment with rG-CSF had lower serum endotoxin levels (7.62 vs. 5.81 log EU/ml at 6 h; P < 0.01) and less cardiovascular dysfunction (P < 0.05 to < 0.002) but similar tumor necrosis factor-alpha levels (P = not significant) compared with controls. Thus prophylactic rG-CSF sufficient to increase circulating neutrophils during bacterial pneumonia may improve cardiovascular function and survival by mechanisms that in part enhance the clearance of bacterial toxins but do not improve lung function. C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 40 TC 37 Z9 37 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD NOV PY 1997 VL 83 IS 5 BP 1467 EP 1475 PG 9 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA YE867 UT WOS:A1997YE86700009 PM 9375307 ER PT J AU Lindle, RS Metter, EJ Lynch, NA Fleg, JL Fozard, JL Tobin, J Roy, TA Hurley, BF AF Lindle, RS Metter, EJ Lynch, NA Fleg, JL Fozard, JL Tobin, J Roy, TA Hurley, BF TI Age and gender comparisons of muscle strength in 654 women and men aged 20-93 yr SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE eccentric strength; gender differences ID STRETCH-SHORTENING CYCLE; QUADRICEPS MUSCLES; PLANTAR FLEXION; KNEE EXTENSION; YOUNG; TORQUE; FEMALES; ENERGY; MALES; ELBOW AB To assess age and gender differences in muscle strength, isometric, concentric (Con), and eccentric (Ecc) peak torque was measured in the knee extensors at a slow (0.52 rad/s) and fast (3.14 rad/s) velocity in 654 subjects (346 men and 308 women, aged 20-93 yr) from the Baltimore Longitudinal Study of Aging. Regression analysis revealed significant (P < 0.001) age-related reductions in Con and Ecc peak torque for men and women at both velocities, but no differences were observed between the gender groups or velocities. Age explained losses in Con better than Ecc peak torque, accounting for 30% (Con) vs. 19% (Ecc) of the variance in men and 28% (Con) vs. 11% (Ecc) in women. To assess age and gender differences in the ability to store and utilize elastic energy, the stretch-shortening cycle was determined in a subset of subjects (it = 47). The older women (mean age = 70 yr) showed a significantly greater enhancement in the stretch-shortening cycle, compared with men of similar age (P < 0.01) and compared with younger men and women (each P < 0.05). Both men and women showed significant declines in muscle quality for Con peak torque (P < 0.01), but no gender differences were observed. Only the men showed a significant decline in muscle quality (P < 0.001) for Ecc peak: torque. Thus both men and women experience age-related losses in isometric, Con, and Ecc knee extensor peak torque; however, age accounted for less of the variance in Ecc peak torque in women, and women tend to better preserve muscle quality with age for Ecc peak torque. In addition, older women have an enhanced capacity to store and utilize elastic energy compared with similarly aged men as well as with younger women and men. C1 UNIV MARYLAND,DEPT KINESIOL,COLL HLTH & HUMAN PERFORMANCE,COLLEGE PK,MD 20742. NIA,GERONTOL RES CTR,NIH,BALTIMORE,MD 21224. RI Fozard, James Leonard/B-3660-2009 NR 35 TC 399 Z9 416 U1 5 U2 24 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD NOV PY 1997 VL 83 IS 5 BP 1581 EP 1587 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA YE867 UT WOS:A1997YE86700025 PM 9375323 ER PT J AU Sandkvist, M Michel, LO Hough, LP Morales, VM Bagdasarian, M Koomey, M DiRita, VJ Bagdasarian, M AF Sandkvist, M Michel, LO Hough, LP Morales, VM Bagdasarian, M Koomey, M DiRita, VJ Bagdasarian, M TI General secretion pathway (eps) genes required for toxin secretion and outer membrane biogenesis in Vibrio cholerae SO JOURNAL OF BACTERIOLOGY LA English DT Article ID LABILE ENTERO-TOXIN; GRAM-NEGATIVE BACTERIA; EXTRACELLULAR PROTEIN SECRETION; ESCHERICHIA-COLI K-12; PSEUDOMONAS-AERUGINOSA; ERWINIA-CHRYSANTHEMI; NEISSERIA-GONORRHOEAE; PREPILIN PEPTIDASE; AEROMONAS-HYDROPHILA; CYTOPLASMIC MEMBRANE AB The general secretion pathway (GSP) of Vibrio cholerae is required for secretion of proteins including chitinase, enterotoxin, and protease through the outer membrane. In this study, we report the cloning and sequencing of a DNA fragment from V. cholerae, containing 12 open reading frames, epsC to -N, which are similar to GSP genes of Aeromonas, Erwinia, Klebsiella, Pseudomonas, and Xanthomonas spp. In addition to the two previously described genes, epsE and epsM (M. Sandkvist, V. Morales, and hi. Bagdasarian, Gene 123: 81-86, 1993; L. J. Overbye, M. Sandkvist, and M. Bagdasarian, Gene 132:101-106, 1993), it is shown here that epsC, epsF, epsG, and epsL also encode proteins essential for GSP function, Mutations in the Eps genes result in aberrant outer membrane protein profiles, which indicates that the GSP, or at least some of its components, is required not only for secretion of soluble proteins but also for proper outer membrane assembly. Several of the Eps proteins have been identified by use of the T7 polymerase-promoter system in Escherichia coli. One of them, a pilin-like protein, EpsG, was analyzed also in V. cholerae and found to migrate as two bands on polyacrylamide gels, suggesting that in this organism it might be processed or otherwise modified by a prepilin peptidase. We believe that TcpJ prepilin peptidase, which processes the subunit of the toxin coregulated pilus, TcpA, is not involved in this event. This is supported by the observations that apparent processing of EpsG occurs in a tcpJ mutant of V. cholerae and that, when coexpressed in E. coli, TcpJ cannot process EpsG although the PilD peptidase from Neisseria gonorrhoeae can. C1 MICHIGAN STATE UNIV, DEPT MICROBIOL, E LANSING, MI 48824 USA. MICHIGAN STATE UNIV, NSF CTR MICROBIOL ECOL, E LANSING, MI 48824 USA. NIDR, ORAL INFECT & IMMUN BRANCH, NIH, BETHESDA, MD 20892 USA. BRIGHAM & WOMENS HOSP, DIV GASTROENTEROL, BOSTON, MA 02115 USA. UNIV MICHIGAN, DEPT MICROBIOL & IMMUNOL, ANN ARBOR, MI 48109 USA. FU NCRR NIH HHS [MO1 RR00042]; NIAID NIH HHS [AI-31645, T32 AI-07360] NR 75 TC 133 Z9 142 U1 1 U2 6 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0021-9193 EI 1098-5530 J9 J BACTERIOL JI J. Bacteriol. PD NOV PY 1997 VL 179 IS 22 BP 6994 EP 7003 PG 10 WC Microbiology SC Microbiology GA YG075 UT WOS:A1997YG07500017 PM 9371445 ER PT J AU Yang, XP He, F Rawson, TY Wilson, SH AF Yang, XP He, F Rawson, TY Wilson, SH TI Human DNA polymerase-beta promoter: Phorbol ester activation is mediated through the cAMP response element and cAMP-response-element-binding protein SO JOURNAL OF BIOMEDICAL SCIENCE LA English DT Article DE promoter; transcription factor; transactivation; signal transduction; phorbol ester; protein kinase A; protein kinase C; DNA repair enzyme ID TRANSCRIPTION FACTOR; CYCLIC-AMP; KINASE-C; LEUCINE ZIPPER; FACTOR CREB; PHOSPHORYLATION; FAMILY; JUN; CONTAINS; COMMON AB That mammalian DNA polymerase-beta (beta-pol) gene transcription is upregulated by activated ras and also by phorbol ester (TPA) treatment suggests the involvement of protein kinase C in the gene expression control for this DNA repair enzyme. Yet, the core promoters of the human, bovine and rodent beta-pol genes do not have a TPA response element or other binding site for the transcriptional activator AP-1. Instead, these beta-pol promoters appear to be regulated mainly by proteins binding to the cAMP response element (CRE) centered within 50 bp 5' of the transcriptional start site. In this study, the CRE in the human beta-pol promoter was found to mediate TPA upregulation of the cloned promoter in HeLa cell transient expression experiments. To further examine the role of this CRE in TPA stimulation, we used several mutated promoters that were either deficient in protein binding to the CRE or contained extra CRE sites arranged as tandem repeats. All constructs with at least one functional CRE were upregulated by TPA, whereas mutants lacking CRE protein-binding function were not TPA upregulated. Analyses of HeLa nuclear extract DNA-binding proteins indicated that the beta-pol CRE was bound by CRE-binding protein (CREB) family members CREB-1 and activating transcription factor-1, but not by AP-1 or complexes containing AP-1 subunits. These results suggest that CREB, rather than AP-1 proteins, are required for the CRE-mediated TPA activation of the beta-pol promoter. C1 Univ Texas, Med Branch, Sealy Ctr Mol Sci, Galveston, TX 77550 USA. RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, B2-06,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA. EM wilson5@niebs.nih.gov NR 33 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1021-7770 J9 J BIOMED SCI JI J. Biomed. Sci. PD NOV-DEC PY 1997 VL 4 IS 6 BP 279 EP 288 DI 10.1007/BF02258351 PG 10 WC Cell Biology; Medicine, Research & Experimental SC Cell Biology; Research & Experimental Medicine GA YR320 UT WOS:000071483400002 ER PT J AU Looker, AC Orwoll, ES Johnston, CC Lindsay, RL Wahner, HW Dunn, WL Calvo, MS Harris, TB Heyse, SP AF Looker, AC Orwoll, ES Johnston, CC Lindsay, RL Wahner, HW Dunn, WL Calvo, MS Harris, TB Heyse, SP TI Prevalence of low femoral bone density in older US adults from NHANES III SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article; Proceedings Paper CT 17th Annual Meeting of the American-Society-for-Bone-and-Mineral-Research CY SEP 09-13, 1995 CL BALTIMORE, MD SP Amer Soc Bone & Mineral Res ID MEXICAN-AMERICAN WOMEN; HIP FRACTURE; MINERAL DENSITY; OSTEOPOROTIC FRACTURES; POSTMENOPAUSAL WOMEN; SEX-DIFFERENCES; SECULAR TRENDS; PREDICTION; MASS; RISK AB Most estimates of osteoporosis in older U.S. adults have been based on its occurrence in white women, even though it is known to affect men and minority women, In the present study, we used dual-energy X-ray absorptiometry measurements of femoral bone mineral density (BMD) from the third National Health and Nutrition Examination Survey (NHANES III, 1988-1994) to estimate the overall scope of the disease in the older U.S. population, Specifically, we estimate prevalences of low femoral BMD in women 50 years and older and explore different approaches for defining low BMD in older men ire that age range, Low BMD levels were defined in accordance with an approach proposed by an expert panel of the World Health Organization and used BMD data from 382 non-Hispanic white (NHW) men or 409 NHW women ages 20-29 years from the NHANES III dataset, For women, estimates indicate 13-18%, or 4-6 million, have osteoporosis (i.e., BMD >2.5 standard deviations [SD] below the mean of young NHW women) and 37-50%, or 13-17 million, have osteopenia (BMD between 1 and 2.5 SD below the mean of young NHW women), For men, these numbers depend on the gender of the reference group used to define cutoff values, When based on male cutoffs, 3-6% (1-2 million) of men have osteoporosis and 28-47% (8-13 million) have osteopenia; when based on female cutoffs, 1-4% (280,000-1 million) have osteoporosis and 15-33% (4-9 million) have osteopenia, Most of the older U.S. adults with low femur BMD are women, but, regardless of which cutoffs are used, the number of men is substantial. C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. PORTLAND VA MED CTR,PORTLAND,OR. INDIANA UNIV,MED CTR,INDIANAPOLIS,IN. HELEN HAYES HOSP,REG BONE CTR,W HAVERSTRAW,NY. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. US FDA,CTR FOOD SAFETY & APPL NUTR,WASHINGTON,DC 20204. NIA,NIH,BETHESDA,MD 20892. NIAID,NIH,BETHESDA,MD 20892. RP Looker, AC (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR HLTH STAT,DIV HLTH EXAMINAT STAT,6525 BELCREST RD,ROOM 900,HYATTSVILLE,MD 20782, USA. OI Orwoll, Eric/0000-0002-8520-7355 NR 47 TC 673 Z9 697 U1 7 U2 20 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD NOV PY 1997 VL 12 IS 11 BP 1761 EP 1768 DI 10.1359/jbmr.1997.12.11.1761 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YE194 UT WOS:A1997YE19400001 PM 9383679 ER PT J AU Goldsmith, PK Fan, GF Miller, JL Rogers, KV Spiegel, AM AF Goldsmith, PK Fan, GF Miller, JL Rogers, KV Spiegel, AM TI Monoclonal antibodies against synthetic peptides corresponding to the extracellular domain of the human Ca2+ receptor: Characterization and use in studying concanavalin A inhibition SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID CALCIUM-SENSING RECEPTOR; BOVINE PARATHYROID CELLS; MESSENGER-RIBONUCLEIC-ACID; CA2+-SENSING RECEPTOR; FUNCTIONAL EXPRESSION; MOLECULAR-CLONING; MUTATIONS; KIDNEY; ACCUMULATION; PROTEINS AB We generated monoclonal antibodies against two synthetic peptides corresponding to residues 214-235 (ADD) and 374-391 (LRG) of the human Ca2+ receptor (hCaR) extracellular domain (ECD). Although both antibodies reacted well with their respective immunizing peptides on peptide-based enzyme linked immunosorbent assay. ADD tvas much more strongly reactive with the hCaR than LRG in assays such as immunoblots done under denaturing conditions. The opposite pattern mas seen in flow cytometry analysis of the native receptor stably expressed in transfected 293 cells. We speculate that the ADD epitope is unexposed in the native receptor while the reverse is true for the LRG epitope. The ability to measure cell surface expression of the hCaR under native conditions using flow cytometry with the LRG monoclonal allowed us to study the basis for Concanavalin A (Con A) inhibition of CaR activation by Ca2+. Our studies show that Con A inhibition is partially accounted far by receptor internalization but, additionally, Con A may prevent Ca2+ stimulation directly by binding to carbohydrate residues in the receptor ECD. C1 NIDDKD, METAB DIS BRANCH, NIH, BETHESDA, MD 20892 USA. NIDDKD, BIOL CHEM LAB, NIH, BETHESDA, MD 20892 USA. NPS PHARMACEUT, SALT LAKE CITY, UT USA. NR 18 TC 40 Z9 40 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD NOV PY 1997 VL 12 IS 11 BP 1780 EP 1788 DI 10.1359/jbmr.1997.12.11.1780 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YE194 UT WOS:A1997YE19400004 PM 9383682 ER PT J AU Malide, D Cushman, SW AF Malide, D Cushman, SW TI Morphological effects of wortmannin on the endosomal system and GLUT4-containing compartments in rat adipose cells SO JOURNAL OF CELL SCIENCE LA English DT Article DE wortmannin; GLUT4; adipose cell; confocal microscopy ID STIMULATED GLUT4 TRANSLOCATION; PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY; GLUCOSE-TRANSPORT; 3T3-L1 ADIPOCYTES; PHOSPHOINOSITIDE 3-KINASE; ENDOCYTIC PATHWAY; GROWTH-FACTOR; 1-PHOSPHATIDYLINOSITOL 3-KINASE; TRANSFERRIN RECEPTORS; INSULIN AB Studies using functional and pharmacological approaches have implicated PI 3-kinase as a key intermediate in the glucose transport and GLUT4 translocation responses to insulin, Confocal microscopy was used to investigate the effects of the PI 3-kinase inhibitor wortmannin in isolated rat adipose cells, Independent of insulin, wortmannin induces the appearance of phase-lucent vacuoles containing the endosomal markers TfR, Rab4, M6PR, and cellubrevin, When added before or with insulin, wortmannin blocks insulin-stimulated GLUT4 translocation, but does not influence the basal VAMP2-containing GLUT4 compartment, These results substantiate the concept of a specialized basal GLUT4 compartment mostly distinct from that of the recycling receptors. However, when added after insulin, wortmannin induces a rapid redistribution of GLUT4 from the cell surface into those endosomal-derived vacuoles where the GLUT4 co-localize with TfR, Rab4, cellubrevin, and VAMP2, but not with clathrin, M6PR, Golgi complex markers TGN38-mannosidase II and gamma-adaptin, and lysosomal marker lgp-120, Therefore, wortmannin also disrupts insulin-stimulated GLUT4 traffic in the recycling endosomal pathway, at a step distal to the sorting of recycling proteins from late endosomal and TGN markers; wortmannin does not appear to affect internalization from the plasma membrane, and delivery from early to late endosomes or from late endosomes to the TGN, Tn combination with previous kinetic biochemical studies, these results suggest that: (i) insulin stimulates the exocytosis of GLUT4 through a direct pathway from a specialized basal compartment to the plasma membrane, (ii) during endocytosis in the presence of insulin, GLUT4 is sorted out of the TfR compartment into a separate recycling pathway back to the plasma membrane, and (iii) both of these pathways involve wortmannin sensitive enzymes. C1 NIDDK, Expt Diabet Metab & Nutr Sect, Diabet Branch, NIH, Bethesda, MD 20892 USA. RP Malide, D (reprint author), NIDDK, Expt Diabet Metab & Nutr Sect, Diabet Branch, NIH, Bethesda, MD 20892 USA. NR 64 TC 37 Z9 38 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD NOV PY 1997 VL 110 BP 2795 EP 2806 PN 22 PG 12 WC Cell Biology SC Cell Biology GA YM087 UT WOS:000071027100003 PM 9427288 ER PT J AU Close, MJ Howlett, AR Roskelley, CD Desprez, PY Bailey, N Rowning, B Teng, CT Stampfer, MR Yaswen, P AF Close, MJ Howlett, AR Roskelley, CD Desprez, PY Bailey, N Rowning, B Teng, CT Stampfer, MR Yaswen, P TI Lactoferrin expression in mammary epithelial cells is mediated by changes in cell shape and actin cytoskeleton SO JOURNAL OF CELL SCIENCE LA English DT Article DE mammary epithelium; lactoferrin; cell shape; cytoskeleton; extracellular matrix; mRNA stability ID RECONSTITUTED BASEMENT-MEMBRANE; CASEIN GENE-EXPRESSION; EXTRACELLULAR-MATRIX; FUNCTIONAL-DIFFERENTIATION; SIGNAL-TRANSDUCTION; GROWTH; FIBRONECTIN; MORPHOGENESIS; COMPONENTS; PROTEIN AB Lactoferrin is a secreted iron binding protein which is expressed during normal functional development of mammary epithelium. Murine mammary epithelial cell lines competent for milk protein expression were used to identify microenvironmental factors that regulate lactoferrin expression. While lactoferrin was not expressed in adherent monolayer cultures under standard subconfluent conditions on plastic, lactoferrin mRNA and protein steadily accumulated when the cells aggregated to form spheroids on a reconstituted basement membrane gel. However, unlike other milk proteins such as beta-casein, lactoferrin expression was also induced at high cell density in the absence of exogenously added basement membrane or prolactin. These results led us to examine whether changes in cell growth, cell-cell interactions and/or cell shape were responsible for regulation of lactoferrin gene expression. Rounded, non-proliferating cells in suspension in serum-free medium expressed lactoferrin even as single cells. Conversely, lactoferrin expression could be inhibited in non-proliferative cells in serum-free medium by maintaining them in contact with an air-dried extracellular matrix which caused the cells to retain flat, spread morphologies. These findings indicated that cessation of cell growth was not sufficient, that cell-cell interactions were not required, and that cell culture conditions which minimize cell spreading may be important in maintaining lactoferrin expression. Additional data supporting this latter concept were generated by treating spread cells with cytochalasin D. The resulting disruption of microfilament assembly induced both cell rounding and lactoferrin expression. Shape-dependent regulation of lactoferrin mRNA was both transcriptional and post-transcriptional. Surprisingly, treatment of rounded cells with a transcription inhibitor, actinomycin D, produced a stabilization of lactoferrin mRNA, suggesting that transcription of an unstable factor is required for degradation of lactoferrin mRNA. Importantly, lactoferrin mRNA expression was regulated similarly in early passage normal human mammary epithelial cells. In vivo, the changing extracellular matrix components of the mammary gland during different stages of normal and abnormal growth and differentiation may provide different physical constraints on the configurations of cell surface molecules. These physical constraints may be communicated to the cell interior through mechanical changes in the cytoskeleton. Unlike beta-casein whose expression is upregulated by specific integrin-mediated signals, lactoferrin may be representative of a class of proteins synthesized in the mammary gland using basal transcriptional and translational machinery. The suppression of lactoferrin expression that is observed in monolayer culture and in malignant tissues may reflect inappropriate cell shapes and cytoskeletal structures that are manifested under these conditions. C1 Univ Calif Berkeley, Lawrence Berkeley Lab, Dept Phys, Div Life Sci, Berkeley, CA 94720 USA. Berlex Biosci, Richmond, CA 94804 USA. Univ British Columbia, Dept Anat, Vancouver, BC V6T 1Z3, Canada. NIEHS, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA. RP Yaswen, P (reprint author), Univ Calif Berkeley, Lawrence Berkeley Lab, Dept Phys, Div Life Sci, Berkeley, CA 94720 USA. RI Roskelley, Calvin /F-4630-2011 FU NCI NIH HHS [CA-24844, CA-57621] NR 72 TC 49 Z9 51 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD NOV PY 1997 VL 110 BP 2861 EP 2871 PN 22 PG 11 WC Cell Biology SC Cell Biology GA YM087 UT WOS:000071027100009 PM 9427294 ER PT J AU Menard, S Castronovo, V Tagliabue, E Sobel, ME AF Menard, S Castronovo, V Tagliabue, E Sobel, ME TI New insights into the metastasis-associated 67 kD laminin receptor SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE adhesion receptors; tumor progression; ribosomal proteins; laminin; cancer ID BREAST-CANCER CELLS; MULTICOPY GENE FAMILY; HUMAN COLON-CANCER; SER-ARG YIGSR; BINDING-PROTEIN; MESSENGER-RNA; LUNG-CANCER; RIBOSOMAL-PROTEIN; DIFFERENTIAL EXPRESSION; PROGNOSTIC-SIGNIFICANCE AB The interactions between tumor cells and laminin or other components of the extracellular matrix have been shown to play an important role in tumor invasion and metastasis. These interactions are mediated by different eel I surface molecules, including the monomeric 67 kD laminin receptor. This molecule appears to be very peculiar since so far only a full-length gene encoding a 37 kD precursor protein has been isolated and the mechanism by which the precursor reaches the mature form is not understood. Based on clinical data, which clearly demonstrate the importance of the receptor in tumor progression, studies were conducted to define the structure, expression, and function of this laminin receptor as a step toward developing therapeutic strategies that target this molecule. The data suggest that acylation of the precursor is the key mechanism in maturation of the 67 kD form. The function of the membrane receptor is to stabilize the binding of laminin to cell surface integrins, acting as an integrin-accessory molecule, although homology of the gene encoding the receptor precursor with other genes suggests additional functions. Downregulation of the receptor expression on tumor cells might open new therapeutic approaches to decrease tumor aggressiveness. (C) 1997 Wiley-Liss, Inc. C1 UNIV LIEGE, METASTASIS RES LAB, LIEGE, BELGIUM. NCI, MOL PATHOL SECT, BETHESDA, MD 20814 USA. RP Menard, S (reprint author), IST NAZL STUDIO & CURA TUMORI, DIV EXPT ONCOL E, VIA VENEZIAN 1, I-20133 MILAN, ITALY. RI Tagliabue, Elda/B-9377-2017 OI Tagliabue, Elda/0000-0001-9877-2903 NR 95 TC 106 Z9 108 U1 0 U2 5 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 NOV 1 PY 1997 VL 67 IS 2 BP 155 EP 165 DI 10.1002/(SICI)1097-4644(19971101)67:2<155::AID-JCB1>3.3.CO;2-O PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA XZ506 UT WOS:A1997XZ50600001 PM 9328821 ER PT J AU Palka, JA Phang, JM AF Palka, JA Phang, JM TI Prolidase activity in fibroblasts is regulated by interaction of extracellular matrix with cell surface integrin receptors SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE prolidase; fibroblasts; collagen; integrins; extracellular matrix-cell interaction ID L-PROLINE; DEFICIENCY; COLLAGEN; PROTEINS; IMINODIPEPTIDURIA; LOCALIZATION; HYDROLYSIS; EXPRESSION; CLEAVAGE; PH AB Prolidase (EC 3.4.13.9) is a ubiquitously distributed imidodipeptidase that catalyzes the hydrolysis of C-terminal proline or hydroxyproline containing dipeptides. The enzyme plays an important role in the recycling of proline for collagen synthesis and cell growth. An increase in enzyme activity is correlated with increased rates of collagen turnover indicative of extracellular matrix (ECM) remodeling, but the mechanism linking prolidase activity and ECM is poorly understood. Thus, the effect of ECM-cell interaction on intracellular prolidase activity is of special interest. In cultured human skin fibroblasts, the interaction with ECM and, more specifically, type I collagen mediated by the beta(1) integrin receptor regulates cellular prolidase activity. Supporting evidence comes from the following observations: 1) in sparse cells with a low amount of ECM collagen or in confluent cells in which ECM collagen was removed by collagenase (but not by trypsin or elastase) treatment, prolidase activity was decreased; 2) this effect was reversed by the addition of type I collagen or beta(1) integrin antibody (agonist for beta(1) integrin receptor); 3) sparse cells (with typically low prolidase activity) showed increased prolidase activity when grown on plates coated with type I collagen or on type IV collagen and laminin, constituents of basement membrane; 4) the relative differences in prolidase activity due to collagenase treatment and subsequent recovery of the activity by beta(1) integrin antibody or type I collagen treatment were accompanied by parallel differences in the amount of the enzyme protein recovered from these cells, as shown by Western immunoblot analysis. Thus, we conclude that prolidase activity responded to ECM metabolism (tissue remodeling) through signals mediated by the integrin receptor. (C) 1997 Wiley-Liss, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,LNMR,DIV BASIC SCI,FREDERICK,MD 21702. NR 35 TC 112 Z9 111 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD NOV 1 PY 1997 VL 67 IS 2 BP 166 EP 175 DI 10.1002/(SICI)1097-4644(19971101)67:2<166::AID-JCB2>3.0.CO;2-V PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA XZ506 UT WOS:A1997XZ50600002 PM 9328822 ER PT J AU Hall, CW McLachlan, KR Krag, SS Robbins, AR AF Hall, CW McLachlan, KR Krag, SS Robbins, AR TI Reduced utilization of Man(5)GlcNAc(2)-P-P-lipid in a Lec9 mutant of Chinese hamster ovary cells: Analysis of the steps in oligosaccharide-lipid assembly SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE dolichol; polyprenol; translocation; glycosylation sites; eukaryotic cells ID STOMATITIS VIRUS-G; RAT-LIVER; GLYCOSYLATION REACTIONS; ENZYMES; MANNOSYLPHOSPHORYLDOLICHOL; GLYCOPROTEIN; PHOSPHATASE; DEFICIENT; DOLICHOL; PROTEIN AB Recently we reported that CHB11-1-3, a Chinese hamster ovary cell mutant defective in glycosylation of asparagine-linked proteins, is defective in the synthesis of dolichol [Quellhorst et al., 343:19-26, 1997: Arch Biochem Biophys]. CHB11-1-3 was found to be in the Lec9 complementation group, which synthesizes polyprenol rather than dolichol. In this paper, levels of various polyprenyl derivatives in CHB11-1-3 are compared to levels of the corresponding dolichyl derivatives in parental cells. CHB11-1-3 was found to maintain near normal levels of Man(5)GlcNAc(2)-P-P-polyprenol and mannosylphosphorylpolyprenol, despite reduced rates of synthesis, by utilizing those intermediates at a reduced rate. The Man(5)GlcNAc(2) oligosaccharide attached to prenol in CHB11-1-3 cells and to dolichol in parental cells is the same structure, as determined by acetolysis. Man(5)GlcNAc(2)-P-P-polyprenol and Man(5)GlcNAc(5)-P-P-dolichol both appeared to be translocated efficiently in an in vitro reaction. Glycosylation of G protein was compared in vesicular stomatitus virus (VSV)-infected parent and mutant; although a portion of G protein was normally glycosylated in CHB11-1-3 cells, a large portion of G was underglycosylated, resulting in the addition of either one or no oligosaccharide to C. Addition of a single oligosaccharide occurred randomly rather than preferentially at one of the two sites. (C) 1997 Wiley-Liss, Inc. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT BIOCHEM,BALTIMORE,MD 21205. NIDDK,BIOCHEM & METAB LAB,NIH,BETHESDA,MD 20892. FU NCI NIH HHS [R01CA20421]; NIEHS NIH HHS [T32ES07141] NR 31 TC 7 Z9 7 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 NOV 1 PY 1997 VL 67 IS 2 BP 201 EP 215 DI 10.1002/(SICI)1097-4644(19971101)67:2<201::AID-JCB5>3.0.CO;2-0 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA XZ506 UT WOS:A1997XZ50600005 PM 9328825 ER PT J AU Wang, XW Harris, CC AF Wang, XW Harris, CC TI p53 tumor-suppressor gene: Clues to molecular carcinogenesis SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article; Proceedings Paper CT 9th International Conference of the International-Society-of-Differentiation on Development, Cell Differentiation and Cancer CY SEP 28-OCT 02, 1996 CL PISA, ITALY SP Int Soc Differentiat Inc ID WILD-TYPE P53; CELL-CYCLE CONTROL; DNA-REPAIR GENE; TRANSCRIPTIONAL ACTIVATION; IN-VIVO; P53-DEPENDENT APOPTOSIS; IONIZING-RADIATION; BINDING PROTEIN; GROWTH ARREST; CDNA CLONE C1 NCI,HUMAN CARCINOGENESIS LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892. RI Wang, Xin/B-6162-2009 NR 153 TC 72 Z9 73 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD NOV PY 1997 VL 173 IS 2 BP 247 EP 255 DI 10.1002/(SICI)1097-4652(199711)173:2<247::AID-JCP30>3.0.CO;2-A PG 9 WC Cell Biology; Physiology SC Cell Biology; Physiology GA YE456 UT WOS:A1997YE45600030 PM 9365531 ER PT J AU De Luca, LM Scita, G Takatsuka, J AF De Luca, LM Scita, G Takatsuka, J TI Retinoic acid downregulates growth, fibronectin and RAR alpha in 3T3 cells: Ha-ras blocks this response and RA metabolism SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article; Proceedings Paper CT 9th International Conference of the International-Society-of-Differentiation on Development, Cell Differentiation and Cancer CY SEP 28-OCT 02, 1996 CL PISA, ITALY SP Int Soc Differentiat Inc ID BREAST-CANCER CELLS; MESSENGER-RNA LEVELS; HUMAN-LEUKEMIA CELLS; INVIVO METABOLISM; LAMININ RECEPTOR; EXPRESSION; IDENTIFICATION; ONCOGENE; GENE; CYTOCHROME-P-450 AB Retinoic acid (RA) reduced growth, fibronectin, and retinoic acid receptor (RAR alpha) in NIH 3T3 cells but not in cells transformed by the Ha-ras oncogene. RA lowered RAR alpha transcript and protein, increased RAR beta transcripts, and had no effect on RAR gamma. H-ras transformation downregulated RAR expression and abolished responsiveness to RA. Ha-ras-transformed cells were as active as normal NIH-3T3 cells in RA uptake but were unable to degrade it to medium oxidation products, so that, paradoxically, the resistant cells accumulated 20-30-fold as much RA as the sensitive cells. RA sensitivity/insensitivity correlated with RA metabolism/lack thereof in 15 cell lines in serum-free medium. These data suggest a relationship between RA inhibition of cell growth and intracellular RA metabolism. (C) 1997 Wiley-Liss, Inc.(dagger) C1 NCI, CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB, NIH, BETHESDA, MD 20892 USA. NR 38 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD NOV PY 1997 VL 173 IS 2 BP 297 EP 300 DI 10.1002/(SICI)1097-4652(199711)173:2<297::AID-JCP39>3.0.CO;2-A PG 4 WC Cell Biology; Physiology SC Cell Biology; Physiology GA YE456 UT WOS:A1997YE45600039 PM 9365540 ER PT J AU Ghizzoni, L Mastorakos, G Street, ME Vottero, A Mazzardo, G Vanelli, M Chrousos, GP Bernasconi, S AF Ghizzoni, L Mastorakos, G Street, ME Vottero, A Mazzardo, G Vanelli, M Chrousos, GP Bernasconi, S TI Spontaneous thyrotropin and cortisol secretion interactions in patients with nonclassical 21-hydroxylase deficiency and control children SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article; Proceedings Paper CT 35th Annual Meeting of the European-Society-for-Pediatric-Endocrinology CY SEP 15-18, 1996 CL MONTPELLIER, FRANCE SP European Soc Pediat Endocrinol ID STRESS-INDUCED INHIBITION; GROWTH-HORMONE SECRETION; ADDISONS-DISEASE; TSH SECRETION; RAT; GLUCOCORTICOIDS; EXPRESSION; PROLACTIN; SYSTEM AB Both exogenous and endogenous hypercortisolism result in reduced TSH secretion and mild hypothyroidism. However, little is known about the relation between endogenous TSH and cortisol secretion under physiological or slightly disturbed conditions. To examine this, we evaluated the pulsatility and circadian rhythmicity and time-cross-correlated the 24-h secretory patterns of cortisol and TSH in eight prepubertal children with nonclassical congenital adrenal hyperplasia (NCCAH) and eight age-matched short normal children. In both groups, TSH and cortisol were secreted in a pulsatile and circadian fashion, with a clear nocturnal TSH surge. Although no difference in mean 24-h TSH levels was observed between the two groups, daytime TSH levels were lower in the NCCAH group than in control children (P < 0.05). The cross-correlation analysis of the 24-h raw data showed that TSH and cortisol were negatively correlated, with a 2.5-h lag time for both groups, with cortisol leading TSH. This correlation might reflect a negative glucocorticoid effect exerted on the hypothalamic-pituitary-thyroid axis under physiological conditions. A significant positive correlation with TSH leading cortisol was observed at 8.5 and 5.5 h lag times for the control and NCCAH groups, respectively. The substantially shorter lag time of this positive correlation in NCCAH children than in controls suggests that in the latter, the nocturnal TSH peak occurs temporally closer to their compromised morning cortisol peak. These data indicate that the hypothalamic-pituitary-adrenal axis has a primarily negative influence on endogenous TSH secretion and that even mild disturbances in cortisol biosynthesis are associated with slight alterations in TSH secretion. C1 UNIV MODENA, DEPT PEDIAT, I-41100 MODENA, ITALY. UNIV ATHENS, SCH MED, EVGENID HOSP, ENDOCRINE UNIT, ATHENS 11528, GREECE. NICHHD, DEV ENDOCRINOL BRANCH, NIH, BETHESDA, MD 20892 USA. RP Ghizzoni, L (reprint author), UNIV PARMA, DEPT PEDIAT, VIA GRAMSCI 14, I-43100 PARMA, ITALY. NR 28 TC 5 Z9 6 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD NOV PY 1997 VL 82 IS 11 BP 3677 EP 3683 DI 10.1210/jc.82.11.3677 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YF271 UT WOS:A1997YF27100025 PM 9360525 ER PT J AU Eisenhofer, G Aneman, A Friberg, P Hooper, D Fandriks, L Lonroth, H Hunyady, B Mezey, E AF Eisenhofer, G Aneman, A Friberg, P Hooper, D Fandriks, L Lonroth, H Hunyady, B Mezey, E TI Substantial production of dopamine in the human gastrointestinal tract SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID LIQUID-CHROMATOGRAPHY; TYROSINE-HYDROXYLASE; CATECHOLAMINES; PLASMA; SECRETION; RECEPTORS; PANCREAS; SYSTEM; 3,4-DIHYDROXYPHENYLALANINE; LYMPHOCYTES AB Considerable urinary excretion of dopamine metabolites indicates that large amounts of dopamine are produced in unknown locations of the body. This study assessed the contribution of mesenteric organs (gastrointestinal tract, spleen, and pancreas) to the total body production of dopamine in humans and examined the presence of the rate-limiting enzyme for dopamine synthesis, tyrosine hydroxylase, in gastrointestinal tissues. Blood sampled from an artery and portal and hepatic veins in eight subjects and from arterial and renal venous sites in other subjects was analyzed for plasma concentrations of dopamine and its metabolites. The activity and distribution of tyrosine hydroxylase was also examined in tissue samples from the stomach and duodenum. Higher concentrations of dopamine and its metabolites in portal venous than arterial plasma indicated substantial production of dopamine by mesenteric organs (12.0 nmol/min) amounting to 42-46% of the renal removal of circulating dopamine metabolites. Tissue samples showed immunoreactive tyrosine hydroxylase in nonneuronal cell bodies and detectable levels of tyrosine hydroxylase enzyme activity. The results show that mesenteric organs produce close to half of the dopamine formed in the body, most of which is unlikely to be derived from sympathetic nerves but may reflect production in a novel nonneuronal dopaminergic system. C1 GOTHENBURG UNIV, DEPT PHYSIOL, GOTHENBURG, SWEDEN. GOTHENBURG UNIV, DEPT CLIN PHYSIOL, GOTHENBURG, SWEDEN. RP Eisenhofer, G (reprint author), NINCDS, CLIN NEUROSCI BRANCH,NIH,BLDG 10,ROOM 4D20, 10 CTR DR, BETHESDA, MD 20892 USA. NR 37 TC 105 Z9 107 U1 0 U2 8 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD NOV PY 1997 VL 82 IS 11 BP 3864 EP 3871 DI 10.1210/jc.82.11.3864 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YF271 UT WOS:A1997YF27100054 PM 9360553 ER PT J AU OShea, JJ Notarangelo, LD Johnston, JA Candotti, F AF OShea, JJ Notarangelo, LD Johnston, JA Candotti, F TI Advances in the understanding of cytokine signal transduction: The role of Jaks and STATs in immunoregulation and the pathogenesis of immunodeficiency SO JOURNAL OF CLINICAL IMMUNOLOGY LA English DT Review DE cytokines; signal transduction; Jaks; STATs; immunoregulation; immunodeficiency ID RECEPTOR-GAMMA-CHAIN; PROTEIN-TYROSINE KINASE; DNA-BINDING ACTIVITY; COLONY-STIMULATING FACTOR; NATURAL-KILLER-CELLS; DEFECTIVE LYMPHOID DEVELOPMENT; ACUTE LYMPHOBLASTIC-LEUKEMIA; X-CHROMOSOME INACTIVATION; GROWTH-HORMONE RECEPTOR; I INTERFERON RECEPTOR AB Cytokines are of great importance in the growth and differentiation of hematopoietic and other cells. Moreover, they are also crucial in immunoregulation and in host defense. Although our understanding of the molecular basis of cytokine action is far from complete, recent advances have substantially improved our knowledge of cytokine-dependent signal transduction. The delineation of the structure of cytokine receptors and the signaling pathways they utilize has provided clues as to how the strikingly specific effects of cytokines are achieved. Additionally, the basis of some of the pleiotropic and redundant effects of cytokines has also become clear. The discovery of the Janus family of protein tyrosine kinases (Jaks) and the STATs (signal transducers and activators of transcription) has also provided key insights into the mechanism by which intracellular signals are transduced. The following paradigm has emerged: cytokines induce dimerization of receptor subunits that are constitutively associated with Jaks. This activates the Jaks, which then phosphorylate the receptors. The phosphorylated receptors are bound by SH2-containing proteins, one class of which is the STATs. Activated STATs, then, translocate to the nucleus to effect gene transcription. Though the Jaks do not explain much in terms of specificity in signaling, the function of the STATs does. The discovery of patients with autosomal recessive severe combined immunodeficiency due to mutations of a particular Jak, Jak3, and the phenotype of knockout mice lacking Jak3 and various STATs demonstrate the specific and critical roles of these molecules in the development and function of the immune system. C1 NIAMSD,LYMPHOCYTE CELL BIOL SECT,ARTHRIT & RHEUMATISM BRANCH,NIH,BETHESDA,MD 20892. UNIV BRESCIA,DEPT PEDIAT,BRESCIA,ITALY. DNAX RES INST MOL & CELLULAR BIOL INC,PALO ALTO,CA 94304. RI Notarangelo, Luigi/F-9718-2016 OI Notarangelo, Luigi/0000-0002-8335-0262 NR 213 TC 30 Z9 31 U1 2 U2 3 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0271-9142 J9 J CLIN IMMUNOL JI J. Clin. Immunol. PD NOV PY 1997 VL 17 IS 6 BP 431 EP 447 DI 10.1023/A:1027388508570 PG 17 WC Immunology SC Immunology GA YK845 UT WOS:A1997YK84500001 PM 9418183 ER PT J AU Adamson, PC Reaman, G Finklestein, JZ Feusner, J Berg, SL Blaney, SM OBrien, M Murphy, RF Balis, FM AF Adamson, PC Reaman, G Finklestein, JZ Feusner, J Berg, SL Blaney, SM OBrien, M Murphy, RF Balis, FM TI Phase I trial and pharmacokinetic study of all-trans-retinoic acid administered on an intermittent schedule in combination with interferon-alpha 2a in pediatric patients with refractory cancer SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACUTE PROMYELOCYTIC LEUKEMIA; HUMAN NEURO-BLASTOMA; THERAPEUTIC ANTICANCER AGENTS; HUMAN NEUROBLASTOMA-CELLS; 13-CIS-RETINOIC ACID; SOLID TUMORS; DIFFERENTIATION; EXPRESSION; CHILDREN; GROWTH AB Purpose: Po determine the maximum-tolerated dose (MTD) of all-trans-retinoic acid (ATRA) administered on an intermittent oral schedule with interferon-alpha 2a (IFN-alpha 2a) in children with refractory cancer, and whether the marked reduction in plasma ATRA concentrations observed with chronic daily oral dosing could be circum vented with an intermittent dosing schedule. Patients and Methods: Thirty-three children with refractory cancer (stratified by age, less than or equal to 12 and > 12 years) were treated with ATRA 3 consecutive days per week and IFN-alpha 2a 3 x 10(6) U/m(2) 5 consecutive days per week, both repeated weekly. The starting dose of ATRA was 60 mg/m(2)/d divided into three doses, with planned escalations to 90 and a 120 mg/m(2)/d. Because severe headaches have been noted to occur on the initial day of ATRA administration, only two of three doses of ATRA were administered on day 1 of each week. Results: Pseudotumor cerebri or dose-limiting headache was observed in two of five patients older than 12 years treated at the a 120-mg/m(2)/d dose: level and in one of six less than or equal to 12 years at the 90-mg/m(2)/d level, Other non-dose-limiting toxicities of ATRA included reversible elevations in hepatic transaminases and triglycerides, dry skin, cheilitis, and nausea/vomiting. One child with recurrent neuroblastoma had an objective response of 6 months' duration, and one with recurrent Wilms' turner had histologic maturation of multiple tumors. This intermittent schedule allowed for exposure to relatively high plasma concentrations of ATRA on a repetitive basis, following 30-mg/m(2) doses, the ATRA area under the concentration-time curve (AUG) decreased from 96+/-14 mu mol/L/min on day a to 26+/-24 mu mol/L/min by day 3 of drug administration, but on day if of the fourth consecutive week of therapy, the AUC averaged 110+/-16 mu mol/L/min. The recommended pediatric phase II dose of ATRA administered an this schedule is 90 mg/m(2)/d. Conclusion: An intermittent schedule of ATRA administration appears 40 circumvent the low plasma drug exposure that is a result of the sustained upregulation of metabolism when this drug is administered an a chronic daily schedule. Based an the results of this trial, a phase II trial of ATRA/IFN-alpha 2a in neuroblastoma and Wilms' tumor using this schedule is in progress. C1 CHILDRENS CANC GRP, ARCADIA, CA USA. RP Adamson, PC (reprint author), NCI, PEDIAT BRANCH, BLDG 10, ROOM 13N240, 10 CTR DR, BETHESDA, MD 20892 USA. FU NCI NIH HHS [CA13539] NR 44 TC 51 Z9 54 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD NOV PY 1997 VL 15 IS 11 BP 3330 EP 3337 PG 8 WC Oncology SC Oncology GA YE015 UT WOS:A1997YE01500006 PM 9363862 ER PT J AU Longo, DL Glatstein, E Duffey, PL Young, RC Ihde, DC Bastian, AW Wilson, WH Wittes, RE Jaffe, ES Hubbard, SM DeVita, VT AF Longo, DL Glatstein, E Duffey, PL Young, RC Ihde, DC Bastian, AW Wilson, WH Wittes, RE Jaffe, ES Hubbard, SM DeVita, VT TI Alternating MOPP and ABVD chemotherapy plus mantle-field radiation therapy in patients with massive mediastinal Hodgkin's disease SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COMBINED MODALITY THERAPY; PROGNOSTIC-SIGNIFICANCE; COMBINATION CHEMOTHERAPY; STAGE-I; INVOLVEMENT; RISK; RADIOTHERAPY; MANAGEMENT; TRIAL AB Purpose: To evaluate Pine efficacy and toxicity of mechlorethamine, vincristine, procarbazine, and prednisone (MOPP)/doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) chemotherapy plus mantle-field radiation therapy in the treatment of patients with massive mediastinal Hodgkin's disease of any stage. Patients and Methods: Eighty patients presented with Hodgkin's disease and a mediastinal mass greater than one third the greatest chest diameter on chest radiograph. Patients were staged and treated with MOPP alternated with ABVD chemotherapy for a total of six cycles. patients then received 10 Gy mantle-field radiation therapy delivered to the original extent of disease followed by 25 to 35 Gy to the residual abnormalities. Results: The complete response (CR) rate was 89%, With a median follow-up duration of 10 years, disease-free survives of the complete responders is 78% at 15 )rears and overall survival is 75% at 15 years, For patients with stage I or II disease, disease-free survival was 76% at 15 years and overall survival was 79%; for those with stage III or IV disease, disease-free survival was 82% at 15 years and overall survival was 64%. age, stage, sew, B symptoms, number of extranodal sites, lactate dehydrogenase (LDH) levels, erythrocyte sedimentation rate, and platelet count did net influence treatment outcome, Treatment-related pneumonitis was noted in 16% of patients (fatal in one), mainly in those alder than age 35 years who received total doses of radiation therapy greater than 42 Gy, Fertility is more often preserved with MOPP/ABVD therapy than with MOPP chemotherapy and there appears to be less pulmonary and cardiac disease than with ABVD chemortherapy, Two patients have developed second solid tumors within radiation ports and one relapsed patient developed acute leukemia after MOPP salvage therapy. Conclusion: MOPP/ABVD followed by mantle-field radiation therapy is an effective treatment for all stages of Hodgkin's disease that present with a large mediastinal mass, Our data suggest that the large mediastinal mass is a more dominant determinant of prognosis than Ann arbor stage or other clinical prognostic factors. C1 USN,MED ONCOL BRANCH,RADIAT ONCOL BRANCH,MED BRANCH,BETHESDA,MD 20084. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 28 TC 38 Z9 39 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD NOV PY 1997 VL 15 IS 11 BP 3338 EP 3346 PG 9 WC Oncology SC Oncology GA YE015 UT WOS:A1997YE01500007 PM 9363863 ER PT J AU Munoz, KA Harlan, LC Trimble, EL AF Munoz, KA Harlan, LC Trimble, EL TI Patterns of care for women with ovarian cancer in the United States SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID PROGNOSTIC FACTORS; RANDOMIZED TRIAL; STAGE-I; CARCINOMA; CISPLATIN; SURVIVAL; MANAGEMENT; AGE; CYCLOPHOSPHAMIDE; CHEMOTHERAPY AB Purpose: To characterize treatments for ovarian cancer, to determine if recommended staging and treatment were provided, and to determine factors that influence receipt of recommended staging and treatment. Methods: A total of 785 women diagnosed with ovarian cancer in 1991 were selected from the National Cancer Institute (NCI) Surveillance, Epidemiology, and End Results (SEER) program, Type and receipt of recommended staging and treatment were examined using data on surgery and physician-verified chemotherapy. Results: Most women with presumptive stage I and II ovarian cancer were treated with surgery alone (58%), while women with stage III or IV disease were treated with surgery plus platinum-based chemotherapy (75% stage III, 56% stage IV). Approximately 10% of women with presumptive stage I and II, 71% with stage III, and 53% with stage IV disease received recommended staging and treatment, The absence of lymphadenectomy and assignment of histologic grade were the primary reasons women with presumptive stage I and II cancer did not receive recommended staging and treatment, whereas for stages III and IV, it was due to older women not receiving surgery plus platinum-based adjuvant chemotherapy, Age, stage, comorbidity, ''other'' race ethnicity, and treatment at a facility with an approved residency training program were associated with whether recommended staging and therapy were received. Conclusion: Older women with late-stage disease did not receive recommended treatment, The majority of women with early-stage disease did not receive recommended staging and treatment. C1 NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,NIH,BETHESDA,MD 20892. NCI,CANC THERAPY EVALUAT PROGRAM,DIV CANC TREATMENT DIAGNOSIS & CTR,NIH,BETHESDA,MD 20892. NR 48 TC 102 Z9 102 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD NOV PY 1997 VL 15 IS 11 BP 3408 EP 3415 PG 8 WC Oncology SC Oncology GA YE015 UT WOS:A1997YE01500017 PM 9363873 ER PT J AU Brown, R Buckley, R Kelley, M AF Brown, R Buckley, R Kelley, M TI Pancreatic panniculitis SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID DISEASE C1 NCI, BETHESDA, MD 20892 USA. RP Brown, R (reprint author), NATL NAVAL MED CTR, BETHESDA, MD 20889 USA. OI Kelley, Michael/0000-0001-9523-6080 NR 5 TC 7 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD NOV PY 1997 VL 15 IS 11 BP 3418 EP 3419 PG 2 WC Oncology SC Oncology GA YE015 UT WOS:A1997YE01500019 PM 9363875 ER PT J AU Denicoff, KD SmithJackson, EE Disney, ER Ali, SO Leverich, GS Post, RM AF Denicoff, KD SmithJackson, EE Disney, ER Ali, SO Leverich, GS Post, RM TI Comparative prophylactic efficacy of lithium, carbamazepine, and the combination in bipolar disorder SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT 2nd International Conference on Bipolar Disorder CY JUN 19, 1997 CL PITTSBURGH, PA ID RECURRENT AFFECTIVE DISORDERS; MANIC-DEPRESSIVE ILLNESS; CARBONATE; PREVENTION; TRIAL; IMIPRAMINE; SYNERGISM AB Background: We compared the prophylactic efficacy of lithium, carbamazepine, and the combination and identified possible clinical markers of response. Method: Fifty-two outpatients who met DSM-III-R criteria for bipolar illness were randomly assigned in a double-blind design fur an intended I year of treatment with lithium or carbamazepine, a crossover to the opposite drug in the second gear, and then a third year on the combination, Patients received monthly detailed evaluations, and daily life chart ratings of the degree of functional incapacity associated with mania or depression were completed. Results: For evaluable patients: 13 (31.0%) of 42 failed to complete a full year of lithium therapy owing to lack of efficacy, and 2 dropped our because of side effects, 13 (37.1%) of 35 withdrew from carbamazepine within the first year owing to lack of efficacy, and 10 dropped out because of side effects (9 of the 10 had a rash; 7 (24.1%) of 29 withdrew from the combination therapy owing to lack of efficacy. The percentage of the evaluable patients who had marked or moderate improvement on the Clinical Global Impressions scale was 33.3% on lithium, 11.4% on carbamazepine, and 55.2% on the combination treatment, which was not significantly different, By a variety of measures, lithium was more effective than carbamazepine in the prophylaxis of mania, Patients with a past history of rapid cycling did poorly on monotherapy (28.0% responded to lithium; 19.0% responded to carbamazepine), but significantly better on the combination (56.3%, p < .05). Conclusion: These prospective, randomized data suggest a high incidence of inadequate response to either mood stabilizer or their combination despite use of adjunctive agents as needed, Additional novel treatment regimens are needed to better decrease affective morbidity in large numbers of bipolar outpatients. RP Denicoff, KD (reprint author), NIMH,SECT PSYCHOBIOL,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI Ali, Syed/0000-0003-3131-3299 NR 54 TC 236 Z9 237 U1 1 U2 4 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD NOV PY 1997 VL 58 IS 11 BP 470 EP 478 DI 10.4088/JCP.v58n1102 PG 10 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA YL173 UT WOS:A1997YL17300002 PM 9413412 ER PT J AU Lakein, DA Fantie, BD Grafman, J Ross, S AF Lakein, DA Fantie, BD Grafman, J Ross, S TI Patients with chronic fatigue syndrome and accurate feeling-of-knowing judgments SO JOURNAL OF CLINICAL PSYCHOLOGY LA English DT Article ID MULTIPLE-SCLEROSIS; HOSPITAL ANXIETY; DEPRESSION SCALE; CUE-FAMILIARITY; KNOWLEDGE; MORBIDITY; RECALL; LEVEL AB Many Chronic Fatigue Syndrome (CFS) patients complain of memory impairments which have been difficult to document empirically Subjective complaints of memory impairment may be due to a deficit in metamemory judgment. CFS patients and matched controls were tested with a computerized Trivia Information Quiz that required them to rate their confidence about correctly recognizing an answer in a multiple choice format that they had been unable to remember in a fact-recall format. Even though CFS patients reported significantly greater amounts of fatigue, cognitive. and physical symptoms. the accuracy of their confidence levels and recognition responses were similar to controls. This finding suggests that a metamemory deficit is not the cause of the memory problems reported by CFS patients. (C) 1997 John Wiley & Sons, Inc. C1 NINCDS,COGNIT NEUROSCI SECT,NIH,MNB,BETHESDA,MD 20892. AMERICAN UNIV,WASHINGTON,DC 20016. OI Grafman, Jordan H./0000-0001-8645-4457 NR 38 TC 5 Z9 5 U1 0 U2 1 PU CLINICAL PSYCHOLOGY PUBL CO PI BRANDON PA 4 CONANT SQUARE, BRANDON, VT 05733 SN 0021-9762 J9 J CLIN PSYCHOL JI J. Clin. Psychol. PD NOV PY 1997 VL 53 IS 7 BP 635 EP 645 DI 10.1002/(SICI)1097-4679(199711)53:7<635::AID-JCLP1>3.0.CO;2-H PG 11 WC Psychology, Clinical SC Psychology GA YB742 UT WOS:A1997YB74200001 PM 9356893 ER PT J AU Ishai, A Sagi, D AF Ishai, A Sagi, D TI Visual imagery: Effects of short- and long-term memory SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID MENTAL-IMAGERY; CORTEX; BRAIN; REPRESENTATION; RECOGNITION; MECHANISMS; PERCEPTION; PATTERNS; CONTRAST; AGNOSIA AB Visual imagery and perception share several functional properties and apparently share common underlying brain structures. A main approach to the scientific study of visual imagery is exploring the effects of mental imagery on perceptual professes. Previous studies have shown that visual imagery interferes with perception (Perky effect). Recently we have shown a direct facilitatory effect of visual imagery on visual perception. In an attempt to differentiate the conditions under which visual imagery interferes or facilitates visual perception, we designed new experimental paradigms, using detection tasks of a Gabor target. We found that imagery-induced interference and facilitation are memory-dependent: Visual recall of common objects from long-term memory can interfere with perception, while on short-term memory tasks facilitation can be obtained. These results support the distinction between low-level and structure representations in visual memory. C1 Weizmann Inst Sci, IL-76100 Rehovot, Israel. RP Ishai, A (reprint author), NIMH, Lab Brain & Cognit, NIH, Bldg 10,Room 4C110, Bethesda, MD 20892 USA. NR 39 TC 18 Z9 18 U1 0 U2 3 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD NOV PY 1997 VL 9 IS 6 BP 734 EP 742 DI 10.1162/jocn.1997.9.6.734 PG 9 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA YM577 UT WOS:000071078700004 PM 23964596 ER PT J AU Casey, BJ Trainor, RJ Orendi, JL Schubert, AB Nystrom, LE Giedd, JN Castellanos, FX Haxby, JV Noll, DC Cohen, JD Forman, SD Dahl, RE Rapoport, JL AF Casey, BJ Trainor, RJ Orendi, JL Schubert, AB Nystrom, LE Giedd, JN Castellanos, FX Haxby, JV Noll, DC Cohen, JD Forman, SD Dahl, RE Rapoport, JL TI A developmental functional MRI study of prefrontal activation during performance of a Go-No-Go task SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; ANTERIOR CINGULATE CORTEX; FRONTAL-LOBE; WORKING-MEMORY; SENSORY STIMULATION; SIGNAL CHANGES; HUMAN INFANTS; LESIONS; CHILDREN; MONKEYS AB This study examines important developmental differences in patterns of activation in the prefrontal cortex during performance of a Go-No-Go paradigm using functional magnetic resonance imaging (fMRI). Eighteen subjects (9 children and 9 adults) were scanned using gradient echo, echo planar imaging during performance of a response inhibition task. The results suggest four general findings. First, the location of activation in the prefrontal cortex was not different between children and adults, which is similar to our earlier pediatric fMRI results of prefrontal activation during a working memory task (Casey et al., 1995). Second, the volume of activation was significantly greater for children relative to adults. These differences in volume of activation were observed predominantly in the dorsal and lateral prefrontal cortices. Third, although inhibitory processes have typically been associated with more ventral or orbital frontal regions, the current study revealed activation that was distributed across both dorsolateral and orbitofrontal cortices. Finally, consistent with animal and human lesion studies, activity in orbital frontal and anterior cingulate cortices correlated with behavioral performance (i.e., number of false alarms). These results further demonstrate the utility of this methodology in studying pediatric populations. C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Med Ctr, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, Pittsburgh, PA 15213 USA. NIMH, Rockville, MD 20857 USA. RP Casey, BJ (reprint author), Univ Pittsburgh, Western Psychiat Inst & Clin, Med Ctr, Room E-735,3811 OHara St, Pittsburgh, PA 15213 USA. EM bjcasey@pitt.edu RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Noll, Douglas/D-8124-2014; Giedd, Jay/J-9644-2015 OI Giedd, Jay/0000-0003-0827-3460; Noll, Douglas/0000-0002-0983-3805; Giedd, Jay/0000-0003-2002-8978 NR 58 TC 610 Z9 620 U1 8 U2 88 PU MIT PRESS PI CAMBRIDGE PA 55 HAYWARD STREET, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD NOV PY 1997 VL 9 IS 6 BP 835 EP 847 DI 10.1162/jocn.1997.9.6.835 PG 13 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA YM577 UT WOS:000071078700011 PM 23964603 ER PT J AU MenottiRaymond, M David, VA Stephens, JC Lyons, LA OBrien, SJ AF MenottiRaymond, M David, VA Stephens, JC Lyons, LA OBrien, SJ TI Genetic individualization of domestic cats using feline STR loci for forensic applications SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE forensic science; feline short tandem repeat forensic panel; genetic individualization of domestic cats ID PERSONAL IDENTIFICATION APPLICATIONS; DEOXYRIBONUCLEIC-ACID DNA; POLYMERASE CHAIN-REACTION; TANDEM REPEAT LOCI; LINKAGE MAP; DINUCLEOTIDE REPEAT; MICROSATELLITE LOCI; PCR AMPLIFICATION; MITOCHONDRIAL-DNA; CONTROL REGION AB A group of ten short tandem repeat (STR) loci suitable for PCR typing from DNA of domestic cats is evaluated for genetic individualization using blinded samples of eight putative feline blood specimens. The ten loci were also typed in a 70 member cat pedigree to demonstrate Mendelian inheritance and independent assortment. A ''match window'' or measurement precision estimate was empirically established by determining the maximum gel migration difference among alleles identical by descent in different individuals of the pedigree. Hardy-Weinberg equilibrium and abundant heterozygosity was observed for each locus in cat population samples from Canada and the USA. The probabilities of two unrelated individuals matching by chance (P-m) at all ten loci was estimated as 1.35 x 10(-10). We present a conservative approach to compute, for forensic consideration, the mathematical likelihood of a chance genotypic match between DNA evidence from a crime scene and the suspect composite STR genotypes for species or populations when genotype frequency information is not available. C1 NCI, INTRAMURAL SUPPORT RES PROGRAM, FREDERICK CANC RES & DEV CTR, SAIC FREDERICK, FREDERICK, MD 21702 USA. RP MenottiRaymond, M (reprint author), NCI, LAB GENOM DIVERS, FREDERICK CANC RES & DEV CTR, BLDG 560, RM 11-38, FREDERICK, MD 21702 USA. NR 54 TC 40 Z9 41 U1 0 U2 9 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0022-1198 EI 1556-4029 J9 J FORENSIC SCI JI J. Forensic Sci. PD NOV PY 1997 VL 42 IS 6 BP 1039 EP 1051 PG 13 WC Medicine, Legal SC Legal Medicine GA YF717 UT WOS:A1997YF71700011 PM 9397545 ER PT J AU Stern, MD Pizzaro, G Rios, E AF Stern, MD Pizzaro, G Rios, E TI Local control model of excitation-contraction coupling in skeletal muscle (vol 110, pg 415, 1997) SO JOURNAL OF GENERAL PHYSIOLOGY LA English DT Correction, Addition C1 NIH,NIA,CTR GERONTOL RES,CARDIOVASC SCI LAB,BALTIMORE,MD 21214. RUSH UNIV,SCH MED,DEPT MOL BIOPHYS & PHYSIOL,CHICAGO,IL 60612. RP Stern, MD (reprint author), UNIV REPUBLICA,FAC MED,DEPT BIOFIS,G FLORES 2125,MONTEVIDEO,URUGUAY. NR 1 TC 0 Z9 0 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1295 J9 J GEN PHYSIOL JI J. Gen. Physiol. PD NOV PY 1997 VL 110 IS 5 BP 641 EP 641 PG 1 WC Physiology SC Physiology GA YF133 UT WOS:A1997YF13300013 ER PT J AU Teien, DE Jones, M Shiota, T Yamada, I Frithiof, D Sahn, DJ AF Teien, DE Jones, M Shiota, T Yamada, I Frithiof, D Sahn, DJ TI Left ventricular stroke work in mitral regurgitation: An animal experimental study SO JOURNAL OF HEART VALVE DISEASE LA English DT Article ID TRANSESOPHAGEAL ECHOCARDIOGRAPHY; DOPPLER ECHOCARDIOGRAPHY; JET SIZE; FLOW; QUANTIFICATION; MODEL; LIMITATIONS; SEVERITY; AREA AB Background and aims of the study: Most studies on mitral regurgitation have focused on evaluating the regurgitant volume. The effects of mitral regurgitation and its associated cardiac workload on left ventricular function and mechanics may be equally important both in assessing the impact of regurgitation as well as in planning and evaluating therapy. The present study was undertaken to investigate the interrelationships of the regurgitant volume, hemodynamics and left ventricular work in an experimental animal model of chronic mitral regurgitation in which the regurgitant volume could be measured directly with electromagnetic flow probes. Methods: A total of 21 hemodynamic states were studied in six sheep with surgically created mitral regurgitation. Regurgitant flow rates were obtained from electromagnetic flow meters. Left ventricular and atrial pressures were recorded using high-fidelity catheters. Regurgitant jet velocity was recorded by continuous wave Doppler. Left ventricular stroke work and energy losses due to the regurgitation were calculated. Results: There was a close correlation between left ventricular stroke work and both jet energy and left atrial systolic pressure rise (r = 0.81, p = 0.0001 and r = 0.92, p = 0.0001, respectively). A moderate correlation to the regurgitant volume was found (r = 0.52, p = 0.01). Conclusions: The regurgitant volume itself is only one of the determinants of left ventricular stroke work in mitral regurgitation. Other factors such as left atrial mechanical properties and the regurgitant kinetic jet energy are at least as important for assessing cardiac work in patients with mitral regurgitation. C1 OREGON HLTH SCI UNIV,CLIN CARE CTR CONGENITAL HEART DIS,PORTLAND,OR 97201. NHLBI,BETHESDA,MD 20892. NR 33 TC 4 Z9 4 U1 0 U2 1 PU I C R PUBLISHERS PI NORTHWOOD PA CRISPIN HOUSE, 12/A SOUTH APPROACH, MOOR PARK, NORTHWOOD, ENGLAND HA6 2ET SN 0966-8519 J9 J HEART VALVE DIS JI J. Heart Valve Dis. PD NOV PY 1997 VL 6 IS 6 BP 613 EP 620 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YG957 UT WOS:A1997YG95700010 PM 9427130 ER PT J AU Herold, KC Lu, J Rulifson, I Vezys, V Taub, D Grusby, MJ Bluestone, JA AF Herold, KC Lu, J Rulifson, I Vezys, V Taub, D Grusby, MJ Bluestone, JA TI Regulation of C-C chemokine production by murine T cells by CD28/B7 costimulation SO JOURNAL OF IMMUNOLOGY LA English DT Article ID AUTOIMMUNE-THYROIDITIS; CYTOKINE FAMILY; TH2 CELLS; MICE; EXPRESSION; RESPONSES; RECEPTOR; RANTES; IDENTIFICATION; MIP-1-ALPHA AB C-C chemokines pray an important role in recruitment of T lymphocytes to inflammatory sites, T lymphocytes secrete chemokines, but the activation requirements for chemokine production by T cells are uncertain, We studied the regulation of C-C chemokine production by CD28 costimulatory signals by murine T lymphocytes. Splenocytes from BALB/c mice cultured with anti-CD3 mAb expressed macrophage-inflammatory protein (MIP)-1 alpha mRNA and secreted MIP-1 alpha, which was inhibited by anti-B7-1 plus anti-B7-2 mAbs. MIP-1 alpha production by Ag-stimulated T cells from DO.11.10 TCR transgenic mice was augmented by anti-CD28 mAb and increased compared with DO.11.10/CD28(-/-) cells, When T cell costimulation was provided by IL-2, MIP-1 alpha was not enhanced, Studies with IL-2, IL-4, STAT4, and STAT6 knock-out mice suggested that chemokine production is controlled by pathways different from those regulating T cell differentiation, Thus, CD28 costimulation may amplify an immune response by stimulating T cell survival, proliferation, and production of chemokines that recruit T cells to inflammatory sites. C1 Univ Illinois, Coll Med, Dept Med, Chicago, IL 60612 USA. NIA, Baltimore, MD 21224 USA. Harvard Univ, Sch Publ Hlth, Dept Canc Biol, Boston, MA 02115 USA. Univ Chicago, Ben May Inst Canc Res, Chicago, IL 60637 USA. Univ Chicago, Comm Immunol, Chicago, IL 60637 USA. RP Herold, KC (reprint author), Univ Illinois, Coll Med, Dept Med, M-C 640,1819 W Polk St, Chicago, IL 60612 USA. OI Vezys, Vaiva/0000-0002-2520-809X FU NIAID NIH HHS [AI41071]; NIDDK NIH HHS [DK49799] NR 29 TC 62 Z9 65 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1997 VL 159 IS 9 BP 4150 EP 4153 PG 4 WC Immunology SC Immunology GA YW260 UT WOS:000071914500003 PM 9379007 ER PT J AU Mason, LH Gosselin, P Anderson, SK Fogler, WE Ortaldo, JR McVicar, DW AF Mason, LH Gosselin, P Anderson, SK Fogler, WE Ortaldo, JR McVicar, DW TI Differential tyrosine phosphorylation of inhibitory versus activating Ly-49 receptor proteins and their recruitment of SHP-1 phosphatase SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NATURAL-KILLER-CELLS; CLASS-I EXPRESSION; T-CELLS; MONOCLONAL-ANTIBODIES; MEMBRANE-PROTEINS; MULTIGENE FAMILY; ANTIGEN RECEPTOR; P58 MOLECULES; TARGET-CELLS; NK CELLS AB Killer cell inhibitory receptors represent a family of p58/70-Ig-like proteins expressed on the surface of human NK cells, Engagement of class I MHC by killer cell inhibitory receptors turns off the lytic machinery of NK cells, This receptor/ligand interaction results in phosphorylation of intracellular tyrosine residues of p58/70 proteins, Murine NK cells express surface receptors of an unrelated family of type II lectin-like proteins, Ly-49, that have similar functions, Ly-49A, -C, and -G2 represent murine inhibitory receptors, However, Ly-49D functions as an activation receptor on the surface of NK cells, This dichotomy of function between Ly-49 family members suggested different signaling events upon receptor/ligand interaction, Here we demonstrate that: 1) in transfected Cos7 and murine NK cells, Ly-49A, -C, and -G2 are phosphorylated following pervanadate stimulation, whereas Ly-49D is not; 2) mAb-induced receptor ligation mediates tyrosine phosphorylation of Ly-49A and -G2, but not Ly-49D; 3) SHP-1 coprecipitates with Ly-49A and -G2 following receptor phosphorylation; and 4) tyrosine phosphorylation of Ly-49 inhibitory receptors depends on tyrosine residues restricted to the immunoreceptor tyrosine-based inhibitory motif, Our data further support the involvement of immunoreceptor tyrosine-based inhibitory motifs as crucial sequences regulating receptor-mediated inhibitory functions in WK cells. C1 NCI, Frederick Canc Res & Dev Ctr, Div Basic Sci, Expt Immunol Lab, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, Sci Applicat Int Corp, Frederick, MD 21702 USA. RP Mason, LH (reprint author), NCI, Frederick Canc Res & Dev Ctr, Div Basic Sci, Expt Immunol Lab, Bldg 560,Room 31-93, Frederick, MD 21702 USA. RI Anderson, Stephen/B-1727-2012; McVicar, Daniel/G-1970-2015 OI Anderson, Stephen/0000-0002-7856-4266; NR 36 TC 63 Z9 64 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1997 VL 159 IS 9 BP 4187 EP 4196 PG 10 WC Immunology SC Immunology GA YW260 UT WOS:000071914500008 PM 9379012 ER PT J AU Moriuchi, M Moriuchi, H Turner, W Fauci, AS AF Moriuchi, M Moriuchi, H Turner, W Fauci, AS TI Cloning and analysis of the promoter region of CXCR4, a coreceptor for HIV-1 entry SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MOLECULAR-CLONING; STIMULATING FACTOR; RECEPTOR GENE; HUMAN HOMOLOG; NPY BINDING; PROTEIN; CELLS; NRF-1; MIP-1-ALPHA; MIP-1-BETA AB The chemokine receptor CXCR4, (also designated fusin and LESTR) is a cofactor for fusion and entry of T cell-tropic strains of HIV-1. CXCR4 is expressed in various cell types; however, the mechanisms involved in the regulation of its expression remain unknown, To delineate these mechanisms, approximately 1.2 kb of DNA from the immediate 5' upstream region of CXCR4 gene was cloned, sequenced, and characterized. Transient expression assays using CXCR4 promoter/luciferase gene reporter constructs revealed that stimulation with PMA plus ionomycin up-regulates the CXCR4 promoter activity in the A3.01 CD4(+) T cell line and PBL and that a DNA fragment from -93 to +59 relative to the transcription start site contributes markedly to the basal and induced activity, This fragment contains a consensus TATA box, two potential GC boxes, and a potential nuclear respiratory factor (NRF)-1 binding site, which were confirmed by gel mobility shift assays and footprinting analysis, Mutagenesis studies revealed that a NRF-1 site is especially important for the basal and induced activity of the CXCR4 promoter, Transient expression assays further revealed that stimulation of PBL with either IL-2 or Abs to CD3 and CD28 enhances the CXCR4 promoter activity, Inducibility of the CXCR4 promoter activity by T cell stimulation suggests that overexpression of CXCR4 may be one of the mechanisms whereby immune activation and/or perturbation of the cytokine network up-regulate HIV expression and replication and thus contribute to the progression of HIV disease. C1 NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. Howard Univ, Coll Med, Dept Microbiol, Washington, DC 20059 USA. RP Moriuchi, H (reprint author), NIAID, Immunoregulat Lab, NIH, Bldg 10,Room 6A11,10 Ctr Dr,MSC-1576, Bethesda, MD 20892 USA. NR 36 TC 65 Z9 66 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1997 VL 159 IS 9 BP 4322 EP 4329 PG 8 WC Immunology SC Immunology GA YW260 UT WOS:000071914500024 PM 9379028 ER PT J AU Plaksin, D Polakova, K Mage, MG Margulies, DH AF Plaksin, D Polakova, K Mage, MG Margulies, DH TI Rigidification of the alpha(2) helix of an MHC class I molecule by a valine to proline mutation in position 165 does not prevent peptide-specific antigen presentation SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HISTOCOMPATIBILITY COMPLEX ANTIGENS; MONOCLONAL-ANTIBODIES; LYMPHOCYTES-T; EXPRESSION; HYBRIDOMA; SURFACE; CELLS; CD1; RECOGNITION; BINDING AB Although classical MHC class I glycoproteins bind peptide Ags for display at the cell surface, some MHC class-I-related molecules such as the neonatal Fc receptor (FcRn) execute their function without binding peptide ligands. The three-dimensional structure of the FcRn suggested that a substitution of the conserved valine at position 165 of the alpha(2) helix by proline contributed to a kink in the position of this helix relative to the cu, helix, and resulted in ceasing of the potential peptide-binding cleft, To test the contribution of proline 165 to the occlusion of the cleft and the binding of potential antigenic peptides, we introduced this mutation into the classical murine MHC class 1 molecule, H-2D(d), and characterized the ability of such a mutant to present peptide Ags to either a peptide-specific, H-2D(d)-restricted T cell hybridoma (B4.2.3), or an allospecific, peptide-dependent T cell hybridoma (3DT52.5.8). We show that the V165P mutation, expressed at the cell surface either in H-2D(d) or in a single chain membrane version of H-2D(d) fails to eliminate recognition of the peptide/MHC complexes by two different T cells, Evaluation of a panel of synthetic substituted peptides suggests that subtle differences in the fine specificity of presentation can be discerned. Thus, the proline substitution at position 165 of FcRn and some other class I-like molecules is not the sole cause of the lack of peptide presentation. C1 NIAID, Immunol Lab, Mol Biol Sect, NIH, Bethesda, MD 20892 USA. NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Margulies, DH (reprint author), NIAID, Immunol Lab, Mol Biol Sect, NIH, Bldg 10,Room 11N311, Bethesda, MD 20892 USA. RI Margulies, David/H-7089-2013; OI Margulies, David/0000-0001-8530-7375 NR 27 TC 4 Z9 4 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1997 VL 159 IS 9 BP 4408 EP 4414 PG 7 WC Immunology SC Immunology GA YW260 UT WOS:000071914500035 PM 9379039 ER PT J AU Kimura, T Zhang, J Sagawa, K Sakaguchi, K Appella, E Siraganian, RP AF Kimura, T Zhang, J Sagawa, K Sakaguchi, K Appella, E Siraganian, RP TI Syk-independent tyrosine phosphorylation and association of the protein tyrosine phosphatases SHP-1 and SHP-2 with the high affinity IgE receptor SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL ANTIGEN RECEPTOR; SRC HOMOLOGY-2 DOMAINS; FC-GAMMA-RIIB; SH2-CONTAINING PHOSPHOTYROSINE PHOSPHATASE; T-CELL; SIGNAL-TRANSDUCTION; MAST-CELLS; HISTAMINE-RELEASE; ZETA-CHAIN; MEDIATED DEGRANULATION AB Aggregation of the high affinity IgE receptor (Fc epsilon RI), a member of the immune receptor family, results in the activation of protein tyrosine kinase and downstream signaling pathways. The two cytoplasmic Src homology 2 domain-containing protein tyrosine phosphatase, SHP-1 (also called SH-PTP1, PTP1C or HCP) and SHP-2 (also known as SH-PTP2, PTP1D, PTP2C, or Syp), are expressed in the RBL-2H3 rat mast cell line. Here we report that aggregation of Fc epsilon RI induced the tyrosine phosphorylation of both SHP-1 and SHP-2. This phosphorylation was independent of the presence of the protein tyrosine kinase Syk. Both SHP-1 and SHP-2 associated with Fc epsilon RI. Whereas SHP-1 was constitutively associated with the receptor, SHP-2 coprecipitated with Fe epsilon RI only after receptor aggregation. Fusion proteins containing either the full-length or the Src homology 2 domains of SHP-2 directly bound to the tyrosine-phosphorylated beta, but not the gamma, subunit of Fc epsilon RI. In the reciprocal experiments, synthetic phosphorylated peptides based on the immunoreceptor tyrosine-based activation motif of the beta, but not the gamma, subunit precipitated SHP-2. In contrast, neither fusion proteins nor synthetic peptides detected interaction between SHP-1 and Fc epsilon RI. In vitro, both SHP-1 and SHP-2 dephosphorylated tyrosine-phosphorylated beta and gamma subunits of Fc epsilon RI. Therefore, SHP-1 and SHP-2 associate with Fc epsilon RI by different mechanisms and can regulate the extent of the tyrosine phosphorlyation of the receptor subunits. Thus, unlike other immune cells in which inhibitory molecules are recruited by accessory proteins, Fc epsilon RI bind molecules that both activate and inhibit signal transduction. C1 NIDR, Immunol Lab, NIH, Bethesda, MD 20892 USA. NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. RP Kimura, T (reprint author), NIDR, Immunol Lab, NIH, Bldg 10,Room 1N106, Bethesda, MD 20892 USA. NR 67 TC 63 Z9 64 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1997 VL 159 IS 9 BP 4426 EP 4434 PG 9 WC Immunology SC Immunology GA YW260 UT WOS:000071914500037 PM 9379041 ER PT J AU Oravecz, T Pall, M Wang, JH Roderiquez, G Ditto, M Norcross, MA AF Oravecz, T Pall, M Wang, JH Roderiquez, G Ditto, M Norcross, MA TI Regulation of anti-HIV-1 activity of RANTES by heparan sulfate proteoglycans SO JOURNAL OF IMMUNOLOGY LA English DT Article ID 7-TRANSMEMBRANE DOMAIN RECEPTOR; T-CELL-LINE; HIV-1 INFECTION; FUNCTIONAL EXPRESSION; HUMAN-MONOCYTES; CHEMOKINE; ENTRY; CLONING; SURFACE; REPLICATION AB The role of cell surface proteoglycans in CC chemokine-mediated anti-HIV-1 activity in T cells and macrophages was investigated. Enzyme digestion of heparan sulfate (HS), but not chondroitin sulfate, from the surface of PM1(CD26H) cells (a human T cell line selected for high CD26 expression) rendered them resistant to the antiviral effects of RANTES and macrophage-inflammatory protein-1 beta at otherwise inhibitory chemokine concentrations. HIV-1 infection of macrophages, however, was inhibited only partially, even at high concentrations of RANTES, and this inhibition was not prevented by HS removal, Flow cytometry revealed that digestion of cell surface proteoglycans, including HS, prevented the binding of RANTES at 10 to 100 nM concentrations to pM1(CD26H) cells, However, the binding of RANTES to activated macrophages occurred only at higher concentrations (100-300 nM) and was mostly chondroitin sulfate, and not HS, dependent. These results support a role for HS in facilitating the interaction of CC chemokines with the cell surface and the consequent inhibition of HIV-1 infection, The absence of HS-dependent binding of RANTES at lower concentrations to macrophages is consistent with the resistance of these cells to the antiviral effects of chemokines. C1 US FDA, Ctr Biol Evaluat & Res, Div Hematol Prod, NIH, Bethesda, MD 20892 USA. RP Oravecz, T (reprint author), US FDA, Ctr Biol Evaluat & Res, Div Hematol Prod, NIH, Bldg 29B,Room 4E12,HPM-541, Bethesda, MD 20892 USA. NR 34 TC 79 Z9 80 U1 2 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1997 VL 159 IS 9 BP 4587 EP 4592 PG 6 WC Immunology SC Immunology GA YW260 UT WOS:000071914500056 PM 9379060 ER PT J AU McLaughlin, JP Abrams, S Kantor, J Dobrzanski, MJ Greenbaum, J Schlom, J Greiner, JW AF McLaughlin, JP Abrams, S Kantor, J Dobrzanski, MJ Greenbaum, J Schlom, J Greiner, JW TI Immunization with a syngeneic tumor infected with recombinant vaccinia virus expressing granulocyte-macrophage colony-stimulating factor (GM-CSF) induces tumor regression and long-lasting systemic immunity SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE GM-CSF; antitumor immunity; recombinant vaccinia; GM-CSF vaccine ID EPIDERMAL LANGERHANS CELLS; ANTITUMOR IMMUNITY; DENDRITIC CELLS; GROWTH-FACTOR; GENE; IMMUNOTHERAPY; CANCER; INDUCTION; PROTEIN; ANTIGEN AB A recombinant vaccinia virus encoding the gene for granulocyte-macrophage colony-stimulating factor (rV-GM-CSF) was used to infect the poorly immunogenic murine colon adenocarcinoma cell line, MC-38. Infection of MC-38 tumor cells with rV-GM-CSF completely suppressed the growth of the MC-38 primary tumors, whereas progressively growing tumors were formed in mice injected with MC-38 cells infected with wild type V-Wyeth. Irradiation of the recipient B6 mice before implantation of rV-GM-CSF-infected tumor cells resulted in the development of progressively growing tumors. Moreover, in vivo T-cell depletion studies revealed that growth suppression of the rV-GM-CSF-infected tumor cells was dependent on the presence of both CD4(+) and CD8(+) T-cell subsets. Subsequent studies established that this immunity was long-lasting and antigen specific, as demonstrated by the protection of rV-GM-CSF-immunized mice from MC-38 tumor challenge but not from challenge with another syngeneic tumor cell type. No such effects were observed when MC-38 tumor cells were infected with recombinant vaccinia viruses expressing interleukin (IL)-2 or IL-6. The results demonstrate that paracrine release of biologically active murine GM-CSF by tumor cells infected with rV-GM-CSF enhances the intrinsic immunogenicity of a poorly immunogenic murine tumor. Presumably the augmentation of tumor immunogenicity induces an antigen-specific T-cell-dependent antitumor response that prevents the formation of primary tumors and protects mice from tumor challenge. Thus in this experimental model, GM-CSF functions as a highly effective vaccine adjuvant. C1 NCI,TUMOR IMMUNOL & BIOL LAB,NIH,BETHESDA,MD 20892. NR 56 TC 29 Z9 29 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD NOV PY 1997 VL 20 IS 6 BP 449 EP 459 DI 10.1097/00002371-199711000-00004 PG 11 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA YJ868 UT WOS:A1997YJ86800004 PM 9409450 ER PT J AU Kageshita, T Kawakami, Y Hirai, S Ono, T AF Kageshita, T Kawakami, Y Hirai, S Ono, T TI Differential expression of MART-1 in primary and metastatic melanoma lesions SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE MART-1; gp100; melanocytic tumor ID INTERCELLULAR-ADHESION MOLECULE-1; TUMOR-INFILTRATING LYMPHOCYTES; ACRAL LENTIGINOUS MELANOMA; CLINICAL-SIGNIFICANCE; ANTIGEN EXPRESSION; IN-VIVO; GENE; IDENTIFICATION; PROGRESSION; ASSOCIATION AB Twenty-eight primary and 29 metastatic melanoma lesions and 18 pigmented nevi lesions were analyzed by using the immunoperoxidase reaction with anti-MART-1 and anti-gp100 monoclonal antibodies (mAbs). The MART-1 was expressed in 28, 29, and 18, and gp100 was expressed in 27, 28, and eight of these lesions, respectively. Intensity and percentage of stained cells with anti-MART-1 mAb were stronger and higher than those with anti-gp100 mAb. MART-1 was expressed homogeneously in primary melanoma and pigmented nevi, whereas it was heterogeneously expressed in metastatic melanoma lesions. The level of expression of MART-1 in primary melanoma lesions did not correlate with any clinicopathologic parameters. These results suggest that anti-MART-1 mAb is a useful tool for immunohistochemical analysis of melanocytic lesions and also is useful for patient's selection and monitoring of antigen-loss variants in clinical trials with the MART-1-based immunotherapy. C1 NCI,SURG BRANCH,NIH,BETHESDA,MD 20892. RP Kageshita, T (reprint author), KUMAMOTO UNIV,SCH MED,DEPT DERMATOL,1-1 HONJO,KUMAMOTO 860,JAPAN. RI Kawakami, Yutaka /E-7429-2013 OI Kawakami, Yutaka /0000-0003-4836-2855 NR 28 TC 43 Z9 43 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD NOV PY 1997 VL 20 IS 6 BP 460 EP 465 DI 10.1097/00002371-199711000-00005 PG 6 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA YJ868 UT WOS:A1997YJ86800005 PM 9409451 ER PT J AU Nicotra, MR Nistico, P Mangoni, A DiFilippo, F Marincola, FM Natali, PG AF Nicotra, MR Nistico, P Mangoni, A DiFilippo, F Marincola, FM Natali, PG TI Melan-A/MART-1 antigen expression in cutaneous and ocular melanomas SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE MART-1; cutaneous melanomas; ocular melanomas ID TUMOR-INFILTRATING LYMPHOCYTES; IDENTIFICATION; MART-1; CELLS AB The human immune repertoire appears to be capable of recognizing normal antigens expressed by tumor cells. Among these antigens, those of differentiation, characterized by a restricted tissue expression, could be of clinical interest since they may represent a target for immunotherapeutic protocols. In this context we have evaluated, in benign and malignant lesions of the melanocytic lineage, the expression of the Melan-A/MART-1 antigen, which has been shown to be recognized by T cells, of HLA-A2 melanoma patients. The immunohistochemical analysis conducted with a Melan-A/MART-1 monoclonal antibody demonstrated that the antigen expression does not correlate with transformation or tumor progression. At variable levels Melan-A/MART-1, differently from other differentiation antigens, is homogeneously expressed by multiple autologous metastases and by melanoma metastases at different body sites. This tissue distribution adds further biological support to the ongoing use of Melan-A/MART-1-related peptides in active immunotherapy. C1 REGINA ELENA INST CANC RES,IMMUNOL LAB,I-00158 ROME,ITALY. CNR,DEPT BIOMED TECHNOL,ROME,ITALY. NCI,SURG BRANCH,NIH,BETHESDA,MD 20892. OI Nistico', Paola/0000-0003-4409-2261 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 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD NOV PY 1997 VL 20 IS 6 BP 466 EP 469 DI 10.1097/00002371-199711000-00006 PG 4 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA YJ868 UT WOS:A1997YJ86800006 PM 9409452 ER PT J AU Straus, SE Wald, A Kost, RG McKenzie, R Langenberg, AGM Hohman, P Lekstrom, J Cox, E Nakamura, M Sekulovich, R Izu, A Dekker, C Corey, L AF Straus, SE Wald, A Kost, RG McKenzie, R Langenberg, AGM Hohman, P Lekstrom, J Cox, E Nakamura, M Sekulovich, R Izu, A Dekker, C Corey, L TI Immunotherapy of recurrent genital herpes with recombinant herpes simplex virus type 2 glycoproteins D and B: Results of a placebo-controlled vaccine trial SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID ORAL ACYCLOVIR; SUBUNIT VACCINE; GUINEA-PIGS; EFFICACY; INFECTIONS; PREVENTION; SUPPRESSION; PROTECTION; RESPONSES; THERAPY AB To determine the safety, immunogenicity, and efficacy of a recombinant herpes simplex virus type 2 glycoprotein D and B vaccine in the treatment of recurrent genital herpes, a randomized, placebo-controlled trial was held at two referral centers. Healthy patients with 4-14 recurrences per year received injections of both glycoproteins in MF59 adjuvant or of MF59 alone at 0, 2, 12, and 14 months. For 18 study months, the rate and number of recurrences, the duration and severity of the first confirmed recurrence, vaccine immunogenicity, and rates of local and systemic reactions were determined. The monthly rate of recurrences was not significantly improved, but the duration and severity of the first study outbreak was reduced significantly by vaccination. Glycoprotein-specific and neutralizing antibodies were boosted by vaccination for the duration of the study. This vaccine is safe and immunogenic and ameliorated an observed first postvaccination genital recurrence, but it does not reduce recurrence frequency. C1 UNIV WASHINGTON,DEPT MED,DIV VIROL,SEATTLE,WA. UNIV WASHINGTON,DEPT LAB MED,SEATTLE,WA. CHIRON VACCINE CO,EMERYVILLE,CA. RP Straus, SE (reprint author), NIAID,CLIN INVEST LAB,NIH,BLDG 10,ROOM 11N228,10 CTR DR,BETHESDA,MD 20892, USA. RI Wald, Anna/B-6272-2012 OI Wald, Anna/0000-0003-3486-6438 NR 39 TC 130 Z9 136 U1 2 U2 7 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD NOV PY 1997 VL 176 IS 5 BP 1129 EP 1134 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA YD809 UT WOS:A1997YD80900001 PM 9359709 ER PT J AU Reinhart, TA Rogan, MJ Huddleston, D Rausch, DM Eiden, LE Haase, AT AF Reinhart, TA Rogan, MJ Huddleston, D Rausch, DM Eiden, LE Haase, AT TI Simian immunodeficiency virus burden in tissues and cellular compartments during clinical latency and AIDS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID INFECTED RHESUS-MONKEYS; CENTRAL-NERVOUS-SYSTEM; HIV-INFECTION; VIRAL REPLICATION; LYMPHOID-TISSUE; IN-VIVO; SIV; MACAQUES; DISEASE; BRAIN AB In the course of human immunodeficiency virus infection or of the related simian immunodeficiency virus (SIV), progression to AIDS is associated with high virus burdens in blood. How virus burden in the bloodstream is related to virus burden in tissue reservoirs was addressed in an animal model of rhesus macaques infected with SIV, In situ hybridization and quantitative image analysis were used to quantitate virus burden, Animals who developed AIDS had high levels of virus production and storage in lymphoid tissue reservoirs and evidence of productive infection of macrophages in the nervous system, With the quantitative approach described, it should be possible to design and assess the impact of treatment and shed light on the outstanding issues in pathogenesis. C1 UNIV MINNESOTA,SCH MED,DEPT MICROBIOL,MINNEAPOLIS,MN 55455. NIMH,OFF AIDS,NIH,ROCKVILLE,MD 20857. NIMH,MOL NEUROSCI SECT,LAB CELLULAR & MOL REGULAT,NIH,BETHESDA,MD 20892. OI Eiden, Lee/0000-0001-7524-944X NR 43 TC 54 Z9 54 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD NOV PY 1997 VL 176 IS 5 BP 1198 EP 1208 PG 11 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA YD809 UT WOS:A1997YD80900011 PM 9359719 ER PT J AU DaCunha, A Jefferson, JJ Tyor, WR Glass, JD Jannotta, FS Cottrell, JR Resau, JH AF DaCunha, A Jefferson, JJ Tyor, WR Glass, JD Jannotta, FS Cottrell, JR Resau, JH TI Transforming growth factor-beta 1 in adult human microglia and its stimulated production by interleukin-1 SO JOURNAL OF INTERFERON AND CYTOKINE RESEARCH LA English DT Article ID POLYMERASE CHAIN-REACTION; CENTRAL-NERVOUS-SYSTEM; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; SUBACUTE AIDS ENCEPHALITIS; PERIPHERAL-BLOOD MONOCYTES; IA-ANTIGEN EXPRESSION; NECROSIS-FACTOR-ALPHA; FACTOR-BETA; HUMAN-BRAIN; CELLULAR-LOCALIZATION AB Ameboid microglia express human immunodeficiency virus 1 (HIV-1) more frequently than do ramified microglia, These two microglial subtypes might also differ in the frequency with which they express transforming growth factor-beta 1 (TGF-beta 1), a cytokine that regulates HIV-1 expression in monocytes. Results described here show that ameboid and ramified microglia express TGF-beta 1. In brain tissues from HIV-1-infected individuals as compared with seronegative controls, ameboid rather than ramified microglia more frequently expressed TGF-beta 1, Ameboid microglia, isolated and cultured from postmortem adult human brain more frequently expressed TGF-beta 1 in presence of interleukin-1(IL-1), a cytokine that is elevated in brains of HIV-1-infected individuals when compared with seronegative controls. The stimulation of TGF-beta 1 by IL-1 was dose and time dependent, occurring with ameboid microglia isolated from either frontal cortex or globus pallidus but not midbrain pens, Ameboid microglia are similar to the RCA-1-positive cells that form clusters, called microglial nodules, in the brain of HIV-1-infected individuals. Pathologic conditions, such as disseminated microglial nodules, are associated with HIV-1 encephalitis, direct infection of the brain, and moderate to severe neurologic impairment. TGF-beta 1 expression in ameboid microglia may play a role in HIV-1 neuropathogenesis. C1 NIMH,CELL BIOL LAB,NIH,BETHESDA,MD 20892. NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. MED UNIV S CAROLINA,DEPT NEUROL,CHARLESTON,SC 29425. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20037. UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. NCI,ABL BASIC RES PROGRAM,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. NR 69 TC 12 Z9 12 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1079-9907 J9 J INTERF CYTOK RES JI J. Interferon Cytokine Res. PD NOV PY 1997 VL 17 IS 11 BP 655 EP 664 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA YG827 UT WOS:A1997YG82700001 PM 9402103 ER PT J AU Richard, G Lin, JP Smith, L Whyte, YM Itin, P Wollina, U Epstein, E Hohl, D Giroux, JM Charnas, L Bale, SJ DiGiovanna, JJ AF Richard, G Lin, JP Smith, L Whyte, YM Itin, P Wollina, U Epstein, E Hohl, D Giroux, JM Charnas, L Bale, SJ DiGiovanna, JJ TI Linkage studies in erythrokeratodermias: Fine mapping, genetic heterogeneity, and analysis of candidate genes SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE ataxia chromosome 1; connexin; erythrokeratodermia variabilis; Greither disease ID GAP JUNCTIONAL PROTEINS; HUMAN GENOME; VARIABILIS; FAMILY; MAP; HYBRIDIZATION; EXPRESSION; SKIN AB Erythrokeratodermias are a clinically heterogeneous group of rare autosomal dominant disorders of cornification with overlapping features including hyperkeratosis and erythema, We ascertained five extended pedigrees with different phenotypes for a linkage study. Three families presented with localized erythrokeratodermia variabilis, and one with erythrokeratodermia and ataxia, Another family had Greither disease associated with variable hyperkeratotic plaques, Despite their phenotypic differences, both erythrokeratodermia variabilis and erythrokeratodermia with ataxia map to a common region in 1p34-p35. Multipoint Linkage and haplotype analyses place erythrokeratodermia variabilis between the marker D1S496 and D1S186 with a maximum LOD score of 12.88, Our linkage results provide compelling evidence for genetic homogeneity among families of mixed European and French-Canadian origin. In contrast, results excluded Greither's disease from the established erythrokeratodermia variabilis gene region indicating genetic heterogeneity of erythrokeratodermias. Based on recombinations, two genes assigned to 1p34-p35 were excluded: cartilage matrix protein and avian myelocytosis viral oncogene. Connexin-37 (GJA4), a member of the connexin gene family, maps within the erythrokeratodermia variabilis region and is an attractive candidate gene. Direct sequencing of the coding region of GJA4 in four patients revealed several variations, including a novel polymorphism within the 5' cytoplasmic domain, but no pathogenic mutations were found, thus excluding Connexin-37 as a candidate, There is evidence, however, that; other epidermally expressed connexins cluster in this region, and one may yet be determined to play a role in the pathogenesis of erythrokeratodermia variabilis. C1 NIAMSD,SKIN BIOL LAB,GENET STUDIES SECT,NIH,BETHESDA,MD. NIAMSD,DERMATOL CLIN RES UNIT,NIH,BETHESDA,MD. UNIV BASEL,DEPT DERMATOL,BASEL,SWITZERLAND. UNIV JENA,DEPT DERMATOL,D-6900 JENA,GERMANY. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,DEPT DERMATOL,SAN FRANCISCO,CA. BEAUMONT HOSP,DEPT DERMATOL,LAUSANNE,SWITZERLAND. HOP HOTEL DIEU,DERMATOL SECT,DEPT MED,MONTREAL,PQ,CANADA. UNIV MONTREAL,MONTREAL,PQ H3C 3J7,CANADA. NICHHD,HERITABLE DIORDERS BRANCH,NIH,BETHESDA,MD 20892. NR 42 TC 45 Z9 46 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD NOV PY 1997 VL 109 IS 5 BP 666 EP 671 DI 10.1111/1523-1747.ep12337713 PG 6 WC Dermatology SC Dermatology GA YB204 UT WOS:A1997YB20400011 PM 9347797 ER PT J AU Yang, JM Yoneda, K Morita, E Imamura, S Nam, K Lee, ES Steinert, PM AF Yang, JM Yoneda, K Morita, E Imamura, S Nam, K Lee, ES Steinert, PM TI An alanine to proline mutation in the 1A rod domain of the keratin 10 chain in epidermolytic hyperkeratosis SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE keratin intermediate filament structure; type I keratin ID INTERMEDIATE FILAMENTS; H1; DISEASE AB We report a mutation in a case of epidermolytic hyperkeratosis that results in a proline for alanine substitution in the residue position 12 of the 1A subdomain of the keratin 10 chain (codon 158). The disease phenotype is consistent with the inappropriate substitution of a proline near the beginning of the rod domain, because it is likely to seriously disrupt the structural organization of coiled-coil molecules within keratin intermediate filaments. Mutations/substitutions in this position have not been reported in any keratin disease. Position 12 is an alanine in all intermediate filament chains, and lies in the outer It heptad position of the coiled-coil. In vitro peptide interference assembly assays revealed that substitutions that alter residue size or charge at this position primarily interfere with keratin filament elongation. C1 SAMSUNG BIOMED RES INST, CLIN & BASIC RES CTR, SEOUL, SOUTH KOREA. KYOTO UNIV, COLL MED, DEPT DERMATOL, KYOTO 606, JAPAN. HIROSHIMA UNIV, COLL MED, DEPT DERMATOL, KYOTO, JAPAN. NIAMSD, SKIN BIOL LAB, NIH, BETHESDA, MD USA. HIROSHIMA UNIV, COLL MED, DEPT DERMATOL, HIROSHIMA, JAPAN. RP Yang, JM (reprint author), SUNGKYUNKWAN UNIV, SAMSUNG MED CTR,COLL MED,DEPT DERMATOL,KANGNAM KU, 50 ILWON DONG, SEOUL 135230, SOUTH KOREA. NR 23 TC 11 Z9 11 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD NOV PY 1997 VL 109 IS 5 BP 692 EP 694 DI 10.1111/1523-1747.ep12338320 PG 3 WC Dermatology SC Dermatology GA YB204 UT WOS:A1997YB20400016 PM 9347802 ER PT J AU Parker, RI Gralnick, HR AF Parker, RI Gralnick, HR TI Energy-dependent expression of platelet-von Willebrand factor on the surface of unstimulated and stimulated platelets SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Article ID GLYCOPROTEIN IIB-IIIA; VONWILLEBRAND-FACTOR; BLOOD-PLATELETS; THROMBIN; AGGREGATION; RESPONSES; BINDING; CONSUMPTION; METABOLISM; ACTIVATION AB We have studied the energy requirements (adenosine triphosphate) for the expression of platelet-van Willbrand factor on platelets under conditions In which glycolysis and/or oxidative phosphorylation were inhibited. We found that platelet-vWf expression on the surfaces of both unstimulated and stimulated platelets required energy and was maximally decreased when metabolic ATP was maximally depleted. Platelet-vWf expression correlated directly with estimates of adenylate energy charge in both unstimulated and stimulated platelets. In addition, platelet shape change and agonist-induced intracellular Ca2+ flux were maintained at lower AECs than were either platelet aggregation or alpha-granule secretion. Our results indicate that the surface expression of platelet-vWf on unstimulated platelets is a dynamic process, and that energy is required to maintain basal amounts of platelet-vWf on the platelet surface. Our data also suggest that the metabolic ATP required to effect changes in platelet shape is less than that necessary to maintain basal platelet-vWf surface expression or to produce full alpha-granule secretion. We show that platelet-shape change in the absence of alpha-granule secretion can result in an increase in platelet-vWf surface expression. C1 NIH,DEPT CLIN PATHOL,CTR CLIN,BETHESDA,MD 20892. RP Parker, RI (reprint author), SUNY STONY BROOK,DEPT PEDIAT,HSC,T11,ROOM 060,STONY BROOK,NY 11794, USA. NR 36 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 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD NOV PY 1997 VL 130 IS 5 BP 520 EP 529 DI 10.1016/S0022-2143(97)90129-3 PG 10 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA YH752 UT WOS:A1997YH75200010 PM 9390640 ER PT J AU Lyon, GR Moats, LC AF Lyon, GR Moats, LC TI Critical conceptual and methodological considerations in reading intervention research SO JOURNAL OF LEARNING DISABILITIES LA English DT Article ID DEVELOPMENTAL DYSLEXIA; PHONOLOGICAL AWARENESS; INDIVIDUAL-DIFFERENCES; LEARNING-DISABILITIES; CHILDREN; SKILLS; GROWTH; INSTRUCTION; ACQUISITION; DEFINITION AB Research designed to identify the instructional and ecological conditions that foster the development of literacy skills in children with reading disabilities reflects a complex, multivariate enterprise. In essence, such research must be able to ultimately identify the teacher characteristics and instructional components that are critical for individual children and the interrelationships among these components. The intensity and duration of instruction will differ according to the severity of deficits in either single-or multiple-component reading processes. Moreover, training in any one component may not be sufficient to produce automatic improvements in other reading skills. This article identifies a number of conceptual and methodological issues that should be considered when conducting and interpreting reading intervention research. C1 UNIV TEXAS, SCH MED, AUSTIN, TX USA. NICHHD, READING INTERVENT PROJECT, WASHINGTON, DC USA. NR 85 TC 95 Z9 96 U1 5 U2 12 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0022-2194 EI 1538-4780 J9 J LEARN DISABIL-US JI J. Learn. Disabil. PD NOV-DEC PY 1997 VL 30 IS 6 BP 578 EP 588 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA YF264 UT WOS:A1997YF26400001 PM 9364895 ER PT J AU Xu, L Rahimpour, R Ran, L Kong, C Biragyn, A Andrews, J Devries, M Wang, JM Kelvin, DJ AF Xu, L Rahimpour, R Ran, L Kong, C Biragyn, A Andrews, J Devries, M Wang, JM Kelvin, DJ TI Regulation of CCR2 chemokine receptor mRNA stability SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE interleukin-8; lipopolysaccharide; deadenylation; macrophage inflammatory protein-1 alpha ID AU-RICH ELEMENTS; MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; MONOCYTE CHEMOATTRACTANT PROTEIN-1; MULTIPLE LEUKOCYTE RECEPTORS; MESSENGER-RNA DEGRADATION; COLONY-STIMULATING FACTOR; INTERLEUKIN-8 RECEPTOR; FUNCTIONAL EXPRESSION; CHEMOTACTIC CYTOKINES; MOLECULAR-BIOLOGY AB During inflammatory and immunological responses, leukocytes respond to external stimuli by altering the stability of cytokine and cytokine receptor messages, Change in message stability is an effective mechanism for rapidly regulating steady state levels of mRNA. Cytokine messages containing A-U-rich elements located in the 3' untranslated region (ARE) are the best studied examples of this process, AREs have been shown to act as targeting motifs for degradation of cytokine and transcription factor messages, We have recently observed that the interleukin-8 (IL-8) receptor messages, IL-8RA and B (CXCR1 and CXCR2), also undergo changes in stability in response to the inflammatory stimulator lipopolysaccharide (LPS), To determine whether regulation of message stability is a common mechanism for modulation of chemokine receptor mRNA we explored whether the stability of the CC chemokine receptor message for CCR2 (monocyte chemotactic protein-1 receptor) is also regulated by LPS. We found that LPS induces a rapid loss of steady state levels of CCR2 message through message degradation, Furthermore, LPS stimulated the decay of Poly(A) CCR2 mRNA faster than total CCR2 RNA, indicating that deadenylation is the first step in LPS-induced CCR2 RNA degradation, We conclude from these experiments that LPS stimulates the rapid degradation of CCR2 messages through a two-step process, deadenylation followed by degradation of the message body, In contrast to the results obtained for CCR2 nRNA, macrophage inflammatory protein-lot messages, which contain an ARE motif, were stabilized by LPS stimulation, indicating that chemokine and chemokine receptor mRNA stability are regulated by different and opposing mechanisms. C1 ROBARTS RES INST,LAB MOL IMMUNOL & INFLAMMAT,LONDON,ON N6G 2V4,CANADA. UNIV WESTERN ONTARIO,DEPT IMMUNOL & MICROBIOL,LONDON,ON N6A 3K7,CANADA. NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BCDP,FREDERICK,MD. NR 42 TC 52 Z9 53 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD NOV PY 1997 VL 62 IS 5 BP 653 EP 660 PG 8 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YF500 UT WOS:A1997YF50000014 PM 9365120 ER PT J AU Brasaemle, DL Barber, T Wolins, NE Serrero, G BlanchetteMackie, EJ Londos, C AF Brasaemle, DL Barber, T Wolins, NE Serrero, G BlanchetteMackie, EJ Londos, C TI Adipose differentiation-related protein is an ubiquitously expressed lipid storage droplet-associated protein SO JOURNAL OF LIPID RESEARCH LA English DT Article DE perilipin; immunocytochemistry; hepatoma cells; fibroblasts; steroidogenic cells; triacylglycerol; cholesteryl ester ID LEYDIG TUMOR-CELLS; OIL BODIES; RAT-LIVER; PERILIPIN; STEROIDOGENESIS; ADIPOCYTES; BIOSYNTHESIS; METABOLISM; MEMBRANE; LUNG AB The adipose differentiation-related protein (ADRP) was first characterized as a mRNA induced early during adipocyte differentiation (Jiang, H. P., and G. Serrero. 1992. Proc. Natl. Acad. Sci. USA. 89:7856-7860). The present study demonstrates that ADRP mRNA is expressed in a variety of tissues and cultured cell lines. Immunocytochemical examination revealed that ADRP localizes to neutral lipid storage droplets in cultured murine 3T3-L1 adipocytes, murine MA-10 Leydig cells, Chinese hamster ovary (CHO) fibroblasts, and human HepG2 hepatoma cells; the association of ADRP with lipid droplets was confirmed by subcellular fractionation of MA-10 Leydig cells. In addition to ADRP, steroidogenic cells and adipocytes express the perilipins, a family of lipid droplet-associated proteins that share a highly related sequence domain with ADRP. ADRP and perilipins co-localize on lipid droplets in MA-10 Leydig cells. While ADRP was found on small lipid droplets in 3T3-L1 preadipocytes and early differentiated adipocytes, it was absent in maturing adipocytes. In contrast, perilipins were absent early during differentiation, but were found on small and large lipid droplets at latero stages. The transition in surface protein composition of adipocyte lipid droplets from ADRP to perilipins occurred 3 days after the initiation of differentiation when cells displayed colocalization of both proteins on the same lipid droplets. The specific localization of adipose differentiation-related protein to lipid droplets in a wide variety of cells suggests that ADRP plays a role in management of neutral lipid stores. C1 NIDDKD,CELLULAR & DEV BIOL LAB,NIH,BETHESDA,MD 20892. NIDDKD,LAB CELL BIOCHEM & BIOL,NIH,BETHESDA,MD 20892. UNIV MARYLAND,SCH PHARM,DEPT PHARMACEUT SCI,BALTIMORE,MD 21201. OI Brasaemle, Dawn/0000-0002-8553-8285 NR 32 TC 405 Z9 414 U1 3 U2 11 PU LIPID RESEARCH INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD NOV PY 1997 VL 38 IS 11 BP 2249 EP 2263 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YF498 UT WOS:A1997YF49800008 PM 9392423 ER PT J AU Ried, T Liyanage, M duManoir, S Heselmeyer, K Auer, G Macville, M Schrock, E AF Ried, T Liyanage, M duManoir, S Heselmeyer, K Auer, G Macville, M Schrock, E TI Tumor cytogenetics revisited: comparative genomic hybridization and spectral karyotyping SO JOURNAL OF MOLECULAR MEDICINE-JMM LA English DT Review DE fluorescence in situ hybridization; comparative genomic hybridization; spectral karyotyping; chromosome aberrations; tumor progression ID FLUORESCENCE INSITU HYBRIDIZATION; IN-SITU HYBRIDIZATION; UNIVERSAL DNA-AMPLIFICATION; GLIOMA CELL-LINES; CHROMOSOMAL GAINS; PROSTATE-CANCER; BREAST-CANCER; COPY NUMBER; PAINTING PROBES; GENETIC CHANGES AB Fluorescence in situ hybridization techniques allow the visualization and localization of DNA target sequences on the chromosomal and cellular level and have evolved as exceedingly valuable tools in basic chromosome research and cytogenetic diagnostics. Recent advances in molecular cytogenetic approaches, namely comparative genomic hybridization and spectral karyotyping, now allow tumor genomes to be surveyed for chromosomal aberrations in a single experiment and permit identification of tumor-specific chromosomal aberrations with unprecedented accuracy. Comparative genomic hybridization utilizes the hybridization of differentially labeled tumor and reference DNA to generate a map of DNA copy number changes in,tumor genomes. Comparative genomic hybridization is in ideal tool for analyzing chromosomal imbalances in archived tumor material and for examining possible correlations between these findings and tumor phenotypes. Spectral karyotyping is based on the simultaneous hybridization of differentially labeled chromosome painting probes (24 in human), followed by spectral imaging that allows the unique display of all human (and other species) chromosomes in different colors. Spectral karyotyping greatly facilitates the characterization of numerical and structural chromosomal aberrations, therefore improving karyotype analysis considerably. We review these new molecular cytogenetic concepts, describe applications of comparative genomic hybridization and spectral karyotyping for the visualization of chromosomal aberrations as they relate to human malignancies and animal models thereof, and provide evidence that fluorescence in situ hybridization has developed as a robust and reliable technique which justifies its translation to cytogenetic diagnostics. C1 KAROLINSKA HOSP & INST,DEPT TUMOR PATHOL,DIV CELL & MOL ANAL,STOCKHOLM,SWEDEN. RP Ried, T (reprint author), NATL HUMAN GENOME RES INST,NIH,49 CONVENT DR,BETHESDA,MD 20892, USA. NR 74 TC 64 Z9 64 U1 0 U2 9 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0946-2716 J9 J MOL MED-JMM JI J. Mol. Med. PD NOV-DEC PY 1997 VL 75 IS 11-12 BP 801 EP 814 DI 10.1007/s001090050169 PG 14 WC Genetics & Heredity; Medicine, Research & Experimental SC Genetics & Heredity; Research & Experimental Medicine GA YH420 UT WOS:A1997YH42000005 PM 9428610 ER PT J AU OKeefe, BR Beutler, JA Cardellina, JH Prather, TR Shoemaker, RH Sowder, RC Henderson, LE Pannell, LK Boyd, MR AF OKeefe, BR Beutler, JA Cardellina, JH Prather, TR Shoemaker, RH Sowder, RC Henderson, LE Pannell, LK Boyd, MR TI Isolation of a novel kunitz family protease inhibitor in association with Tethya hemolysin from the sponge Tethya ingalli SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID MARINE SPONGE; SEA-ANEMONE; IN-VITRO; PURIFICATION; PRECURSOR; PROTEINS; COMPLEX; TOXIN; FISH AB Aqueous extracts from the New Zealand sponge Tethya ingalli (Hadromerida) displayed potent cytotoxicity in the NCI's 60-cell-line human tumor panel. Fractionation of the extract by ammonium sulfate precipitation, gel filtration, ultrafiltration, and both hydrophobic interaction and reversed-phase chromatography resulted in the isolation of two biologically active proteins. The first protein, Tethya protease inhibitor (TPI), which was purified to homogeneity, inhibited trypsin with an EC50 of 65 nM. TPI had a molecular mass of 11 431 Ba, and an isoelectric point of 8.2. A partial N-terminal amino acid sequence determined for TPI showed significant homology with protease inhibitors of the Kunitz family. The second isolated protein displayed potent cytotoxicity, with pronounced selectivity for certain tumor cell lines (e.g., ovarian, renal, CNS, and breast). The latter protein, which had an apparent molecular weight of 21 kDa (SDS-PAGE), also lysed human red blood cells (EC50 Of 39 nM) and was similar to a hemolysin previously isolated from the sponge Tethya lycinurium. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC BIOL DIAG & CTR,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,SAIC,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RI Beutler, John/B-1141-2009 OI Beutler, John/0000-0002-4646-1924 NR 27 TC 3 Z9 3 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD NOV PY 1997 VL 60 IS 11 BP 1094 EP 1099 DI 10.1021/np970242l PG 6 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA YH852 UT WOS:A1997YH85200006 PM 9392878 ER PT J AU Rall, JE AF Rall, JE TI This is biology, the science of the living world - Mayr,E SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Book Review RP Rall, JE (reprint author), NIDDK,NIH,BETHESDA,MD, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD NOV PY 1997 VL 185 IS 11 BP 707 EP 708 PG 2 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA YE933 UT WOS:A1997YE93300011 ER PT J AU Holz, A Frank, M Copeland, NG Gilbert, DJ Jenkins, NA Schwab, ME AF Holz, A Frank, M Copeland, NG Gilbert, DJ Jenkins, NA Schwab, ME TI Chromosomal localization of the myelin-associated oligodendrocytic basic protein and expression in the genetically linked neurological mouse mutants ducky and tippy SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE myelin gene; oligodendrocytes; chromosomal localization; in situ hybridization; expression; dysmyelination ID CENTRAL-NERVOUS-SYSTEM; PROTEOLIPID PROTEIN; X-CHROMOSOME; GENE; MICE; ASSIGNMENT; DISEASE; LINKAGE; MOBP AB The alternatively spliced cDNAs encoding the myelin-associated/oligodendrocytic basic proteins (MOBPs) have recently been identified in rat. The Mobp gene maps to the distal part of mouse chromosome 9 at a region syntenic with the human chromosome 3p22-p21.3. Two nonallelic mouse mutants, tippy and ducky, with severe neurological phenotypes map to the vicinity of the Mobp locus. We therefore tested whether MOBP malfunction could explain the tippy and ducky defects. In tippy mutant animals, MOBP expression and that of other myelin markers were indistinguishable from wild type. The ultrastructure of tippy myelin was shown to be normal. Ducky animals showed a slight reduction of the brain size, most evident in the spinal cord, but normal progress of myelination. Both MOBP and myelin basic protein expression were lowered only regionally in the CNS, but were mostly normal in the anterior parts of the brain. Ultrastructurally, ducky myelin appeared normal. MOBP transcript sizes and the molecular weights of the encoded proteins were shown to be normal in both mutants. Finally, the nucleotide sequence of the abundant MOBP-81 cDNA was determined and compared with tippy and ducky MOBP-81. Wild-type mouse MOBP-81 protein was 99% identical to the rat homologue, and tippy and ducky MOBP-81 were identical to the wild-type sequence. Our results suggest that alterations in the Mobp gene are not the cause for the severe neurological phenotypes of ducky and tippy mice. C1 UNIV ZURICH,BRAIN RES INST,CH-8029 ZURICH,SWITZERLAND. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21701. RI Schwab, Martin/B-6818-2016 FU NCI NIH HHS [N01-CO-46000] NR 37 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD NOV PY 1997 VL 69 IS 5 BP 1801 EP 1809 PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA YC168 UT WOS:A1997YC16800003 PM 9349522 ER PT J AU Saunders, PA ChaleckaFranaszek, E Chuang, DM AF Saunders, PA ChaleckaFranaszek, E Chuang, DM TI Subcellular distribution of glyceraldehyde-3-phosphate dehydrogenase in cerebellar granule cells undergoing cytosine arabinoside-induced apoptosis SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE glyceraldehyde; 3-phosphate dehydrogenase; DNA laddering; apoptosis; subcellular distribution; cerebellar granule cells ID AGE-INDUCED APOPTOSIS; DNA GLYCOSYLASE; NEURONS; GENE; ANTISENSE; SURVIVAL; CULTURE; RAT; TRANSCRIPTION; MEMBRANE AB We have previously shown that cytosine arabinoside (AraC)-induced apoptosis of cerebellar granule cells (CGCs) results in an increase of a 38-kDa band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH; EC 1.2.1.12). Antisense oligonucleotides to GAPDH mRNA afford acutely plated CGCs significant protection against AraC-induced apoptosis. We used differential centrifugation to examine which subcellular components are affected, Treated and untreated cells were sonicated in 0.32 M sucrose and sequentially centrifuged at 1,000, 20,000, and 200,000 g, to obtain crude nuclear, mitochondrial, microsomal, and cytosolic fractions. Western blotting showed that the levels of GAPDH protein were markedly increased in the 1,000- and 20,000-g pellets, The levels in the cytosolic supernatant were decreased dramatically by AraC in acutely plated CGCs but not in cells 24 h after plating. It is noteworthy that although GAPDH protein in the pellet fractions increased, the dehydrogenase activity of GAPDH decreased. Two other dehydrogenases, lactate dehydrogenase (EC 1.1.1.27)and glucose-6-phosphate dehydrogenase (EC 1.1.1.49), were not similarly affected, suggesting that the effect was GAPDH specific. These observations suggest that GAPDH levels change in specific organelles during apoptosis for reasons that are separate from its function as a glycolytic enzyme. The accumulation of GAPDH protein in specific subcellular loci may play a role in neuronal apoptosis. C1 NIMH,MOL NEUROBIOL SECT,BIOL PSYCHIAT BRANCH,NIH,BETHESDA,MD 20892. NR 49 TC 73 Z9 73 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD NOV PY 1997 VL 69 IS 5 BP 1820 EP 1828 PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA YC168 UT WOS:A1997YC16800005 PM 9349524 ER PT J AU Bigner, SH Schrock, E AF Bigner, SH Schrock, E TI Molecular cytogenetics of brain tumors SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE brain tumors; chromosomes; comparative genomic hybridization; fluorescence in situ hybridization; genes; glioma; medulloblastoma ID COMPARATIVE GENOMIC HYBRIDIZATION; IN-SITU HYBRIDIZATION; PRIMITIVE NEUROECTODERMAL TUMORS; HUMAN GLIOBLASTOMA-MULTIFORME; NONRANDOM CHROMOSOMAL GAINS; MALIGNANT HUMAN GLIOMAS; GENETIC ALTERATIONS; P53 MUTATIONS; SOLID TUMORS; CELL-LINES AB Molecular cytogenetics includes a spectrum of methodologies that use molecular reagents to better define chromosomal alterations in normal and neoplastic cells. Brain tumors are a group of neoplasms for which there is a wealth of cytogenetic and molecular genetic information, and some of the newer techniques have extended the types of samples from which genetic information which can be obtained to biopsies and even paraffin-embedded sections. Fluorescence in situ hybridization on interphase nuclei has been used to confirm gains of chromosome 7, loss of chromosome 10, 9p deletion and gene amplification in malignant gliomas, and to visualize isochromosome 17q in medulloblastomas. Comparative genomic hybridization uses genomic DNA to determine gains and losses of chromosomes and chromosomal regions. This approach is particularly useful for identifying gene amplification. For cases in which chromosomal spreads are obtained, chromosomal painting is helpful in determining the origin of chromosomal segments. Several methods are now available in which each of the 22 autosomes and the sex chromosome can be identified by unique colors, termed Spectral karyotyping and multiplex-FISH. These molecular cytogenetic techniques are important clinical and experimental tools that have provided new insight into the genetic alterations of brain tumors. C1 NATL HUMAN GENOME RES INST,BETHESDA,MD. RP Bigner, SH (reprint author), DUKE UNIV,MED CTR,DEPT PATHOL,BOX 3712,DURHAM,NC 27710, USA. FU NCI NIH HHS [CA 68119, CA 43722] NR 74 TC 21 Z9 21 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD NOV PY 1997 VL 56 IS 11 BP 1173 EP 1181 DI 10.1097/00005072-199711000-00001 PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA YG291 UT WOS:A1997YG29100001 PM 9370227 ER PT J AU Jagadeesh, B Wheat, HS Kontsevich, LL Tyler, CW Ferster, D AF Jagadeesh, B Wheat, HS Kontsevich, LL Tyler, CW Ferster, D TI Direction selectivity of synaptic potentials in simple cells of the cat visual cortex SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID RECEPTIVE-FIELD STRUCTURE; STRIATE CORTEX; SPATIAL SUMMATION; AREA 17; MOTION; NEURONS; MODEL; INHIBITION; RESPONSES; MECHANISM AB The direction selectivity of simple cells in the visual cortex is generated at least in part by nonlinear mechanisms. If a neuron were spatially linear, its responses to moving stimuli could be predicted accurately from linear combinations of its responses to stationary stimuli presented at different positions within the receptive field. In extracellular recordings, this has not been found to be the case. Although the extracellular experiments demonstrate the presence of a nonlinearity, the cellular process underlying the nonlinearity, whether an early synaptic mechanism such as a shunting inhibition or simply the spike threshold at the output is not known. To differentiate between these possibilities, we have recorded intracellularly from simple cells of the intact cat with the whole cell patch technique. A linear model of direction selectivity was used to analyze the synaptic potentials evoked by stationary sine-wave gratings. The model predicted the responses of cells to moving gratings with considerable accuracy. The degree of direction selectivity and the time course of the responses to moving gratings were both well matched by the model. The direction selectivity of the synaptic potentials was considerably smaller than that of the intracellularly recorded action potential, indicating that a nonlinear mechanism such as threshold enhances the direction selectivity of the cell's output over that of its synaptic inputs. At the input stage, however, the cells apparently sum their synaptic inputs in a highly linear fashion. A more constrained test of linearity of synaptic summation based on principal component analysis was applied to the responses of direction-selective cells to stationary gratings. The analysis confirms that the summation in these cells is highly linear. The principal component analysis is consistent with a model in which direction selectivity in cortical simple cells is generated by only two subunits, each with a different receptive-held position and response time course. The response time course for each of the two subunits is derived for four analyzed cells. Each derived subunit is linear in spatial summation, suggesting that the neurons that comprise each subunit are either geniculate X-cells or receive their primary synaptic input from X-cells. The amplitude of the response of each subunit is linearly related to the contrast of the stimulus. The subunits are nonlinear in the time domain, however: the response to a stationary stimulus whose contrast is modulated sinusoidally in time is nonsinusoidal. The principal component analysis does not exclude models of direction selectivity based on more than two subunits, but such higher-order models would have to include the constraint that the extra subunits form a smooth continuum of interpolation between the properties derived from the two subunit solution. C1 NORTHWESTERN UNIV,DEPT NEUROBIOL & PHYSIOL,EVANSTON,IL 60208. NIMH,NEUROPSYCHOL LAB,NIH,BETHESDA,MD 20892. SMITH KETTLEWELL EYE RES INST,SAN FRANCISCO,CA 94115. FU NEI NIH HHS [R01-EY-04716] NR 56 TC 92 Z9 92 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD NOV PY 1997 VL 78 IS 5 BP 2772 EP 2789 PG 18 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA YG939 UT WOS:A1997YG93900049 PM 9356425 ER PT J AU Staley, JK Rothman, RB Rice, KC Partilla, J Mash, DC AF Staley, JK Rothman, RB Rice, KC Partilla, J Mash, DC TI kappa(2) Opioid receptors in limbic areas of the human brain are upregulated by cocaine in fatal overdose victims SO JOURNAL OF NEUROSCIENCE LA English DT Article DE cocaine; human brain; kappa opioid receptor; IOXY; delirium; dopamine ID GUINEA-PIG BRAIN; PRODYNORPHIN MESSENGER-RNA; OPIATE RECEPTOR; BINDING-SITES; DOPAMINE RELEASE; PHARMACOLOGICAL CHARACTERIZATION; BEHAVIORAL SENSITIZATION; NUCLEUS-ACCUMBENS; RAT; PEPTIDES AB Cocaine is thought to be addictive because chronic use leads to molecular adaptations within the mesolimbic dopamine (DA) circuitry that affect motivated behavior and emotion. Although the reinforcing effects of cocaine are mediated primarily by blocking DA reuptake into the presynaptic nerve terminal, reciprocal signaling between DA and endogenous opioids has important implications for cocaine dependence. The present study used the opioid antagonist 6 beta-[125iodo]-3,14-dihydroxy-17-cyclopropylmethyl-4,5 alpha-epoxymorphinan ([I-125]IOXY) after pretreatment with the site-directed acylating agents 2-(p-ethoxybenzyl)-1-diethylaminoethyl-5-isothiocyanato-benzimidiazole-HCl (mu-selective) and N-phenyl-N-[1-(2-(4-isothiocyanato)-phenethyl)-4-piperidinyl]-propanamide-HCl (delta-selective) to examine the effect of cocaine exposure on the distribution and density of kappa(2) receptors in autopsy studies of human cocaine fatalities. The selective labeling of the kappa(2) receptor subtype was demonstrated by competition binding studies, which gave a pharmacological signature (IOXY greater than or equal to (+)-bremazocine much greater than U50,488 greater than or equal to U69,593) distinct from either the kappa(1) or kappa(3) receptor subtypes. Visualization of [I-125]IOXY labeling revealed that kappa(2) receptors localize to mesocortical and subcortical limbic areas, including the cingulate, entorhinal, insular, and orbitofrontal cortices and the nucleus accumbens and amygdala. The number of kappa(2) receptors in the nucleus accumbens and other limbic brain regions from cocaine fatalities was increased twofold as compared with age-matched and drug-free control subjects. Cocaine overdose victims, who experienced paranoia and marked agitation before death, also had elevated densities of kappa(2) receptors in the amygdala. These findings demonstrate for the first time that kappa(2) receptor numbers are upregulated by cocaine exposure. The molecular adaptation of kappa(2) receptor numbers may play a role in the motivational incentive associated with episodes of binge cocaine use and in the dysphoria that follows abrupt cocaine withdrawal. C1 UNIV MIAMI,SCH MED,DEPT NEUROL & MOL & CELLULAR PHARMACOL,MIAMI,FL 33101. UNIV MIAMI,SCH MED,COMPREHENS DRUG RES CTR,MIAMI,FL 33101. NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,DIV INTRAMURAL RES,NIH,BALTIMORE,MD 21224. NIDDKD,MED CHEM LAB,NIH,BETHESDA,MD 20892. FU NIDA NIH HHS [DA-06227] NR 59 TC 49 Z9 50 U1 1 U2 2 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 1 PY 1997 VL 17 IS 21 BP 8225 EP 8233 PG 9 WC Neurosciences SC Neurosciences & Neurology GA YC947 UT WOS:A1997YC94700017 PM 9334398 ER PT J AU Johren, O Sanvitto, GL Egidy, G Saavedra, JM AF Johren, O Sanvitto, GL Egidy, G Saavedra, JM TI Angiotensin II AT(1A) receptor mRNA expression is induced by estrogen-progesterone in dopaminergic neurons of the female rat arcuate nucleus SO JOURNAL OF NEUROSCIENCE LA English DT Article DE angiotensin II receptors; catecholamines; tyrosine hydroxylase; in situ hybridization; anterior pituitary; prolactin ID MESSENGER-RNA LEVELS; ANTERIOR-PITUITARY; TYROSINE-HYDROXYLASE; PROLACTIN SECRETION; GENE-EXPRESSION; INSITU HYBRIDIZATION; LUTEINIZING-HORMONE; MEDIAN-EMINENCE; BRAIN; RELEASE AB Brain angiotensin II (Ang II) inhibits pituitary prolactin release by an indirect mechanism requiring stimulation of dopamine formation and release. We report that [I-125]Sar(1)-Ang II binding to AT(1) receptors and AT(1A) receptor mRNA expression increase selectively in the dorsomedial arcuate nucleus of 17 beta-estradiol-primed ovariectomized rats after treatment with progesterone. In hormone-treated rats, arcuate nucleus AT(1A) receptor mRNA expression is associated with tyrosine hydroxylase-positive neurons. No AT(1A) receptor mRNA was detected in tyrosine hydroxylase-positive cells of the arcuate nucleus of intact male rats. Conversely, in the anterior pituitary, where local or circulating Ang II stimulates prolactin release, [I-125]Sar(1)-Ang II binding to AT(1) receptors and AT(1B) receptor mRNA expression are decreased in 17 beta-estradiol/progesterone-treated ovariectomized rats. Thus, AT(1A) receptors in the dorsal arcuate nucleus and AT(1B) receptors in the anterior pituitary are regulated inversely by estrogen/progesterone treatment, supporting the hypothesis of a dual role for brain and pituitary Ang II on prolactin release. The colocalization of AT(1A) receptor mRNA and tyrosine hydroxylase in neurons of the arcuate nucleus furthermore indicates that within this area central Ang II acts directly on dopaminergic neurons. These results support the hypothesis that central Ang II inhibits pituitary prolactin release indirectly via modulation of dopaminergic activity in the arcuate nucleus. RP Johren, O (reprint author), NIMH,PHARMACOL SECT,10 CTR DR,MSC 1514,BLDG 10,ROOM 2D-57,BETHESDA,MD 20892, USA. RI Johren, Olaf/G-6967-2011 NR 54 TC 41 Z9 41 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 1 PY 1997 VL 17 IS 21 BP 8283 EP 8292 PG 10 WC Neurosciences SC Neurosciences & Neurology GA YC947 UT WOS:A1997YC94700022 PM 9334403 ER PT J AU Widenfalk, J Nosrat, C Tomac, A Westphal, H Hoffer, B Olson, L AF Widenfalk, J Nosrat, C Tomac, A Westphal, H Hoffer, B Olson, L TI Neurturin and glial cell line-derived neurotrophic factor receptor-beta (GDNFR-beta), novel proteins related to GDNF and GDNFR-alpha with specific cellular patterns of expression suggesting roles in the developing and adult nervous system and in peripheral organs SO JOURNAL OF NEUROSCIENCE LA English DT Article DE GDNF; neurturin; GDNFR alpha; GDNFR beta; RET; in situ hybridization; CNS; development; kidney; gastrointestinal tract; gonads; kainic acid; GFR alpha-1; GFR alpha-2 ID MICE LACKING GDNF; RET PROTOONCOGENE; MESSENGER-RNA; TYROSINE KINASE; HIRSCHSPRUNG DISEASE; MUTATIONS; NEURONS; RAT; HYBRIDIZATION; SURVIVAL AB Cloning strategies were used to identify a gene termed glial cell line-derived neurotrophic factor receptor-beta (GDNFR-beta) related to GDNFR-alpha. In situ hybridization was then used to map cellular expression of the GDNF-related trophic factor neurturin (NTN) and GDNFR-beta mRNA in developing and adult mice, and comparisons with GDNFR-alpha and RET were made. Neurturin is expressed in postnatal cerebral cortex, striatum, several brainstem areas, and the pineal gland. GDNFR-beta mRNA was more widely expressed in the developing and adult CNS, including cerebral cortex, cerebellum, thalamus, zona incerta, hypothalamus, brainstem, and spinal cord, and in subpopulations of sensory neurons and developing peripheral nerves. NTN colocalized with RET and GDNFR-alpha in ureteric buds of the developing kidney. The circular muscle layer of the developing intestines, smooth muscle of the urether, and developing bronchiolae also expressed NTN. GDNFR-beta was found in myenteric but not submucosal intestinal plexuses. in developing salivary glands NTN had an epithelial expression, whereas GDNFR-beta was expressed in surrounding tissue. Neurturin and GDNFR-beta were present in developing sensory organs. In the gonads, NTN appeared to be expressed in Sertoli cells and in the epithelium of the oviduct, whereas GDNFR-beta was expressed by the germ cell line. Our findings suggest multiple roles for NTN and GDNFR-beta in the developing and adult organism. Although NTN and GDNFR-beta expression patterns are sometimes complementary, this is not always the case, suggesting multiple modi operandi of GDNF and NTN in relation to RET and the two binding proteins, GDNFR-alpha and GDNFR-beta. C1 KAROLINSKA INST,DEPT NEUROSCI,S-17177 STOCKHOLM,SWEDEN. NICHHD,BETHESDA,MD 20892. NIDA,NIH,BALTIMORE,MD 21224. NR 35 TC 199 Z9 201 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 1 PY 1997 VL 17 IS 21 BP 8506 EP 8519 PG 14 WC Neurosciences SC Neurosciences & Neurology GA YC947 UT WOS:A1997YC94700042 PM 9334423 ER PT J AU Thornton, JA Rothblat, LA Murray, EA AF Thornton, JA Rothblat, LA Murray, EA TI Rhinal cortex removal produces amnesia for preoperatively learned discrimination problems but fails to disrupt postoperative acquisition and retention in rhesus monkeys SO JOURNAL OF NEUROSCIENCE LA English DT Article DE visual discrimination; stimulus memory; retrograde amnesia; entorhinal cortex; perirhinal cortex; rhesus monkey ID RETROGRADE-AMNESIA; ENTORHINAL CORTEX; INTERTRIAL INTERVALS; ANTEROGRADE AMNESIA; FORNIX TRANSECTION; SPATIAL DISCRIMINATION; TEMPORAL GRADIENT; MEMORY IMPAIRMENT; PERIRHINAL CORTEX; PARIETAL CORTEX AB To test whether the rhinal cortex (i.e., entorhinal and perirhinal cortex) plays a time-limited role in information storage, eight rhesus monkeys were trained to criterion on two sets of 60 object discrimination problems, one set at each of two different time periods separated by 15 weeks. After the monkeys had learned both sets, two groups balanced for preoperative acquisition rates were formed. One group received bilateral ablation of the rhinal cortex (n = 4), and the other was retained as an unoperated control group (n = 4). After a 2 week rest period, monkeys were assessed for retention of the object discrimination problems. Retention was significantly poorer in monkeys with removals of the rhinal cortex relative to the controls (68 vs 91 %). Although both groups showed slightly better retention of problems from the more recently learned set, there was no evidence of a differential effect of the cortical removal across sets (i.e., no temporal gradient). In addition, the monkeys with rhinal cortex lesions subsequently learned three new sets of 10 object discrimination problems as quickly as the controls did, thus ruling out the possibility of a gross impairment in visual perception or discrimination abilities. Furthermore, they retained these postoperatively learned object discriminations as well as the controls did. The findings indicate that the rhinal cortex is critical for the storage and/or retrieval of object discrimination problems that were learned up to 16 weeks before rhinal cortex ablation; however, in the absence of the rhinal cortex, efficient learning and retention of new discrimination problems can still occur. C1 NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,DEPT PSYCHOL,WASHINGTON,DC 20052. OI Murray, Elisabeth/0000-0003-1450-1642 NR 51 TC 72 Z9 72 U1 0 U2 1 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 1 PY 1997 VL 17 IS 21 BP 8536 EP 8549 PG 14 WC Neurosciences SC Neurosciences & Neurology GA YC947 UT WOS:A1997YC94700045 PM 9334426 ER PT J AU Jiang, H Guroff, G AF Jiang, H Guroff, G TI Actions of the neurotrophins on calcium uptake SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Review DE neurotrophins; calcium uptake; nerve growth factor; neuronal survival ID NERVE GROWTH-FACTOR; PROTEIN-KINASE-C; SENSORY NEURON DEVELOPMENT; ARACHIDONIC-ACID RELEASE; PC12 CELLS; SIGNAL-TRANSDUCTION; CHROMAFFIN CELLS; FACTOR INCREASES; FIBER OUTGROWTH; TRK RECEPTORS AB The neurotrophins are important for their long-term effects on the survival and differentiation of many types of neurons during development, They also appear to protect mature neurons from injury caused by nutrient or oxygen deprivation, More recently, the neurotrophins have been implicated in such shortterm processes as synaptic plasticity, A great deal of evidence suggests that intracellular calcium levels play a key role in neuronal survival during normal development, in neuronal injury following nutrient or oxygen deprivation, and in synaptic plasticity as well, Maintaining appropriate intracellular levels of calcium is important for proper biological function and it has been shown that one of the actions of the neurotrophins is to modulate intracellular calcium levels in a number of in vivo and in vitro systems, Some information about the mechanism(s) by which this is accomplished is now available, Understanding the mechanisms of neurotrophin action should provide insights into the processes by which the brain functions and, further, provide therapeutic tools for the treatment of neuronal injury and neurodegenerative diseases, (C) 1997 Wiley-Liss, Inc.dagger C1 NICHHD, GROWTH FACTORS SECT, NIH, BETHESDA, MD 20892 USA. NR 59 TC 21 Z9 22 U1 2 U2 2 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD NOV 1 PY 1997 VL 50 IS 3 BP 355 EP 360 DI 10.1002/(SICI)1097-4547(19971101)50:3<355::AID-JNR1>3.0.CO;2-H PG 6 WC Neurosciences SC Neurosciences & Neurology GA YE049 UT WOS:A1997YE04900001 PM 9364320 ER PT J AU Pluta, RM Oldfield, EH Boock, RJ AF Pluta, RM Oldfield, EH Boock, RJ TI Reversal and prevention of cerebral vasospasm by intracarotid infusions of nitric oxide donors in a primate model of subarachnoid hemorrhage SO JOURNAL OF NEUROSURGERY LA English DT Article DE nitric oxide; cerebral vasospasm; cerebral blood flow; nitric oxide donor; subarachnoid hemorrhage; Macaca cynomolgus ID INTRAVENOUS NITROGLYCERIN; ARTERIAL SPASM; NITROPRUSSIDE; ENDOTHELIUM; HEMOGLOBIN; RELEASE; UPDATE; BRAIN; BLOOD; NO AB Decreased endothelium-derived relaxing factor, nitric oxide (NO), in the arterial wall has been hypothesized to be a potential cause of cerebral vasospasm following subarachnoid hemorrhage (SAH). The authors sought to determine whether intracarotid infusions of newly developed NO-donating compounds (NONOates) could reverse vasospasm or prevent the occurrence of cerebral vasospasm in a primate model of SAH. Twenty-one cynomolgus monkeys were studied in two experimental settings. In an acute infusion experiment, saline or NONOate was infused intracarotidly in four normal monkeys and in four monkeys after onset of SAH. During the infusions regional cerebral blood flow (rCBF) was measured in eight animals and CBF velocity in two. In a chronic infusion experiment, saline (four animals) or NONOate (diethylamine-NO [three animals] or proli-NO [six animals]) was infused intracarotidly in monkeys for 7 days after SAH. In acute infusion experiments, 3-minute intracarotid diethylamine-NO infusions reversed arteriographically confirmed vasospasm of the right middle cerebral artery (MCA) (as viewed on anteroposterior projection, the decrease in area was 8.4 +/- 4.3% in the treatment group compared with 35 +/- 12% in the control group; p < 0.004), increased rCBF by 31 +/- 1.9% (p < 0.002), and decreased the mean systolic CBF velocity in the right MCA. In a long-term infusion experiment, the area of the right MCA in control animals decreased by 63 +/- 5%. In animals undergoing a 7-day continuous glucantime-NO intracarotid infusion, the area of the right MCA decreased by 15 +/- 6.2%, and in animals undergoing a 7-day proli-NO infusion, the area of the right MCA decreased by 11 +/- 2.9% (p < 0.05). The mean arterial blood pressure decreased in the glucantime-NO group from 75 +/- 12 mm Hg (during saline infusion) to 57 +/- 10 mm Hg (during glucantime-NO infusion; p < 0.05), but it was unchanged in animals undergoing proli-NO infusion (76 +/- 12 mm Hg VS, 78 +/- 12 mm Hg). Results of these experiments show that cerebral vasospasm is both reversed and completely prevented by NO replacement. However, only the use of regional infusion of the NONOate with an extremely shea half-life avoided a concomitant decrease in arterial blood pressure, which could produce cerebral ischemia in patients with impaired autoregulation of CBF after the rupture of an intracranial aneurysm. C1 NINCDS,SURG NEUROL BRANCH,NIH,BETHESDA,MD 20892. NR 31 TC 126 Z9 128 U1 0 U2 2 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD NOV PY 1997 VL 87 IS 5 BP 746 EP 751 DI 10.3171/jns.1997.87.5.0746 PG 6 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA YC367 UT WOS:A1997YC36700014 PM 9347984 ER PT J AU Gallant, PE Galbraith, JA AF Gallant, PE Galbraith, JA TI Axonal structure and function after axolemmal leakage in the squid giant axon SO JOURNAL OF NEUROTRAUMA LA English DT Article DE axonal protection; axoplasmic transport; degeneration; electroporation; membrane resealing ID AXOPLASMIC-TRANSPORT; OPTIC-NERVE; MEMBRANE-PERMEABILITY; STRETCH-INJURY; IN-VITRO; REDISTRIBUTION; VESICULATION; CONSTRICTION; MITOCHONDRIA; COMPRESSION AB Membrane leakage is a common consequence of traumatic nerve injury, In order to measure the early secondary effects of different levels of membrane leakage on axonal structure and function we studied the squid giant axon after electroporation at field strengths of 0.5, 1.0, 1.6, or 3.3 kV/cm, Immediately after mild electroporation at 0.5 kV/cm, 40% of the axons had no action potentials, but by 1 h all of the mildly electroporated axons had recovered their action potentials. Many large organelles (mitochondria) were swollen, however, and their transport was reduced by 62% 1 h after this mild electroporation, One hour after moderate electroporation at 1.0 kV/cm, most of the axons had no action potentials, most large organelles were swollen, and their transport was reduced by 98%, whereas small organelle transport was reduced by 75%, Finally at severe electroporation levels of 1.65-3.0 kV/cm all conduction and transport was lost and the gel-like axoplasmic structure was clumped or liquefied, The structural damage and transport block seen after severe and moderate poration were early secondary injuries that could be prevented by placing the porated axons in an intracellular-type medium (low in Ca2+, Na+, and Cl-) immediately after poration. In moderately, but not severely, porated axons this protection of organelle transport and structure persisted, and action potential conduction returned when the axons were returned to the previously injurious extracellular-type medium, This suggests that the primary damage, the axolemmal leak, was repaired while the moderately porated axons were in the protective intracellular-type medium. C1 MARINE BIOL LAB,WOODS HOLE,MA 02543. UNIV CALIF SAN DIEGO,DEPT BIOENGN,LA JOLLA,CA 92093. RP Gallant, PE (reprint author), NINCDS,NEUROBIOL LAB,NIH,BLDG 36,ROOM 2A-21,BETHESDA,MD 20892, USA. NR 42 TC 15 Z9 15 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0897-7151 J9 J NEUROTRAUM JI J. Neurotrauma PD NOV PY 1997 VL 14 IS 11 BP 811 EP 822 DI 10.1089/neu.1997.14.811 PG 12 WC Critical Care Medicine; Clinical Neurology; Neurosciences SC General & Internal Medicine; Neurosciences & Neurology GA YK511 UT WOS:A1997YK51100001 PM 9421453 ER PT J AU Villemagne, VL Horti, A Scheffel, U Ravert, HT Finley, P Clough, DJ London, ED Wagner, HN Dannals, RF AF Villemagne, VL Horti, A Scheffel, U Ravert, HT Finley, P Clough, DJ London, ED Wagner, HN Dannals, RF TI Imaging nicotinic acetylcholine receptors with fluorine-18-FPH, an epibatidine analog SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE nicotinic receptors; PET; nonhuman primate; brain; epibatidine ID POSITRON EMISSION TOMOGRAPHY; LIVING HUMAN-BRAIN; BINDING-SITES; RAT-BRAIN; CHOLINERGIC RECEPTORS; ALZHEIMERS-DISEASE; CEREBRAL-CORTEX; H-3 EPIBATIDINE; AUTORADIOGRAPHIC LOCALIZATION; ALPHA-BUNGAROTOXIN AB Nicotinic acetylcholine receptors (nAChRs) have been implicated in a variety of central processes, such as learning and memory and analgesia. These receptors also mediate the reinforcing properties of nicotine in tobacco products and are increased in postmortem samples of brains of smokers, On the other hand, brains of individuals who have died from dementia of the Alzheimer type show abnormally low densities of nAChRs. In this study, the distribution and kinetics of [(+/-)-exo-2-(2-[F-18] fluoro-5-pyridyl)-7-azabicyclo[2.2.1]heptane (F-18-FPH), a high-affinity nAChR agonist, was evaluated in a baboon using PET. Methods: After intravenous injection of 5 mCi [185 MBq] F-18-FPH into a 25-kg anesthetized baboon, sequential quantitative tomographic data were acquired over a period of 150 min. Regions of interest were placed and time-activity curves were generated, Brain kinetics of the radiotracer were calculated, and the in vivo regional binding in the baboon brain was compared with the known in vitro regional distribution of nAChRs in the rat and human brain. Results: Brain activity reached a plateau within 60 min after injection of the tracer, and the binding was reversible. Elimination of F-18-FPH was relatively rapid from the cerebellum (clearance t(1/2) = 3 hr), intermediate from the hypothalamus/midbrain (t(1/2) = 7 hr) and slow from the thalamus (t(1/2) = 16 hr). Radioactivity due to F-18-FPH at 130 min postinjection was highest in the thalamus and hypothalamus/midbrain, intermediate in the neocortex and hippocampus and lowest in the cerebellum. Subcutaneous injection of 1 mg/kg cytisine 45 min after injection of the radiotracer reduced brain activity at 130 min by 67%, 64%, 56% and 52% of control values in the thalamus, hypothalamus/midbrain, hippocampus and cerebellum, respectively. The regional binding of F-18-FPH at 130 min was highly correlated with the known densities of nAChR measured in vitro in human (r = 0.81) and rat brain (r = 0.90). Conclusion: These results demonstrate the feasibility of imaging nAChRs in vivo. Fluorine-18-FPH appears to be a suitable tracer to study nAChRs in the human brain. C1 JOHNS HOPKINS MED INST, DIV NUCL MED, BALTIMORE, MD 21205 USA. JOHNS HOPKINS MED INST, DIV RADIAT HLTH SCI, BALTIMORE, MD 21205 USA. NIDA, BRAIN IMAGING SECT, INTRAMURAL RES PROGRAM, NIH, BALTIMORE, MD USA. FU NCI NIH HHS [CA 32845] NR 42 TC 56 Z9 57 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 EI 1535-5667 J9 J NUCL MED JI J. Nucl. Med. PD NOV PY 1997 VL 38 IS 11 BP 1737 EP 1741 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA YF971 UT WOS:A1997YF97100021 PM 9374343 ER PT J AU Zahm, SH AF Zahm, SH TI Mortality study of pesticide applicators and other employees of a lawn care service company SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Article ID NON-HODGKINS-LYMPHOMA; SOFT-TISSUE SARCOMAS; AGRICULTURAL RISK-FACTORS; PHENOXY HERBICIDES; CANCER MORTALITY; CASE-REFERENT; MALIGNANT-LYMPHOMA; WESTERN WASHINGTON; COHORT MORTALITY; CHEMICAL WORKERS AB In response to reports linking non-Hodgkin's lymphoma (NHL) and the herbicide 2, 4-dichlorophenoxyacetic acid, a retrospective cohort mortality study of 32,600 employees of a lawn. care company was conducted, The cohort was generally young with short-duration employment and follow-up. In comparison to the US population, the cohort had significantly decreased mortality from all cases of death combined (307 deaths), arteriosclerotic heart disease, and accidents. There were 45 cancer-deaths (59.6 expected, standardized mortality ratio [SMR] = 0.76, 95% confidence interval [CI] = 0.5, 1.01). Bladder cancer mortality was significantly increased but two of the three observed deaths had no direct occupational contact with pesticides. There were four deaths due to NHL (SMR = 1.14, CI = 0.31, 2.91); three were male lawn applicators (SMR = 1.63, CI = 0.33, 4.77), with two of the applicators employed for three or more years (SMR = 7.11, CI = 1.78, 28, 42). No other cause of death was significantly elevated among lawn applicators as a group or among those employed for three or more years. Although based on very small numbers and perhaps due to chance, the NHL excess is consistent with several earlier studies. RP Zahm, SH (reprint author), NATL CANC INST,DIV CANC EPIDEMIOL & GENET,OCCUPAT EPIDEMIOL BRANCH,6130 EXECUT BLVD,EPN 418,ROCKVILLE,MD 20892, USA. RI Zahm, Shelia/B-5025-2015 NR 72 TC 42 Z9 43 U1 2 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1076-2752 J9 J OCCUP ENVIRON MED JI J. Occup. Environ. Med. PD NOV PY 1997 VL 39 IS 11 BP 1055 EP 1067 DI 10.1097/00043764-199711000-00006 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YF515 UT WOS:A1997YF51500006 PM 9383716 ER PT J AU Skolnick, P Hu, RJ Cook, CM Hurt, SD Trometer, JD Lu, RY Huang, Q Cook, JM AF Skolnick, P Hu, RJ Cook, CM Hurt, SD Trometer, JD Lu, RY Huang, Q Cook, JM TI [H-3]RY 80: A high-affinity, selective ligand for gamma-aminobutyric acid(A) receptors containing alpha-5 subunits SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article; Proceedings Paper CT 35th Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 09-13, 1996 CL SAN JUAN, PR SP Amer Coll Neuropsychopharm ID RECOMBINANT GABA(A) RECEPTOR; RAT-BRAIN; A RECEPTORS; BENZODIAZEPINE RECEPTORS; PHARMACOLOGICAL PROPERTIES; SUBTYPES; BINDING; IMIDAZOBENZODIAZEPINES; STOICHIOMETRY; HETEROGENEITY AB The radiochemical synthesis and pharmacological properties are described of[H-3]RY 80 (ethyl-8-acetylene-5,6-dihydro-5-methyl-6-oxo-4H-imidazo[1,5a] [1,4]benzodiazepine-3-carboxylate, [ethyl-H-3]). This compound is one of a series of 8-substituted imidazobenzodiazepines that exhibits both high affinity and selectivity for gamma-aminobutyric acid (GABA)(A) receptors containing alpha-5 subunits. Saturable, high-affinity (K-d similar to 0.7 nM) binding of [H-3]RY 80 was observed in hippocampal membranes. The maximum number (B-max) of [H-3]RY 80 binding sites was similar to 18% of that obtained with [H-3]flunitrazepam, a radioligand that labels all ''diazepam-sensitive'' GABA(A) receptors. This value is consistent with previous estimates (10-20%) of the proportion of rat hippocampal GABA(A) receptors containing alpha-5 subunits determined by immunoprecipitation with selective antibodies and competition experiments using an alpha-5-selective ligand. In recombinant GABA(A) receptors composed of alpha-5 beta-3 gamma-2 subunits, the K-d of [H-3]RY 80 (similar to 0.5 nM) was consistent with the value obtained in hippocampus, whereas the B-max value was not significantly different from that obtained with [H-3]flunitrazepam. The potencies of several benzodiazepine site ligands to inhibit [H-3]RY 80 binding to hippocampal membranes were in agreement with the values obtained in recombinant (alpha-5 beta-3 gamma-2) GABA(A) receptors. [H-3]RY 80 was used both in a ''GABA shift'' assay to correctly predict the in vivo actions of a novel, alpha-5-selective ligand and to characterize a population of GABA(A) receptors containing alpha-5 subunits in neonatal rat cortex. These findings demonstrate that [H-3]RY 80 can be used as a radioligand to examine the properties of GABA(A) receptors containing alpha-5 subunits. C1 NEW ENGLAND NUCL,BOSTON,MA. UNIV WISCONSIN,DEPT CHEM,MILWAUKEE,WI. RP Skolnick, P (reprint author), NIDDKD,NEUROSCI LAB,NIH,BLDG 8-111,BETHESDA,MD 20892, USA. FU NIMH NIH HHS [MH-46851] NR 40 TC 52 Z9 52 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 1997 VL 283 IS 2 BP 488 EP 493 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YF254 UT WOS:A1997YF25400009 PM 9353361 ER PT J AU Sadeque, AJM Fisher, MB Korzekwa, KR Gonzalez, FJ Rettie, AE AF Sadeque, AJM Fisher, MB Korzekwa, KR Gonzalez, FJ Rettie, AE TI Human CYP2C9 and CYP2A6 mediate formation of the hepatotoxin 4-ene-valproic acid SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID HUMAN-LIVER-MICROSOMES; VALPROIC ACID; METABOLIC-ACTIVATION; 2-NORMAL-PROPYL-4-PENTENOIC ACID; SPECIES-DIFFERENCES; HEPATIC FATALITIES; CYTOCHROME P4502C9; TOXIC METABOLITE; RAT HEPATOCYTES; IDENTIFICATION AB Cytochrome P450-dependent desaturation of the anticonvulsant drug valproic acid (VPA) results in formation of the hepatotoxin, 4-ene-VPA. Polytherapy with other anticonvulsants which are known P450 inducers increases the flux through this bioactivation pathway. The aim of the present study was to identify specific, inducible forms of human liver P450 which catalyze terminal desaturation of VPA. Oxidized VPA metabolites formed in an NADPH-dependent manner by human liver microsomes were quantified by gas-chromatography/mass spectrometry. In vitro reaction conditions were established which reflected the product profile found in vivo. Production of 4-ene-VPA by microsomal P450s could be inhibited significantly by coumarin, sulfaphenazole and diethyldithiocarbamate, but not by triacetyloleandomycin, quinidine or furafylline. Recombinant human CYP3A4 did not form detectable levels of 4-ene-VPA and, of nine additional isoforms expressed in either HepG2 or lymphoblastoid cells which were screened for VPA desaturase activity, only CYP2C9 and CYP2A6 formed detectable levels of metabolite. Consequently, CYP3A4, the isoform usually associated with induction by anticonvulsants cannot be responsible for the enhanced 4-ene-VPA formation that occurs during polytherapy. Instead, enhanced activity in vivo likely results from induction of CYP2A6 and/or CYP2C9. C1 UNIV WASHINGTON,DEPT MED CHEM,SEATTLE,WA 98195. NCI,MOL CARCINOGENESIS LAB,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM07750, GM32165, GM49054] NR 37 TC 86 Z9 93 U1 0 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 1997 VL 283 IS 2 BP 698 EP 703 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YF254 UT WOS:A1997YF25400036 PM 9353388 ER PT J AU Blanchet, PJ Konitsiotis, S Chase, TN AF Blanchet, PJ Konitsiotis, S Chase, TN TI Motor response to a dopamine D3 receptor preferring agonist compared to apomorphine in levodopa-primed 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine monkeys SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID PARKINSONS-DISEASE; INDUCED DYSKINESIA; D-3 RECEPTORS; RAT; FLUCTUATIONS; BRAIN; MPTP; LOCALIZATION; PHARMACOLOGY; EXPRESSION AB The profile of dopamine receptor subtype activation contributing to the therapeutic efficacy and motor response complications of levodopa (nonselective pro-agonist) in Parkinson's disease remains unclear. Potent, selective, short-acting dopamine D2 receptor subfamily agonists show good antiparkinsonian efficacy but produce dyskinesias comparable to levodopa. Nonetheless, agonists displaying higher affinity for dopamine receptors other than the D2 subtype may have a better therapeutic index. To clarify this issue, we compared the nonselective dopamine D1/D2 receptor subfamilies agonist apomorphine to the dopamine D3 receptor preferring agonist [R-(+)trans-3,4,4a,10b-tetrahydro-4-propyl-2H,5H-[1]benzopyrano[4,3b]-1,4-oxazin-9-ol] (PD 128,907) in 6 levodopa-primed, 1-methyl4-phenyl-1,2,3,6-tetrahydropyridine-lesioned parkinsonian monkeys with reproducible dyskinesias. Single s.c. dosing with the lowest fully effective dose of apomorphine (averaging 27.9 +/- 4.5 mu g/kg) and PD 128,907 (averaging 41.7 +/- 4.4 mu g/kg) yielded equivalent antiparkinsonian efficacy on the behavioral scale and portable activity monitoring used. A comparable significant dose-dependent increase in the response magnitude and duration was seen with two higher doses. The severity of dyskinesia was also similar between the two drugs. When the lower dose for each drug was administered six times at a fixed 90-min interval, both drugs remained efficacious with no significant tolerance observed. The D3 receptor preferring antagonist U-99194A significantly reduced the motor effects of both apomorphine and PD 128,907. Thus, increased D3 receptor tone does not acutely ameliorate dyskinesias in levodopaprimed parkinsonian monkeys. Given the reported lack of affinity of PD 128,907 for central D1 receptors, our data support the concept that the pharmacological activation of D1 receptors is not mandatory for relief of parkinsonism and production of dyskinesia. C1 NINCDS,EXPT THERAPEUT BRANCH,NIH,BETHESDA,MD 20892. NR 50 TC 35 Z9 35 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 1997 VL 283 IS 2 BP 794 EP 799 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YF254 UT WOS:A1997YF25400048 PM 9353400 ER PT J AU Vaupel, DB Jasinski, DR AF Vaupel, DB Jasinski, DR TI l-alpha-acetylmethadol, l-alpha-acetyl-N-normethadol and l-alpha-acetyl-N,N-dinormethadol: Comparisons with morphine and methadone in suppression of the opioid withdrawal syndrome in the dog SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID NALORPHINE-LIKE DRUGS; CHRONIC SPINAL DOG; PHENCYCLIDINE; ENANTIOMERS AB 1-alpha-Acetyl-N-normethadol (nor-LAAM) and 1-alpha-acetyl-N,N-dinormethadol (dinor-LAAM) are active metabolites of the opiate 1-alpha-acetylmethadol (LAAM), and they contribute to the prolonged actions of the parent compound. Single doses of nor-LAAM, dinor-LAAM, LAAM, methadone and morphine were given intravenously to the chronic spinal dog to determine acute, single-dose effects and their ability to suppress withdrawal in morphine-dependent dogs. These opioids produced dose-dependent antinociception, decreases in body temperature and pupillary constriction. For these measures, dinor-LAAM was 1.5 to 3 times and nor-LAAM 6 to 12 times as potent as LAAM. Five hours after the acute administration of LAAM or either of the metabolites, a 1-mg/kg dose of naltrexone given intravenously produced withdrawal, indicating the presence of acute physical dependence. In dogs physically dependent on a daily dose of 125 mg of morphine, nor-LAAM was 9 times as potent as either LAAM or dinor-LAAM in suppressing spontaneous withdrawal 40 hr after the last dose of morphine. The efficacies of LAAM and its demethylated metabolites in the dog for producing acute opiate effects were comparable with those of morphine and methadone. There was a trend, however, for LAAM to suppress the expression of abstinence more fully than either metabolite. The usefulness of LAAM as a treatment for opiate addiction is likely due in part to the equivalent efficacies and higher potencies of its nor and diner metabolites. C1 JOHNS HOPKINS BAYVIEW MED CTR,CTR CHEM DEPENDENCE,BALTIMORE,MD. RP Vaupel, DB (reprint author), NIDA,INTRAMURAL RES PROGRAM,BRAIN IMAGING SECT,5500 NATHAN SHOCK DR,BALTIMORE,MD 21224, USA. NR 30 TC 10 Z9 10 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 1997 VL 283 IS 2 BP 833 EP 842 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YF254 UT WOS:A1997YF25400053 PM 9353405 ER PT J AU Jones, S Yakel, JL AF Jones, S Yakel, JL TI Functional nicotinic ACh receptors on interneurones in the rat hippocampus SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Article ID NEURONS; ACETYLCHOLINE AB 1. Neuronal nicotinic ACh receptors (nAChRs) were studied in the rat hippocampal slice preparation using whole-cell patch-clamp recording techniques. 2. Responses to ACh (100 mu M) were detected on inhibitory interneurones in the CA1 field of the hippocampus proper and in the dentate gyrus, but not on principal excitatory neurones in either region. The different neuronal types were identified based on their morphology and location. 3. ACh excited interneurones in the hippocampus and dentate gyrus in current-clamp recordings. In voltage-clamp recordings, ACh-activated inward currents were recorded from interneurones in the presence of blockers of synaptic transmission and the muscarinic ACh receptor antagonist atropine. The zero current potential for this response to ACh was near 0 mV. 4. The effect of ACh was mimicked by the nAChR-selective agonists nicotine (100 mu M) and 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP, 100 mu M). The response to ACh was reversibly antagonized by the neuronal nAChR antagonist mecamylamine (10 mu M). The nAChR alpha 7 subunit-selective antagonists alpha-bungarotoxin (100 nM) and methyllycaconitine (10 nM) also inhibited the response to ACh. 5. These observations demonstrate the presence of functional nAChRs on inhibitory interneurones in the rat hippocampus. Thus, a novel mechanism by which ACh can regulate neuronal activity in the hippocampus is revealed. C1 NIEHS,LAB SIGNAL TRANSDUCT,NIH,RES TRIANGLE PK,NC 27709. NR 22 TC 214 Z9 217 U1 0 U2 2 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD NOV 1 PY 1997 VL 504 IS 3 BP 603 EP 610 DI 10.1111/j.1469-7793.1997.603bd.x PG 8 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA YG079 UT WOS:A1997YG07900010 PM 9401968 ER PT J AU Jia, M Li, MX Nelson, PG AF Jia, M Li, MX Nelson, PG TI Thrombin receptor activation and protein kinase C (PKC) are involved in selective activity-dependent synapse loss in mouse motoneuron and muscle co-culture. SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Meeting Abstract C1 NICHHD,LDN,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD NOV PY 1997 VL 504P SI SI BP P213 EP P214 PG 2 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA YJ424 UT WOS:A1997YJ42400290 ER PT J AU McDonald, MP Crawley, JN AF McDonald, MP Crawley, JN TI Galanin-acetylcholine interactions in rodent memory tasks and Alzheimer's disease SO JOURNAL OF PSYCHIATRY & NEUROSCIENCE LA English DT Review ID CENTRAL-NERVOUS-SYSTEM; RAT VENTRAL HIPPOCAMPUS; GROWTH-HORMONE SECRETION; LOCUS COERULEUS NEURONS; NONMATCHING-TO-SAMPLE; MEDIAL SEPTAL AREA; MUDPUPPY PARASYMPATHETIC NEURONS; INVITRO RECEPTOR AUTORADIOGRAPHY; DOPAMINE-BETA-HYDROXYLASE; BASAL FOREBRAIN COMPLEX AB Galanin is a 29-amino-acid neuropeptide that is widely distributed in the mammalian central nervous system. Galanin-immunoreactive cell bodies, fibres and terminals, and galanin binding sites, are located in the basal forebrain of rats, monkeys and humans. Galanin fibres hyperinnervate the surviving cholinergic cell bodies in patients with Alzheimer's disease (AD). In rats, galanin inhibits acetylcholine release and produces deficits in learning and memory. These findings suggest that overexpressed galanin may contribute to the cognitive impairments exhibited by patients with AD. This paper reviews the literature on galanin distribution and function in light of its putative role in the mnemonic deficits in patients with AD, the effects of galanin on tests of learning and memory, and preliminary experiments with galanin antagonists in animal models of AD. C1 NIMH,SECT BEHAV NEUROPHARMACOL,EXPT THERAPEUT BRANCH,BETHESDA,MD 20892. NR 245 TC 26 Z9 27 U1 0 U2 0 PU CANADIAN PSYCHIATRIC ASSOC PI OTTAWA PA SUITE 200, 237 ARGYLE AVE, OTTAWA ON K2P 1B8, CANADA SN 1180-4882 J9 J PSYCHIATR NEUROSCI JI J. Psychiatry Neurosci. PD NOV PY 1997 VL 22 IS 5 BP 303 EP 317 PG 15 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA YH416 UT WOS:A1997YH41600003 PM 9401311 ER PT J AU Schechtman, KB Kutner, NG Wallace, RB Buchner, DM Ory, MG Miller, JP Province, MA Arfken, CL RossiterFornoff, JE Hornbrook, MC Stevens, VJ Wingfield, DJ Greenlick, MR Tinetti, ME Baker, DI Claus, EB Horwitz, RI AF Schechtman, KB Kutner, NG Wallace, RB Buchner, DM Ory, MG Miller, JP Province, MA Arfken, CL RossiterFornoff, JE Hornbrook, MC Stevens, VJ Wingfield, DJ Greenlick, MR Tinetti, ME Baker, DI Claus, EB Horwitz, RI TI Gender, self-reported depressive symptoms, and sleep disturbance among older community-dwelling persons SO JOURNAL OF PSYCHOSOMATIC RESEARCH LA English DT Article DE FICSIT trials; gender differences; depression; sleep problems; elderly adults ID DISORDERS; PATTERNS; ADULTS; HEALTH; LIFE; COMPLAINTS; INSOMNIA; EXERCISE; SUPPORT; ILLNESS AB The purposes of this report are: (1) to investigate the association between sleep disturbances. and depressive symptomatology in older adults; (2) to evaluate the degree to which gender serves to mediate this relationship; and (3) to determine whether several predefined covariates help to explain the association between sleep disturbance and depressive symptoms. This is a retrospective and cross-sectional analysis of baseline data from 485 elderly adults enrolled in three of the eight clinical sites participating in the Frailty and Injuries: Cooperative Studies of Intervention Techniques (FICSIT) trials, FICSIT was a linked series of randomized clinical trials which evaluated the impact of various exercise interventions on several measures of frailty in older adults. Women reported more depressive symptoms and more sleep disturbances than men. Sleep disturbances were independently associated with depressive symptoms, bodily pain, a history of falling, limited education, being married, and being female. Gender interactions suggest that, although women reported more depressive symptoms and more chronic health conditions than men, both may be more important predictors of sleep disturbance in men. By contrast, being married may be more predictive in women. Finally, the data suggest a stronger relationship between sleep disturbance and depressive symptoms in men than in women. (C) 1997 Elsevier Science Inc. C1 EMORY UNIV,SCH MED,ATLANTA,GA 30322. UNIV IOWA,COLL MED,IOWA CITY,IA 52242. UNIV WASHINGTON,SEATTLE,WA 98195. NIA,BETHESDA,MD 20892. KAISER PERMANENTE,CTR HLTH RES,LOS ANGELES,CA. YALE UNIV,SCH MED,PROGRAM AGING,NEW HAVEN,CT 06520. UNIV WASHINGTON,DEPT HLTH SCI,SEATTLE,WA 98195. RP Schechtman, KB (reprint author), WASHINGTON UNIV,SCH MED,DIV BIOSTAT,BOX 8067,660 S EUCLID AVE,ST LOUIS,MO 63110, USA. NR 41 TC 21 Z9 21 U1 2 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0022-3999 J9 J PSYCHOSOM RES JI J. Psychosomat. Res. PD NOV PY 1997 VL 43 IS 5 BP 513 EP 527 DI 10.1016/S0022-3999(97)00117-7 PG 15 WC Psychiatry SC Psychiatry GA YC753 UT WOS:A1997YC75300009 PM 9394268 ER PT J AU Hirsch, R Fernandes, RJ Pillemer, SR Hochberg, MC Lane, NE Altman, RD Knowler, WC Bennett, PH AF Hirsch, R Fernandes, RJ Pillemer, SR Hochberg, MC Lane, NE Altman, RD Knowler, WC Bennett, PH TI Enlarged acetabular labra in the Pima Indians SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE acetabulum; radiographic; epidemiology ID OSTEOARTHRITIS; INSULIN AB Objective, To report the descriptive epidemiology of acetabular labral enlargement and analyze associations of other variables with this variant. Methods, Pelvis radiographs from 761 Pima Indians aged greater than or equal to 45 years enrolled in a population based study were read by Kellgren-Lawrence global and individual radiographic features grading scales for osteoarthritis (OA) at separate sittings. In total, 722 radiographs remained eligible for this study after excluding 12 unreadable radiographs and 27 cases of radiographic hip OA (Kellgren-Lawrence grade greater than or equal to 2). Enlarged acetabular labra were recorded during readings of individual radiographic features. Results. Enlarged acetabular labra were present in 16% of study participants without OA and were significantly associated with female sex, but not with the variables age, body mass index, clinical hip joint involvement, diabetes, or serum insulin concentrations. Conclusion. Acetabular labral enlargement is common in the Pima Indians, and although not in excess of other reported acetabular margin anomalies, it differs in appearance and is not associated with age. Recognition of this structural variant is important because it can mimic fractures or osteophytes. C1 NIDDK, PHOENIX EPIDEMIOL & CLIN RES BRANCH, BETHESDA, MD 20892 USA. UNIV MARYLAND, SCH MED, BALTIMORE, MD 21201 USA. BALTIMORE VET MED AFFAIRS MED CTR, BALTIMORE, MD USA. UNIV CALIF SAN FRANCISCO, SAN FRANCISCO, CA 94143 USA. UNIV MIAMI, SCH MED, CORAL GABLES, FL 33124 USA. NR 14 TC 1 Z9 1 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 365 BLOOR ST E, STE 901, TORONTO, ONTARIO M4W 3L4, CANADA SN 0315-162X EI 1499-2752 J9 J RHEUMATOL JI J. Rheumatol. PD NOV PY 1997 VL 24 IS 11 BP 2210 EP 2212 PG 3 WC Rheumatology SC Rheumatology GA YD326 UT WOS:A1997YD32600027 PM 9375885 ER PT J AU Leapman, RD Jarnik, M Steven, AC AF Leapman, RD Jarnik, M Steven, AC TI Spatial distributions of sulfur-rich proteins in cornifying epithelia SO JOURNAL OF STRUCTURAL BIOLOGY LA English DT Article DE loricrin; cornified cell envelope; keratinocyte; energy-filtered electron microscopy; electron energy-loss spectroscopy ID ELECTRON-ENERGY-LOSS; X-RAY-MICROANALYSIS; POSTCOLUMN IMAGING FILTER; CELL-ENVELOPE; KERATOHYALIN GRANULES; EPIDERMAL-KERATINOCYTES; QUANTITATIVE ASSAY; LOSS SPECTROSCOPY; EXPRESSION; LORICRIN AB We have used energy-filtered electron microscopy and electron energy loss spectroscopy (EELS) to characterize the distributions of sulfur-rich proteins in granular layer cells of squamous stratifying epithelia and their redistribution in the cornified layer, with particular attention to assembly of the cornified cell envelope (CE). Our measurements provide quantitative information that complements highly specific but qualitative data from immunocytochemistry. Spatial distributions of sulfur, phosphorus, and nitrogen were mapped in unstained thin sections of mouse epidermis and forestomach, using a postcolumn energy filter. Nitrogen images were indicative of total protein while phosphorus images provided a control to validate the algorithms used to calculate the elemental maps. Sulfur was found at high levels in round L-granules in the granulocyte cytoplasm and in the cornified CE, correlating with the presence of the protein, loricrin (similar to 7% Cys/Met residues). EELS confirmed these observations quantitatively: either L-granules consist exclusively of loricrin or any additional components must have an equally high net sulfur content. These data also confirm the large fraction (similar to 75%) of loricrin in the CE, as inferred from modeling of its amino acid composition. We also observed extracellular deposits between cornified squames in fetal mouse epidermis that we call peripheral granules. Their sulfur content is at least as high as that of L-granules but they do not label with anti-loricrin antibodies, suggesting the presence of another sulfur-rich protein. C1 NIH, Natl Ctr Res Resources, Biomed Engn & Instrumentat Program, Bethesda, MD 20892 USA. NIAMSD, Struct Biol Lab, NIH, Bethesda, MD 20892 USA. RP Leapman, RD (reprint author), NIH, Natl Ctr Res Resources, Biomed Engn & Instrumentat Program, Bldg 13,Rm 3N17, Bethesda, MD 20892 USA. NR 49 TC 24 Z9 24 U1 0 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1047-8477 J9 J STRUCT BIOL JI J. Struct. Biol. PD NOV PY 1997 VL 120 IS 2 BP 168 EP 179 DI 10.1006/jsbi.1997.3937 PG 12 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA YP849 UT WOS:000071322000005 PM 9417981 ER PT J AU Chadwick, RS AF Chadwick, RS TI What should be the goals of cochlear modeling? SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Letter AB The recent thought-provoking paper by de Beer, ''Classical and nonclassical models of the cochlea,'' not only deserves comment on its own right, but more generally it should cause cochlea modelers to reflect on their ultimate goals. While his claim that a ''classical'' model can be found that has the same response as a ''nonclassical'' model is mathematically correct for linear, single degree-of-freedom models, this paper argues that his algorithm produces a ''nonrealizable'' and hence less useful model. Also, his assertion of uniqueness needs to be qualified. RP Chadwick, RS (reprint author), NIDCD,LCB,NIH,9 CTR DR,MSC 0922,BETHESDA,MD 20892, USA. NR 1 TC 1 Z9 1 U1 0 U2 1 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD NOV PY 1997 VL 102 IS 5 BP 3054 EP 3054 DI 10.1121/1.420363 PN 1 PG 1 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA YG922 UT WOS:A1997YG92200062 ER PT J AU Iwasa, KH Chadwick, RS AF Iwasa, KH Chadwick, RS TI Does nonlinear capacitance of the outer hair cell really improve its high-frequency response? SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Letter ID MOTILITY AB There is a conceptual error in the paper, ''A theoretical basis for the high-frequency performance of the outer hair cell's receptor potential'' by El S. Hassan [J. Acoust. Soc. Am. 101, 2129-2134 (1997)]. Correcting the error reverses the conclusion, and reveals that the nonlinear capacitance in the outer hair cell is a factor that degrades, rather than improves, the high-frequency response of the receptor potential of the outer hair cell. (C) 1997 Acoustical Society of America. RP Iwasa, KH (reprint author), NIDCD,BIOPHYS SECT,LCB,NIH,9 CTR DR,MSC 0922,BETHESDA,MD 20892, USA. OI Iwasa, Kuni/0000-0002-9397-7704 NR 8 TC 1 Z9 1 U1 0 U2 0 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD NOV PY 1997 VL 102 IS 5 BP 3055 EP 3056 DI 10.1121/1.420364 PN 1 PG 2 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA YG922 UT WOS:A1997YG92200063 ER PT J AU Darling, TN AF Darling, TN TI Mutational analysis of the bullous pemphigoid antigen 2 type XVII collagen gene in patients with generalized atrophic benign epidermolysis bullosa SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article RP Darling, TN (reprint author), NCI,DERMATOL BRANCH,DIV CLIN SCI,NIH,BLDG 10,ROOM 12N238,10 CTR DR MSC-1908,BETHESDA,MD 20892, USA. OI Darling, Thomas/0000-0002-5161-1974 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 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD NOV PY 1997 VL 37 IS 5 BP 773 EP 774 PN 1 PG 2 WC Dermatology SC Dermatology GA YF084 UT WOS:A1997YF08400013 PM 9366826 ER PT J AU Walker, PS AF Walker, PS TI Direct targeting of skin with DNA vaccines for genetic immunization against Leishmania in a murine model SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article RP Walker, PS (reprint author), NCI,DERMATOL BRANCH,NIH,BLDG 10,ROOM 12N238,10 CTR DR MSC-1908,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD NOV PY 1997 VL 37 IS 5 BP 776 EP 777 PN 1 PG 2 WC Dermatology SC Dermatology GA YF084 UT WOS:A1997YF08400016 PM 9366829 ER PT J AU Quyyumi, AA Dakak, N Diodati, JG Gilligan, DM Panza, JA Cannon, RO AF Quyyumi, AA Dakak, N Diodati, JG Gilligan, DM Panza, JA Cannon, RO TI Effect of L-arginine on human coronary endothelium-dependent and physiologic vasodilation SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID ORAL L-ARGININE; NITRIC-OXIDE PRECURSOR; RELAXING FACTOR; HYPERCHOLESTEROLEMIC PATIENTS; HEART-FAILURE; RABBIT AORTA; RISK-FACTORS; ACETYLCHOLINE; CELLS; RELEASE AB Objectives. We hypothesized that L-arginine would improve abnormal coronary vasodilation in response to physiologic stress in patients with atherosclerosis and its risk factors by reversing coronary endothelial dysfunction. Background. Studies have demonstrated that physiologic coronary vasodilation correlates with endothelial function and that L-arginine, the substrate for nitric oxide synthesis, improves the response to acetylcholine (Ach). Methods. Changes in coronary blood flow and epicardial diameter response to Ach, adenosine and cardiac pacing were measured in 32 patients with coronary atherosclerosis or its risk factors and in 7 patients without risk factors and normal coronary angiograms. Results. Intracoronary L-arginine did not alter baseline coronary vascular tone, but the epicardial and microvascular responses to Ach were enhanced (both p < 0.001). The improvement after L-arginine was greater in epicardial segments that initially constricted with Ach; similarly L-arginine abolished microvascular constriction produced by higher doses of Ach. Thus, there mas a negative correlation between the initial epicardial and vascular resistance responses to Ach and the magnitude of improvement with L-arginine (r = -0.55 and r = -0.50, respectively, p < 0.001). D-Arginine did not affect the responses to Ach, and adenosine responses were unchanged with L-arginine. Cardiac pacing-induced epicardial constriction was abolished ba L-arginine, hut microvascular dilation remained unaffected. Conclusions. Thus, L-arginine improved endothelium dependent coronary epicardial and microvascular function in patients with endothelial dysfunction. Prevention of epicardial constriction during physiologic stress by L-arginine in patients with endothelial dysfunction may be of therapeutic value in the treatment of myocardial ischemia. (C) 1997 by the American College of Cardiology. RP Quyyumi, AA (reprint author), NHLBI,NIH,CARDIOL BRANCH,BLDG 10,ROOM 7B15,10 CTR DR,MSC 1650,BETHESDA,MD 20892, USA. NR 43 TC 71 Z9 72 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD NOV 1 PY 1997 VL 30 IS 5 BP 1220 EP 1227 DI 10.1016/S0735-1097(97)00279-9 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YD802 UT WOS:A1997YD80200012 PM 9350919 ER PT J AU Rehman, A Zalos, G Andrews, NP Mulcahy, D Quyyumi, AA AF Rehman, A Zalos, G Andrews, NP Mulcahy, D Quyyumi, AA TI Blood pressure changes during transient myocardial ischemia: Insights into mechanisms SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; DAILY LIFE; HEART-RATE; MENTAL STRESS; CIRCADIAN VARIATION; NOCTURNAL ANGINA; STABLE ANGINA; THRESHOLD; FREQUENCY AB Objectives. We investigated the contribution of changes in systemic blood pressure to the genesis of spontaneous myocardial ischemia. Background. Although increases in heart rate often precede the development of spontaneous myocardial ischemia, it remains a subject of controversy whether these are accompanied by simultaneous changes in blood pressure. Methods. Using an ambulatory monitoring device that triggered blood pressure recordings from the level of the ST segment, we documented systolic and diastolic blood pressure and heart rate changes related to episodes of ST segment depression in 17 patients with stable coronary artery disease. Results. Systolic blood pressure and heart rate, but not diastolic pressure, increased significantly before the onset of ST segment depression and persisted throughout the ischemic episode. There was a significant correlation between the changes in heart rate and systolic blood pressure during episodes of myocardial ischemia (r = 0.5, p = 0.0005) and between heart rate and systolic blood pressure changes at 1-mm ST segment depression during treadmill exercise testing and ambulatory monitoring (r = 0.73, p = 0.0005 for heart rate; r = 0.77, p = 0.0008 for systolic blood pressure), indicating that patients with a low heart rate threshold during ischemic episodes also had a lower systolic blood pressure threshold before ischemia during both tests. Circadian changes in systolic blood pressure paralleled the variations in heart rate and ischemic episodes, with the lowest values at night. Conclusions. Significant increases in myocardial oxygen demand, including systolic blood pressure, occur during episodes of spontaneous myocardial ischemia, Patients with a lower heart rate threshold during ischemic episodes had a lower systolic blood pressure threshold during both ambulatory monitoring and treadmill exercise, The effects of antianginal therapy on blood pressure changes during ischemia need to be explored further. (C) 1997 by the American College of Cardiology. C1 NHLBI,CARDIOL BRANCH,NIH,BETHESDA,MD 20892. NR 22 TC 16 Z9 17 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD NOV 1 PY 1997 VL 30 IS 5 BP 1249 EP 1255 DI 10.1016/S0735-1097(97)00289-1 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YD802 UT WOS:A1997YD80200016 PM 9350923 ER PT J AU Zhou, XD Jones, M Shiota, T Yamada, I Teien, D Sahn, DJ AF Zhou, XD Jones, M Shiota, T Yamada, I Teien, D Sahn, DJ TI Vena contracts imaged by Doppler color flow mapping predicts the severity of eccentric mitral regurgitation better than color jet area: A chronic animal study SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID AORTIC REGURGITATION; VALVULAR REGURGITATION; VALVE REPAIR; IN-VITRO; INVITRO; ECHOCARDIOGRAPHY; QUANTIFICATION; VARIABILITY; SIZE; INSUFFICIENCY AB Objectives. This study sought to evaluate the relation between the color Doppler-imaged vena contracta and the severity of mitral regurgitation (MR) in a chronic animal model of MR. Background. The vena contracta, which is defined as the smallest connection between the laminar flow acceleration zone and the turbulent regurgitant jet, has been reported to be a clinically useful marker for evaluating the severity of valvular regurgitation, Methods. Six sheep with chronic MR produced by previous operation severing the chordae tendineae were examined. MR jet hows and vena contracta widths were imaged using a Vingmed 775 scanner with a 5-MHz transducer. Image data were directly transferred in digital format to a microcomputer for off-line measurement. MR was quantified as peak and mean regurgitant how rates, regurgitant stroke volumes and regurgitant fractions determined using mitral and aortic electromagnetic how probes and flowmeters balanced against each other. Results. Vena contracta width correlated well,vith regurgitant severity determined by electromagnetic flowmeters (r = 0.95, SEE = 0.05 cm, p < 0.0001 for peak regurgitant flow rate; r = 0.85, SEE = 0.08 cm, p < 0.0001 for regurgitant stroke volume; r = 0.90, SEE = 0.07 cm, p < 0.0001 for regurgitant fraction). Conclusions. This study shows that the vena contracta width method is useful for predicting the severity of MR. It is simple and conveniently available with high resolution equipment. The quantitative comparisons in the present study lay the foundation for future clinical and research studies using this vena contracta technique. (C) 1997 by the American College of Cardiology. C1 NHLBI,LAB ANIM MED & SURG,NIH,BETHESDA,MD 20892. OREGON HLTH SCI UNIV,CLIN CARE CTR CONGENITAL HEART DIS,PORTLAND,OR 97201. NR 39 TC 24 Z9 29 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD NOV 1 PY 1997 VL 30 IS 5 BP 1393 EP 1398 DI 10.1016/S0735-1097(97)00304-5 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YD802 UT WOS:A1997YD80200038 PM 9350945 ER PT J AU Slavkin, HC AF Slavkin, HC TI Chronic disabling diseases and disorders: The challenges of fibromyalgia SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article RP Slavkin, HC (reprint author), NIDR,31 CTR DR,MSC 2290,BLDG 31,ROOM 2C39,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD NOV PY 1997 VL 128 IS 11 BP 1583 EP 1589 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YE453 UT WOS:A1997YE45300024 PM 9368446 ER PT J AU Pennington, JAT Wilkening, VL AF Pennington, JAT Wilkening, VL TI Final regulations for the nutrition labeling of raw fruits, vegetables, and fish SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Review AB In August 1996, the US Food and Drug Administration published regulations that revised the guidelines for voluntary nutrition labeling of raw fruits, vegetables, and fish; revised the criteria for retailers' compliance with the guidelines; and updated the nutrition labeling values for the 20 most frequently consumed raw fruits, vegetables, and fish. These actions were in response to the requirements of the Nutrition Labeling and Education Act of 1990 and make the voluntary nutrition labeling program more consistent with mandatory nutrition labeling of other foods. The provisions of the final rule are important for dietitians who develop nutrition education materials for retail stores and for dietitians who instruct patients and clients in selecting foods according to nutrition labeling information. C1 US FDA,CTR FOOD SAFETY & APPL NUTR,OFF FOOD LABELING,DIV TECH EVALUAT,WASHINGTON,DC 20204. NIDDKD,DIV NUTR RES COORDINAT,NIH,BETHESDA,MD 20892. RP Pennington, JAT (reprint author), NIDDKD,DIV NUTR RES COORDINAT,NIH,NATCHER BLDG,45 CTR DR,MSC 6600,BETHESDA,MD 20892, USA. NR 18 TC 6 Z9 7 U1 0 U2 1 PU AMER DIETETIC ASSOC PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD NOV PY 1997 VL 97 IS 11 BP 1299 EP 1305 DI 10.1016/S0002-8223(97)00310-6 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA YE622 UT WOS:A1997YE62200018 PM 9366869 ER PT J AU Humphreys, BL McCray, AT Cheh, ML AF Humphreys, BL McCray, AT Cheh, ML TI Evaluating the coverage of controlled health data terminologies: Report on the results of the NLM/AHCPR large scale vocabulary test SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article ID AGREEMENT AB Objective: To determine the extent to which a combination of existing machine-readable health terminologies cover the concepts and terms needed for a comprehensive controlled vocabulary for health information systems by carrying out a distributed national experiment using the Internet and the UMLS Knowledge Sources,lexical programs, and server. Methods: Using a specially designed Web-based interface to the UMLS Knowledge Source Server, participants searched the more than 30 vocabularies in the 1996 UMLS Metathesaurus and three planned additions to determine if concepts for which they desired controlled terminology were present or absent. For each term submitted, the interface presented a candidate exact match or a set of potential approximate matches from which the participant selected the most closely related concept. The interface captured a profile of the terms submitted by the participant and for each term searched, information about the concept (if any) selected by the participant. The term information was loaded into a database at NLM for review and analysis and was also available to be downloaded by the participant. A team of subject experts reviewed records to identify matches missed by participants and to correct any obvious errors in relationships. The editors of SNOMED International and the Read Codes were given a random sample of reviewed terms for which exact meaning matches were not found to identify exact matches that were missed or any valid combinations of concepts that were synonymous to input terms. The 1997 UMLS Metathesaurus was used in the semantic type and vocabulary source analysis because it included most of the three planned additions. Results: Sixty-three participants submitted a total of 41,127 terms, which represented 32,679 normalized strings. Mure than 80% of the terms submitted were wanted for parts of the patient record related to the patient's condition. Following review, 58% of all submitted terms had exact meaning matches in the controlled vocabularies in the test, 41% had related concepts, and 1% were not found. Of the 28% of the terms which were narrower in meaning than a concept in the controlled vocabularies, 86% shared lexical items with the broader concept, but had additional modification; The percentage of exact meaning matches varied by specialty from 45% to 71%. Twenty-nine different vocabularies contained meanings for some of the 23,837 terms (a maximum of 12,707 discrete concepts) with exact meaning matches. Based on preliminary data and analysis, individual vocabularies contained <1% to 63% of the terms and <1% to 54% of the concepts. Only SNOMED International and the Read Codes had more than 60% of the terms and more than 50% of the concepts. Conclusions: The combination of existing controlled vocabularies included in the test represents the meanings of the majority of the terminology needed to record patient conditions, providing substantially more exact matches than any individual vocabulary in the set. From a technical and organizational perspective, the test was successful and should serve as a useful model, both for distributed input to the enhancement of controlled vocabularies and for other kinds of collaborative informatics research. RP Humphreys, BL (reprint author), NATL LIB MED, 8600 ROCKVILLE PIKE, BETHESDA, MD 20894 USA. NR 16 TC 69 Z9 69 U1 1 U2 5 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PD NOV-DEC PY 1997 VL 4 IS 6 BP 484 EP 500 PG 17 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA YG267 UT WOS:A1997YG26700009 PM 9391936 ER PT J AU Nguyen, VQ Chen, XG Yergey, AL AF Nguyen, VQ Chen, XG Yergey, AL TI Observations of magic numbers in gas phase hydrates of alkylammonium ions SO JOURNAL OF THE AMERICAN SOCIETY FOR MASS SPECTROMETRY LA English DT Article ID COLLISION-INDUCED DISSOCIATION; PROTONATED WATER CLUSTERS; ELECTROSPRAY-IONIZATION; CLATHRATE STRUCTURES; ENHANCED STABILITY; MASS-SPECTROMETRY; METAL-IONS; ENERGIES; QUADRUPOLE; COMPLEXES AB Hydration of alkylammonium ions under nonanalytical electrospray ionization conditions has been found to yield cluster ions with more than 20 water molecules associated with the central ion. These cluster ion species are taken to be an approximation of the conditions in liquid water. Many of the alkylammonium cation mass spectra exhibit water cluster numbers that appear to be particularly favorable, i.e., ''magic number clusters'' (MNC). We have found MNC in hydrates of mono-and tetra-alkyl ammonium ions, NH3(CmH2m+1)(+)(H2O)(n), m = 1-8 and N(CmH2m+1)(4)(+) (H2O)(n), m = 2-8. In contrast, NH2(CH3)(2)(+)(H2O)(n), NH(CH3)(3)(+)(H2O)(n), and N(CH3)(4)(+)(H2O)(n) do not exhibit any MNC. We conjecture that the structures of these magic number clusters correspond to exohedral structures in which the ion is situated on the surface of the water cage in contrast to the widely accepted caged ion structures of H3O+(H2O)(n) and NH4+(H2O)(n). C1 NICHHD,SECT METAB ANAL & MASS SPECTROMETRY,BETHESDA,MD 20892. NR 35 TC 26 Z9 26 U1 1 U2 7 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1044-0305 J9 J AM SOC MASS SPECTR JI J. Am. Soc. Mass Spectrom. PD NOV PY 1997 VL 8 IS 11 BP 1175 EP 1179 DI 10.1016/S1044-0305(97)00188-8 PG 5 WC Chemistry, Analytical; Chemistry, Physical; Spectroscopy SC Chemistry; Spectroscopy GA YB445 UT WOS:A1997YB44500008 ER PT J AU Walther, MM Yang, JC Pass, HI Linehan, WM Rosenberg, SA AF Walther, MM Yang, JC Pass, HI Linehan, WM Rosenberg, SA TI Cytoreductive surgery before high dose interleukin-2 based therapy in patients with metastatic renal cell carcinoma SO JOURNAL OF UROLOGY LA English DT Article DE carcinoma, renal cell; interleukin-2; metastasis; nephrectomy ID SUBCUTANEOUS RECOMBINANT INTERLEUKIN-2; ACTIVATED KILLER-CELLS; ADOPTIVE IMMUNOTHERAPY; PROGNOSTIC FACTORS; ALPHA-INTERFERON; CANCER; NEPHRECTOMY; TRIAL; TUMOR AB Purpose: We defined the outcome of a strategy using cytoreductive surgery before high dose interleukin-2 (IL-2) therapy in patients with metastatic renal cell carcinoma. Materials and Methods: During an Ii-year period, 195 patients underwent cytoreductive surgery as preparation for high dose IL-2 based therapy. The renal primary and locoregional metastatic disease that could be safely resected was removed. Results: Because of the large size 176 of 195 renal tumors (90%) were resected through transabdominal incision and in 45 patients (23%) a second additional significant procedure was performed. Five cases (2.6%) were unresectable and 2 (1%) perioperative deaths occurred. After surgery 121 of 195 patients (62%) were eligible for treatment with high dose IL-2 based protocols. Overall response rate to IL-2 based protocols was 18%. Conclusions: Cytoreductive surgery can be performed safely in patients with metastatic renal cell carcinoma. Although the impact of cytoreductive surgery on response to immunotherapy remains undefined, this combination of primary debulking and systemic IL-2 can result in durable complete tumor regression in some patients with metastatic renal cell carcinoma. C1 NCI,SURG BRANCH,BETHESDA,MD 20892. RP Walther, MM (reprint author), NCI,UROL ONCOL BRANCH,BETHESDA,MD 20892, USA. NR 26 TC 74 Z9 76 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD NOV PY 1997 VL 158 IS 5 BP 1675 EP 1678 DI 10.1016/S0022-5347(01)64091-6 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA XZ996 UT WOS:A1997XZ99600004 PM 9334576 ER PT J AU Wagner, JR Merino, MJ Pass, HI Linehan, WM Walther, MM AF Wagner, JR Merino, MJ Pass, HI Linehan, WM Walther, MM TI Pulmonary infarcts mimic pulmonary metastases from renal cancer SO JOURNAL OF UROLOGY LA English DT Article DE carcinoma, renal cell; neoplasm metastasis; pulmonary disease ID CELL-CARCINOMA; SPONTANEOUS REGRESSION AB Purpose: Spontaneous regression of pulmonary metastases from renal cell carcinoma is a rare but well documented event. We present 2 recent cases that were radiographically consistent with pulmonary metastases from renal cell carcinoma but were pathologically shown to be pulmonary infarcts with no evidence of metastatic cells. Stable pulmonary infarcts can be misconstrued as metastatic disease in patients with renal cell carcinoma while resolving pulmonary infarcts may represent a subpopulation of patients with apparent spontaneous regression. Clinical implications of these findings are discussed, Materials and Methods: Clinical and pathological data from 2 patients with large primary renal tumors, venous thrombi and lung masses were reviewed. Data from these cases, as well as pertinent urological and pathological literature, are presented, Results: Although preoperative assessment was consistent with stage TV renal cell carcinoma, pathological examination of the lung masses in these patients showed no evidence of tumor cells. Conclusions: Pulmonary infarcts may mimic resolving or stable pulmonary metastasis in patients with renal cell carcinoma, Accurate clinical staging is crucial for the prognosis and treatment of renal cell carcinoma. Mistaking pulmonary infarcts for metastatic lesions can lead to inaccurate prognoses and inappropriate treatment. C1 NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. RP Wagner, JR (reprint author), NCI,UROL ONCOL BRANCH,THORAC SURG SECT,SURG BRANCH,NIH,BETHESDA,MD 20892, USA. NR 14 TC 6 Z9 7 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD NOV PY 1997 VL 158 IS 5 BP 1688 EP 1690 DI 10.1016/S0022-5347(01)64096-5 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA XZ996 UT WOS:A1997XZ99600009 PM 9334579 ER PT J AU Han, JY Cannon, PM Lai, KM Zhao, Y Eiden, MV Anderson, WF AF Han, JY Cannon, PM Lai, KM Zhao, Y Eiden, MV Anderson, WF TI Identification of envelope protein residues required for the expanded host range of 10A1 murine leukemia virus SO JOURNAL OF VIROLOGY LA English DT Article ID CELL-SURFACE RECEPTORS; PHOSPHATE TRANSPORTER; RETROVIRUS INFECTION; BINDING; GLYCOPROTEINS; VECTORS; FAMILY; EXPRESSION; ENTRY AB The 10A1 murine leukemia virus (MuLV) is a recombinant type C retrovirus isolated from a mouse infected with amphotropic MuLV (A-MuLV). 10A1 and A-MuLV have 91% amino acid identity in their envelope proteins yet display different host ranges. For example, CHO-K1 cells are resistant to A-MuLV but susceptible to infection by 10A1. We have now determined that retroviral vectors bearing altered A-MuLV envelope proteins containing 10A1-derived residues at positions 71 (A71G), 74 (Q74K), and 139 (V139M) transduce CHO-K1 cells at efficiencies similar to those achieved with 10A1 enveloped vectors. A-MuLV enveloped retroviral vectors with these three 10A1 residues were also able to transduce A-MuLV-infected NIH 3T3 cells. This observation is consistent with the ability of vectors bearing this altered A-MuLV envelope protein to recognize the 10A1-specific receptor present on NIH 3T3 cells and supports the possibility that residues at positions 71, 74, and 139 of the 10A1 envelope SU protein account for the expanded host range of 10A1. C1 UNIV SO CALIF, SCH MED, NORRIS CANC CTR, GENE THERAPY LABS, LOS ANGELES, CA 90033 USA. UNIV SO CALIF, SCH MED, DEPT BIOCHEM & MOL BIOL, LOS ANGELES, CA 90033 USA. NIMH, LAB CELLULAR & MOL REGULAT, BETHESDA, MD 20892 USA. FU NCI NIH HHS [CA59318-04] NR 36 TC 40 Z9 45 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X EI 1098-5514 J9 J VIROL JI J. Virol. PD NOV PY 1997 VL 71 IS 11 BP 8103 EP 8108 PG 6 WC Virology SC Virology GA YB143 UT WOS:A1997YB14300003 PM 9343159 ER PT J AU Boomer, S Eiden, M Burns, CC Overbaugh, J AF Boomer, S Eiden, M Burns, CC Overbaugh, J TI Three distinct envelope domains, variably present in subgroup B feline leukemia virus recombinants, mediate Pit1 and Pit2 receptor recognition SO JOURNAL OF VIROLOGY LA English DT Article ID HOST RANGE; NUCLEOTIDE-SEQUENCES; CELLULAR RECEPTOR; HUMAN-CELLS; MURINE; GENE; RETROVIRUS; GLYCOPROTEIN; DETERMINANTS; INTERFERENCE AB Subgroup B feline leukemia viruses (FeLV-Bs) evolve from subgroup A FeLV (FeLV-A) by recombining with portions of endogenous FeLV envelope sequences in the cat genome, The replication properties of FeLV-B are distinct from those of FeLV-A; FeLV-B infects many nonfeline cell lines and recognizes the human Pit1 (HuPit1) receptor, whereas FeLV-A infects primarily feline cells, using a distinct but as yet undefined receptor. Here, we demonstrate that some FeLV-Bs can also use human Pit2 (HuPit2) and hamster Pit2 (HaPit2) for entry. By making viruses that contain chimeric surface (SU) envelope proteins from FeLV-A and FeLV-B, and testing their infectivity, we have defined genetic determinants that confer host range and specific receptor recognition, HuPit1 receptor recognition determinants localize to the N-terminal region of the FeLV-B SU, amino acids 83 to 116, encompassing the N-terminal portion of variable region A (VRA), While this 34-amino-acid domain of the FeLV-B VRA is sufficient for infection of some cells (feline, canine,and human), amino acids 146 to 249 of FeLV-B, which include variable region B (VRB), were required for efficient infection in other cell types (hamster, bovine, and rat), Chimeras encoding FeLV-B VRA and VRB also infected cells expressing HaPit2 and HuPit2 receptors more efficiently than chimeras encoding only the VRA of FeLV-B, suggesting that VRB provides a secondary determinant that is both cell and receptor specific, However, viruses containing additional FeLV-B sequences in the C terminus of SU could not recognize HuPit2, implying that there is a determinant beyond VRB that negatively affects HuPit2 interactions, Thus, Pit2 recognition may drive selection for the generation of specific FeLV-B recombinants, offering an explanation for the two major classes of FeLV-B that have been observed in vivo. Furthermore, the finding that some FeLV-Bs can use both Pit1 and Pit2 may explain previous observations that FeLV-B and GALV, which primarily uses Pit1, display nonreciprocal interference on many cell types. C1 UNIV WASHINGTON,DEPT MICROBIOL,SEATTLE,WA 98195. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA51080, F32 CA62771-01]; NIGMS NIH HHS [T32 GM07270] NR 57 TC 55 Z9 55 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1997 VL 71 IS 11 BP 8116 EP 8123 PG 8 WC Virology SC Virology GA YB143 UT WOS:A1997YB14300005 PM 9343161 ER PT J AU Shibata, R Siemon, C Czajak, SC Desrosiers, RC Martin, MA AF Shibata, R Siemon, C Czajak, SC Desrosiers, RC Martin, MA TI Live, attenuated simian immunodeficiency virus vaccines elicit potent resistance against a challenge with a human immunodeficiency virus type 1 chimeric virus SO JOURNAL OF VIROLOGY LA English DT Article ID BLOOD MONONUCLEAR-CELLS; RHESUS MACAQUES; SIV INFECTION; PROTECTION; IMMUNIZATION; CHIMPANZEES; ENVELOPE; RECOMBINANT; HIV-1; GP160 AB Three rhesus macaques, previously immunized with SIV Delta 3 or SIV Delta 2, each an attenuated derivative of SIVmac239, and two naive monkeys were challenged with 30,000 50% tissue culture infective doses of SHIV, an SIV/human immunodeficiency virus type 1 (HIV-1) chimeric virus bearing the dual-tropic envelope of HIV-1(DH12). By several criteria, including virus isolation, serological assays, and PCR (both DNA and reverse transcriptase), SHIV levels were reduced to barely detectable levels in the circulating blood of vaccinated animals. The resistant SIV-vaccinated macaques had no preexisting neutralizing antibodies directed against SHIV, nor did they produce neutralizing antibodies at any time over a 14-month observation period following SHIV challenge. Interestingly, SIV sequences, derived from the vaccine, could be amplified from numerous tissue samples collected at the conclusion of the experiment, 60 weeks postchallenge, but SHIV-specific sequences (viz., HIV-1 env) could not. These results demonstrate that live attenuated SIV vaccines provide strong long-term protection even against challenge strains with highly divergent envelope sequences. C1 HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. RP Shibata, R (reprint author), NIAID,MOL MICROBIOL LAB,NIH,4 CTR DR,BLDG 4,ROOM 305,BETHESDA,MD 20892, USA. FU NCRR NIH HHS [RR00168]; NIAID NIH HHS [AI35365] NR 61 TC 103 Z9 104 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1997 VL 71 IS 11 BP 8141 EP 8148 PG 8 WC Virology SC Virology GA YB143 UT WOS:A1997YB14300008 PM 9343164 ER PT J AU Ciarlet, M Hoshino, Y Liprandi, F AF Ciarlet, M Hoshino, Y Liprandi, F TI Single point mutations may affect the serotype reactivity of serotype G11 porcine rotavirus strains: a widening spectrum? SO JOURNAL OF VIROLOGY LA English DT Article ID AMINO-ACID-SEQUENCE; NEUTRALIZATION EPITOPES; GENOMIC CHARACTERIZATION; MONOCLONAL-ANTIBODIES; RHESUS ROTAVIRUS; EQUINE ROTAVIRUSES; SURFACE-PROTEINS; VP7; SITES; SPECIFICITY AB A panel of single and double neutralization-resistant escape mutants of serotype G11 porcine rotavirus strains A253 and YM, selected with G11 monotype-and serotype-specific neutralizing monoclonal antibodies (MAbs) to VP7, was tested in neutralization assays with hyperimmune sera raised against rotavirus strains of different serotypes, Escape mutants with an amino acid substitution in antigenic region A (amino acids [aa] 87 to 101) resulting in a residue identical or chemically similar to those present at the same positions in serotype G3 strains, at positions 87 for strain A253 and 96 for strain YM, were significantly more sensitive than the parental strains to neutralization with sera against some serotype G3 strains, Also, one YM antigenic variant (YM-5E6.1) acquired reactivity by enzyme-linked immunosorbent assay with MAbs 159, 57/8, and YO-1E2, which react with G3 strains, but not with the serotype G11 parental strain YM, Cross-adsorption studies suggested that the observed cross-neutralization by the G3-specific sera was due to the sera containing antibodies reactive with the parental strain plus antibodies reactive,vith the epitope(s) on the antigenic variant that mimick the serotype G3 specific one(s), Moreover, antibodies reactive with antigenic region F (aa 235 to 242) of VP7 might also be involved since cross-reactivity to serotype G3 was decreased in double mutants carrying an additional mutation, which creates a potential glycosylation site at position 238. Thus, single point mutations can affect the serotype reactivity of G11 porcine rotavirus strains with both monoclonal and polyclonal antibodies and may explain the origin of rotavirus strains with dual serotype specificity based on sequence divergence of VP7. C1 NIAID,INFECT DIS LAB,BETHESDA,MD 20892. INST VENEZOLANO INVEST CIENT,CTR MICROBIOL & BIOL CELULAR,LAB BIOL VIRUS,CARACAS 1020A,VENEZUELA. NR 39 TC 48 Z9 49 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1997 VL 71 IS 11 BP 8213 EP 8220 PG 8 WC Virology SC Virology GA YB143 UT WOS:A1997YB14300016 PM 9343172 ER PT J AU Buge, SL Richardson, E Alipanah, S Markham, P Cheng, S Kalyan, N Miller, CJ Lubeck, M Udem, S Eldridge, J RobertGuroff, M AF Buge, SL Richardson, E Alipanah, S Markham, P Cheng, S Kalyan, N Miller, CJ Lubeck, M Udem, S Eldridge, J RobertGuroff, M TI An adenovirus simian immunodeficiency virus env vaccine elicits humoral, cellular, and mucosal immune responses in rhesus macaques and decreases viral burden following vaginal challenge SO JOURNAL OF VIROLOGY LA English DT Article ID RECOMBINANT HUMAN ADENOVIRUS; LYMPH-NODE IMMUNIZATION; CYTOTOXIC T-LYMPHOCYTES; IMMUNOGLOBULIN-A; HIV-INFECTION; SIV ENVELOPE; HTLV-III/LAV; P27 ANTIGEN; GLYCOPROTEIN; AIDS AB Six female rhesus macaques were immunized orally and intranasally at 0 weeks and intratracheally at 12 weeks with an adenovirus type 5 host range mutant (Ad5hr)-simian immunodeficiency virus SIVsm env recombinant and at 24 and 36 weeks with native SIV(mac251)gp120 in Syntex adjuvant. Four macaques received the Ad5hr vector and adjuvant alone; two additional controls were naive. In vivo replication of the Ad5hr wild-type and recombinant vectors occurred with detection of Ad5 DNA in stool samples and/or nasal secretions in all macaques and increases in Ad5 neutralizing antibody in 9 of 10 macaques following Ad administrations. SIV-specific neutralizing antibodies appeared after the second recombinant immunization and rose to titers > 10,000 following the second subunit boost. Immunoglobulin G (IgG) and IgA antibodies able to bind gp120 developed in nasal and rectal secretions, and SIV-specific IgGs were also observed in vaginal secretions and saliva. T-cell proliferative responses to SIV gp140 and T-helper epitopes were sporadically detected in all immunized macaques. Following vaginal challenge with SIVmac251, transient or persistent infection resulted in both immunized and control monkeys. The mean viral burden in persistently infected immunized macaques was significantly decreased in the primary infection period compared to that of control macaques. These results establish in vivo use of the Ad5hr vector, which overcomes the host range restriction of human Ads for rhesus macaques, thereby providing a new model for evaluation of Ad-based vaccines. In addition, they show that a vaccine regimen using the Ad5hr-SIV env recombinant and gp120 subunit induces strong humoral, cellular, and mucosal immunity in rhesus macaques. The reduced viral burden achieved solely with an env-based vaccine supports further development of Ad-based vaccines comprising additional viral components for immune therapy and AIDS vaccine development. C1 NCI,BASIC RES LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD 20895. WYETH AYERST RES,RADNOR,PA 19087. WYETH LEDERLE VACCINES & PEDIAT,PEARL RIVER,NY 10965. UNIV CALIF DAVIS,DAVIS,CA 95616. WYETH LEDERLE VACCINES & PEDIAT,MARIETTA,PA 17547. LEDERLE PRAXIS BIOL,W HENRIETTA,NY 14586. NR 60 TC 115 Z9 119 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1997 VL 71 IS 11 BP 8531 EP 8541 PG 11 WC Virology SC Virology GA YB143 UT WOS:A1997YB14300055 PM 9343211 ER PT J AU Lavignon, M Richardson, J Evans, LH AF Lavignon, M Richardson, J Evans, LH TI A small region of the ecotropic murine leukemia virus (MuLV) gag gene profoundly influences the types of polytropic MuLVs generated in mice SO JOURNAL OF VIROLOGY LA English DT Article ID FOCUS-FORMING VIRUSES; NUCLEOCAPSID PROTEIN; ZINC-FINGER; ENV GENE; MONOCLONAL-ANTIBODIES; INFECTED MICE; MCF VIRUSES; VIRAL-RNA; FRIEND; DNA AB The vast majority of recombinant polytropic murine leukemia viruses (MuLVs) generated in mice after infection by ecotropic MuLVs can be classified into two major antigenic groups based on their reactivities to two monoclonal antibodies (MAbs) termed Hy 7 and 516. These groups very likely correspond to viruses formed by recombination of the ecotropic MuLV with two distinct sets of polytropic env genes present in the genomes of inbred mouse strains. We have found that nearly all polytropic MuLVs identified in mice infected with a substrain of Friend MuLV (F-MuLV(57)) are reactive with Hy 7, whereas mice infected with Moloney MuLV (Mo-MuLV) generate major populations of both Hy 7- and 516-reactive polytropic MuLVs. We examined polytropic MuLVs generated in NFS/N mice after inoculation with Mo-MuLV-F-MuLV(57) chimeras to determine which regions of the viral genome influence this difference between the two ecotropic MuLVs. These studies identified a region of the MuLV genome which encodes the nucleocapsid protein and a portion of the viral protease as the only region that influenced the difference in polytropic-MuLV generation by Mo-MuLV and F-MuLV(57). C1 NIAID, ROCKY MT LABS, PERSISTENT VIRAL DIS LAB, HAMILTON, MT 59840 USA. INST COCHIN GENET MOL, INSERM, U363, F-75014 PARIS, FRANCE. NR 48 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X EI 1098-5514 J9 J VIROL JI J. Virol. PD NOV PY 1997 VL 71 IS 11 BP 8923 EP 8927 PG 5 WC Virology SC Virology GA YB143 UT WOS:A1997YB14300104 PM 9343260 ER PT J AU Wang, GH Bertin, J Wang, Y Martin, DA Wang, J Tomaselli, KJ Armstrong, RC Cohen, JI AF Wang, GH Bertin, J Wang, Y Martin, DA Wang, J Tomaselli, KJ Armstrong, RC Cohen, JI TI Bovine herpesvirus 4 BORFE2 protein inhibits fas- and tumor necrosis factor receptor 1-induced apoptosis and contains death effector domains shared with other gamma-2 herpesviruses SO JOURNAL OF VIROLOGY LA English DT Article ID CELL-DEATH; BCL-2 HOMOLOG; VIRUS; TYPE-4; GENE; E1B; PROTEASES; SEQUENCE; FADD; HOST AB Fas- and tumor necrosis factor receptor 1 (TNFR1)-induced apoptosis is mediated by the interaction of FADD with caspase-8. Here, we report that the bovine herpesvirus 4 (BHV4) BORFE2 gene encodes a protein that inhibits Fas- and TNFR1-induced apoptosis and contains death effector domains (DEDs). Using the yeast two-hybrid system, we found that the BORFE2 protein interacts with the prodomain of caspase-8. Furthermore, we show that BHV4 BORFE2 is a member of a family of DED-containing proteins that includes other gamma-2 herpesviruses, such as Kaposi's sarcoma-associated herpesvirus and herpesvirus saimiri. C1 NIAID,IMMUNOL LAB,NIH,BETHESDA,MD 20892. IDUN PHARMACEUT INC,LA JOLLA,CA 92037. RP Wang, GH (reprint author), NIAID,CLIN IMMUNOL LAB,NIH,BLDG 10,RM 11N228,MSC 1888,9000 ROCKVILLE PK,BETHESDA,MD 20892, USA. NR 33 TC 59 Z9 60 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1997 VL 71 IS 11 BP 8928 EP 8932 PG 5 WC Virology SC Virology GA YB143 UT WOS:A1997YB14300105 PM 9343261 ER PT J AU Juhasz, K Whitehead, SS Bui, PT Biggs, JM Crowe, JE Boulanger, CA Collins, PL Murphy, BR AF Juhasz, K Whitehead, SS Bui, PT Biggs, JM Crowe, JE Boulanger, CA Collins, PL Murphy, BR TI The temperature-sensitive (ts) phenotype of a cold-passaged (cp) live attenuated respiratory syncytial virus vaccine candidate, designated cpts530, results from a single amino acid substitution in the L protein (vol 71, pg 5814, 1997) SO JOURNAL OF VIROLOGY LA English DT Correction, Addition RP Juhasz, K (reprint author), NIAID,INFECT DIS LAB,BETHESDA,MD 20892, USA. RI Crowe, James/B-5549-2009 OI Crowe, James/0000-0002-0049-1079 NR 1 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1997 VL 71 IS 11 BP 8953 EP 8953 PG 1 WC Virology SC Virology GA YB143 UT WOS:A1997YB14300112 ER PT J AU Yancik, R AF Yancik, R TI Integration of aging and cancer research in geriatric medicine SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES LA English DT Article ID OLDER RP Yancik, R (reprint author), NIA,CANC SECT,GERIATR PROGRAM,NIH,GATEWAY BLDG,ROOM 3E327,7201 WISCONSON AVE,MSC 92,BETHESDA,MD 20892, USA. NR 15 TC 19 Z9 19 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 1079-5006 J9 J GERONTOL A-BIOL JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci. PD NOV PY 1997 VL 52 IS 6 BP M329 EP M332 PG 4 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA YK498 UT WOS:A1997YK49800009 PM 9402937 ER PT J AU Haseley, LA Wisnieski, JJ Denburg, MR MichaelGrossman, AR Ginzler, EM Gourley, MF Hoffman, JH Kimberly, RP Salmon, JE AF Haseley, LA Wisnieski, JJ Denburg, MR MichaelGrossman, AR Ginzler, EM Gourley, MF Hoffman, JH Kimberly, RP Salmon, JE TI Antibodies to C1q in systemic lupus erythematosus: Characteristics and relation to Fc gamma RIIA alleles SO KIDNEY INTERNATIONAL LA English DT Article DE systemic lupus erythematosus; lupus; antibody; Fc gamma RIIA; complement; IgG2 ID COLLAGEN-LIKE REGION; URTICARIAL VASCULITIS SYNDROME; IGG SUBCLASS DISTRIBUTION; SOLID-PHASE C1Q; RHEUMATIC DISEASES; IMMUNOGLOBULIN-G; AUTOANTIBODIES; NEPHRITIS; GLOMERULONEPHRITIS; POLYMORPHISM AB Autoantibodies to the collagen-like region of the first complement component (C1qAB) are found in patients with systemic lupus erythematosus (SLE), particularly those with renal disease. In a cohort of 46 SLE patients with diffuse proliferative glomerulonephritis, we found declining C1qAB titers in 77% of treatment responders and in only 38% of treatment non-responders (P < 0.03). To further characterize this autoantibody, we tested 240 SLE patients for the presence of C1qAB. Positive titers were found in 44% of patients with renal disease and 18% of patients without renal disease (X-2 P < 0.0003). Analysis of IgG subclass revealed IgG2 C1qAB alone in 34%, IgG1 C1qAB alone in 20%, and both IgG1 and IgG2 in 46% of patients. Fewer than 10% of patients had measurable titers of IgG3 or IgG4 C1qAB. The pathogenic role of these IgG2-skewed C1qAB may relate to impaired immune complex clearance by the mononuclear phagocyte system: IgG2 antibodies are efficiently recognized by only one IgG receptor, the H131 allele of Fc gamma RIIa (Fc gamma RIIa-H131). In contrast, Fc gamma RIIa-R131, which is characterized by minimal IgG2 binding, has recently been associated with lupus nephritis. In our C1qAB positive patients, the presence of Fc gamma RIIA-R131 was associated with an increased risk for renal disease. Autoantibodies to C1q may have pathogenic significance in SLE patients with genetic defects in the ability to clear IgG2 containing immune complexes. C1 HOSP SPECIAL SURG,DEPT MED,DIV NEPHROL,NEW YORK,NY 10021. HOSP SPECIAL SURG,DEPT MED,DIV RHEUMATOL,NEW YORK,NY 10021. CORNELL UNIV MED COLL,NEW YORK HOSP,NEW YORK,NY. CASE WESTERN RESERVE UNIV,VET ADM MED CTR,DEPT MED,DIV RHEUMATOL,CLEVELAND,OH 44106. SUNY HLTH SCI CTR,DEPT MED,DIV RHEUMATOL,BROOKLYN,NY 11203. NIAMSD,NIH,BETHESDA,MD 20892. FU NIAMS NIH HHS [R01-AR38889] NR 39 TC 63 Z9 65 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD NOV PY 1997 VL 52 IS 5 BP 1375 EP 1380 DI 10.1038/ki.1997.464 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA YC339 UT WOS:A1997YC33900023 PM 9350662 ER PT J AU Eknoyan, G Kopple, J Levey, A Levin, N Schulman, G Beck, G Kusek, J Daugirdas, JT Depner, TA Gotch, FA Greene, T Keshaviah, P Levin, NW AF Eknoyan, G Kopple, J Levey, A Levin, N Schulman, G Beck, G Kusek, J Daugirdas, JT Depner, TA Gotch, FA Greene, T Keshaviah, P Levin, NW TI Comparison of methods to predict equilibrated Kt/V in the HEMO pilot study SO KIDNEY INTERNATIONAL LA English DT Article DE urea kinetics; pharmacokinetics; hemodialysis; modeling; rebound; clearance; organ blood flow ID REGIONAL BLOOD-FLOW; UREA KINETIC-MODEL; CARDIOPULMONARY RECIRCULATION; HEMODIALYSIS; EFFICIENCY; REMOVAL; DIFFUSION AB The ongoing HEMO Study, a National Institutes of Health (NIH) sponsored multicenter trial to test the effects of dialysis dosage and membrane flux on morbidity and mortality, was preceded by a Pilot Study (called the MMHD Pilot Study) designed to test the reliability of methods for quantifying hemodialysis. Dialysis dose was defined by the fractional urea clearance per dialysis determined by the predialysis BUN and the equilibrated postdialysis BUN after urea rebound is completed (eKt/V). In the Pilot Study the blood side standard for eKt/V was calculated from the predialysis, postdialysis, and 30-minute postdialysis BUN. Four techniques of approximating eKt/V that eliminated the requirement for the 30-minute postdialysis sample were also evaluated. The first adjusted the single compartment Kt/V using a linear equation with slope based on the relative rate of solute removal (K/V) to predict eKt/V (rate method). The second and third techniques used equations or mathematical curve fitting algorithms to fit data that included one or more samples drawn during dialysis (intradialysis methods). The fourth technique (dialysate-side) predicted eKt/V from an analysis of the time-dependent profile of dialysate urea nitrogen concentrations (BioStat method; Baxter Healthcare, Inc., Round Lake, IL, USA). The Pilot Study demonstrated the feasibility of conventional and high dose targets of about 1.0 and 1.4 far eKt/V. Based on the blood side standard method, the mean +/- SD eKt/V for patients randomized to these targets was 1.14 +/- 0.11 and 1.52 +/- 0.15 (N = 19 and 16 patients, respectively). Single-pool Kt/Vs were about 0.2 Kt/V units higher. Results were similar when eKt/V was based on dialysate side measurements: 1.10 +/- 0.11 and 1.50 +/- 0.11. The approximations of eKt/V by the three blood side methods that eliminated the delayed 30-minute post-dialysis sample correlated well with eKt/V from the standard blood side method: r = 0.78 and 0.76 for the single-sample (Smye) and multiple-sample intradialysis methods (N = 295 and 229 sessions, respectively) and 0.85 for the rate method (N = 295). The median absolute difference between eKt/V computed using the standard blood side method and eKt/V from the four other methods ranged from 0.064 to 0.097, with the smallest difference (and hence best accuracy) for the rate method. The results suggest that, in a dialysis patient population selected for ability to achieve an equilibrated Kt/V of about 1.45 in less than a 4.5 hour period, use of the pre and postdialysis samples and a kinetically derived rate equation gives reasonably good prediction of equilibrated Kt/V. Addition of one or more intradialytic samples does not appear to increase accuracy of predicting the equilibrated Kt/V in the majority of patients. A method based on dialysate urea analysis and curve-fitting yields results for equilibrated Kt/V that are similar to those obtained using exclusively blood-based techniques of kinetic modelling. C1 NIDDK,NIH,BETHESDA,MD. NR 29 TC 116 Z9 117 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD NOV PY 1997 VL 52 IS 5 BP 1395 EP 1405 PG 11 WC Urology & Nephrology SC Urology & Nephrology GA YC339 UT WOS:A1997YC33900026 ER PT J AU Sandor, V AF Sandor, V TI Chronotherapy with 5-fluorouracil, oxaliplatin, and folinic acid in colorectal cancer SO LANCET LA English DT Letter RP Sandor, V (reprint author), NCI,NIH,MED BRANCH,BETHESDA,MD 20892, USA. NR 3 TC 9 Z9 9 U1 1 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD NOV 1 PY 1997 VL 350 IS 9087 BP 1325 EP 1326 DI 10.1016/S0140-6736(05)62486-5 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA YD689 UT WOS:A1997YD68900053 PM 9357429 ER PT J AU Linnekin, D Mou, S Deberry, CS Weiler, SR Keller, JR Ruscetti, FW Longo, DL AF Linnekin, D Mou, S Deberry, CS Weiler, SR Keller, JR Ruscetti, FW Longo, DL TI Stem cell factor, the JAK-STAT pathway and signal transduction SO LEUKEMIA & LYMPHOMA LA English DT Review DE cytokines; growth factors; signal transduction; hematopoiesis ID COLONY-STIMULATING FACTOR; EPIDERMAL GROWTH-FACTOR; C-KIT LIGAND; TYROSINE PHOSPHORYLATION; HEMATOPOIETIC-CELLS; FACTOR RECEPTOR; SI-LOCUS; KINASE; ACTIVATION; INTERLEUKIN-3 AB Recent work has demonstrated the importance of Janus family kinases (JAKs) and signal transducers and activators of transcription (STATs) in the stimulus-response coupling of receptors lacking intrinsic tyrosine kinase activity. In particular, the JAK-STAT pathway appears critical in signal transduction by interferon as well as numerous hematopoietic growth factors interacting with members of the hemapoietin receptor superfamily. Although ligands that interact with receptor tyrosine kinases (RTK), such as epidermal growth factor (EGF), platelet-derived growth factor (PDGF) and colony stimulating factor-1 (CSF-1), have been shown to induce increases in phosphorylation of both JAKs and STATs, little is known about activation of this pathway by stem cell factor (SCF). This review will summarize what is known about the JAK/STAT pathway in relation to SCF signal transduction. C1 NCI, Lab Leukocyte Biol, Div Basic Sci, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. RP Linnekin, D (reprint author), NCI, Lab Leukocyte Biol, Div Basic Sci, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. NR 39 TC 28 Z9 29 U1 0 U2 2 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-8194 J9 LEUKEMIA LYMPHOMA JI Leuk. Lymphoma PD NOV PY 1997 VL 27 IS 5-6 BP 439 EP 444 PG 6 WC Oncology; Hematology SC Oncology; Hematology GA YP493 UT WOS:000071282800006 PM 9477125 ER PT J AU Gilgenkrantz, S Schrock, E Liyanage, M duManoir, S Ried, T AF Gilgenkrantz, S Schrock, E Liyanage, M duManoir, S Ried, T TI All that FISH can do for you SO M S-MEDECINE SCIENCES LA French DT Review ID FLUORESCENCE INSITU HYBRIDIZATION; HUMAN-CHROMOSOMES; PROBES C1 NIH,NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892. NR 16 TC 4 Z9 4 U1 0 U2 0 PU JOHN LIBBEY EUROTEXT LTD PI MONTROUGE PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE SN 0767-0974 J9 M S-MED SCI JI M S-Med. Sci. PD NOV PY 1997 VL 13 IS 11 BP 1294 EP 1298 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YF169 UT WOS:A1997YF16900008 ER PT J AU Jezzard, P Rauschecker, JP Malonek, D AF Jezzard, P Rauschecker, JP Malonek, D TI An in vivo model for functional MRI in cat visual cortex SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE fMRI; animal model; visual cortex; BOLD ID HUMAN BRAIN; SENSORY STIMULATION; INTRINSIC SIGNALS; NEURONAL-ACTIVITY; DOMAINS; LAYOUT; EPI AB A protocol is described for obtaining functional magnetic resonance images in anesthetized cat brain based on the blood oxygenation level dependent (BOLD) contrast mechanism. A visual stimulus was used, which consisted of a high-contrast drifting grating, whose speed and spatial frequency was optimized for cat area 18 (V2). Experiments were conducted at 4.7 Tesla using a gradient echo EPI sequence with a 29-ms echo time, yielding signal changes of between 0.7% and 2% in area 18. C1 GEORGETOWN UNIV,GICCS,WASHINGTON,DC. WEIZMANN INST SCI,DEPT NEUROBIOL,IL-76100 REHOVOT,ISRAEL. RP Jezzard, P (reprint author), NIMH,UNIT MRI PHYS,LBC,NIH,BLDG 10 ROOM 4C104,BETHESDA,MD 20892, USA. RI Rauschecker, Josef/A-4120-2013; OI Jezzard, Peter/0000-0001-7912-2251 NR 22 TC 39 Z9 41 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD NOV PY 1997 VL 38 IS 5 BP 699 EP 705 DI 10.1002/mrm.1910380504 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA YD911 UT WOS:A1997YD91100003 PM 9358442 ER PT J AU Crawford, MJ Lanctot, C Tremblay, JJ Jenkins, N Gilbert, D Copeland, N Beatty, B Drouin, J AF Crawford, MJ Lanctot, C Tremblay, JJ Jenkins, N Gilbert, D Copeland, N Beatty, B Drouin, J TI Human and murine PTX1/Ptx1 gene maps to the region for Treacher Collins Syndrome SO MAMMALIAN GENOME LA English DT Article ID INSITU HYBRIDIZATION; CHROMOSOMES; MOUSE; DNA; TRANSCRIPTION AB Ptx1 belongs to an expanding family of bicoid-related vertebrate homeobox genes. These genes, like their Drosophila homolog, seem to play a role in the development of anterior structures and, in particular, the brain and facies. We report the chromosomal localization of mouse Ptx1, and the cloning, sequencing, and chromosomal localization of the human homolog PTX1. The putative encoded proteins share 100% homology in the homeodomain and are 88% and 97% conserved in the N- and C-termini respectively. Intron/exon boundaries are also conserved. Murine Ptx1 was localized, by interspecific backcrossing, to Chr 13 within 2.6 cM of Caml. The gene resides centrally on Chromosome (Chr) 13 in a region syntenic with human Chr 5q. Subsequent analysis by fluorescent in situ hybridization places the human gene, PTX1, on 5q31, a region associated with Treacher Collins Franceschetti Syndrome. Taken together with the craniofacial expression pattern of Ptx1 during early development, the localization of the gene in this chromosomal area is consistent with an involvement in Treacher Collins Franceschetti Syndrome. C1 INST RECH CLIN MONTREAL,GENET MOL LAB,MONTREAL,PQ H2W 1R7,CANADA. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. HOSP SICK CHILDREN,TORONTO,ON M5G 1X8,CANADA. NR 27 TC 25 Z9 26 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD NOV PY 1997 VL 8 IS 11 BP 841 EP 845 DI 10.1007/s003359900589 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA YC460 UT WOS:A1997YC46000009 PM 9337397 ER PT J AU Russell, MW Baker, P Izumo, S AF Russell, MW Baker, P Izumo, S TI Cloning, chromosomal mapping, and expression of the human eHAND gene SO MAMMALIAN GENOME LA English DT Article ID MYOGENESIS; PROTEINS C1 UNIV MICHIGAN,MED CTR,DEPT PEDIAT,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT COMMUNICABLE DIS,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,ANN ARBOR,MI 48109. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. RP Russell, MW (reprint author), UNIV MICHIGAN,MED CTR,CARDIOVASC RES CTR,1500 E MED CTR DR,F1310 MCHC BOX 0204,ANN ARBOR,MI 48109, USA. NR 15 TC 12 Z9 13 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD NOV PY 1997 VL 8 IS 11 BP 863 EP 865 DI 10.1007/s003359900596 PG 3 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA YC460 UT WOS:A1997YC46000016 PM 9337404 ER PT J AU Rhim, H Savagner, P Thibaudeau, G Thiery, JP Pavan, WJ AF Rhim, H Savagner, P Thibaudeau, G Thiery, JP Pavan, WJ TI Localization of a neural crest transcription factor, Slug, to mouse Chromosome 16 and human Chromosome 8 SO MAMMALIAN GENOME LA English DT Article C1 NIH,LAB GENET DIS RES,NATL HUMAN GENOME RES INST,BETHESDA,MD 20892. NIDR,CRANIOFACIAL DEV BIOL & REGENERAT BRANCH,NIH,BETHESDA,MD 20892. INST CURIE,CNRS,UMR 144,F-75248 PARIS 05,FRANCE. NR 6 TC 9 Z9 9 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD NOV PY 1997 VL 8 IS 11 BP 872 EP 873 DI 10.1007/s003359900601 PG 2 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA YC460 UT WOS:A1997YC46000021 PM 9337409 ER PT J AU Johnson, MR Wilkin, DJ Vos, HL DeLuna, RIO Dehejia, AM Polymeropoulos, MH Francomano, CA AF Johnson, MR Wilkin, DJ Vos, HL DeLuna, RIO Dehejia, AM Polymeropoulos, MH Francomano, CA TI Characterization of the human extracellular matrix protein 1 gene on chromosome 1q21 SO MATRIX BIOLOGY LA English DT Article DE bone; cartilage; chromosome 1q21; extracellular matrix protein 1 ID PYCNODYSOSTOSIS; EXPRESSION; ALBUMIN; GENOMES; FAMILY AB Ecm1, the mouse gene encoding extracellular matrix protein 1, is highly expressed in bone and cartilage as well as in osteogenic, preosteoblastic and chondroblastic cell lines. Ecm1 was recently localized to a chromosomal region in mouse syntenic to human chromosome 1q21, establishing this gene as a prime candidate gene for pycnodysostosis, a rare, autosomal recessive sclerosing skeletal dysplasia. Shortly thereafter, it was determined that cathepsin K is the pycnodysostosis gene. We now report the radiation hybrid mapping of human ECM1 to 1q21, and the gene structure and coding sequence of human ECM1. C1 NHGRI,MED GENET BRANCH,NIH,BETHESDA,MD. NETHERLANDS CANC INST,AMSTERDAM,NETHERLANDS. HOSP INFANTIL MEXICO DR FEDERICO GOMEZ,MEXICO CITY,DF,MEXICO. NHGRI,LAB GENET DIS BRANCH,NIH,BETHESDA,MD. NR 9 TC 25 Z9 28 U1 0 U2 1 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0945-053X J9 MATRIX BIOL JI Matrix Biol. PD NOV PY 1997 VL 16 IS 5 BP 289 EP 292 DI 10.1016/S0945-053X(97)90017-2 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA YH992 UT WOS:A1997YH99200006 PM 9501329 ER PT J AU Levin, JS Glass, TA Kushi, LH Schuck, JR Steele, L Jonas, WB AF Levin, JS Glass, TA Kushi, LH Schuck, JR Steele, L Jonas, WB TI Quantitative methods in research on complementary and alternative medicine - A methodological manifesto SO MEDICAL CARE LA English DT Article; Proceedings Paper CT NIH Conference on Complementary and Alternative Medicine Research Methodology CY APR 26-28, 1995 CL BETHESDA, MD SP NIH DE alternative medicine; research; methodology; statistics ID CHAOS THEORY; HEALTH; PHYSICIANS; BIOLOGY; TRIALS AB OBJECTIVES. This article summarizes the deliberations of the Quantitative Methods Working Group convened by the National Institutes of Health (NIH) in support of the NIH Office of Alternative Medicine. METHODS. The working group was charged with identifying methods of study design and data analysis that can be applied to empirical research on complementary and alternative medicine. This charge was broad and inclusive and addressed the evaluation of alternative therapies, the investigation of the basic science of complementary medical systems, studies of health promotion and disease prevention, and health services research. RESULTS. The working group produced a ''methodological manifesto,'' a summary list of seven recommended methodological guidelines for research on alternative medicine. These recommendations emphasize the robustness of existing research methods and analytic procedures despite the substantive unconventionality of alternative medicine. CONCLUSIONS. Contrary to the assertions of many researchers and alternative practitioners, established methodologies (eg, experimental trials, observational epidemiology, social survey research) and data-analytic procedures (eg, analysis of variance, logistic regression, multivariate modeling techniques) are quite satisfactory for addressing the majority of study questions related to alternative medicine, from clinical research on therapeutic efficacy to basic science research on mechanisms of pathogenesis and recovery. C1 NATL INST HEALTHCARE RES,ROCKVILLE,MD. HARVARD UNIV,SCH PUBL HLTH,DEPT HLTH & SOCIAL BEHAV,BOSTON,MA 02115. UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. BOWLING GREEN STATE UNIV,DEPT PSYCHOL,BOWLING GREEN,OH 43403. KANSAS COMMISS VET AFFAIRS,TOPEKA,KS. NIH,OFF ALTERNAT MED,BETHESDA,MD 20892. OI Glass, Thomas/0000-0003-4399-612X; Kushi, Lawrence/0000-0001-9136-1175 FU NIA NIH HHS [R01-AG10135, R29-AG09462] NR 54 TC 74 Z9 91 U1 1 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD NOV PY 1997 VL 35 IS 11 BP 1079 EP 1094 DI 10.1097/00005650-199711000-00001 PG 16 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA YE813 UT WOS:A1997YE81300001 PM 9366888 ER PT J AU DePamphilis, ML AF DePamphilis, ML TI The search for origins of DNA replication SO METHODS-A COMPANION TO METHODS IN ENZYMOLOGY LA English DT Article ID DIHYDROFOLATE-REDUCTASE DOMAIN; ANIMAL-CELLS; EGG EXTRACTS; CHO CELLS; GENE; IDENTIFICATION; INITIATION; SITES; AMPLIFICATION; CHROMOSOMES AB The past decade has witnessed an explosion of new information about the nature of DNA replication in eukaryotic cells. Much of this information has resulted from the advent of novel methods for identifying and characterizing origins of DNA replication in the genomes of viruses, plasmids, and cells. These methods can map with remarkable precision sites where replication begins. In addition, they provide assays for origin activity that can be used to identify the sequence of events leading to the formation and activation of prereplication complexes at specific sites in chromosomal DNA. I summarize briefly the current view of eukaryotic replication origins and the methods that have been used to identify and characterize them. Selected methods that show promise for future applications are then described in detail in subsequent articles. (C) 1997 Academic Press. C1 NICHHD, NIH, Bethesda, MD 20892 USA. RP DePamphilis, ML (reprint author), NICHHD, NIH, Bldg 6,Room 416, Bethesda, MD 20892 USA. NR 50 TC 24 Z9 25 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1046-2023 J9 METHODS JI Methods PD NOV PY 1997 VL 13 IS 3 BP 211 EP 219 DI 10.1006/meth.1997.0521 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YQ758 UT WOS:000071420300002 PM 9441848 ER PT J AU Stephens, NL Jiang, H AF Stephens, NL Jiang, H TI Velocity of translation of single actin filaments (AF) by myosin heads from antigen-sensitized airway smooth muscle SO MOLECULAR AND CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Meeting on Cellular Basis of Cardiovascular Function in Health and Disease CY AUG 23-25, 1996 CL KENORA, CANADA DE allergic bronchospasm; motility assay; maximum velocity of shortening of crossbridges ID INVITRO; SUBFRAGMENT-1; MOVE AB We have previously reported increased velocity of shortening (V-0) in the sensitized airway (0.36 1(0)/s, +/- SE) smooth muscle compared to the control (0.26 1(0)/s, +/- 0.017 SE) and subsequent experiments indicated this was due to increased phosphorylation of the 20 kDa myosin light chain resulting from increased total myosin light chain kinase activity. The motility assay technique described by Kron and Spudich was employed to determine whether additionally the molecular motor (actomyosin crossbridge) itself was altered in airway smooth muscle by ragweed pollen sensitization. The motility assay measures the velocity of actin filament translation by myosin molecules. The negative results of the motility assay were valuable in determining that the pathogenesis of allergic bronchospasm is not at contractile protein level but at regulatory enzyme level. C1 NHLBI,MOL CARDIOL LAB,NIH,BETHESDA,MD 20892. RP Stephens, NL (reprint author), UNIV MANITOBA,DEPT PHYSIOL,425 BASIC MED SCI BLDG,730 WILLIAM AVE,WINNIPEG,MB R3E 3J7,CANADA. NR 16 TC 6 Z9 6 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0300-8177 J9 MOL CELL BIOCHEM JI Mol. Cell. Biochem. PD NOV PY 1997 VL 176 IS 1-2 BP 41 EP 46 DI 10.1023/A:1006866626607 PG 6 WC Cell Biology SC Cell Biology GA YH288 UT WOS:A1997YH28800007 PM 9406143 ER PT J AU Wu, L Good, PJ Richter, JD AF Wu, L Good, PJ Richter, JD TI The 36-kilodalton embryonic-type cytoplasmic polyadenylation element-binding protein in Xenopus laevis is ElrA, a member of the ELAV family of RNA-Binding proteins SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MATURATION-SPECIFIC POLYADENYLATION; MOS MESSENGER-RNA; TRANSLATIONAL CONTROL; OOCYTE MATURATION; C-MOS; DROSOPHILA; SEQUENCE; REGIONS; PRODUCT; HEL-N1 AB The translational activation of several maternal mRNAs in Xenopus laevis is dependent on cytoplasmic poly(A) elongation. Messages harboring the UUUUUAU-type cytoplasmic polyadenylation element (CPE) in their 3' untranslated regions (UTRs) undergo polyadenylation and translation during oocyte maturation. This CPE is bound by the protein CPEB, which is essential for polyadenylation. mRNAs that have the poly(U)(12-27) embryonic-type CPE (eCPE) in their 3' UTRs undergo polyadenylation and translation during the early cleavage and blastula stages. A 36-kDa eCPE-binding protein in oocytes and embryos ties been identified by UV cross-linking. We now report that this 36-kDa protein if ElrA, a member of the ELAV family of RNA-binding proteins. The proteins are identical in size, antibody directed against ElrA immunoprecipitates the 36-kDa protein, and the two proteins have the same RNA binding specificity in vitro. Cl2 and activin receptor mRNAs, both of which contain eCPEs, are detected in immunoprecipitated ElrA-mRNP complexes from eggs and embryos. In addition, this in vivo interaction requires the eCPE. Although a number of experiments failed to define a role for ElrA in cytoplasmic polyadenylation, the expression of a dominant negative ElrA protein in embryos results in an exogastrulation phenotype. The possible functions of ElrA in gastrulation are discussed. C1 UNIV MASSACHUSETTS,MED CTR,DEPT MOL GENET & MICROBIOL,WORCESTER,MA 01655. NICHHD,MOL GENET LAB,BETHESDA,MD 20892. LOUISIANA STATE UNIV,MED CTR,DEPT BIOCHEM & MOL BIOL,SHREVEPORT,LA 71130. LOUISIANA STATE UNIV,MED CTR,CTR EXCELLENCE CANC RES,SHREVEPORT,LA 71130. FU NCI NIH HHS [CA40189]; NIGMS NIH HHS [GM17932, GM46779] NR 43 TC 53 Z9 55 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 NOV PY 1997 VL 17 IS 11 BP 6402 EP 6409 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA YC255 UT WOS:A1997YC25500022 PM 9343402 ER PT J AU Bhattacharyya, N Dey, A Minucci, S Zimmer, A John, S Hager, G Ozato, K AF Bhattacharyya, N Dey, A Minucci, S Zimmer, A John, S Hager, G Ozato, K TI Retinoid-induced chromatin structure alterations in the retinoic acid receptor beta 2 promoter SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID TUMOR VIRUS PROMOTER; TRANSCRIPTION FACTOR ACCESS; EMBRYONAL CARCINOMA-CELLS; IN-VIVO; HISTONE ACETYLATION; NUCLEOSOME DISRUPTION; HYPERSENSITIVE SITES; GENE-REGULATION; MMTV PROMOTER; PHO5 PROMOTER AB Transcription of the retinoic acid receptor beta 2 (RAR beta 2) gene is induced by retinoic acid (RA) in mouse P19 embryonal carcinoma (EC) cells. Here we studied RA-induced chromatin structure alterations in the endogenous RAR beta 2 promoter and in an integrated, multicopy RAR beta 2 promoter in EC cells, RA markedly increased restriction site accessibility within the promoter, including a site near the RA responsive element (RARE) to which the nuclear receptor retinoid X receptor (RXR)-RAR heterodimer binds, These changes coincided with RA-induced alterations in the DNase I hypersensitivity pattern in and around the promoter. These changes became undetectable upon removal of RA, which coincided with the extinction of transcription, Analyses with receptor-selective ligands and an antagonist showed that increase in restriction site accessibility correlates with transcriptional activation, which parallels the RA-induced in vivo footprint of the promoter. Despite these changes, the micrococcal nuclease digestion profile of this promoter was not altered by RA, These results indicate that concurrent with the binding of the RXR-RAR heterodimer to the RARE, the local chromatin structure undergoes dynamic, reversible changes in and around the promoter without globally affecting the nucleosomal organization. C1 NICHHD,LAB MOL GROWTH & REGULAT,NIH,BETHESDA,MD 20892. NIMH,PEOPLE INVESTIGATING GENES,BETHESDA,MD 20892. NCI,LAB RECEPTOR BIOL & GENE EXPRESS,NIH,BETHESDA,MD 20892. RI Zimmer, Andreas/B-8357-2009; Minucci, Saverio/J-9669-2012 NR 65 TC 38 Z9 38 U1 1 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD NOV PY 1997 VL 17 IS 11 BP 6481 EP 6490 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA YC255 UT WOS:A1997YC25500031 PM 9343411 ER PT J AU Wolfgang, CD Chen, BPC Martindale, JL Holbrook, NJ Hai, T AF Wolfgang, CD Chen, BPC Martindale, JL Holbrook, NJ Hai, T TI gadd153/Chop10, a potential target gene of the transcriptional repressor ATF3 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID NF-KAPPA-B; PROTEIN (C/EBP)-RELATED GENE; NITRIC-OXIDE SYNTHASE; DNA-BINDING; C-JUN; OXIDATIVE STRESS; GROWTH ARREST; MESSENGER-RNA; EXPRESSION; RAT AB Recently, we demonstrated that the function of ATF3, a stress-inducible transcriptional repressor, is negatively regulated by a bZip protein, gadd153/Chop10. In this report, we present evidence that ATF3 can repress the expression of its own inhibitor, gadd153/Chop10. First, ATF3 represses a chloramphenicol acetyltransferase reporter gene driven by the gadd153/Chop10 promoter when assayed by a transfection assay in vivo and a transcription assay in vitro, Second, the gadd153/Chop10 promoter contains two functionally important binding sites for ATF3: an AP-1 site and a C/EBP-ATF composite site, a previously unidentified binding site for ATF3, The absence of either site reduces the ability of ATF3 to repress the promoter, Third, overexpression of ATF3 by transient transfection results in a reduction of the endogenous gadd153/Chop10 mRNA level. Fourth, as described previously, ATM is induced in the liver upon CCl4 treatment. Intriguingly, we show in this report that gadd153/Chop10 mRNA is not present in areas where ATF3 is induced, Taken together, these results strongly suggest that ATF3 represses the expression of gadd153/Chop10. The mutual negative regulation between ATF3 and gadd153/Chop10 is discussed. C1 OHIO STATE UNIV,CTR NEUROBIOTECHNOL,COLUMBUS,OH 43210. OHIO STATE UNIV,OHIO STATE BIOCHEM PROGRAM,COLUMBUS,OH 43210. OHIO STATE UNIV,DEPT MED BIOCHEM,COLUMBUS,OH 43210. NIA,SECT GENE EXPRESS & AGING,CTR GERONTOL RES,BALTIMORE,MD 21224. RI Hai, Tsonwin/H-4480-2011; Hai, Tsonwin/E-3185-2011 OI Hai, Tsonwin/0000-0003-4510-0315; Hai, Tsonwin/0000-0003-4510-0315 FU NIEHS NIH HHS [ES08690] NR 48 TC 117 Z9 118 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD NOV PY 1997 VL 17 IS 11 BP 6700 EP 6707 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA YC255 UT WOS:A1997YC25500054 PM 9343434 ER PT J AU Braga, EA Kotova, EY Pugacheva, EM Gizatullin, RZ Kashuba, VI Lerman, MI Aksenova, MG Efremov, IA Zabarovsky, ER Kiselev, LL AF Braga, EA Kotova, EY Pugacheva, EM Gizatullin, RZ Kashuba, VI Lerman, MI Aksenova, MG Efremov, IA Zabarovsky, ER Kiselev, LL TI Microsatellite di-, tri-, and tetrameric motifs on human chromosome 3: Study of distribution and design of markers SO MOLECULAR BIOLOGY LA English DT Article DE human chromosome 3; NotI linking and jumping clones; di-, tri-, and tetranucleotide microsatellites; gene markers; carcinogenesis ID NOTI-LINKING CLONES; CELL LUNG-CANCER; POLYMERASE CHAIN-REACTION; IN-SITU HYBRIDIZATION; HUMAN GENOME; TRINUCLEOTIDE REPEATS; DYNAMIC MUTATIONS; 3P21 REGION; SHORT ARM; DNA AB Nine microsatellite motifs were studied in DNA inserts of 150 NotI linking and jumping clones of human chromosome 3, and also in the contig of 22 overlapping cosmids related to the region of homozygous deletions in small-cell lung carcinoma (locus 3p21.3, 570 kbp). Compared with the human genome in total, the NotI clones had three times less CA repeats and more GAG, GGA, AAT, CAC, AAAG, AATG, and GATG motifs, More than 11 kbp of subcloned DNA fragments from clones NL1-212, NLM-216, NL-026, J32-135H and cosmids 6, 7, and 16 were sequenced. Allele polymorphism was studied in 10 microsatellite loci identified on human chromosome 3 and in 8 CAG/CTG(n), loci of the brain cDNA (data from GenBank). Polymorphic loci were rather rare near the NotI sites (one of seven) and in cDNA (one of eight). This phenomenon and the distribution patterns of some microsatellites suggest that the NotI clones of human chromosome 3 and the cosmids related to the 3p21.3 region are rich in genes. Two polymorphic and nine STS markers were generated for the human chromosome 3; three of them were located in regions frequently affected in various solid tumors and four were related to genes. Polymorphic markers were related to the murine neuropeptide gene encoding receptor Y-YI gene (93.3% homology, 62 bp) and to the gene EST04896 expressed in brain. C1 State Genet Ctr, Moscow 113545, Russia. Karolinska Inst, S-17177 Stockholm, Sweden. NCI, Ctr Canc Res & Dev, Frederick, MD 21702 USA. VA Engelhardt Mol Biol Inst, Moscow 117984, Russia. RP Braga, EA (reprint author), State Genet Ctr, Moscow 113545, Russia. EM EBraga@vnigen.msk.su RI Zabarovsky, Eugene/A-6645-2010; Braga, Eleonora/P-5574-2016 NR 58 TC 0 Z9 0 U1 0 U2 2 PU PLENUM PUBL CORP PI NEW YORK PA CONSULTANTS BUREAU, 233 SPRING ST, NEW YORK, NY 10013 USA SN 0026-8933 J9 MOL BIOL+ JI Mol. Biol. PD NOV-DEC PY 1997 VL 31 IS 6 BP 838 EP 848 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YX655 UT WOS:000072063000009 ER PT J AU Mannen, H Tsoi, SCM Krushkal, JS Li, WH Li, SSL AF Mannen, H Tsoi, SCM Krushkal, JS Li, WH Li, SSL TI The cDNA cloning and molecular evolution of reptile and pigeon lactate dehydrogenase isozymes SO MOLECULAR BIOLOGY AND EVOLUTION LA English DT Article DE alligator; lizard; turtle; bird; protein sequence; phylogeny ID PHYLOGENETIC TREES; AMNIOTE PHYLOGENY; SEQUENCE-ANALYSIS; GENE FAMILY; TURTLES; TESTIS; SUBSTITUTION; MAMMALS; MUSCLE; SITES AB The cDNAs encoding lactate dehydrogenase isozymes LDH-A (muscle) and LDH-B (heart) from alligator and turtle and LDH-A, LDH-B, and LDH-C (testis) from pigeon were cloned and sequenced. The evolutionary relationships among vertebrate LDH isozymes were analyzed. Contrary to the traditional belief that the turtle lineage branched off before the divergence between the lizard/alligator and bird lineages, the turtle lineage was found to be clustered with either the alligator lineage or the alligator-bird clade, while the lizard lineage was found to have branched off before the divergence between the alligator/turtle and bird lineages. The pigeon testicular LDH-C isozyme was evidently duplicated from LDH-B (heart), so it is not orthologous to the mammalian testicular LDH-C isozymes. C1 NATL SUN YAT SEN UNIV, INST LIFE SCI, KAOHSIUNG 80824, TAIWAN. NIH, GENET MOL LAB, INST ENVIRONM HLTH SCI, RES TRIANGLE PK, NC USA. UNIV TEXAS, CTR HUMAN GENET, HOUSTON, TX USA. OI Li, Wen-Hsiung/0000-0003-1086-1456 FU NIGMS NIH HHS [GM30998] NR 39 TC 34 Z9 40 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0737-4038 J9 MOL BIOL EVOL JI Mol. Biol. Evol. PD NOV PY 1997 VL 14 IS 11 BP 1081 EP 1087 PG 7 WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity GA YE818 UT WOS:A1997YE81800001 PM 9364765 ER PT J AU Prahlad, V Yoon, M Marekov, L Steinert, P Goldman, RD AF Prahlad, V Yoon, M Marekov, L Steinert, P Goldman, RD TI Interactions between vimentin and microtubules (MT) during the formation of an intermediate filament (IF) network in vivo SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NORTHWESTERN UNIV,SCH MED,DEPT CELL & MOL BIOL,EVANSTON,IL 60208. NIAMS,NIH,SKIN BIOL GRP,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 15 EP 15 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600016 ER PT J AU Melloy, PG Ewart, JL Cohen, MF Desmond, ME Kuehn, MR Lo, CW AF Melloy, PG Ewart, JL Cohen, MF Desmond, ME Kuehn, MR Lo, CW TI No turning, a left/right patterning mutant displaying abnormal notochordal function SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV PENN,DEPT BIOL,PHILADELPHIA,PA 19104. VILLANOVA UNIV,DEPT BIOL,VILLANOVA,PA 19085. NICHHD,NIH,MOL GENET LAB,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 40 EP 40 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600038 ER PT J AU Wallace, WC Luo, JJ Wallace, MS Kusiak, JW AF Wallace, WC Luo, JJ Wallace, MS Kusiak, JW TI Amyloid precursor protein (APP) protects against serum deprivation in PC12 cells and sustains primary cortical neurons SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA,BIOL CHEM LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 58 EP 58 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600056 ER PT J AU Cai, H Zelenka, PS AF Cai, H Zelenka, PS TI Overexpression of 14-3-3eta isoform increases PKC activity in vivo SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 65 EP 65 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600064 ER PT J AU Lorenzo, PS Bogi, K Acs, P Blumberg, PM AF Lorenzo, PS Bogi, K Acs, P Blumberg, PM TI The catalytic domain of PKC delta confers protection from down-regulation induced by bryostatin 1 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,NIH,LCCTP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 66 EP 66 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600067 ER PT J AU Ahmad, F Gao, G Wang, LM Pierce, JH Degerman, E Manganiello, VC AF Ahmad, F Gao, G Wang, LM Pierce, JH Degerman, E Manganiello, VC TI Regulation of cyclic nucleotide phosphodiesterases PDE3 and PDE4 by cytokines in FDCP2 cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 82 EP 82 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600081 ER PT J AU Brown, KD Barlow, C Deng, CX Tagle, DA WynshawBoris, A AF Brown, KD Barlow, C Deng, CX Tagle, DA WynshawBoris, A TI ATM selectivity regulates distinct downstream p53-dependent pathways of cell cycle progression and apoptosis in vivo SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHGRI,LGT,BETHESDA,MD. NHGRI,LGDR,BETHESDA,MD. NIDDK,NIH,LBM,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 95 EP 95 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600096 ER PT J AU Kohn, KW AF Kohn, KW TI Functional capabilities of molecular network components controlling the mammalian G1/S cell cycle phase transition SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NATL CANC INST,DIV BASIC SCI,MOL PHARMACOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 96 EP 96 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600094 ER PT J AU Park, MH Joe, YA Wolff, EC AF Park, MH Joe, YA Wolff, EC TI Deoxyhypusine synthase plays a critical role in eukaryotic cell proliferation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,ORAL & PHARYNGEAL CANC BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 102 EP 102 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600100 ER PT J AU Gao, CY Kantorow, M Piatigorsky, J Zelenka, PS AF Gao, CY Kantorow, M Piatigorsky, J Zelenka, PS TI alpha beta-Crystallin is an in vitro substrate for Cdk5-associated kinase activity of lens fiber cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 113 EP 113 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600111 ER PT J AU Ohshima, T Gilmore, E Jacobowitz, D Herrup, K Brady, R Kulkarni, A AF Ohshima, T Gilmore, E Jacobowitz, D Herrup, K Brady, R Kulkarni, A TI Abnormal neuronal migration in Cdk5(-/-) mice SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS,NIH,BETHESDA,MD 20892. NIDR,GENE TARGETING RES CORE FACIL,NIH,BETHESDA,MD 20892. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. NIMH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 121 EP 121 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600118 ER PT J AU Racz, A Barsony, J AF Racz, A Barsony, J TI Hormone-dependent translocation of vitamin D receptors SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,LAB CELL BIOL & BIOCHEM,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 138 EP 138 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600134 ER PT J AU Kino, T Kopp, JB Stauber, RH Alexander, K Pavlakis, GN Chrousos, GP AF Kino, T Kopp, JB Stauber, RH Alexander, K Pavlakis, GN Chrousos, GP TI HIV-1 VPR gene product is a coactivator of the nuclear receptor and cause glucocorticoid hypersensitivity: Implication for AIDS patients SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,SECT PEDIAT ENDOCRINOL,DEB,BETHESDA,MD. NIDDKD,KIDNEY DIS SECT,MDB,NIH,BETHESDA,MD. NCI,HUMAN RETROVIRUS SECT,ABL BASIC RES PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 147 EP 147 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600147 ER PT J AU Kim, SY Steinert, PM AF Kim, SY Steinert, PM TI The expression of transglutaminases 1, 2 and 3 in normal human brain SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 175 EP 175 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600173 ER PT J AU Jarnik, M Simon, MN Fan, E Lichti, C Steven, AC AF Jarnik, M Simon, MN Fan, E Lichti, C Steven, AC TI Cornified cell envelope assembly: Inferences from electron microscopy of mature, immature and cultured CEs SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMS,LSBR,BETHESDA,MD 20892. NIH,ECB,NCI,BETHESDA,MD 20892. BROOKHAVEN NATL LAB,UPTON,NY 11973. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 189 EP 189 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600186 ER PT J AU Sesso, A TeixeiraMonteiro, MM Fujiwara, D Jaeger, MM Correa, H Schumacher, I Kachar, B AF Sesso, A TeixeiraMonteiro, MM Fujiwara, D Jaeger, MM Correa, H Schumacher, I Kachar, B TI The fragmentation of the Golgi complex into vesicles is an additional structural resemblance between mitosis and apoptosis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV SAO PAULO,SAO PAULO,BRAZIL. NATL INST HLTH,BETHESDA,MD 20852. RI Marques, Marcia/F-3780-2012 OI Marques, Marcia/0000-0002-9398-1252 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 190 EP 190 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600189 ER PT J AU Kudryashov, DS Vorotnikov, AV Flicker, PF Silver, DL Sellers, JR Watterson, DM Shirinsky, VP AF Kudryashov, DS Vorotnikov, AV Flicker, PF Silver, DL Sellers, JR Watterson, DM Shirinsky, VP TI Opposite action of kinase-related protein and caldesmon on smooth muscle myosin filament assembly. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 CTR CARDIOL,MOSCOW,RUSSIA. NHLBI,NIH,BETHESDA,MD 20892. VANDERBILT UNIV,NASHVILLE,TN. NORTHWESTERN UNIV,CHICAGO,IL 60611. RI Vorotnikov, Alexander/A-8392-2014 OI Vorotnikov, Alexander/0000-0002-1460-971X NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 225 EP 225 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600221 ER PT J AU Buxton, DB Adelstein, RS AF Buxton, DB Adelstein, RS TI Interaction of mammalian nonmuscle myosin II-B with plasma membranes. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,MOL CARDIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 226 EP 226 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600224 ER PT J AU Brzeska, H Young, R Knaus, U Korn, ED AF Brzeska, H Young, R Knaus, U Korn, ED TI Acanthamoeba myosin I heavy chain kinase (MIHCK) is a member of the PAK family and is activated by small GTP-binding proteins SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI, CELL BIOL LAB, NIH, BETHESDA, MD 20892 USA. SCRIPPS RES INST, LA JOLLA, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 228 EP 228 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600228 ER PT J AU Ramachandran, U Szczepanowska, J Herring, CJ Qin, JD Korn, ED Brzeska, H AF Ramachandran, U Szczepanowska, J Herring, CJ Qin, JD Korn, ED Brzeska, H TI Ser and Thr residues required for activity of Acanthamoeba myosin I heavy chain kinase (MIHCK) catalytic domain SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. NHLBI,BIOPHYS CHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 229 EP 229 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600226 ER PT J AU Ralston, E Ploug, T AF Ralston, E Ploug, T TI Fiber-type specific distribution of microtubules and microtubule-organizing centers (MTOC) in skeletal muscle fibers. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS,LN,NIH,BETHESDA,MD 20492. COPENHAGEN MUSCLE RES CTR,COPENHAGEN,DENMARK. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 239 EP 239 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600239 ER PT J AU Ogilvie, MK Liu, C Chin, K Noguchi, CT AF Ogilvie, MK Liu, C Chin, K Noguchi, CT TI Erythropoietin receptor responsiveness in mouse myoblasts SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,BIOL CHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 243 EP 243 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600241 ER PT J AU Bai, R Ewell, JB Nguyen, NY Hamel, E AF Bai, R Ewell, JB Nguyen, NY Hamel, E TI Localization of the nonexchangeable GTP binding site on alpha-tubulin. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,LAB DRUG DISCOVERY RES & DEV,FREDERICK,MD 21702. US FDA,FACIL BIOTECHNOL RESOURCES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 268 EP 268 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600266 ER PT J AU VerdierPinard, P Gerwick, H Hamel, E AF VerdierPinard, P Gerwick, H Hamel, E TI Interaction of curacin A with tubulin. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,LAB DRUG DISCOVERY RES & DEV,FREDERICK,MD 21702. OREGON STATE UNIV,COLL PHARM,CORVALLIS,OR 97331. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 272 EP 272 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600268 ER PT J AU Zambito, AM Wolff, J AF Zambito, AM Wolff, J TI Tubulin palmitoylation and its regulation. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 274 EP 274 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600272 ER PT J AU Barsony, J Lenherr, S Shih, K Smith, CL Sackett, DL AF Barsony, J Lenherr, S Shih, K Smith, CL Sackett, DL TI Importin alpha mediates steroid receptor interaction with microtubules during translocation. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,LAB CELL BIOCHEM & BIOL,BETHESDA,MD 20892. NCI,LAB RECEPTOR BIOL & GENE EXPRESS,NIH,BETHESDA,MD 20892. NCI,MED BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 283 EP 283 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600282 ER PT J AU Hoffman, MP Rogue, E Nomizu, M Yamada, Y Kleinman, HK AF Hoffman, MP Rogue, E Nomizu, M Yamada, Y Kleinman, HK TI Laminin-1 and laminin-2 G domain synthetic peptides bind syndecan-1 and promote acinar-like development of a human submandibular gland cell line. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,CDBRB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 391 EP 391 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600389 ER PT J AU Giacomello, E Neumayer, J Yin, Z Zardi, L Aota, S Yamada, KM Lazarowitz, A Colombatti, A Perris, R AF Giacomello, E Neumayer, J Yin, Z Zardi, L Aota, S Yamada, KM Lazarowitz, A Colombatti, A Perris, R TI Interaction of human B cell lymphomas with fibronectin involves recognition of multiple cooperating sites. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 REFERENCE CTR ONCOL,AVIANO,ITALY. TECAN,SALZBURG,AUSTRIA. IST,GENOA,ITALY. NIH,BETHESDA,MD 20892. UNIV WESTERN ONTARIO,LONDON,ON,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 397 EP 397 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600395 ER PT J AU Takahashi, I Shum, L Takahashi, K Dashner, R Slavkin, HC Nuckolls, GH AF Takahashi, I Shum, L Takahashi, K Dashner, R Slavkin, HC Nuckolls, GH TI Compression force induces type II collagen and aggrecan transcription during embryonic mouse limb chrondrogenesis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIMH,CRANIOFACIAL DEV SECT,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 411 EP 411 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600411 ER PT J AU Satomura, K Kuznetsov, SA deRubeis, AR Erlacher, R Robey, PG AF Satomura, K Kuznetsov, SA deRubeis, AR Erlacher, R Robey, PG TI In vitro expression of CBFA-1 and BMP family members in osteogenic, non-osteogenic, and osteoinductive human cells. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,CRANOFACIAL & SKELETAL DIS BRANCH,NIH,BETHESDA,MD 20892. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 421 EP 421 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600419 ER PT J AU Mueller, SC Ghersi, G Akiyama, SK Sang, QZA Howard, L PineiroSanchez, M Nakahara, H Yeh, Y Chen, WT AF Mueller, SC Ghersi, G Akiyama, SK Sang, QZA Howard, L PineiroSanchez, M Nakahara, H Yeh, Y Chen, WT TI Collagen induces beta 1 integrin docking of a membrane-bound gelatinase, seprase, at plasma membrane sites of tumor cell invasion. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. NIEHS,MOL CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. FLORIDA STATE UNIV,DEPT CHEM,TALLAHASSEE,FL 32306. RI Howard, Linda/B-2463-2009 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 438 EP 438 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600434 ER PT J AU Sasaki, CY Passaniti, A AF Sasaki, CY Passaniti, A TI Interaction of breast cancer cells with ECM regulates cell-cell adhesion and fibrinolysis by urokinase-type plasminogen activator (u-PA). SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA,BIOL CHEM LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 439 EP 439 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600437 ER PT J AU Albini, A Fassina, G Melchiori, A Masiello, L Santi, L Noonan, DM StetlerStevenson, WG Valente, P AF Albini, A Fassina, G Melchiori, A Masiello, L Santi, L Noonan, DM StetlerStevenson, WG Valente, P TI TIMP-2 overexpression reduces B16F10 melanoma cell invasion and angiogenesis yet protects them from apoptosis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 IST NAZL RIC CANC,I-16132 GENOA,ITALY. CTR ADV RES BIOTECHNOL,GENOA,ITALY. CNR,CTR STUDIO NEUROFISIOL CEREBRALE,GENOA,ITALY. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 440 EP 440 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600438 ER PT J AU Huster, D Gawrisch, K AF Huster, D Gawrisch, K TI Influence of docosahexaenoic acid and cholesterol on lateral lipid organization in phospholipid mixtures. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAAA,LAB MEMBRANE BIOCHEM & BIOPHYS,NIH,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 450 EP 450 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600446 ER PT J AU Tremper, KE Gershfeld, NL AF Tremper, KE Gershfeld, NL TI Selective trafficking of phospholipids in nascent membranes of L-pictus embryos SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMS,PHYS BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 453 EP 453 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600453 ER PT J AU Avramoglu, RK Nimpf, J Ko, KWS McLeod, RS Wang, Y FitzGerald, DJ Yao, Z AF Avramoglu, RK Nimpf, J Ko, KWS McLeod, RS Wang, Y FitzGerald, DJ Yao, Z TI Functional expression of recombinant chicken LDL receptor-related protein mutants in a deficient cell line SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV OTTAWA,INST HEART,OTTAWA,ON,CANADA. UNIV VIENNA,A-1010 VIENNA,AUSTRIA. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 467 EP 467 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600463 ER PT J AU Yoon, H Lee, M Grollman, EF Philp, NJ AF Yoon, H Lee, M Grollman, EF Philp, NJ TI Expression and localization of proton coupled monocarboxylate transporters, MCT1 and MCT3, in retinal pigment epithelial cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 PENN COLL OPTOMETRY,PHILADELPHIA,PA 19141. NIDDK,BIOCHEM & METAB LAB,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 478 EP 478 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600475 ER PT J AU Wojda, U Miller, JL AF Wojda, U Miller, JL TI Endocytosis mediated by biotin-avidin crosslinking of surface proteins does not require GPI-proteins. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,BIOL CHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 497 EP 497 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600495 ER PT J AU Richard, G Andreoli, JM Smith, LE Compton, JG AF Richard, G Andreoli, JM Smith, LE Compton, JG TI Characterization and gene mapping of two human connexins expressed in epidermis. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMS,GENET STUDIES SECT,SKIN BIOL LAB,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 551 EP 551 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600551 ER PT J AU Harris, AL Fitzgerald, W Baibakov, B Margolis, LB Zimmerberg, J AF Harris, AL Fitzgerald, W Baibakov, B Margolis, LB Zimmerberg, J TI Inhibition of specific antibody production by gap junction inhibitors SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,NASA,NIH,CTR 3 DIMENS CULTURE,LCMB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 556 EP 556 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600554 ER PT J AU King, C Eisenberg, E Greene, L AF King, C Eisenberg, E Greene, L TI Interaction between HSC70 and DnaJ homologs: Evidence for weak binding of DnaJ homologs to HSC70 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,CELL BIOL LAB,NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 560 EP 560 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600556 ER PT J AU Peculis, BA AF Peculis, BA TI The sequence of the 5' end of the U8 snoRNA is critical for 5.8S and 28S maturation. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,GENET & BIOCHEM BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 575 EP 575 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600573 ER PT J AU ScidmoreCarlson, MA Fischer, ER Hackstadt, T AF ScidmoreCarlson, MA Fischer, ER Hackstadt, T TI Early dissociation from the endocytic compartment by endocytosed chlamydia trachomatis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,INTRACELLULAR PARASITES LAB,ROCKY MT LABS,HAMILTON,MT 59840. NIAID,MICROSCOPY BRANCH,ROCKY MT LABS,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 678 EP 678 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600675 ER PT J AU Yamage, M Dwyer, DM Debrabant, A AF Yamage, M Dwyer, DM Debrabant, A TI Crithidia luciliae 3-nucleotidase/nuclease: Gene structure and regulation. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 693 EP 693 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600691 ER PT J AU Chen, M Mansoura, M FitzGerald, D Rosenfeld, M AF Chen, M Mansoura, M FitzGerald, D Rosenfeld, M TI A novel bifunctional protein, TGF alpha/TRF, specifically binds telomeric DNA and mediates gene transfer into mammalian cells via EGF receptors. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NATL HUMAN GENOME RES INST,NIH,BETHESDA,MD 20892. NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 701 EP 701 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600698 ER PT J AU Bonifacino, JS AF Bonifacino, JS TI Protein sorting in the endosomal/lysosomal system. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 704 EP 704 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600702 ER PT J AU LippincottSchwartz, J Presley, JF Cole, NB Hirschberg, K AF LippincottSchwartz, J Presley, JF Cole, NB Hirschberg, K TI Membrane trafficking and recycling within the secretory pathway. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 705 EP 705 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600705 ER PT J AU Yamada, KM Miyamoto, S Katz, BZ Lafrenie, RM AF Yamada, KM Miyamoto, S Katz, BZ Lafrenie, RM TI Integrin signaling and cytoskeletal complexes. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,CDBRB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 708 EP 708 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600706 ER PT J AU Sciacchitano, S Kulansky, R Taylor, SI AF Sciacchitano, S Kulansky, R Taylor, SI TI Cloning, tissue distribution, chromosomal localization, and expression of the mouse IRS-3 gene. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,NIDDK,DIABET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 746 EP 746 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600746 ER PT J AU Romanova, LY Alexandrov, IA Nguyen, PM Nordan, RP Trepel, J Mushinski, JF AF Romanova, LY Alexandrov, IA Nguyen, PM Nordan, RP Trepel, J Mushinski, JF TI PKC-delta induces rounding and cell cycle arrest of lymphoid cells by disrupting growth factor-mediated assembly of actin-rich ruffled protrusions SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,GENET LAB,NIH,BETHESDA,MD 20892. NCI,MED BRANCH,NIH,BETHESDA,MD 20892. US FDA,DIV MONOCLONAL ANTIBODIES,CBER,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 763 EP 763 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600763 ER PT J AU deMendez, I Abo, A Leto, T AF deMendez, I Abo, A Leto, T TI Down-regulation of a phagocyte host defense system, the NADPH oxidase, by PAK2. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. ONYX PHARMACEUT,RICHMOND,CA 94806. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 772 EP 772 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600768 ER PT J AU Haque, RM Lee, SJ Nguyen, PM Choi, YH Pernia, F Jang, JS Wang, XF Kim, SJ Trepel, JB AF Haque, RM Lee, SJ Nguyen, PM Choi, YH Pernia, F Jang, JS Wang, XF Kim, SJ Trepel, JB TI Regulation of the cyclin-dependent kinase inhibitor p21 by an inhibitor of the mevalonate pathway SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,MED BRANCH,CELL SIGNALLING & ONCOGNESIS SECT,BETHESDA,MD 20892. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 801 EP 801 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600797 ER PT J AU Topol, LZ Clausen, PA Bogdanova, N Marx, M Calothy, G Blair, DG AF Topol, LZ Clausen, PA Bogdanova, N Marx, M Calothy, G Blair, DG TI A novel cell cycle-regulated nuclear protein, drm is involved in growth inhibition. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,IRSP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. ST LOUIS UNIV,ST LOUIS,MO 63104. INST CURIE,F-91405 ORSAY,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 812 EP 812 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600811 ER PT J AU Ha, MJ Kim, HJ Mushinski, FJ Kim, SJ Chang, SH Chun, JS AF Ha, MJ Kim, HJ Mushinski, FJ Kim, SJ Chang, SH Chun, JS TI Inhibition of cyclin A expression by ectopic expression of protein kinase C delta in NIH3T3 cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 AJOU UNIV,MED GENET LAB,SUWON 441749,SOUTH KOREA. NCI,GENET LAB,NIH,BETHESDA,MD 20892. KYUNGPOOK NATL UNIV,DEPT BIOL,TAEGU,SOUTH KOREA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 814 EP 814 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600812 ER PT J AU George, KM Small, PLC AF George, KM Small, PLC TI Purification of a lipid toxin produced by Mycobacterium ulcerans which causes L929 cells to undergo cell cycle arrest SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,MICROSCOPY BRANCH,HAMILTON,MT 59840. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 815 EP 815 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600813 ER PT J AU AlAwar, OS Donaldson, JG AF AlAwar, OS Donaldson, JG TI Structural analysis of ARF1 and ARF6: Mapping localization and functional domains. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 825 EP 825 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600823 ER PT J AU Rao, PV Wawrousek, E Zigler, JS AF Rao, PV Wawrousek, E Zigler, JS TI Rho GTPase function is critical for lens growth and development. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 835 EP 835 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600834 ER PT J AU Takahashi, K Nuckolls, GH Tanaka, O Semba, I Takahashi, I Dashner, R Shum, L Slavkin, HC AF Takahashi, K Nuckolls, GH Tanaka, O Semba, I Takahashi, I Dashner, R Shum, L Slavkin, HC TI Ectopic expression of Msx2 in even-numbered rhombomeres resulted in apoptotic elimination of cranial neural crest cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMS,CRANIOFACIAL DEV SECT,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 850 EP 850 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600847 ER PT J AU Chang, SH Phelps, PC Coursen, JD Wang, XW Berezesky, IK Harris, CC Trump, BF AF Chang, SH Phelps, PC Coursen, JD Wang, XW Berezesky, IK Harris, CC Trump, BF TI Deregulation of cytosolic ionized calcium [Ca2+]i following overexpression of p53 in normal rat kidney (NRK-52E) cells. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. NCI,HUMAN CARCINOGENESIS LAB,NIH,BALTIMORE,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 856 EP 856 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600853 ER PT J AU Yamamoto, A Kumakura, S Uchida, M Annab, L Barrett, JC Tsutsui, T AF Yamamoto, A Kumakura, S Uchida, M Annab, L Barrett, JC Tsutsui, T TI Extended lifespan and immortalization of normal human fibroblasts by introduction of human papillomavirus (HPV) type 16 E6, E7 or E6/E7 gene. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIPPON DENT UNIV TOKYO,DEPT ORAL & MAXILLOFACIAL SURG,TOKYO 102,JAPAN. NIPPON DENT UNIV TOKYO,DEPT PHARMACOL,TOKYO 102,JAPAN. NIEHS,ENVIRONM CARCINOGENESIS PROGRAM,MOL CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 872 EP 872 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600872 ER PT J AU Adams, CS Horton, WE AF Adams, CS Horton, WE TI Chondrocyte apoptosis increases with age in the articular cartilage of adult animals SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA,LBC,GRC,NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 879 EP 879 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600876 ER PT J AU Herrera, AH Horowits, R AF Herrera, AH Horowits, R TI Cloning and expression of the amino termini of mouse nebulin SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 899 EP 899 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600895 ER PT J AU Luo, G Herrera, AH Horowits, R AF Luo, G Herrera, AH Horowits, R TI Sequence analysis, localization, and protein binding properties of N-RAP, a nebulin-related protein of striated muscle SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 900 EP 900 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600898 ER PT J AU Wang, F Conti, MA Jiang, H Harvey, EV Wei, DF Sellers, JR AF Wang, F Conti, MA Jiang, H Harvey, EV Wei, DF Sellers, JR TI Mutations of an actin binding loop in human nonmuscle myosin IIA. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,LMC,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 912 EP 912 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600910 ER PT J AU Tullio, AN Accili, D Ferrans, VJ Yu, ZX Takeda, K Preston, YA Adelstein, RS AF Tullio, AN Accili, D Ferrans, VJ Yu, ZX Takeda, K Preston, YA Adelstein, RS TI Nonmuscle myosin II-B is required for normal development of the mouse heart. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 913 EP 913 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600911 ER PT J AU Lin, H Jiang, H Poetter, K Sellers, JR Epstein, ND AF Lin, H Jiang, H Poetter, K Sellers, JR Epstein, ND TI Expression of naturally occurring mutant human cardiac light chains. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CARDIOL BRANCH,NIH,BETHESDA,MD 20892. NHLBI,MOL CARDIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 914 EP 914 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600914 ER PT J AU Jiang, H Lin, H Wang, F Epstein, ND Sellers, JR AF Jiang, H Lin, H Wang, F Epstein, ND Sellers, JR TI Functional analysis of human beta-cardiac myosin with E-coli. Expressed regulatory light chain (RLC) mutations in familial hypertrophic cardiomyopathy (HCM). SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,MOL CARDIOL LAB,NIH,BETHESDA,MD 20892. NHLBI,CARDIOL BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 915 EP 915 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09600912 ER PT J AU DeGiorgis, JA Medeiros, NA Nascimento, AAC Bearer, EL AF DeGiorgis, JA Medeiros, NA Nascimento, AAC Bearer, EL TI Two myosins are tightly associated with squid axoplasmic organelles SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 BROWN UNIV,DEPT PATHOL,PROVIDENCE,RI 02912. NINCDS,NIH,BETHESDA,MD 20892. UNIV SAO PAULO,SAO PAULO,BRAZIL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1005 EP 1005 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601003 ER PT J AU Giannelli, G Gardner, HA StetlerStevenson, WG Pozzi, A Quaranta, V AF Giannelli, G Gardner, HA StetlerStevenson, WG Pozzi, A Quaranta, V TI Laminin-5 and matrix metalloprotease-2 induce rearrangement of epithelial architecture in the mammary gland. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Scripps Res Inst, DEPT CELL BIOL, LA JOLLA, CA 92037 USA. NIH, PATHOL LAB, NCI, BETHESDA, MD 20892 USA. RI giannelli, gianluigi/A-8169-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1031 EP 1031 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601030 ER PT J AU Wilson, KE Krutzsch, HC Roberts, DD AF Wilson, KE Krutzsch, HC Roberts, DD TI Thrombospondin modulates adhesion, motility and proliferation of Jurkat T-lymphoma cells. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NATL INST HLTH,PATHOL LAB,NATL CANC INST,BETHESDA,MD 20892. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1039 EP 1039 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601037 ER PT J AU Ponce, ML Malinda, KM Delgado, MC Nomizu, M Yamada, Y Kleinman, HK AF Ponce, ML Malinda, KM Delgado, MC Nomizu, M Yamada, Y Kleinman, HK TI Peptide sequences from the laminin gamma 1 chain promote angiogenesis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NATL INST DENTAL RES,CDBRB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1044 EP 1044 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601040 ER PT J AU Hrycyna, CA Ramachandra, M Pastan, I Gottesman, MM AF Hrycyna, CA Ramachandra, M Pastan, I Gottesman, MM TI Functional characterization of human P-glycoprotein: Evidence for the non-equivalency of the two ATP binding domains. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. NCI,MOL BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1107 EP 1107 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601106 ER PT J AU Dey, S Ramachandra, M Pastan, I Gottesman, MM Ambudkar, SV AF Dey, S Ramachandra, M Pastan, I Gottesman, MM Ambudkar, SV TI Photoaffinity labeling of human P-glycoprotein: Evidence for two non-identical drug interaction sites. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,CELL BIOL LAB,BETHESDA,MD 20892. NIH,MOL BIOL LAB,NATL CANC INST,BETHESDA,MD 20892. RI Ambudkar, Suresh/B-5964-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1108 EP 1108 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601104 ER PT J AU Rhodes, MA Kahn, RA Xie, M Rosenwald, AG AF Rhodes, MA Kahn, RA Xie, M Rosenwald, AG TI Characterization of the ARL1 locus of Saccharomyces cerevisiae SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 GEORGETOWN UNIV,DEPT BIOL,WASHINGTON,DC 20057. EMORY UNIV,DEPT BIOCHEM,ATLANTA,GA 30322. NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1113 EP 1113 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601109 ER PT J AU Hirschberg, K Presley, J Cole, N Lippincott, J AF Hirschberg, K Presley, J Cole, N Lippincott, J TI Golgi to plasma membrane trafficking in living cells: Characterization of post-Golgi intermediates. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,CBMB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1121 EP 1121 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601119 ER PT J AU Lee, FJS Huang, CF Yu, WL Buu, LM Lin, CY Huang, MC Moss, J Vaughn, M AF Lee, FJS Huang, CF Yu, WL Buu, LM Lin, CY Huang, MC Moss, J Vaughn, M TI Characterization of an ADP-ribosylation factor-like 1 protein in Saccharomyces cerevisiae. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NATL TAIWAN UNIV,SCH MED,INST MOL MED,TAIPEI 10764,TAIWAN. NHLBI,PULM CRIT CARE MED BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1154 EP 1154 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601152 ER PT J AU Fletcher, PL Fletcher, MD Fainter, LK Martin, BM AF Fletcher, PL Fletcher, MD Fainter, LK Martin, BM TI Pancreatic secretory protein pathways stimulated by scorpion venom: Modulation of GPCR, PKC, and RAB's. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 E CAROLINA UNIV,SCH MED,DEPT MICROBIOL,GREENVILLE,NC 27858. NIMH,SECT MOL NEUROGENET,ADAMHA,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1156 EP 1156 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601156 ER PT J AU Jaeger, MM LacazVieira, F Farshori, P Kachar, B AF Jaeger, MM LacazVieira, F Farshori, P Kachar, B TI Small synthetic peptides homologous to segments of occludin impair tight junction resealing in a Ca+2-switch assay in A6 cell monolayers. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV SAO PAULO,SAO PAULO,BRAZIL. NIH,BETHESDA,MD 20892. RI Marques, Marcia/F-3780-2012 OI Marques, Marcia/0000-0002-9398-1252 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1189 EP 1189 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601187 ER PT J AU Murray, D Horton, WE AF Murray, D Horton, WE TI Evidence for E-box motifs involved in chondrocyte-specific expression of type II collagen SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA,NIH,LBC,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1221 EP 1221 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601220 ER PT J AU Sachs, LM Shi, YB AF Sachs, LM Shi, YB TI Regulation and function of thyroid hormone receptors during amphibian development. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,NIH,MOL EMBRYOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1228 EP 1228 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601224 ER PT J AU Lu, Z McLaren, RS Winters, CA Ralston, E AF Lu, Z McLaren, RS Winters, CA Ralston, E TI Association with ribosomes seems to restrict mRNAs to the cell body of rat hippocampal neurons. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS,NIH,NEUROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1241 EP 1241 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601239 ER PT J AU Masumi, A Horn, V Wang, IM Yang, XJ Nakatani, Y Ozato, K AF Masumi, A Horn, V Wang, IM Yang, XJ Nakatani, Y Ozato, K TI Interferon regulatory factors recruit nuclear proteins that alter histone acetylation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,LAB MOL GROWTH REGULAT,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1245 EP 1245 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601241 ER PT J AU Wu, W Hanover, JA AF Wu, W Hanover, JA TI Identification of the proteins interacting with O-linked GlcNAc transferase. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,NIH,LAB CELL BIOCHEM & BIOL,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1252 EP 1252 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601250 ER PT J AU Nehls, S Cole, N Ellenberg, J Presley, J Siggia, E LippincottSchwartz, J AF Nehls, S Cole, N Ellenberg, J Presley, J Siggia, E LippincottSchwartz, J TI Diffusional mobility of misfolded membrane proteins in the ER. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1310 EP 1310 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601309 ER PT J AU Malinda, KM Sidhu, GS Banaudha, KK Gaddipati, JP Maheshwari, RK Goldstein, AL Kleinman, HK AF Malinda, KM Sidhu, GS Banaudha, KK Gaddipati, JP Maheshwari, RK Goldstein, AL Kleinman, HK TI Thymosin alpha 1 stimulates endothelial cell migration, angiogenesis and wound healing. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT BIOCHEM & MOL BIOL,WASHINGTON,DC 20037. UNIFORMED SERV UNIV HLTH SCI,DEPT PATHOL,CTR COMBAT CASUALTY & LIFE SUSTAINMENT RES,BETHESDA,MD 20814. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1334 EP 1334 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601332 ER PT J AU Pu, RT Dasso, M AF Pu, RT Dasso, M TI The balance of RanBP1 and RCC1 is critical for nuclear assembly and nuclear transport SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,MOL EMBRYOL LAB,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1368 EP 1368 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601366 ER PT J AU Kyriakides, TR Zhu, YH Smith, LT Bain, SD Yang, Z Lin, M LaMarca, M McKinney, CE Ginns, EI Bornstein, P AF Kyriakides, TR Zhu, YH Smith, LT Bain, SD Yang, Z Lin, M LaMarca, M McKinney, CE Ginns, EI Bornstein, P TI Thrombospondin 2 (TSP2), a newly appreciated modulator of cell-matrix interactions and collagen fibrillogeneis. Mice that lack TSP2 display a pleiotrop IC phenotype. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV WASHINGTON,DEPT BIOCHEM,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. ZYMOGENET INC,SEATTLE,WA 98105. NIMH,CLIN NEUROSCI BRANCH,NIH,BETHESDA,MD 20982. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1376 EP 1376 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601373 ER PT J AU Harada, S Machwate, M Wesolowski, G Moalli, M LaRochelle, WJ Rodan, GA AF Harada, S Machwate, M Wesolowski, G Moalli, M LaRochelle, WJ Rodan, GA TI Keratinocyte growth factor FGF7 and its receptor are expressed in osteoblastic cells in vitro and in vivo. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MERCK RES LABS,DEPT BONE BIOL,W POINT,PA 19486. UNIV MICHIGAN,ANN ARBOR,MI 48109. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1400 EP 1400 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601399 ER PT J AU Samuel, KP Hodge, DR AF Samuel, KP Hodge, DR TI Demonstration of direct physical interaction between the HIV-1 Nef protein and c-Raf1 kinase. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MORGAN STATE UNIV,DEPT BIOL,BALTIMORE,MD 21239. NCI,DIV BASIC SCI,LAB LEUKOCYTE BIOL,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1417 EP 1417 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601416 ER PT J AU Gadina, M Bacon, CM Larner, AC OShea, JJ AF Gadina, M Bacon, CM Larner, AC OShea, JJ TI SHP-2 positively regulates IL-2 signaling SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMSD,LYMPHOCYTE CELL BIOL SECT,ARTHRIT & RHEUMATISM BRANCH,NIH,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1422 EP 1422 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601419 ER PT J AU Su, Y Shi, YF Stolow, MA Shi, YB AF Su, Y Shi, YF Stolow, MA Shi, YB TI Thyroid hormone induces apoptosis in primary cell cultures of tadpole intestine: Cell type specificity and effects of extracellular matrix. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,MOL EMBRYOL LAB,NIH,BETHESDAM,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1443 EP 1443 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601438 ER PT J AU Sarin, A Zacharchuk, CM Henkart, PA AF Sarin, A Zacharchuk, CM Henkart, PA TI Cell death via the cytotoxic lymphocyte granule exocytosis pathway shows an apoptotic phenotype in which only nuclear damage is blocked by caspase inhibitors SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 EIB,BETHESDA,MD 20892. NCI,LICB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1454 EP 1454 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601452 ER PT J AU Srivastava, RK Khan, L Longo, DL AF Srivastava, RK Khan, L Longo, DL TI Bcl-2 and Bcl-X-L antagonize the thapsigargin induced cell cycle arrest and apoptosis in Jurkat T lymphocytes. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA,LAB CLIN PHYSIOL,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1455 EP 1455 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601450 ER PT J AU Kirshman, P Wrathall, L Le, P Han, J Basolo, F Sobel, ME AF Kirshman, P Wrathall, L Le, P Han, J Basolo, F Sobel, ME TI Inverse modulation of IL6 and IL6 alpha receptor mRNA levels in human breast cancer cell lines. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1461 EP 1461 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601458 ER PT J AU Schwartz, GN Liao, F Ballon, D Farber, JM Gress, RE AF Schwartz, GN Liao, F Ballon, D Farber, JM Gress, RE TI Suppressive effects of chemokines on insulin-like growth factor II (IGF-II)-enhanced proliferation and differentiation of megakaryoblastic cell lines. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,DEPT EXPT TRANSPLANTAT & IMMUNOL,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1468 EP 1468 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601465 ER PT J AU Soon, LL Evans, CH AF Soon, LL Evans, CH TI Search for anti-defence homologue genes as adaptive immune evasion strategies in cervical cancer. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1470 EP 1470 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601466 ER PT J AU Wolffe, EJ Katz, E Weisberg, A Moss, B AF Wolffe, EJ Katz, E Weisberg, A Moss, B TI Role of EEV-specific proteins in the induction of specialized actin-containing microvilli and cell-to cell transmission of virus SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,NIH,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT VIROL,IL-91120 JERUSALEM,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1486 EP 1486 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601485 ER PT J AU Kim, AC Lutchman, M Zhuang, ZP Chishti, AH AF Kim, AC Lutchman, M Zhuang, ZP Chishti, AH TI Overexpression of dematin alters cell morphology of normal and prostate tumor epithelial cells. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. TUFTS UNIV,ST ELIZABETHS MED CTR,SCH MED,TUMOR CELL BIOL LAB,BOSTON,MA 02135. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1497 EP 1497 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601593 ER PT J AU Elmendorf, HG Nash, TE AF Elmendorf, HG Nash, TE TI Elements of the cytoskeleton in Giardia lamblia. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1571 EP 1571 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601565 ER PT J AU Radhakrishna, H Khachikian, Z Donaldson, JG AF Radhakrishna, H Khachikian, Z Donaldson, JG TI A requirement for ARF6 in Rac1-stimulated membrane ruffling. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1572 EP 1572 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601568 ER PT J AU Loomis, P Amin, N Pant, HC Goldman, RD AF Loomis, P Amin, N Pant, HC Goldman, RD TI Alterations in the neurofilament cytoskeleton of dorsal root ganglia neurons consequent to microinjection of cdk5/p35 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS,NEUROCHEM LAB,NIH,BETHESDA,MD 20892. NORTHWESTERN UNIV,DEPT CELL & MOL BIOL,CHICAGO,IL 60611. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1614 EP 1614 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601610 ER PT J AU Sihag, RK Jaffe, H Nixon, RA Rong, XH AF Sihag, RK Jaffe, H Nixon, RA Rong, XH TI Serine-23 is the major protein kinase a phosphorylation site on the N-terminal head domain of NF-M subunit of neurofilaments. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MCLEAN HOSP,BELMONT,MA 02178. NINCDS,PROT SEQUENCING FACIL,NIH,BETHESDA,MD 20892. NINCDS,NEUROBIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1622 EP 1622 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601617 ER PT J AU Forlino, A Cabral, WA Marini, JC AF Forlino, A Cabral, WA Marini, JC TI Synthesis, secretion and extracellular matrix analysis of mutant type I collagen produced by cultured osteoblasts and fibroblasts from two type IV OI probands SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,SECT CONNECT TISSUE DISORDERS,HDB,NIH,BETHESDA,MD. RI Forlino, Antonella/H-5385-2015 OI Forlino, Antonella/0000-0002-6385-1182 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1629 EP 1629 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601626 ER PT J AU Crow, MT Bilato, C Curto, KA Lakatta, EG Monticone, R AF Crow, MT Bilato, C Curto, KA Lakatta, EG Monticone, R TI Integrin-mediated signaling in migrating vascular smooth muscle cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA,CARDIOVASC SCI LAB,NIH,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1641 EP 1641 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601638 ER PT J AU Coorssen, JR Tahara, M Blank, P Zimmerberg, J AF Coorssen, JR Tahara, M Blank, P Zimmerberg, J TI Role of SNARE proteins in membrane fusion SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,LCMB,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1715 EP 1715 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601710 ER PT J AU Blank, PS Vogel, SS Malley, J Zimmerberg, J AF Blank, PS Vogel, SS Malley, J Zimmerberg, J TI Heterogeneity in calcium-triggered exocytosis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,LCMB,BETHESDA,MD 20892. NIH,CBEL,DCRT,BETHESDA,MD 20892. RI Vogel, Steven/A-3585-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1724 EP 1724 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601720 ER PT J AU StDenis, JF Cabaniols, JP Cushman, SW Roche, PA AF StDenis, JF Cabaniols, JP Cushman, SW Roche, PA TI Identification and characterization of SNAP-23 in rat adipose cells. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NCI,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1727 EP 1727 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601722 ER PT J AU AlHasani, H Hinck, CS Cushman, SW AF AlHasani, H Hinck, CS Cushman, SW TI Endocytosis of the glucose transporter GLUT4 is mediated by the GTPase dynamin SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1742 EP 1742 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601738 ER PT J AU Malide, D DaviesHill, TM Levine, M Simpson, IA AF Malide, D DaviesHill, TM Levine, M Simpson, IA TI Distinct localization of GLUT1, GLUT3, and GLUT5 in human monocyte-derived macrophages: Modulation by cell-activation. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,EDMNS,DB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1743 EP 1743 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601736 ER PT J AU McKee, ML FitzGerald, DJ AF McKee, ML FitzGerald, DJ TI Reduction of nicked Pseudomonas exotoxin A SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,BIOTHERAPY SECT,LMB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1750 EP 1750 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601745 ER PT J AU Yazar, O Sandoval, JJ Jones, TLZ AF Yazar, O Sandoval, JJ Jones, TLZ TI Intracellular distribution of XL alpha s SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,METAB DIS BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1773 EP 1773 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601766 ER PT J AU Aguilar, RC Ohno, H Roche, KW Bonifacino, JS AF Aguilar, RC Ohno, H Roche, KW Bonifacino, JS TI Bipartite structure of the clathrin-associated adaptor medium chains mu(1) and mu(2) SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1777 EP 1777 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601771 ER PT J AU Shakarian, AM Ellis, SL Dwyer, DM AF Shakarian, AM Ellis, SL Dwyer, DM TI Allelic polymorphisms are involved in differential targeting of acid phosphatases in Leishmania donovani SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,CELL BIOL SECT,PARASIT DIS LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1780 EP 1780 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601775 ER PT J AU Nambiar, MP Tedder, TF Pastan, IH FitzGerald, DJ AF Nambiar, MP Tedder, TF Pastan, IH FitzGerald, DJ TI Cloning, expression and characterization of recombinant PE38 immunotoxins directed against CD19 antigen for the therapy of B-cell malignancies SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,MOL BIOL LAB,NIH,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT IMMUNOL,DURHAM,NC 27710. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1788 EP 1788 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601785 ER PT J AU Putilina, T Wong, P Gentleman, S AF Putilina, T Wong, P Gentleman, S TI Identification of a protein with a unique cysteine-rich domain localized in endocrine and neuroendocrine tissues SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 INST BIOL LILLE,F-59021 LILLE,FRANCE. UNIV ALBERTA,DEPT BIOL,EDMONTON,AB,CANADA. NEI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1789 EP 1789 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601783 ER PT J AU Sperbeck, S Segovia, L Horwitz, J Gasser, R Wistow, G AF Sperbeck, S Segovia, L Horwitz, J Gasser, R Wistow, G TI The gene for mu-crystallin: A novel component of retina. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,SECT MOL STRUCT & FUNCT,NIH,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,JULES STEIN EYE INST,LOS ANGELES,CA 90024. UNIV MELBOURNE,PARKVILLE,VIC 3052,AUSTRALIA. RI Segovia, Lorenzo/A-5206-2008 OI Segovia, Lorenzo/0000-0002-4291-4711 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1815 EP 1815 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601810 ER PT J AU Sinha, D Kozak, C Jaworski, C Lyon, M Wistow, G AF Sinha, D Kozak, C Jaworski, C Lyon, M Wistow, G TI Mutation of gamma s-crystallin in the Opj cataract. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NIAID,NIH,BETHESDA,MD 20892. MRC,HARWELL,OXON,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1816 EP 1816 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601811 ER PT J AU Deming, MS Dyer, KD Rosenberg, HF AF Deming, MS Dyer, KD Rosenberg, HF TI Evolutionary analysis of ribonuclease k6: Diverging rates within the ribonuclease a gene superfamily. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1822 EP 1822 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601817 ER PT J AU Kawamoto, S Beohar, N Pyenson, A Bekelman, J AF Kawamoto, S Beohar, N Pyenson, A Bekelman, J TI Identification of cis-regulatory elements that activate nonmuscle myosin heavy chain-A gene transcription. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1826 EP 1826 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601819 ER PT J AU Kwon, S Eddy, EM AF Kwon, S Eddy, EM TI The expression of a membrane associated progesterone receptor (MAPR) in the male mouse reproductive system SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIEHS,NIH,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1849 EP 1849 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601845 ER PT J AU Rogakou, EP Boon, C Bonner, WM AF Rogakou, EP Boon, C Bonner, WM TI Formation of a novel histone derivative, H2AX phosphorylated on serine-139, is an immediate cellular response to non-lethal and lethal amounts of ionizing radiation, and is also found during apoptosis and in germ cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,MOL PHARMACOL LAB,DBS,NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1858 EP 1858 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601853 ER PT J AU Mori, C Nakamura, N Welch, JE Gotoh, H Goulding, EH Fujioka, M Eddy, EM AF Mori, C Nakamura, N Welch, JE Gotoh, H Goulding, EH Fujioka, M Eddy, EM TI Alternative exon use during transcription of the type 1 hexokinase gene in mouse spermatogenic cells. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 KYOTO UNIV,FAC MED,DEPT ANAT & DEV BIOL,KYOTO 60601,JAPAN. KYOTO UNIV,FAC MED,CENT LAB ELECT MICROSCOPY,KYOTO 60601,JAPAN. NIEHS,LRDT,NIH,RES TRIANGLE PK,NC 27709. US EPA,DTD,NHEERL,RES TRIANGLE PK,NC 27711. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1890 EP 1890 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601885 ER PT J AU Semba, I Shum, L Takahashi, K Tanaka, O Takahashi, I Nagata, M Dashner, R Nonaka, K Nuckolls, GH Slavkin, HC AF Semba, I Shum, L Takahashi, K Tanaka, O Takahashi, I Nagata, M Dashner, R Nonaka, K Nuckolls, GH Slavkin, HC TI BMP4 induces ectopic chondrogenesis during embryonic mouse mandibular morphogenesis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMS,CRANIOFACIAL DEV SECT,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1916 EP 1916 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601912 ER PT J AU Abe, K Callahan, R AF Abe, K Callahan, R TI Differential display of genes expressed in normal and transgenic WAP-NOTCH4/INT3 pregnant mammary glands and WAP-NOTCH4/INT3 mammary tumors. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1924 EP 1924 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601919 ER PT J AU Shu, Y Callahan, R AF Shu, Y Callahan, R TI Proteins that interact with the intracellular domain of NOTCH4/INT3. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1925 EP 1925 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601917 ER PT J AU Kordon, EC Smith, GH AF Kordon, EC Smith, GH TI Clonal expansion of mutated mammary epithelial stem cells. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1926 EP 1926 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601920 ER PT J AU Stevens, B Tanner, S Fields, RD AF Stevens, B Tanner, S Fields, RD TI Control of myelination and Schwann cell-axon interactions by specific patterns of neural impulses SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,DEV NEUROBIOL LAB,NINDS,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1928 EP 1928 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601924 ER PT J AU Altevogt, BM Itoh, K Stevens, B Fields, RD AF Altevogt, BM Itoh, K Stevens, B Fields, RD TI Developmental profile of the neural cell adhesion molecule L1 in mouse dorsal root ganglia neurons. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,DEV NEUROBIOL LAB,NIH,BETHESDA,MD 20892. TOKYO METROPOLITAN INST MED SCI,TOKYO 113,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1934 EP 1934 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601930 ER PT J AU Davenport, RW Thies, E AF Davenport, RW Thies, E TI Growth cone collapse is correlated with filopodial and lamellipodial extension from the axonal shaft SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,DEV NEUROBIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1939 EP 1939 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601933 ER PT J AU Bascom, RA Srinivasan, S Nussbaum, RL AF Bascom, RA Srinivasan, S Nussbaum, RL TI A novel Golgi protein: Golgin-84. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHGRI,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1963 EP 1963 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601957 ER PT J AU Steinert, PM Marekov, LN AF Steinert, PM Marekov, LN TI omega-hydroxy-ceramides of variable size are ester-linked to involucrin on the foreskin epidermal cornified cell envelope. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMSD,SKIN BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1970 EP 1970 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601964 ER PT J AU Kenney, NJ Washburn, T Afshari, C Buffusino, W Karach, K Barrett, JC AF Kenney, NJ Washburn, T Afshari, C Buffusino, W Karach, K Barrett, JC TI The response of null estrogen receptor mammary parenchyma and mesenchyme in vivo SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIEHS,NIH,RES TRIANGLE PK,NC 27550. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 1976 EP 1976 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601969 ER PT J AU Lo, CS Ginsburg, E Vonderhaar, BK AF Lo, CS Ginsburg, E Vonderhaar, BK TI Triiodothyronine enhances prolactin-induced human breast cancer cell proliferation. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PHYSIOL,BETHESDA,MD 20814. NCI,TUMOR IMMUNOL & BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2004 EP 2004 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602000 ER PT J AU Jamur, MC Siraganian, RP Oliver, C AF Jamur, MC Siraganian, RP Oliver, C TI Culture of immunomagnetically isolated mouse bone marrow derived mast cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV FED PARANA,BR-80060000 CURITIBA,PARANA,BRAZIL. NIDR,NIH,BETHESDA,MD 20892. OFF NAVAL RES,ARLINGTON,VA. RI Jamur, Maria Celia/L-5520-2016 OI Jamur, Maria Celia/0000-0001-7065-8543 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2007 EP 2007 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601999 ER PT J AU Malecki, M AF Malecki, M TI Multiple labeling of complex macromolecular bioassemblies for electron spectroscopic imaging. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV WISCONSIN,IMR,NIH,BIOTECHNOL RESOURCE & MOL BIOL LAB,MADISON,WI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2016 EP 2016 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602009 ER PT J AU Fauci, AS AF Fauci, AS TI Host factors in the pathogenesis of HIV disease. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2025 EP 2025 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602019 ER PT J AU Hsu, YT Wolter, KG Smith, CL Nechushtan, A Marrone, L Xi, XG Youle, RJ AF Hsu, YT Wolter, KG Smith, CL Nechushtan, A Marrone, L Xi, XG Youle, RJ TI Novel structural and functional relationships among members of the Bcl-2 family SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS,NIH,BIOCHEM SECT,SURG NEUROL BRANCH,BETHESDA,MD 20892. NINCDS,NIH,LIGHT MICROSCOPY FACIL,MOL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2035 EP 2035 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602029 ER PT J AU Liyanage, M Barlow, C Moens, PB Wangsa, D Deng, CX WynshawBoris, A Ried, T AF Liyanage, M Barlow, C Moens, PB Wangsa, D Deng, CX WynshawBoris, A Ried, T TI Molecular mechanisms for infertility and cancer in ataxia telangiectasia SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. YORK UNIV,DOWNSVIEW,ON,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2050 EP 2050 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602045 ER PT J AU Snyder, GA Brooks, AG Sun, PD AF Snyder, GA Brooks, AG Sun, PD TI Structure determination of p58 C143 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,NIH,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2076 EP 2076 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602072 ER PT J AU Chiantore, MV De Luca, LM AF Chiantore, MV De Luca, LM TI N-(4-hydroxyphenyl)-retinamide inhibits cell growth and induces apoptosis in retinoic acid-resistant cell lines: Correlation with transglutaminase II induction. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NATL INST HLTH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2115 EP 2115 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602107 ER PT J AU Ostap, EM Maupin, P Doberstein, SK Baines, IC Korn, ED Pollard, TD AF Ostap, EM Maupin, P Doberstein, SK Baines, IC Korn, ED Pollard, TD TI Acanthamoeba myosin-I isoforms concentrate to phagocytic and macropinocytic structures. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV PENN,SCH MED,DEPT PHYSIOL,PHILADELPHIA,PA 19104. JOHNS HOPKINS SCH MED,DEPT CELL BIOL & ANAT,BALTIMORE,MD. NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. SALK INST BIOL STUDIES,LA JOLLA,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2147 EP 2147 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602141 ER PT J AU Wang, ZY Wang, F Sobota, A Korn, ED Hammer, JA AF Wang, ZY Wang, F Sobota, A Korn, ED Hammer, JA TI Analysis of the regulatory phosphorylation site in Acanthamoeba myosin IC using site-directed mutagenesis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. NHLBI,MOL CARDIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2151 EP 2151 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602143 ER PT J AU Wu, X Kocher, B Wei, Q Lu, F Hammer, J AF Wu, X Kocher, B Wei, Q Lu, F Hammer, J TI Myosin V associates with microtubule-rich domains in both interphase and dividing cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,LCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2156 EP 2156 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602151 ER PT J AU Bonafe, N Sellers, JR AF Bonafe, N Sellers, JR TI Analyses of Drosophila myosin V. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,LMC,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2160 EP 2160 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602156 ER PT J AU Medeiros, NA Jaffe, H Reese, TS Bearer, EL AF Medeiros, NA Jaffe, H Reese, TS Bearer, EL TI Primary amino acid sequence information of a large brain myosin. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS,NIH,BETHESDA,MD 20892. BROWN UNIV,DEPT PATHOL,PROVIDENCE,RI 02912. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2166 EP 2166 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602162 ER PT J AU Muresan, V Lyass, A Zerfas, P Morreira, J Reese, TS Schnapp, BJ AF Muresan, V Lyass, A Zerfas, P Morreira, J Reese, TS Schnapp, BJ TI Conventional kinesin is not the motor for plus-end movement of vesicles purified from squid axoplasm. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,NEUROBIOL LAB,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2199 EP 2199 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602191 ER PT J AU Muresan, V Zerfas, P Lyass, A Reese, TS Schnapp, BJ AF Muresan, V Zerfas, P Lyass, A Reese, TS Schnapp, BJ TI Different vesicle populations in squid axoplasm contain different kinesin motors. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,NEUROBIOL LAB,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2204 EP 2204 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602199 ER PT J AU Lundberg, MS Brown, KD Curto, KA Monticone, R Spurgeon, H Crow, MT AF Lundberg, MS Brown, KD Curto, KA Monticone, R Spurgeon, H Crow, MT TI Mitogen-activated protein kinase and calcium/calmodulin protein kinase II signaling pathways in migrating vascular smooth muscle cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA,CARDIOVASC SCI LAB,NIH,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2235 EP 2235 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602227 ER PT J AU Adachi, M Iwasa, KH AF Adachi, M Iwasa, KH TI Force generation of the cochlear outer hair cell SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDCD,BIOPHYS SECT,LCB,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2249 EP 2249 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602243 ER PT J AU Yan, S Rodrigues, RG CahnHidalgo, D Walsh, TJ Roberts, DD AF Yan, S Rodrigues, RG CahnHidalgo, D Walsh, TJ Roberts, DD TI Hemoglobin induces a common receptor on Candida albicans for several extracellular matrix proteins SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2297 EP 2297 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602290 ER PT J AU Damjanovski, S Shi, YG AF Damjanovski, S Shi, YG TI Metalloproteinase stromelysin-3 in thyroid hormone induced apoptosis and morphogenesis. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,MOL EMBRYOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1997 VL 8 SU S BP 2346 EP 2346 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602338 ER PT J AU Morinaga, N Moss, J Vaughan, M AF Morinaga, N Moss, J Vaughan, M TI Cloning and expression of the cDNA encoding bovine brain brefeldin A-sensitive guanine nucleotide-exchange protein for ADP-ribosylation factor SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. 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