FN Thomson Reuters Web of Science™ VR 1.0 PT J AU BACIU, PC ACASTER, C GOETINCK, PF AF BACIU, PC ACASTER, C GOETINCK, PF TI MOLECULAR-CLONING AND GENOMIC ORGANIZATION OF CHICKEN SYNDECAN-4 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEPARAN-SULFATE PROTEOGLYCAN; HUMAN-LUNG FIBROBLASTS; ROUS-SARCOMA VIRUS; CELL-SURFACE; MEMBRANE PROTEOGLYCAN; CORE PROTEIN; SEQUENCE-ANALYSIS; GROWTH-FACTOR; RECEPTOR; INTEGRIN AB We have cloned and determined the genomic organization of the core protein of the chicken transmembrane proteoglycan, syndecan-4. Identification of the initial cDNA was accomplished using polyclonal antibodies directed against the cytoplasmic domain of murine syndecan-1 core protein. The cDNA for chicken syndecan-4 encodes a putative core protein of 197 amino acids which consists of a 19-amino acid signal peptide, a 125-amino acid ectodomain, a 25-amino acid transmembrane domain, and a 28-amino acid cytoplasmic domain. The predicted molecular mass of the mature core protein is 19,639 daltons. The ectodomain of chicken syndecan-4 core protein contains three potential sites for glycosaminoglycan attachment, two sites for N-glycosylation, and lacks a dibasic protease cleavage site proximal to the membrane-spanning region found in other syndecan family members. Comparison of the complete amino acid sequence with human syndecan-4 (amphlican (David, G., van der Schueren, B., Marynen, P., Cassiman, J. J., and van den Berghe, H. (1992) J. Cell Biol. 118, 961-969)) and rat syndecan-4 (ryudocan (Kojima, T., Shworak, N. W., and Rosenberg, R. D. (1992) J. Biol. Chem. 267, 4870-4877)) indicates an overall identity of 58 and 56%, respectively, with a 91 and 92% identity in the highly conserved transmembrane and cytoplasmic domains. The core protein of chicken syndecan-4 synthesized by chicken cells is modified with heparan sulfate side chains yielding a proteoglycan with a molecular mass of >200 kDa in LMH cells (immortalized male leghorn LM strain hepatocytes) and primary skin fibroblasts. Syndecan-4 isolated from chondrocyte cultures runs as a diffuse band between 100 and 200 kDa. Northern analysis of chicken syndecan-4 indicates three messages with distinct sizes of 0.9, 1.3, and 2.9 kb and a wide mRNA tissue distribution. The chicken syndecan-4 gene is divided into 5 exons encoding distinct regions which contain the signal peptide, the glycosaminoglycan attachment sites, a small spacer of unknown function, the glycosylation sites and the transmembrane and cytoplasmic domains. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED, CUTANEOUS BIOL RES CTR,MAH E BLDG 149, 13TH ST, BOSTON, MA 02129 USA. FU NCI NIH HHS [T32 CA 09579]; NICHD NIH HHS [HD 22050, HD 25938] NR 45 TC 34 Z9 35 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 7 PY 1994 VL 269 IS 1 BP 696 EP 703 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MR219 UT WOS:A1994MR21900109 PM 8276871 ER PT J AU GREEN, R SZOSTAK, JW AF GREEN, R SZOSTAK, JW TI IN-VITRO GENETIC-ANALYSIS OF THE HINGE REGION BETWEEN HELICAL ELEMENTS P5-P4-P6 AND ELEMENTS P7-P3-P8 IN THE STATE-UNIVERSITY-OF-NEW-YORK GROUP-I SELF-SPLICING INTRON SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE RIBOZYME; STRUCTURE; IN-VITRO SELECTION; BASE-TRIPLE; BULGE ID COMPLEMENTARY-STRAND RNA; RIBOSOMAL-RNA; TETRAHYMENA RIBOZYME; MINOR GROOVE; SECONDARY STRUCTURE; BINDING-SITE; SEQUENCE; CONFORMATION; SELECTION; GUANOSINE C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 36 TC 41 Z9 41 U1 1 U2 3 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 JAN 7 PY 1994 VL 235 IS 1 BP 140 EP 155 DI 10.1016/S0022-2836(05)80022-1 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MR304 UT WOS:A1994MR30400017 PM 7507168 ER PT J AU BASSING, CH YINGLING, JM HOWE, DJ WANG, TW HE, WW GUSTAFSON, ML SHAH, P DONAHOE, PK WANG, XF AF BASSING, CH YINGLING, JM HOWE, DJ WANG, TW HE, WW GUSTAFSON, ML SHAH, P DONAHOE, PK WANG, XF TI A TRANSFORMING GROWTH-FACTOR-BETA TYPE-I RECEPTOR THAT SIGNALS TO ACTIVATE GENE-EXPRESSION SO SCIENCE LA English DT Article ID CELL-PROLIFERATION; FAMILY AB Transforming growth factor beta (TGF-beta) is a multifunctional factor that regulates many aspects of cellular functions. TGF-beta signals through a heteromeric complex of the type I and type II TGF-beta receptors. However, the molecular mechanism of signal transduction by this receptor complex remains unresolved. The type II receptor belongs to a transmembrane receptor serine-threonine kinase family. A new member of this receptor family (R4) was identified and shown to be a functional TGF-beta type I receptor on the basis of its ability to restore a TGF-beta-induced gene response in mutant cell lines lacking endogenous type I receptor. Both ligand binding and signaling of the R4 protein were dependent on the presence of a functional type II receptor. The type I receptor has an intrinsic serine-threonine kinase activity, which was essential for signal transduction. C1 DUKE UNIV, MED CTR, DEPT PHARMACOL, DURHAM, NC 27710 USA. MASSACHUSETTS GEN HOSP, PEDIAT SURG RES LAB, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. FU NICHD NIH HHS [NICHD T32HD07396]; NIDDK NIH HHS [DK45746] NR 18 TC 282 Z9 286 U1 0 U2 3 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD JAN 7 PY 1994 VL 263 IS 5143 BP 87 EP 89 DI 10.1126/science.8272871 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MQ301 UT WOS:A1994MQ30100036 PM 8272871 ER PT J AU KOROSHETZ, WJ AF KOROSHETZ, WJ TI CASE-27-1993 - CEREBRAL VASCULITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP KOROSHETZ, WJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JAN 6 PY 1994 VL 330 IS 1 BP 67 EP 68 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MP649 UT WOS:A1994MP64900028 ER PT J AU KOPANS, DB AF KOPANS, DB TI RADIATION-INDUCED BREAST-CANCER SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 EI 1460-2105 J9 JNCI-J NATL CANCER I JI JNCI-. Natl. Cancer Inst. PD JAN 5 PY 1994 VL 86 IS 1 BP 66 EP 67 PG 2 WC Oncology SC Oncology GA MP650 UT WOS:A1994MP65000026 ER PT J AU KOPANS, DB AF KOPANS, DB TI ORGANOCHLORINES AND BREAST-CANCER SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 EI 1460-2105 J9 JNCI-J NATL CANCER I JI JNCI-. Natl. Cancer Inst. PD JAN 5 PY 1994 VL 86 IS 1 BP 66 EP 66 PG 1 WC Oncology SC Oncology GA MP650 UT WOS:A1994MP65000025 ER PT J AU DANDREA, AD CARROLL, M ZHU, Y MATHEYPREVOT, B AF DANDREA, AD CARROLL, M ZHU, Y MATHEYPREVOT, B TI THE ERYTHROPOIETIN RECEPTOR (EPO-R) DRIVES ERYTHROID-SPECIFIC DIFFERENTIATION IN A HEMATOPOIETIC PROGENITOR-CELL LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 4 EP 4 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200009 ER PT J AU HURFORD, RK PERVAIZ, S KLEINFIELD, R TEPPER, RL AF HURFORD, RK PERVAIZ, S KLEINFIELD, R TEPPER, RL TI IL-4 AS A MEDIATOR OF LOCALIZED INFLAMMATION AND TUMOR-CYTOTOXICITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,TUMOR BIOL LAB,BOSTON,MA 02129. RI Pervaiz, Shazib/C-4188-2015 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 5 EP 5 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200012 ER PT J AU HASS, R HIRANO, M KHARBANDA, S RUBIN, E MEINHARDT, G KUFE, D AF HASS, R HIRANO, M KHARBANDA, S RUBIN, E MEINHARDT, G KUFE, D TI RESISTANCE TO PHORBOL ESTER-INDUCED DIFFERENTIATION OF A U-937 MYELOID-LEUKEMIA CELL VARIANT WITH A SIGNALING DEFECT UPSTREAM TO RAF-1 KINASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 28 EP 28 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200097 ER PT J AU LORENZ, U RAVICHANDRAN, KS BURAKOFF, SJ CHANG, S NEEL, BG AF LORENZ, U RAVICHANDRAN, KS BURAKOFF, SJ CHANG, S NEEL, BG TI INVOLVEMENT OF SHPTP-1 IN T-CELL SIGNALING SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,MOLEC MED UNIT,BOSTON,MA 02215. DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 29 EP 29 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200101 ER PT J AU MILLER, SI AF MILLER, SI TI SALMONELLA COORDINATE GENE-REGULATION WITHIN MACROPHAGE PHAGOSOMES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 41 EP 41 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200138 ER PT J AU EFRAT, S LEISER, M SURANA, M FUSCODEMANE, D EMRAN, OA WU, YJ WEIR, G FLEISCHER, N AF EFRAT, S LEISER, M SURANA, M FUSCODEMANE, D EMRAN, OA WU, YJ WEIR, G FLEISCHER, N TI TRANSGENIC MOUSE MODELS FOR STUDYING THE ROLE OF GLUCOSE PHOSPHORYLATION IN BETA-CELL FUNCTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ALBERT EINSTEIN COLL MED,BRONX,NY 10461. JOSLIN DIABET CTR,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 124 EP 124 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200426 ER PT J AU RHODES, CJ AF RHODES, CJ TI THE UNIQUE REGULATION OF PROINSULIN BIOSYNTHESIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,JOSLIN RES LAB,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 125 EP 125 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200428 ER PT J AU HABENER, JF LEECH, CA HOLZ, GG AF HABENER, JF LEECH, CA HOLZ, GG TI MECHANISMS OF ACTION OF INSULINOTROPIC GLUCAGON-LIKE PEPTIDE-1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,HARVARD MED SCH,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA. RI Holz, George/A-3386-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 126 EP 126 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200430 ER PT J AU KAHN, CR CHUANG, LM REYNET, C BIRNBAUM, MJ AF KAHN, CR CHUANG, LM REYNET, C BIRNBAUM, MJ TI INTERACTIONS BETWEEN IRS-1, RAS AND RAS-RELATED PROTEINS IN INSULIN ACTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 129 EP 129 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200441 ER PT J AU MILLER, CP LIN, JC HABENER, JF AF MILLER, CP LIN, JC HABENER, JF TI CHARACTERIZATION OF HOMEOBOX PROTEINS EXPRESSED IN RAT PANCREATIC-ISLETS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 136 EP 136 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200463 ER PT J AU BASKIN, DG SCHWARTZ, MW GOLDSTEIN, BJ WHITE, MF AF BASKIN, DG SCHWARTZ, MW GOLDSTEIN, BJ WHITE, MF TI IRS-1 IN RAT-BRAIN - COLOCALIZATION WITH INSULIN-RECEPTORS AND PHOSPHOTYROSINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 VET AFFAIRS MED CTR,SEATTLE,WA 98195. UNIV WASHINGTON,SEATTLE,WA 98195. JEFFERSON MED COLL,PHILADELPHIA,PA 19107. JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. RI Schwartz, Michael/H-9950-2012 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 138 EP 138 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200472 ER PT J AU CHEATHAM, B VLAHOS, CJ CHEATHAM, L BLENIS, J KAHN, CR AF CHEATHAM, B VLAHOS, CJ CHEATHAM, L BLENIS, J KAHN, CR TI INHIBITION OF PI-3 KINASE BLOCKS INSULIN-STIMULATED DNA-SYNTHESIS, GLUCOSE-UPTAKE AND ACTIVATION OF PP70-S6 KINASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02215. JOSLIN DIABET CTR,BOSTON,MA 02215. LILLY CORP CTR,RES LABS,INDIANAPOLIS,IN 46285. RI Cheatham, Lynn/I-7649-2014 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 139 EP 139 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200473 ER PT J AU REYNET, C KAHN, CR AF REYNET, C KAHN, CR TI RAD - A NOVEL MEMBER OF THE RAS/GTPASE FAMILY OVER-EXPRESSED IN MUSCLE OF TYPE-II DIABETIC HUMANS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 143 EP 143 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200489 ER PT J AU HABENER, JF RON, D AF HABENER, JF RON, D TI INTERACTION OF THE NUCLEAR-PROTEIN CHOP WITH TRANSCRIPTIONAL FACTORS DURING ADIPOCYTE DIFFERENTIATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 150 EP 150 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200510 ER PT J AU KAHN, CR CHUANG, LM REYNET, C BIRNBAUM, MJ AF KAHN, CR CHUANG, LM REYNET, C BIRNBAUM, MJ TI INTERACTIONS BETWEEN IRS-1, RAS AND RAS-RELATED PROTEINS IN INSULIN ACTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 156 EP 156 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200528 ER PT J AU HOTAMISLIGIL, GH MURRAY, D CHOY, L SPIEGELMAN, BM AF HOTAMISLIGIL, GH MURRAY, D CHOY, L SPIEGELMAN, BM TI TNF-ALPHA INHIBITS SIGNALING FROM THE INSULIN-RECEPTOR - IMPLICATIONS FOR DIABETES-MELLITUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 169 EP 169 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200576 ER PT J AU CHEN, SY BAGLEY, J MARASCO, WA AF CHEN, SY BAGLEY, J MARASCO, WA TI HUMAN-LYMPHOCYTES INTRACELLULARLY EXPRESSING AN ANTI-GP120 SINGLE-CHAIN ANTIBODY ARE RESISTANT TO HIV-1 INFECTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED & PATHOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 249 EP 249 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200855 ER PT J AU TEDDER, TF SAUNDERS, KB KANSAS, GS LEY, K ZAKRZEWICZ, A GIBSON, RM FURIE, BC FURIE, B AF TEDDER, TF SAUNDERS, KB KANSAS, GS LEY, K ZAKRZEWICZ, A GIBSON, RM FURIE, BC FURIE, B TI MOLECULAR-BASIS FOR L-SELECTIN FUNCTION IN COMPARISON WITH P-SELECTIN AND E-SELECTIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DURHAM,NC 27710. DANA FARBER CANC INST,BOSTON,MA. FREE UNIV BERLIN,INST PHYSIOL,BERLIN,GERMANY. TUFTS UNIV,SCH MED,NEW ENGLAND MED CTR,BOSTON,MA 02111. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 261 EP 261 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200887 ER PT J AU JAIN, RK AF JAIN, RK TI AN IN-VIVO LOOK AT MICROCIRCULATION IN HEALTH AND DISEASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract ID NEOPLASTIC TISSUES; TUMOR MICROCIRCULATION; DIFFUSION; GROWTH; FLOW C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 14 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 262 EP 262 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200889 ER PT J AU UTANS, U ARCECI, RJ YAMASHITA, Y RUSSELL, ME AF UTANS, U ARCECI, RJ YAMASHITA, Y RUSSELL, ME TI IDENTIFICATION, CLONING AND CHARACTERIZATION OF A NOVEL GENE, ALLOGRAFT INFLAMMATORY FACTOR-I (AIF-1), UP-REGULATED IN RAT CARDIAC ALLOGRAFTS WITH TRANSPLANT ARTERIOSCLEROSIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH PUBL HLTH,CARDIOVASC BIOL LAB,BOSTON,MA 02115. DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 4 Z9 4 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 281 EP 281 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41200960 ER PT J AU ZAKRZEWICZ, A WALZOG, B KANSAS, GS TEDDER, TF GAEHTGENS, P LEY, K AF ZAKRZEWICZ, A WALZOG, B KANSAS, GS TEDDER, TF GAEHTGENS, P LEY, K TI L-SELECTIN PROMOTES NEUTROPHIL ADHESION TO FIBRONECTIN AND FIBRINOGEN UNDER CONDITION OF FLOW SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 FREE UNIV BERLIN,DEPT PHYSIOL,D-14194 BERLIN,GERMANY. DANA FABER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 301 EP 301 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41201034 ER PT J AU TEDDER, TF SAUNDERS, KB KANSAS, GS LEY, K ZAKRZEWICZ, A GIBSON, RM FURIE, BC FURIE, B AF TEDDER, TF SAUNDERS, KB KANSAS, GS LEY, K ZAKRZEWICZ, A GIBSON, RM FURIE, BC FURIE, B TI MOLECULAR-BASIS FOR L-SELECTIN FUNCTION IN COMPARISON WITH P-SELECTIN AND E-SELECTIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DURHAM,NC 27710. DANA FARBER CANC INST,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. FREE UNIV BERLIN,INST PHYSIOL,BERLIN,GERMANY. TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 311 EP 311 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41201057 ER PT J AU JAIN, RK AF JAIN, RK TI AN IN-VIVO LOOK AT MICROCIRCULATION IN HEALTH AND DISEASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract ID NEOPLASTIC TISSUES; TUMOR MICROCIRCULATION; DIFFUSION; GROWTH; FLOW C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 13 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 4 PY 1994 SU 18A BP 312 EP 312 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MV412 UT WOS:A1994MV41201059 ER PT J AU TAKAHASHI, T NOWAKOWSKI, RS CAVINESS, VS AF TAKAHASHI, T NOWAKOWSKI, RS CAVINESS, VS TI MODE OF CELL-PROLIFERATION IN THE DEVELOPING MOUSE NEOCORTEX SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DEVELOPING CEREBRAL-CORTEX; VENTRICULAR ZONE; PRECURSOR CELLS; STEM-CELLS; NEURONS; GENERATION; EXPRESSION; MIGRATION; MONKEY; CYCLE AB There are two proliferative populations in the developing cerebral wall: the pseudostratified ventricular epithelium (PVE) and the secondary proliferative population (SPP). The present experiments provide on embryonic day 14 (E14) in the mouse direct measures of the values for the proportions of daughter cells that continue to proliferate (proliferative, P fraction, or P) and for those that leave the cell cycle (quiescent, Q fraction, or Q; Q = 1 - P) for both of these populations. The range of values of P for the PVE, 0.62-0.66, would provide for the relatively low rate of neuronal output and for an expansion of the proliferative population appropriate for E14. The even higher values of P for the SPP, 0.73-1.0, would expand this population rapidly in preparation for the high glial cell output to occur later in cerebral histogenesis. C1 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT NEUROSCI & CELL BIOL,PISCATAWAY,NJ 08854. RP TAKAHASHI, T (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114, USA. RI Nowakowski, Richard/C-3217-2016; OI Nowakowski, Richard/0000-0002-5006-3670 FU NINDS NIH HHS [NS12005, NS28061] NR 38 TC 96 Z9 96 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 JAN 4 PY 1994 VL 91 IS 1 BP 375 EP 379 DI 10.1073/pnas.91.1.375 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MQ479 UT WOS:A1994MQ47900077 PM 8278397 ER PT B AU MCDERMOTT, T MACLEAN, J HUANG, FM BLOCH, KJ AF MCDERMOTT, T MACLEAN, J HUANG, FM BLOCH, KJ BE Healy, S TI EVALUATION OF TOTAL IMMUNOGLOBULIN-E LEVELS IN A PATIENT WITH ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS (ABPA) SO 20TH NATIONAL MEETING, CLINICAL LIGAND ASSAY SOCIETY, APRIL 26-30, 1994, KISSIMMEE, FLORIDA: SYLLABUS LA English DT Meeting Abstract CT 20th National Meeting of the Clinical Ligand Assay Society CY APR 26-30, 1994 CL KISSIMMEE, FL SP CLIN LIGAND ASSAY SOC C1 MASSACHUSETTS GEN HOSP,CLIN IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CLINICAL LIGAND ASSAY SOC INC PI WAYNE PA PO BOX 67, WAYNE, MI 48184 PY 1994 BP 108 EP 108 PG 1 WC Endocrinology & Metabolism; Medical Laboratory Technology SC Endocrinology & Metabolism; Medical Laboratory Technology GA BA98L UT WOS:A1994BA98L00045 ER PT B AU OBRIEN, CP JONES, RT AF OBRIEN, CP JONES, RT BE Pletscher, A Ladewig, D TI METHODOLOGICAL ISSUES IN THE EVALUATION OF A MEDICATION FOR ITS POTENTIAL BENEFITS IN ENHANCING PSYCHOTHERAPY SO 50 YEARS OF LSD: CURRENT STATUS AND PERSPECTIVES OF HALLUCINOGENS LA English DT Proceedings Paper CT Symposium of the Swiss-Academy-of-Medical-Science - 50-Years of LSD - Current Status and Perspectives of Hallucinogens CY OCT 21-22, 1993 CL LUGANO-AGNO, SWITZERLAND SP SWISS ACAD MED SCI C1 UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA BN 1-85070-569-0 PY 1994 BP 213 EP 221 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA BC46P UT WOS:A1994BC46P00015 ER PT J AU EISENTHAL, S STOECKLE, JD EHRLICH, CM AF EISENTHAL, S STOECKLE, JD EHRLICH, CM TI ORIENTATION OF MEDICAL RESIDENTS TO THE PSYCHOSOCIAL-ASPECTS OF PRIMARY-CARE - INFLUENCE OF TRAINING-PROGRAM SO ACADEMIC MEDICINE LA English DT Article ID INTERNAL-MEDICINE; DEPRESSION; PATIENT; ATTITUDES; MORBIDITY; ANXIETY; CHOICE AB Purpose. To describe the attitudes of residents in general medicine to the psychosocial dimensions of primary care and to evaluate the influences of selected variables. Method. A cross-sectional analysis-of-variance design (two training programs involving residents in all three residency years) was used in the analysis of 21 psychosocial attitude items from a survey questionnaire completed by general medicine residents. In 1991-92, 77 general medicine residents in ambulatory care group practices associated with the Massachusetts General Hospital were surveyed. Eighteen of the residents were in a primary care program (PCP), and 59 were in a traditional medicine program (TMP). Results. The overall response late was 82% (63 of 77 residents), with slightly lower rates for four items. The residents' attitudes to the psychosocial role of the primary care physician were positive but with reservations: 55 (87%) endorsed asking psychosocial questions, while only 28 (44%) indicated that most internists felt competent to diagnose and treat. Most residents did not feel defensive about enacting the role (neither uncomfortable asking questions in ambulatory care settings, 58, 92%; nor nosey, 56, 89%; nor personally interfering, 47, 76%). Fifty-two residents (83%) perceived patients to be receptive to psychosocial questions, yet 31 (49%) indicated that patients were resistant to psychosocial attributions, and 48 (76%) indicated that patients need to be prompted to talk about life problems. The dearest and strongest influence on attitudes was setting: ambulatory care over inpatient (p <.0001). Overall, the responses of the residents from the PCP and TMP were more similar than different. Conclusion. The residents accepted the psychosocial role of the primary care physician, found it most appropriate in ambulatory care settings, felt ambivalent about their ability to carry it out, and assigned it a secondary priority in patient care. To interest residents in primary care, more training should be based in ambulatory care settings and more emphasis should be placed on improving residents' competency in psychosocial skills. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. RP EISENTHAL, S (reprint author), MASSACHUSETTS GEN HOSP,W END HOUSE,BOSTON,MA 02114, USA. NR 32 TC 16 Z9 16 U1 3 U2 3 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD JAN PY 1994 VL 69 IS 1 BP 48 EP 54 DI 10.1097/00001888-199401000-00014 PG 7 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA MR125 UT WOS:A1994MR12500019 PM 8286000 ER PT J AU PIERCE, ET CARR, DB DATTA, S AF PIERCE, ET CARR, DB DATTA, S TI EFFECTS OF EPHEDRINE AND PHENYLEPHRINE ON MATERNAL AND FETAL ATRIAL-NATRIURETIC-PEPTIDE LEVELS DURING ELECTIVE CESAREAN-SECTION SO ACTA ANAESTHESIOLOGICA SCANDINAVICA LA English DT Article DE ANESTHETIC TECHNIQUES, SPINAL; DRUGS, EPHEDRINE AND PHENYLEPHRINE; HORMONES, ATRIAL NATRIURETIC PEPTIDE; PREGNANCY, MATERNAL AND FETAL PLASMA ATRIAL PEPTIDE ID PLASMA-LEVELS; HUMAN-FETUS; HORMONE; BLOOD AB The effects of ephedrine and phenylephrine on fetal and maternal plasma atrial natriuretic peptide (ANP) concentrations were studied during 30 elective cesarean sections. After induction of spinal anesthesia, reductions from baseline maternal blood pressure were corrected with one of these presser agents administered in a double-blinded, randomized manner. Immediately following deliver), umbilical artery (UA) ANP concentrations were significantly higher than umbilical vein (UV) concentrations (pg/ml) for both groups (ephedrine, 120.8 +/- 64.0 vs. 86.8 +/- 40.8, phenylephrine, 125.0 +/- 54.2 vs. 72.4 +/- 31.7), but there were no differences between groups for UA and UV ANP levels. Postpartum maternal ANP concentrations were significantly higher than baseline values in both groups, but again there were no differences between groups. Correlations between total doses of ephedrine or phenylephrine and UA or UV ANP levels did not reach significance. Postpartum maternal (MV2), UA, and UV blood gas variables (pH, Pco(2), and Po-2) were also not different between groups. These data suggest that effects of presser doses of ephedrine (beta and alpha agonist) and phenylephrine (alpha agonist) on maternal and fetal ANP levels are not different. Therefore, 1) assuming these presser drugs stimulate ANP release, this stimulation is not solely mediated by beta receptors and 2) to the extent that fetal ANP influences feto-placental circulatory homeostasis, the effects of ephedrine and phenylephrine on this regulatory mechanism do not appear to be different. C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA. MASSACHUSETTS GEN HOSP,ANALGES PEPTIDE RES UNIT,BOSTON,MA. RP PIERCE, ET (reprint author), NEW ENGLAND DEACONESS HOSP,DEPT ANAESTHESIA,185 PILGRIM RD,BOSTON,MA 02215, USA. NR 13 TC 15 Z9 16 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-5172 J9 ACTA ANAESTH SCAND JI Acta Anaesthesiol. Scand. PD JAN PY 1994 VL 38 IS 1 BP 48 EP 51 PG 4 WC Anesthesiology SC Anesthesiology GA MR578 UT WOS:A1994MR57800009 PM 8140873 ER PT J AU STROOP, WG BANKS, MC AF STROOP, WG BANKS, MC TI HERPES-SIMPLEX VIRUS TYPE-1 STRAIN KOS-63 DOES NOT CAUSE ACUTE OR RECURRENT OCULAR DISEASE AND DOES NOT REACTIVATE GANGLIONIC LATENCY IN-VIVO SO ACTA NEUROPATHOLOGICA LA English DT Article DE CORNEA; HSV-1; HERPESVIRUS; KERATITIS OCULAR DISEASE ID CENTRAL-NERVOUS-SYSTEM; INSITU HYBRIDIZATION; INFECTED NEURONS; DELETION MUTANT; RABBIT; MOUSE; TRANSCRIPT; ENCEPHALITIS; MODEL; RNA AB The virological, clinical, and histopathological manifestations of acute and experimentally reactivated infections of eyes and trigeminal ganglia have been studied following intranasal infection of rabbits with herpes simplex virus type 1 (strain KOS-63). All animals shed virus in nasal secretions, but only three shed virus in tear film during the first 12 days of infection. No animal developed clinical or histological evidence of corneal or retinal ocular disease at any time after infection. KOS-63 established trigeminal ganglionic latency; viral RNA, restricted to neuronal nuclei, was detected by in situ hybridization, and virus was recovered from co-cultivation cultures of nervous tissue, but not from cell-free homogenates. Reactivation of latent trigeminal ganglionic infection was attempted by intravenous administration of cyclophosphamide, followed by dexamethasone 24 h later. Injection of the drugs failed to reactivate KOS-63 latency; no animal shed virus in nasal or ocular secretions, and no animal developed gross or microscopic corneal lesions. In addition, viral antigens were not detected by immunofluorescence microscopy in ganglia from rabbits subjected to the drug protocol, and virus was only recovered from ganglia by in vitro co-cultivation reactivation techniques. The failure of KOS-63 to reactivate was not due to an inherent failure of populate and infect the ganglion, because the virus did not reactivate from ganglia that contained many latently infected cells. These studies demonstrate that, although KOS-63 is neuroinvasive and capable of establishing latency, it is virtually nonvirulent for the eye, and cannot be reactivated by a systemic immunosuppressive trigger known to reactivate other HSV-1 strains. C1 BAYLOR COLL MED,DEPT NEUROL,DEPT OPHTHALMOL,DIV MOLEC VIROL,HOUSTON,TX 77030. RP STROOP, WG (reprint author), BAYLOR COLL MED,CULLEN EYE INST,DEPT VET AFFAIRS MED CTR,OPHTHALMOL RES LAB,6501 FANNIN NC200,HOUSTON,TX 77030, USA. FU NIDCD NIH HHS [1R01 DC1706] NR 41 TC 13 Z9 13 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0001-6322 J9 ACTA NEUROPATHOL JI Acta Neuropathol. PD JAN PY 1994 VL 87 IS 1 BP 14 EP 22 PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA MP030 UT WOS:A1994MP03000003 PM 8140892 ER PT J AU NUECHTERLEIN, KH DAWSON, ME GREEN, MF AF NUECHTERLEIN, KH DAWSON, ME GREEN, MF TI INFORMATION-PROCESSING ABNORMALITIES AS NEUROPSYCHOLOGICAL VULNERABILITY INDICATORS FOR SCHIZOPHRENIA SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE SCHIZOPHRENIA; VULNERABILITY; INFORMATION PROCESSING; ATTENTION; MEMORY; NEUROPSYCHOLOGY ID CONTINUOUS PERFORMANCE-TEST; SUSTAINED ATTENTION; STARTLE-REFLEX; BACKWARD-MASKING; CHILDREN; RISK; DISORDERS AB Studies of schizophrenic patients in psychotic and clinically remitted states and of biological relatives indicate that subtle anomalies in information processing may be critical components of neuropsychological vulnerability to schizophrenia. We describe a conception of possible abnormalities and several recent strategies to differentiate these possibilities. Within Continuous Performance Test conditions, varying the perceptual load vs. the active, working memory load yields a distinction between a stable vulnerability factor across clinical states and a potential mediating vulnerability factor. Specialized backward masking paradigms offer ways to separate two initial sensory-perceptual processes from attentional shifting processes. Top-down attentional influences on sensorimotor gating allow examination of the role of central executive processes in modulating early sensory processes. Initial results are discussed. C1 UNIV SO CALIF, DEPT PSYCHOL, LOS ANGELES, CA 90089 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. RP UNIV CALIF LOS ANGELES, DEPT PSYCHIAT & BIOBEHAV SCI, 300 UCLA MED PLAZA, LOS ANGELES, CA 90024 USA. NR 40 TC 98 Z9 100 U1 1 U2 3 PU WILEY PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0001-690X EI 1600-0447 J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PY 1994 VL 90 SU 384 BP 71 EP 79 DI 10.1111/j.1600-0447.1994.tb05894.x PG 9 WC Psychiatry SC Psychiatry GA PW216 UT WOS:A1994PW21600011 PM 7879647 ER PT J AU MARDER, SR AF MARDER, SR TI THE ROLE OF DOSAGE AND PLASMA-LEVELS IN NEUROLEPTIC RELAPSE PREVENTION SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article; Proceedings Paper CT Lundbeck Symposium on the Role of Compliance in the Treatment of Schizophrenia CY NOV 12-13, 1993 CL COPENHAGEN, DENMARK SP LUNDBECK A S DE SCHIZOPHRENIA; ANTIPSYCHOTIC; FLUPHENAZINE; HALOPERIDOL ID FLUPHENAZINE DECANOATE; SCHIZOPHRENICS; THERAPY AB Recent research has focused on strategies for optimizing the long-term treatment of schizophrenia by decreasing relapse rates at the same time that antipsychotic drug side effects are minimized. Studies have suggested that substantially lowering the dose by as much as 80% can result in fewer side effects, less anxiety and depression, and improved compliance. However, dosage reduction can also lead to increases in the vulnerability to mild exacerbation of psychosis. A recent study from our laboratory indicates that supplementing low dose depot antipsychotic medications with oral supplementation at the time of prodromal symptoms may improve the safety of low doses. For patients who are treated with fluphenazine decanoate, monitoring plasma fluphenazine levels may also help to minimize relapse rates. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP MARDER, SR (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHIAT SERV 116A,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 9 TC 8 Z9 8 U1 6 U2 6 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-690X J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PY 1994 VL 89 SU 382 BP 25 EP 27 DI 10.1111/j.1600-0447.1994.tb05861.x PG 3 WC Psychiatry SC Psychiatry GA NU464 UT WOS:A1994NU46400005 ER PT J AU PARDEE, AB AF PARDEE, AB TI GROWTH DYSREGULATION IN CANCER-CELLS SO ADVANCES IN CANCER RESEARCH, VOL 65 SE ADVANCES IN CANCER RESEARCH LA English DT Review ID THYMIDINE KINASE PROMOTER; RESTRICTION POINT CONTROL; LABILE PROTEIN; DNA-SYNTHESIS; G1/S PHASE; TRANSCRIPTION; PROLIFERATION; STABILITY; BINDING; CYCLE RP PARDEE, AB (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM 24571] NR 40 TC 8 Z9 8 U1 1 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0065-230X J9 ADV CANCER RES JI Adv.Cancer Res. PY 1994 VL 65 BP 213 EP 228 DI 10.1016/S0065-230X(08)60070-6 PG 16 WC Oncology SC Oncology GA BB94M UT WOS:A1994BB94M00007 PM 7879668 ER PT J AU GARG, HG VONDEMBRUCH, K KUNZ, H AF GARG, HG VONDEMBRUCH, K KUNZ, H TI DEVELOPMENTS IN THE SYNTHESIS OF GLYCOPEPTIDES CONTAINING GLYCOSYL L-ASPARAGINE, L-SERINE, AND L-THREONINE SO ADVANCES IN CARBOHYDRATE CHEMISTRY AND BIOCHEMISTRY, VOL 50 SE ADVANCES IN CARBOHYDRATE CHEMISTRY AND BIOCHEMISTRY LA English DT Review ID SOLID-PHASE SYNTHESIS; CARBOXY PROTECTING GROUPS; SELECTIVE ENZYMATIC REMOVAL; BOVINE SERUM-ALBUMIN; ANTIGEN SIDE-CHAIN; O-GLYCOPEPTIDES; PEPTIDE-SYNTHESIS; ALLYL ESTER; STEREOSELECTIVE SYNTHESIS; LINKED GLYCOPEPTIDES C1 UNIV MAINZ,INST ORGAN CHEM,D-55128 MAINZ,GERMANY. RP GARG, HG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. NR 114 TC 85 Z9 85 U1 1 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0065-2318 J9 ADV CARBOHYD CHEM BI JI Adv.Carbohydr.Chem.Biochem. PY 1994 VL 50 BP 277 EP 310 DI 10.1016/S0065-2318(08)60153-5 PG 34 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA BB09N UT WOS:A1994BB09N00006 PM 7942256 ER PT B AU SCHOMACKER, KT FLOTTE, TJ DEUTSCH, TF AF SCHOMACKER, KT FLOTTE, TJ DEUTSCH, TF BE Alfano, RR Katzir, A TI DETECTION OF CHEMICALLY-INDUCED DYSPLASIA IN RAT URINARY-BLADDER WITH LASER-INDUCED FLUORESCENCE SO ADVANCES IN LASER AND LIGHT SPECTROSCOPY TO DIAGNOSE CANCER AND OTHER DISEASES SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Advances in Laser and Light Spectroscopy to Diagnose Cancer and Other Diseases CY JAN 23-24, 1994 CL LOS ANGELES, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1430-1 J9 P SOC PHOTO-OPT INS PY 1994 VL 2135 BP 76 EP 79 DI 10.1117/12.175983 PG 4 WC Oncology; Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Engineering; Radiology, Nuclear Medicine & Medical Imaging GA BA44F UT WOS:A1994BA44F00009 ER PT J AU LIPTON, SA YEH, M DREYER, EB AF LIPTON, SA YEH, M DREYER, EB TI UPDATE ON CURRENT MODELS OF HIV-RELATED NEURONAL INJURY - PLATELET-ACTIVATING-FACTOR, ARACHIDONIC-ACID AND NITRIC-OXIDE SO ADVANCES IN NEUROIMMUNOLOGY LA English DT Article; Proceedings Paper CT 3rd Workshop on Neuro-AIDS CY AUG 16-19, 1993 CL PORTLAND, ME SP NIAID, DIV AIDS ID RECEPTOR-MEDIATED NEUROTOXICITY; TUMOR-NECROSIS-FACTOR; VIRUS-INFECTED MACROPHAGES; NMDA RECEPTOR; COAT PROTEIN; MONONUCLEAR PHAGOCYTES; GLUTAMATE UPTAKE; CELL-CULTURES; GLIAL-CELLS; GP120 AB This review aims to summarize recent work related to the pathogenesis and possible treatment of neuronal injury in the acquired immunodeficiency syndrome (AIDS), especially with reference to potential neurotoxic substances released by HIV-infected or gp120-stimulated macrophages/microglia. Approximately a third of adults and half of children with AIDS eventually suffer from neurological manifestations, including dysfunction of cognition, movement, and sensation. Among the various pathologies reported in brains of patients with AIDS is neuronal injury and loss. A paradox arises, however, because neurons themselves are for all intents and purposes not infected by human immunodeficiency virus type 1 (HIV-1). This paper reviews recent evidence suggesting that at least part of the neuronal injury observed in the brains of AIDS patients is related to excessive influx of Ca2+ after the release of potentially noxious substances from HIV-infected or gp120-stimulated macrophages/microglia. There is growing support for the existence of HIV- or immune-related toxins that lead indirectly to the injury or demise of neurons via a potentially complex web of interactions between macrophages (or microglia), astrocytes, and neurons. HIV-infected monocytoid cells (macrophages, microglia or monocytes), especially after interacting with astrocytes, secrete substances that potentially contribute to neurotoxicity. Not all of these substances are yet known, but they may include eicosanoids, i.e. arachidonic acid and its metabolites, as well as platelet-activating factor. Other candidate toxins include nitric oxide (NO), superoxide anion (O-2.(-)), and the N-methyl-D-aspartate (NMDA) agonist, cysteine. Similarly, macrophages activated by HIV-1 envelope protein gp120 also appear its factors can lead to increased glutamate release or decreased glutamate re-uptake. In addition, interferon-gamma (IFN-gamma) stimulation of macrophages induces release of the NMDA-like agonist, quinolinate. HIV-infected or gp120-stimulated macrophages also produce cytokines, including TNF-alpha and IL1-beta which contribute to astrocytosis. A final common pathway for neuronal susceptibility appears to be operative, similar to that observed in stroke, trauma, epilepsy, neuropathic pain and several neurodegenerative diseases, possibly including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves the activation of voltage-dependent Ca2+ channels and NMDA receptor-operated channels with resultant generation of free radicals, and therefore offers hope for future pharmacological intervention. C1 BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. RP LIPTON, SA (reprint author), CHILDRENS HOSP,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115, USA. NR 43 TC 47 Z9 47 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-5428 J9 ADV NEUROIMMUNOL JI Adv. Neuroimmunol. PY 1994 VL 4 IS 3 BP 181 EP 188 DI 10.1016/S0960-5428(06)80255-X PG 8 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA PP109 UT WOS:A1994PP10900006 PM 7874385 ER PT S AU MERAYOLLOVES, J FOSTER, CS AF MERAYOLLOVES, J FOSTER, CS BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI MURINE MODEL OF SEASONAL ALLERGIC CONJUNCTIVITIS (SAC) TO RAGWEED SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,HILLES IMMUNOL LAB,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 107 EP 110 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00027 ER PT S AU PEDROZASERES, M GOEI, S MERAYOLLOVES, J DUTT, JE ARRUNATEGUICORREA, V FOSTER, CS AF PEDROZASERES, M GOEI, S MERAYOLLOVES, J DUTT, JE ARRUNATEGUICORREA, V FOSTER, CS BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI EXPRESSION OF V beta T-CELL RECEPTOR (TCR) TRANSCRIPTS IN EYES, LYMPH NODES, AND SPLEEN IN EXPERIMENTAL MURINE KERATITIS SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,RHOADS MOLEC & HILLES IMMUNOL LABS,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 293 EP 296 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00070 ER PT S AU NEVES, RA RODRIGUEZ, A POWER, WJ PEDROZASERES, M FOSTER, CS AF NEVES, RA RODRIGUEZ, A POWER, WJ PEDROZASERES, M FOSTER, CS BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI THE VALUE OF COMBINED SERUM ANGIOTENSIN CONVERTING ENZYME AND GALLIUM SCAN IN THE DIAGNOSIS OF OCULAR SARCOIDOSIS SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,IMMUNOL SERV,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 353 EP 356 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00084 ER PT S AU POWER, WJ RODRIGUEZ, A NEVES, RA LANE, L FOSTER, CS AF POWER, WJ RODRIGUEZ, A NEVES, RA LANE, L FOSTER, CS BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI PROGNOSTIC VALUE OF ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES IN LIMITED OCULAR WEGENERS GRANULOMATOSIS SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,IMMUNOL & UVEITIS SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 365 EP 368 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00087 ER PT S AU FOSTER, CS DRAKE, M TURNER, FD CRABB, JL SANTOS, CI AF FOSTER, CS DRAKE, M TURNER, FD CRABB, JL SANTOS, CI BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI EFFICACY AND SAFETY OF 1% RIMEXOLONE OPHTHALMIC SUSPENSION VS PREDNISOLONE ACETATE (PRED-FORTE%) FOR TREATMENT OF UVEITIS SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 411 EP 415 PG 5 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00098 ER PT S AU NEVES, RA DUTT, JE RODRIGUEZ, A MERAYOLLOVES, J BELFORT, R FOSTER, CS AF NEVES, RA DUTT, JE RODRIGUEZ, A MERAYOLLOVES, J BELFORT, R FOSTER, CS BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI IMMUNOHISTOPATHOLOGY OF THE LACRIMAL GLAND IN AIDS-RELATED SICCA SYNDROME SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,IMMUNOL & UVEITIS SERV,BOSTON,MA 02114. RI Belfort Jr, Rubens/E-2252-2012 OI Belfort Jr, Rubens/0000-0002-8422-3898 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 453 EP 456 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00107 ER PT S AU RODRIGUEZ, A POWER, WJ NEVES, RA FOSTER, CS AF RODRIGUEZ, A POWER, WJ NEVES, RA FOSTER, CS BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI LONG-TERM SYSTEMIC ACYCLOVIR IN THE MANAGEMENT OF RECURRENT HERPES SIMPLEX KERATOUVEITIS SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,IMMUNOL & UVEITIS SERV,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 465 EP 468 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00110 ER PT B AU YOSHIKAWA, TT AF YOSHIKAWA, TT BE Powers, DC Morley, JE Coe, RM TI INFECTIOUS DISEASES, IMMUNITY, AND AGING - PERSPECTIVES AND PROSPECTS SO AGING, IMMUNITY, AND INFECTION LA English DT Proceedings Paper CT Aging, Immunity, and Infection Symposium CY SEP, 1992 CL ST LOUIS, MO C1 US DEPT VET AFFAIRS,OFF GERIATR & EXTENDED CARE,WASHINGTON,DC. NR 0 TC 10 Z9 10 U1 0 U2 0 PU SPRINGER PUBL CO PI NEW YORK PA 536 BROADWAY, NEW YORK, NY 10012 BN 0-8261-8180-5 PY 1994 BP 1 EP 11 PG 11 WC Geriatrics & Gerontology; Immunology SC Geriatrics & Gerontology; Immunology GA BB77C UT WOS:A1994BB77C00001 ER PT J AU HARRER, E HARRER, T BUCHBINDER, S MANN, DL FEINBERG, M YILMA, T JOHNSON, RP WALKER, BD AF HARRER, E HARRER, T BUCHBINDER, S MANN, DL FEINBERG, M YILMA, T JOHNSON, RP WALKER, BD TI HIV-1-SPECIFIC CYTOTOXIC T-LYMPHOCYTE RESPONSE IN HEALTHY, LONG-TERM NONPROGRESSING SEROPOSITIVE PERSONS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INFECT DIS UNIT,BOSTON,MA 02114. DEPT PUBL HLTH,SAN FRANCISCO,CA 94102. NCI,FREDERICK,MD 21702. UNIV CALIF SAN FRANCISCO,GLADSTONE INST VIROL & IMMUNOL,SAN FRANCISCO,CA 94141. UNIV CALIF DAVIS,DAVIS,CA 95616. NR 0 TC 42 Z9 42 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. PY 1994 VL 10 SU 2 BP S77 EP S78 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800037 PM 7532426 ER PT J AU JOHNSON, RP HAMMOND, SA TROCHA, A SILICIANO, RF WALKER, BD AF JOHNSON, RP HAMMOND, SA TROCHA, A SILICIANO, RF WALKER, BD TI EPITOPE SPECIFICITY OF MHC RESTRICTED CYTOTOXIC T-LYMPHOCYTES INDUCED BY CANDIDATE HIV-1 VACCINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS ID TYPE-1 ENVELOPE GLYCOPROTEIN; IDENTIFICATION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. RP JOHNSON, RP (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,149 13TH ST,BOSTON,MA 02129, USA. NR 7 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S73 EP S75 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800036 PM 7532425 ER PT J AU RABINOWITZ, JL BRAND, JG COWART, BJ ENGEN, RL AF RABINOWITZ, JL BRAND, JG COWART, BJ ENGEN, RL TI HEPATIC LIPID PROFILES IN MINIATURE PIGS AFTER ALCOHOL FEEDING SO ALCOHOL LA English DT Article DE ALCOHOL; LIVER LIPIDS; NEUTRAL LIPIDS; POLAR LIPIDS; PHOSPHOLIPIDS; SATURATED FATTY ACIDS; UNSATURATED FATTY ACIDS; MINIATURE PIG AB Changes in lipid profiles have not been reported for the known increases in total lipid content in livers of alcoholics. We have reported a lowering of the P-oxidative capacity of alcoholic livers, and therefore would expect a lower turnover of fatty acids in these livers, and thus a change in lipid profile. The percentage composition of saturated and unsaturated fatty acids in the liver of alcohol-fed miniature pigs versus the controls, as well as the function of distance from the main hepatic vein, have both been determined in this study involving the feeding of ethanol for one year. Livers of alcohol-fed miniature pigs contained more total lipids than those of controls. Results also indicated significantly higher percentages of free fatty acids and triglycerides in the alcohol-fed miniature pigs, and also an increase in percentage total neutral lipids. The effect of distance from the main blood source (and therefore oxygenation) gave a fatty acid profile that showed an increase in the ratio of saturated to unsaturated fatty acids with increasing distance from the right hepatic vein. This change in ratio was independent of alcohol feeding. C1 UNIV PENN,SCH DENT MED,PHILADELPHIA,PA 19104. MONELL CHEM SENSES CTR,PHILADELPHIA,PA 19104. IOWA STATE UNIV,DEPT VET PHYSIOL,AMES,IA 50011. RP RABINOWITZ, JL (reprint author), VET AFFAIRS MED CTR,UNIV & WOODLANDS AVE,PHILADELPHIA,PA 19104, USA. NR 27 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0741-8329 J9 ALCOHOL JI Alcohol PD JAN-FEB PY 1994 VL 11 IS 1 BP 25 EP 29 DI 10.1016/0741-8329(94)90007-8 PG 5 WC Substance Abuse; Pharmacology & Pharmacy; Toxicology SC Substance Abuse; Pharmacology & Pharmacy; Toxicology GA MV745 UT WOS:A1994MV74500005 PM 8142063 ER PT J AU SASAKI, Y HAYASHI, N ITO, T FUSAMOTO, H KAMADA, T WANDS, JR AF SASAKI, Y HAYASHI, N ITO, T FUSAMOTO, H KAMADA, T WANDS, JR TI INFLUENCE OF ETHANOL ON INSULIN-RECEPTOR SUBSTRATE-1-MEDIATED SIGNAL-TRANSDUCTION DURING RAT-LIVER REGENERATION SO ALCOHOL AND ALCOHOLISM LA English DT Article; Proceedings Paper CT 14th Annual Conference of the Japanese-Society-for-Biomedical-Research-on-Alcohol CY FEB 02-03, 1994 CL SAPPORO, JAPAN SP Japanese Soc Biomed Res Alcohol ID GROWTH-FACTOR; PHOSPHATIDYLINOSITOL 3'-KINASE; HEPATIC REGENERATION; FACTOR-I; EXPRESSION; PROTEIN; PHOSPHORYLATION; STIMULATION; IRS-1; CELL AB Chronic ethanol exposure inhibits the capacity of the liver to regenerate. Insulin is a potent hepatotrophic factor, and tyrosyl phosphorylation (TP) of the intracellular insulin receptor substrate-1 (IRS-1) protein plays a crucial role in hepatocyte growth. The present investigation determined whether ethanol interferes with IRS-1-mediated signal transduction during liver regeneration induced by partial hepatectomy (PH) using the chronic ethanol-fed rat model. Tyrosyl phosphorylation of IRS-1 was strikingly increased and two peaks of TP were observed at 2 and 12 hr prior to the major wave of DNA synthesis in isocaloric pair-fed control animals; a blunted and delayed response was found in the ethanol-fed group. Furthermore, association of IRS-1 with phosphatidylinositol 3-kinase (PtdIns 3-kinase), a Src homology 2 (SH2) domain containing signal transduction molecule, was enhanced at 2 and 12 hr after PH in controls. In ethanol-fed rats, a single peak of association at 4 hr was observed. More important, PtdIns 3-kinase enzymatic activity was strikingly enhanced by the association with tyrosyl phosphorylated IRS-1 at 2 and 12 hr after PH, whereas in ethanol-fed animals this activity was greatly diminished and delayed to 6 and 36 hr, respectively. The biological consequence of this ethanol effect on TP of IRS-1 was a reduction and delay of the hepatic regenerative response after PH. These results indicate that one potential molecular mechanism whereby ethanol inhibits hepatocyte DNA synthesis is through its action on the IRS-1-mediated signal transduction pathway. C1 OSAKA UNIV,SCH MED,DEPT MED,SUITA,OSAKA 565,JAPAN. RP SASAKI, Y (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,SCH MED,MOLEC HEPATOL LAB,BOSTON,MA 02129, USA. NR 33 TC 13 Z9 13 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0735-0414 J9 ALCOHOL ALCOHOLISM JI Alcohol Alcohol. PY 1994 VL 29 SU 1 BP 99 EP 106 PG 8 WC Substance Abuse SC Substance Abuse GA RL748 UT WOS:A1994RL74800017 PM 9063828 ER PT J AU ROSENBERG, AE BROWN, GA BHAN, AK LEE, JM AF ROSENBERG, AE BROWN, GA BHAN, AK LEE, JM TI CHONDROID CHORDOMA - A VARIANT OF CHORDOMA - A MORPHOLOGIC AND IMMUNOHISTOCHEMICAL STUDY SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE BASE OF THE SKULL; CHONDROID CHORDOMA; CHONDROSARCOMA; CHORDOMA; IMMUNOHISTOCHEMISTRY ID EPITHELIAL MEMBRANE ANTIGEN; ECCHORDOSIS-PHYSALIPHORA; DIFFERENTIAL-DIAGNOSIS; CYTOKERATINS; ANTIBODIES; TUMORS AB In 1973, Heffelfinger and coworkers(6) described a variant of chordoma that contained cartilaginous areas indistinguishable from hyaline type chondrosarcoma. They designated these tumors chondroid chordomas and found that they had a better prognosis than classic (nonchondroid) chordomas. Since that time, there has been an ongoing debate over whether chondroid chordoma is best considered a distinct clinicopathologic entity separable from chondrosarcoma or a misdiagnosed chondrosarcoma whose concept developed from the erroneous interpretation of morphology. In an attempt to clarify the issue, the authors used light microscopy and immunohistochemistry to study 12 chondroid chordomas, 38 classic chordomas, and 28 chondrosarcomas that arose in the base of the skull or spine. As a reference, they also analyzed the immunohistochemical profile of fetal notochord, ecchordosis physaliphora, and fetal hyaline cartilage. They found that all chondroid and nonchondroid chordomas were positive for cytokeratin, and the majority werealso positive for epithelial membrane antigen (EMA) and carcinoembryonic antigen (CEA). In contrast, none of the chondrosarcomas stained for cytokeratin, EMA or CEA. Vimentin and S-100 were positive in more than 95% of both classic and chondroid chordomas and chondrosarcomas. The immunohistochemical profile of these tumors was similar to the pattern of immunoreactivity of their nonneoplastic counterparts. The authors conclude that chondroid chordomas is a variant of chordoma and should not be confused with chondrosarcoma. Because chondroid chordomas have been reported to have a better prognosis, they felt that this nosologic term should be preserved and that chondroid chordoma should continue to be a focus of clinical and pathologic study. C1 HARVARD UNIV,SCH MED,DIV HLTH SCI,BOSTON,MA. HARVARD UNIV,SCH MED,DIV TECHNOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT PATHOL,KUBRIK LAB NEUROPATHOL,BOSTON,MA. RP ROSENBERG, AE (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT LAB,WARREN 2,14 FRUIT ST,BOSTON,MA 02114, USA. NR 27 TC 97 Z9 104 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD JAN PY 1994 VL 101 IS 1 BP 36 EP 41 PG 6 WC Pathology SC Pathology GA MR302 UT WOS:A1994MR30200008 PM 7506477 ER PT J AU JONES, MA CLEMENT, PB YOUNG, RH AF JONES, MA CLEMENT, PB YOUNG, RH TI PRIMARY YOLK-SAC TUMORS OF THE MESENTERY - A REPORT OF 2 CASES SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE EXTRAGONADAL GERM CELL TUMORS; INTESTINES; MESENTERY; YOLK SAC TUMORS ID ENDODERMAL SINUS TUMOR; GERM-CELL TUMORS; SACROCOCCYGEAL TERATOMAS; INFANT VAGINA; CHILDREN; LIVER; CHEMOTHERAPY; MEDIASTINUM; CHILDHOOD; EXPERIENCE AB Two yolk sac tumors that arose in the mesentery of the jejunum and the mesentery of the transverse colon of two male patients, aged 2 and 17 years, are reported. Both patients had abdominal masses. The tumors measured 9 and 11 cm in maximum dimension. One of them grew into the bowel lumen. Microscopically, both neoplasms exhibited several of the typical patterns of yolk sac tumor and stained immunohistochemically for alpha-fetoprotein. Both patients received chemotherapy postoperatively and are alive, but follow-up is short. The subject of extragonadal yolk sec tumors is reviewed, and histogenetic implications of their occasional origin in the mesentery is discussed. C1 UNIV BRITISH COLUMBIA,VANCOUVER GEN HOSP,DEPT PATHOL,VANCOUVER V5Z 1M9,BC,CANADA. MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA. RP JONES, MA (reprint author), MAINE MED CTR,DEPT PATHOL,PORTLAND,ME 04102, USA. NR 78 TC 13 Z9 13 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD JAN PY 1994 VL 101 IS 1 BP 42 EP 47 PG 6 WC Pathology SC Pathology GA MR302 UT WOS:A1994MR30200009 PM 7506478 ER PT J AU JONES, EC YOUNG, RH AF JONES, EC YOUNG, RH TI THE DIFFERENTIAL-DIAGNOSIS OF PROSTATIC-CARCINOMA - ITS DISTINCTION FROM PREMALIGNANT AND PSEUDOCARCINOMATOUS LESIONS OF THE PROSTRATE GLAND SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Review DE ADENOSIS; ATYPICAL ADENOMATOUS HYPERPLASIA; BASAL CELL HYPERPLASIA; CRIBRIFORM HYPERPLASIA; MESONEPHRIC HYPERPLASIA; PROSTATIC CARCINOMA; PROSTATIC INTRAEPITHELIAL NEOPLASIA; PSEUDOCARCINOMATOUS PROSTATIC LESIONS; SCLEROSING ADENOSIS ID ADENOID CYSTIC CARCINOMA; BASAL-CELL HYPERPLASIA; TRANS-URETHRAL RESECTION; DUCT-ACINAR DYSPLASIA; INTRAEPITHELIAL NEOPLASIA; SCLEROSING ADENOSIS; CRIBRIFORM HYPERPLASIA; TOTAL PROSTATECTOMIES; ATYPICAL HYPERPLASIA; SEMINAL-VESICLE AB Prostate gland specimens account for a significant percentage of diagnostically challenging cases in surgical pathology practice. The understanding of prostate pathology has progressed, and the differential diagnosis of prostatic carcinoma has expanded to include possible premalignant lesions and several recently described pseudocarcinomatous lesions. The authors discuss the histopathology of prostatic intraepithelial neoplasia and atypical adenomatous hyperplasia, review the evidence for their role as premalignant lesions, and discuss the criteria that allow for their distinction from prostatic adenocarcinoma. Pseudocarcinomatous lesions that must be recognized when assessing prostatic tissue include sclerosing adenosis, cribriform hyperplasia, mesonephric hyperplasia, and basal cell hyperplasia. The pathologic features end diagnostic challenges of these and other pseudocarcinomatous lesions are reviewed. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV BRITISH COLUMBIA,DEPT PATHOL,VANCOUVER,BC,CANADA. RP JONES, EC (reprint author), VANCOUVER GEN HOSP,DEPT PATHOL,855 W 12TH AVE,VANCOUVER V5Z 1M9,BC,CANADA. NR 137 TC 36 Z9 38 U1 2 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD JAN PY 1994 VL 101 IS 1 BP 48 EP 64 PG 17 WC Pathology SC Pathology GA MR302 UT WOS:A1994MR30200010 PM 7506479 ER PT J AU WORNER, TM AF WORNER, TM TI PROPRANOLOL VERSUS DIAZEPAM IN THE MANAGEMENT OF THE ALCOHOL-WITHDRAWAL SYNDROME - DOUBLE-BLIND CONTROLLED TRIAL SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID CLINICAL MANAGEMENT; CEREBROSPINAL-FLUID; DRUG-THERAPY; IV-CLONIDINE; BENZODIAZEPINES; INTOXICATION; LOFEXIDINE AB Thirty-seven male alcoholics admitted electively for detoxification were randomized to treatment with either diazepam or propranolol. Subjects were comparable both in age and in duration and quantity of alcohol consumed. Admission laboratory parameters did not distinguish between the groups. Eleven subjects required no medication to control withdrawal signs/symptoms. Both groups showed improvement in blood pressure, pulse, and withdrawal tremor. None of the subjects randomized to diazepam manifested withdrawal seizures or hallucinations. By contrast, one subject in the propranolol group had a single withdrawal seizure. Another subject manifested increasing withdrawal that required parenteral paraldehyde treatment. Thus, this study confirms that a significant number of subjects admitted electively for alcohol withdrawal can be managed without medication. Minor tranquilizers still remain the ''gold standard'' for management of the withdrawal syndrome. C1 BRONX VET ADM MED CTR,DEPT MED,BRONX,NY. MT SINAI SCH MED,DEPT MED,NEW YORK,NY. NR 29 TC 25 Z9 25 U1 3 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1994 VL 20 IS 1 BP 115 EP 124 DI 10.3109/00952999409084061 PG 10 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA MY615 UT WOS:A1994MY61500009 PM 8192130 ER PT J AU TSUANG, JW SHAPIRO, E SMITH, TL SCHUCKIT, MA AF TSUANG, JW SHAPIRO, E SMITH, TL SCHUCKIT, MA TI DRUG-USE AMONG PRIMARY ALCOHOLIC VETERANS SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID TREATMENT PROGRAM; YOUNG ADULTHOOD; PATTERNS; ABUSE; PROGRESSION; ADOLESCENCE; RELAPSE; INVOLVEMENT; POPULATION; DEPENDENCE AB Many people with alcohol dependence use other drugs. However, not much is known about the relationship between their past drug use (not necessarily dependence) and their prognosis following treatment. The goal of this study is first to determine the drug use rates among primary alcoholic men and then to evaluate the possible relationship between past drug use and future alcohol or drug use relapse. As a result, 630 primary alcoholic veterans were recruited from a 28-day inpatient Alcohol and Drug Treatment Program at the San Diego VA Medical Center. Among them, almost two-thirds also had a history of drug use. Subjects were divided into the following four groups which were determined by their lifetime drug use histories: Group I (N = 226) consisted of drug abstainers, Group 2 (N = 142) was made up of alcoholics who had used only marijuana, Group 3 (N = 210) contained stimulant users who had never used opiates, and Group 4 (N = 52) included all opiate users. Comparisons of the four groups at a 3-month follow-up revealed that alcoholic men who had a history of stimulant or opiate use (Groups 3 and 4) were more likely to have had a drug use relapse. However, the four groups had similar alcohol relapse rates. C1 VET AFFAIRS MED CTR,DEPT PSYCHIAT,PSYCHIAT SERV 116A,SAN DIEGO,CA 92161. UNIV CALIF SAN DIEGO,SCH MED,SAN DIEGO,CA 92103. W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. FU NIAAA NIH HHS [NIAAA 05226, NIAAA 08403, NIAAA 08401] NR 35 TC 11 Z9 11 U1 4 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1994 VL 20 IS 4 BP 483 EP 493 DI 10.3109/00952999409109185 PG 11 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA PN615 UT WOS:A1994PN61500006 PM 7832181 ER PT J AU LERNER, TJ BOUSTANY, RMN MACCORMACK, K GLEITSMAN, J SCHLUMPF, K BREAKEFIELD, XO GUSELLA, JF HAINES, JL AF LERNER, TJ BOUSTANY, RMN MACCORMACK, K GLEITSMAN, J SCHLUMPF, K BREAKEFIELD, XO GUSELLA, JF HAINES, JL TI LINKAGE DISEQUILIBRIUM BETWEEN THE JUVENILE NEURONAL CEROID-LIPOFUSCINOSIS GENE AND MARKER LOCI ON CHROMOSOME 16P12.I SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID DISEASE; REGION; CLN3; MAPS AB The neuronal ceroid lipofuscinoses (NCL; Batten disease) are a collection of autosomal recessive disorders characterized by the accumulation of autofluorescent lipopigments in the neurons and other cell types. Clinically, these disorders are characterized by progressive encephalopathy, loss of vision, and seizures. CLN3, the gene responsible for juvenile NCL, has been mapped to a 15-cM region flanked by the marker loci D16S148 and D16S150 on human chromosome 16. CLN2, the gene causing the late-infantile form of NCL (LNCL), is not yet mapped. We have used highly informative dinucleotide repeat markers mapping between D16S148 and D16S150 to refine the localization of CLN3 and to test for linkage to CLN2. We find significant linkage disequilibrium between CLN3 and the dinucleotide repeat marker loci D16S288 (chi2(7) = 46.5, P < .005), D16S298 (chi2(6) = 36.6, P < .005), and D16S299 (chi2(7) = 73.8, P < .005), and also a novel RFLP marker at the D16S272 locus (chi2(1) = 5.7, P = .02). These markers all map to 16p12.1. The D16S298/D16S299 haplotype ''5/4'' is highly overrepresented, accounting for 54% of CLN3 chromosomes as compared with 8% of control chromosomes (chi2 = 117, df = 1, P < .001). Examination of the haplotypes suggests that the CLN3 locus can be narrowed to the region immediately surrounding these markers in 16p12.1. Analysis of D16S299 in our LNCL pedigrees supports our previous finding that CLN3 and CLN2 are different genetic loci. This study also indicates that dinucleotide repeat markers play a valuable role in disequilibrium studies. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. DUKE UNIV,MED CTR,DIV PEDIAT NEUROL,DURHAM,NC 27710. RP LERNER, TJ (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BLDG 149,13TH ST,BOSTON,MA 02129, USA. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00324]; NINDS NIH HHS [NINDS NS24279] NR 23 TC 45 Z9 47 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JAN PY 1994 VL 54 IS 1 BP 88 EP 94 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA MQ700 UT WOS:A1994MQ70000012 PM 8279474 ER PT J AU CRAIG, DJ AF CRAIG, DJ TI JOHNNY COMES HOME SO AMERICAN JOURNAL OF NURSING LA English DT Editorial Material RP CRAIG, DJ (reprint author), PORTLAND VET AFFAIRS MED CTR,NURSING HOME CARE UNIT,VANCOUVER,WA, 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 0002-936X J9 AM J NURS JI Am. J. Nurs. PD JAN PY 1994 VL 94 IS 1 BP 50 EP 51 PG 2 WC Nursing SC Nursing GA MQ529 UT WOS:A1994MQ52900020 PM 8273816 ER PT J AU LU, CB SCHUKNECHT, HF AF LU, CB SCHUKNECHT, HF TI PATHOLOGY OF PRELINGUAL PROFOUND DEAFNESS - MAGNITUDE OF LABYRINTHITIS FIBRO-OSSIFICANS SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article ID SENSORINEURAL HEARING-LOSS; MULTICHANNEL COCHLEAR IMPLANTS; SPIRAL GANGLION; CHILDREN AB Quantitative histologic studies were performed on 15 temporal bones from eight adult persons who were known to have prelingual bilateral profound hearing loss. The pathologic changes are characterized by severe degeneration of the structures of the cochlear duct, often with degeneration of the vestibular sense organs, causing a reparative host response that features osteoneogenesis and fibrous proliferation followed by retrograde neuronal degeneration. The pathology is consistent with meningogenic bacterial or viral labyrinthitis that occurred subclinically or went undiagnosed. Bone and fibrous tissue are present in varying extent in the scala tympani of 12 of the 15 temporal bones. Six cochleae from four subjects with fibro-osseous proliferation in the scala tympani extending as far as the ascending part of the basal turn have neuronal populations ranging from 963 to 5,355 (mean 2,826, 8% of neonatal normal, 35,500). In three cochleae from two subjects with no fibro-osseous proliferation in any area of the scala tympani the neuronal population ranges from 11,322 to 20,484 (mean 15,438, 43% of neonatal normal). Relative to cochlear implantation, computed tomographic imaging provides a means for determining the extent of fibro-osseous proliferation in the scala tympani, which in turn alerts the surgeon to surgical obstacles to optimal implantation as well as providing a basis for judging the extent of loss of cochlear neuronal population. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. TAINAN AF GEN HOSP,DEPT EAR NOSE & THROAT,TAINAN,TAIWAN. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. FU NIDCD NIH HHS [R01 DC00079] NR 29 TC 8 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD JAN PY 1994 VL 15 IS 1 BP 74 EP 85 PG 12 WC Otorhinolaryngology SC Otorhinolaryngology GA MP900 UT WOS:A1994MP90000018 PM 8109636 ER PT J AU LAKE, FR DEMPSEY, EC SPAHN, JD RICHES, DWH AF LAKE, FR DEMPSEY, EC SPAHN, JD RICHES, DWH TI INVOLVEMENT OF PROTEIN-KINASE-C IN MACROPHAGE ACTIVATION BY POLY(I-CENTER-DOT-C) SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE COMPLEMENT BF; INTERFERON-BETA; TUMOR NECROSIS FACTOR-ALPHA ID TUMOR-NECROSIS-FACTOR; MURINE PERITONEAL-MACROPHAGES; MESSENGER-RNA EXPRESSION; TUMORICIDAL ACTIVITY; INTERFERON-BETA; BACTERIAL LIPOPOLYSACCHARIDE; DOWN-REGULATION; PHORBOL ESTERS; CALCIUM; GAMMA AB The expression of cytocidal activity is initiated by the interaction of macrophages with priming [e.g., interferon (IFN)] and triggering stimuli (polyinosinic-polycytidylic acid). We have shown that the triggering step can be initiated in a Ca2+-dependent fashion and hypothesized that protein kinase C (PKC) may couple the Ca2+ signal to the expression of a gene product, Bf, that accompanies the expression of macrophage cytocidal activity. Exposure of IFN-primed macrophages to polyinosinic-polycytidylic acid in the presence of the PKC inhibitors H-7 or sphingosine or after downregulation of PKC with phorbol myristate acetate markedly inhibited Bf synthesis. Western blots of macrophage lysates revealed the presence of the alpha-, delta-, and zeta-isozymes of PKC, and all were found to be downregulated by phorbol myristate acetate. Inhibition of PKC also prevented the increase in IFN-beta mRNA levels and partially blocked the response to IFN-beta. These data suggest that the alpha-, delta-, and zeta-isozymes of PKC are involved in signaling leading to Bf expression and that the level of involvement is restricted to the induction and response to IFN-beta. C1 DENVER VET AFFAIRS MED CTR,DEPT MED,DIV PULM SCI,DENVER,CO 80206. UNIV COLORADO,HLTH SCI CTR,CARDIOVASC PULM RES LAB,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT BIOCHEM BIOPHYS & GENET,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT PHARMACOL,DENVER,CO 80262. RP LAKE, FR (reprint author), NATL JEWISH CTR IMMUNOL & RESP MED,DEPT PEDIAT,DIV BASIC SCI,DENVER,CO 80206, USA. FU DRS NIH HHS [BRSG-05357]; NCI NIH HHS [CA-50107] NR 37 TC 11 Z9 11 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP C134 EP C142 PN 1 PG 9 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100015 PM 8304411 ER PT J AU PIQUERAS, AI SOMERS, M HAMMOND, TG STRANGE, K HARRIS, HW GAWRYL, M ZEIDEL, ML AF PIQUERAS, AI SOMERS, M HAMMOND, TG STRANGE, K HARRIS, HW GAWRYL, M ZEIDEL, ML TI PERMEABILITY PROPERTIES OF RAT RENAL LYSOSOMES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE KIDNEY; MEMBRANE PERMEABILITY; PROTON ADENOSINE-TRIPHOSPHATASE; WATER PERMEABILITY; WATER CHANNELS ID LIPID BILAYER-MEMBRANES; CELL CHIP28 PROTEIN; WATER CHANNELS; TOAD BLADDER; PROTON PUMP; NONELECTROLYTE PERMEATION; URINARY-BLADDER; H+-ATPASE; VESICLES; INHIBITORS AB Although lysosomes maintain large pH gradients and may be subjected to significant osmotic gradients in vivo, little is known about their passive permeability properties. In recent studies, vacuolar H+-adenosinetriphosphatases (ATPases), such as those found in lysosomes, have been suggested to act as water channels. In addition, the erythrocyte and proximal tubule water channel CHIP28 is present on the plasma membrane of proximal tubule cells and may undergo endocytosis so that it is incorporated in lysosomes. We therefore examined water, proton, and small nonelectrolyte permeabilities in freshly purified lysosomes from rat renal proximal tubule. Lysosomes were purified by differential and Percoll gradient centrifugation. The preparation contained only lysosomes when examined by electron microscopy. Moreover, analysis by flow cytometry showed virtually all particles to be positive for acid phosphatase and cathepsin B activities. Permeabilities were measured on a stopped-flow fluorimeter by monitoring the self-quenching or pH-sensitive quenching of entrapped fluorescein derivatives. Osmotic water permeability (P-f) averaged 0.011 +/- 0.003 cm/s (n = 6), a value similar to that of biological membranes containing water channels. However, P-f was insensitive to the organic mercurial reagent p-chloromercuribenzene-sulfonate and to HgCl2 and exhibited an activation energy of 10.8 +/- 0.8 kcal/mol. These results indicate that water flux in lysosomes occurred via the lipid bilayer, and not via water channels. Addition of ATP led to lysosomal acidification (proton flux = 4.6 +/- 0.8 x 10(-11) mmol H+.s(-1).cm(-2)), which was completely inhibited by 0.1 mu M bafilomycin. P-f was insensitive to this agent as was the passive proton permeability (0.36 +/- 0.18 cm/s, n = 4). Permeabilities to small nonelectrolytes varied in proportion to the oil-water partition coefficient, confirming the applicability of Overton's rule to lysosomes. We conclude that proximal tubular lysosomes exhibit high P-f, which occurs via the lipid bilayer and not via vacuolar H+-ATPase. C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. BIOPURE CORP,BOSTON,MA 02111. VET ADM MED CTR W ROXBURY,BOSTON,MA 02132. UNIV WISCONSIN,MED & RES SERV,WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP PIQUERAS, AI (reprint author), CHILDRENS HOSP MED CTR,DEPT MED,BOSTON,MA 02111, USA. FU NIDDK NIH HHS [DK-38744, DK-43955, DK-46117] NR 55 TC 18 Z9 19 U1 1 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP C121 EP C133 PN 1 PG 13 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100014 PM 8304410 ER PT J AU GWOSDOW, AR OCONNELL, NA ABOUSAMRA, AB AF GWOSDOW, AR OCONNELL, NA ABOUSAMRA, AB TI INTERLEUKIN-1 INCREASES PROTEIN-KINASE-A ACTIVITY BY A CAMP-INDEPENDENT MECHANISM IN ATT-20 CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ADRENOCORTICOTROPIC HORMONE; ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE; 2ND MESSENGERS ID ANTERIOR-PITUITARY-CELLS; RECOMBINANT HUMAN INTERLEUKIN-1-ALPHA; CORTICOTROPIN-RELEASING FACTOR; NECROSIS-FACTOR-ALPHA; SIGNAL TRANSDUCTION; LINE ATT-20; BETA-ENDORPHIN; ACTH RELEASE; CYCLIC-AMP; IL-1 AB A recent study from this laboratory has shown that the inflammatory mediator, interleukin-1 alpha (IL-1 alpha), stimulates protein kinase A (PKA) activity and adrenocorticotropic hormone (ACTH) secretion from AtT-20 cells without any detectable increase in intracellular cAMP accumulation. The present studies were conducted to determine if cAMP is involved in IL-1 alpha activation of PKA and if PKA is responsible for IL-1 alpha-induced ACTH release from AtT-20 cells. The data are consistent with a novel, mechanism of PKA. activation that does not involve cAMP. Inhibition of adenylate cyclase with 2'5'-dideoxyadenosine (2'5'-DDA) did not affect IL-1 alpha-induced increases in PKA activity and ACTH secretion. In contrast, CRF-stimulated PKA activity and ACTH secretion were inhibited by 2'5'-DDA. Additional evidence was obtained using the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX). IBMX did not alter IL-1 alpha-induced PKA activity or ACTH secretion, yet IBMX potentiated CRF-induced cAMP accumulation. Inhibition of PKA with the PKA. inhibitor, H-8, blocked activation of PKA and ACTH secretion by both IL-1 alpha and CRF in AtT-20 cells. These observations demonstrate that 1) the mechanism of IL-1 alpha activation of PKA. is independent of adenylate cyclase or cAMP and 2) PKA is used by IL-1 alpha to induce ACTH secretion from AtT-20 cells. C1 SHRINERS BURNS INST,BOSTON,MA 02114. RP GWOSDOW, AR (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BULFINCH 3,FRUIT ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [NIDDK 1-R29-DK-41419] NR 30 TC 26 Z9 26 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP E79 EP E84 PN 1 PG 6 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100046 PM 7508195 ER PT J AU JAFFA, AA LEROITH, D ROBERTS, CT RUST, PF MAYFIELD, RK AF JAFFA, AA LEROITH, D ROBERTS, CT RUST, PF MAYFIELD, RK TI INSULIN-LIKE GROWTH-FACTOR-I PRODUCES RENAL HYPERFILTRATION BY A KININ-MEDIATED MECHANISM SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE RENAL KALLIKREIN; KININ RECEPTOR ANTAGONIST; RENAL VASODILATION ID GLOMERULAR MESANGIAL CELLS; DIETARY-PROTEIN; FILTRATION RATE; PLASMA-FLOW; KIDNEY; KALLIKREIN; EXPRESSION; BINDING; RNA AB Insulin-like growth factor-I (IGF-I) infusion into rats and humans reduces renal vascular resistance and raises glomerular filtration rate (GFR) and renal plasma flow (RPF). To investigate whether kinins mediate the renal vasodilatory effects of IGF-I, we infused rats with IGF-I alone or in the presence of a B-2 kinin receptor antagonist. Left kidney GFR, RPF, and kinin excretion were measured during infusion of vehicle and subsequently during 60-min infusion ofIGF-I or IGF-I plus kinin antagonist. IGF-I was given as a bolus (150 mu g/kg body wt), followed by infusion at a rate of 8.3 mu g.kg(-1).min(-1) for 60 min. The kinin antagonist was infused at a dose of 1 mu g.kg(-1).min(-1) for 60 min before the start of IGF-I infusion. GFR and RPF increased significantly after IGF-I infusion was begun, from baseline levels of 1.70 +/- 0.12 and 6.21 +/- 0.34 to 2.12 +/- 0.11 and 7.91 +/-: 0.29 ml/min, respectively, at 20 min (P < 0.001). This effect was maintained throughout 60 min of infusion. The increase in GFR and RPF was associated with a marked rise in urinary kinin excretion, from a baseline of 8.51 +/- 6.7 to 24.7 +/- 6.7 pg/min at 20 min and 40.3 +/- 10.4 pg/min at 40 min (P < 0.001). Pretreatment with the kinin receptor antagonist blocked the rise in GFR and RPF in response to IGF-I. These data suggest that the renal vasodilatory effect of IGF-I is mediated by kinins. C1 MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT BIOMETRY,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29425. NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. RP JAFFA, AA (reprint author), MED UNIV S CAROLINA,DEPT MED,DIV ENDOCRINOL DIABET & METAB,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 27 TC 26 Z9 26 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP F102 EP F107 PN 2 PG 6 WC Physiology SC Physiology GA NA598 UT WOS:A1994NA59800096 PM 8304475 ER PT J AU CENTORRINO, F BALDESSARINI, RJ KANDO, J FRANKENBURG, FR VOLPICELLI, SA PUOPOLO, PR FLOOD, JG AF CENTORRINO, F BALDESSARINI, RJ KANDO, J FRANKENBURG, FR VOLPICELLI, SA PUOPOLO, PR FLOOD, JG TI SERUM CONCENTRATIONS OF CLOZAPINE AND ITS MAJOR METABOLITES - EFFECTS OF COTREATMENT WITH FLUOXETINE OR VALPROATE SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Note ID DISORDER AB Serum concentrations of clozapine, norclozapine, and clozapine-N-oxide were assayed in psychotic patients treated with clozapine alone (N=17), clozapine with fluoxetine added (N=6), or clozapine with valproic acid added (N=11). Subjects were matched for age and other treatments, and concentrations were corrected for daily dose of clozapine (milligrams per kilogram of body weight). With valproic acid, there was a minor increase in total clozapine metabolites, which was even less with dose correction. Fluoxetine increased all clozapine analytes, in some cases to twice the levels in the subjects given only clozapine. C1 MCLEAN HOSP,MAILMAN RES CTR,BELMONT,MA 02178. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CLIN CHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. FU NIMH NIH HHS [NIMH MH-31154, NIMH MH-47370] NR 12 TC 162 Z9 162 U1 1 U2 2 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 JAN PY 1994 VL 151 IS 1 BP 123 EP 125 PG 3 WC Psychiatry SC Psychiatry GA MN949 UT WOS:A1994MN94900023 PM 8267110 ER PT J AU GAZELLE, GS GOLDBERG, MA WITTENBERG, J HALPERN, EF PINKNEY, L MUELLER, PR AF GAZELLE, GS GOLDBERG, MA WITTENBERG, J HALPERN, EF PINKNEY, L MUELLER, PR TI EFFICACY OF CT IN DISTINGUISHING SMALL-BOWEL OBSTRUCTION FROM OTHER CAUSES OF SMALL-BOWEL DILATATION SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article AB OBJECTIVE. Dilatation of the small bowel is a common finding on plain abdominal radiographs. In such cases, it is often difficult to determine if the cause of the dilatation is small bowel obstruction, paralytic ileus, or another intraabdominal disorder. Accordingly, we studied the efficacy of CT in making this distinction. MATERIALS AND METHODS. The medical records of 75 patients with small-bowel dilatation seen on CT scans (more than three segments > 2.5 cm in diameter) were reviewed. The patients were divided into three groups (obstruction [27 patients], other surgical diagnosis [16 patients], and no surgery [32 patients]) on the basis of clinical course, findings at surgery, or both. CT scans were retrospectively evaluated by two gastrointestinal radiologists who did not know the results of the chart review. They evaluated the images with regard to the following specific criteria for obstruction: presence/continuity of duodenal, small-bowel, and colonic dilatation; presence of air-fluid levels; amount of intestinal fluid; presence of prestenotic dilatation; presence of transition zone; and cause of obstruction. In addition, each radiologist gave an overall impression regarding the presence or absence of obstruction (criteria not specified to the observers) and its site, or other cause of bowel dilatation. The CT interpretations of each of the radiologists were compared with the patients' subsequent clinical course. RESULTS. Observer A was correct in 89%, 88%, and 72% of cases in the obstruction, other surgical diagnosis, and no surgery groups, respectively. Observer B was correct in 78%, 81%, and 69% of cases in the obstruction, other surgical diagnosis, and no surgery groups, respectively. Observer agreement regarding the proposed criteria for obstruction ranged from 65% to 91%. For both observers, only the presence of continuous small-bowel dilatation, prestenotic dilatation, and a transition zone correlated significantly with the presence of small-bowel obstruction. CONCLUSION. CT can be a useful test for evaluating small-bowel dilatation and can aid both the diagnosis of small-bowel obstruction and its differentiation from other conditions resulting in small-bowel dilatation. RP GAZELLE, GS (reprint author), MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 5 TC 86 Z9 90 U1 1 U2 1 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 JAN PY 1994 VL 162 IS 1 BP 43 EP 47 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MQ207 UT WOS:A1994MQ20700010 PM 8273687 ER PT J AU RIEUMONT, MJ WHITMAN, GJ AF RIEUMONT, MJ WHITMAN, GJ TI MESOBLASTIC NEPHROMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 5 TC 4 Z9 5 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 JAN PY 1994 VL 162 IS 1 BP 76 EP 76 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MQ207 UT WOS:A1994MQ20700018 PM 8273694 ER PT J AU BARBORIAK, DP PROVENZALE, JM BOYKO, OB AF BARBORIAK, DP PROVENZALE, JM BOYKO, OB TI MR DIAGNOSIS OF CREUTZFELDT-JAKOB-DISEASE - SIGNIFICANCE OF HIGH SIGNAL INTENSITY OF THE BASAL GANGLIA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID INVOLVEMENT AB OBJECTIVE, Creutzfeldt-Jakob disease is a rare dementing illness that usually affects older adults. Currently, neuroradiologic examinations play a minor role in the diagnosis of Creutzfeldt-Jakob disease. Several single case reports have noted a distinctive finding of hyperintense signal abnormalities in the basal ganglia on T2-weighted MR images of patients with Creutzfeldt-Jakob disease. In order to assess the diagnostic utility of this finding, we studied the imaging features of four patients with Creutzfeldt-Jakob disease in whom this MR finding was present. MATERIALS AND METHODS. Two neuroradiologists retrospectively reviewed the MR images of four patients who had pathologically proved Creutzfeldt Jakob disease and signal abnormalities in the basal ganglia on TS-weighted MR images. The patients' clinical findings were also analyzed. RESULTS. The four patients had MR examinations between 6 months and 1 year after the onset of symptoms. In all four cases, the hyperintense signal abnormalities in the basal ganglia on T2-weighted images were diffuse and bilaterally symmetric. The T1-weighted images were normal. A CT scan was obtained on a single patient and was normal. CONCLUSION. Although a lack of signal abnormality in the basal ganglia on MR imaging cannot be used to rule out a diagnosis of Creutzfeldt-Jakob disease, our experience and review of published reports suggest that in the proper clinical setting, bilaterally symmetric, diffuse hyperintense abnormalities in the basal ganglia on T2-weighted images may be a specific sign of Creutzfeldt-Jakob disease. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. DUKE UNIV,MED CTR,DEPT RADIOL,DURHAM,NC 27710. NR 12 TC 51 Z9 52 U1 0 U2 1 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 JAN PY 1994 VL 162 IS 1 BP 137 EP 140 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MQ207 UT WOS:A1994MQ20700030 PM 8273652 ER PT J AU FRANK, H WEISSLEDER, R BRADY, TJ AF FRANK, H WEISSLEDER, R BRADY, TJ TI ENHANCEMENT OF MR-ANGIOGRAPHY WITH IRON-OXIDE - PRELIMINARY STUDIES IN WHOLE-BLOOD PHANTOM AND IN ANIMALS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID CONTRAST AGENT AB OBJECTIVE. We hypothesized that the previously observed T1 effect of a small monocrystalline iron oxide preparation can be exploited to decrease T1 relaxation time of blood. Such a decrease, particularly if present for a long time, could be used to improve the quality of MR angiograms. To test the hypothesis, we performed phantom studies and in vivo animal experiments. MATERIALS AND METHODS. The effect of the monocrystalline iron oxide preparation on the MR signal intensity (spoiled gradient-recalled acquisition in the steady state pulse sequences, various timing parameters) of human whole blood was first tested in a phantom (dose range of monocrystalline iron oxide preparation, 0-3 mu mol Fe/ml). Subsequent experiments were performed in rats (n=7) and in rabbits (n=6) to determine whether predicted changes in signal intensity could be observed in vivo. RESULTS. Dose optimization studies in rats indicate that injected doses of 15-50 mu mol Fe/kg (0.8-2.8 mg Fe/kg) of monocrystalline iron oxide preparation resulted in threefold to fourfold increases of aortic signal-to-noise ratio. Because of its long plasma half-life (180 min in rats), the iron oxide preparation markedly improved the quality of images of the vasculature of the lungs, abdomen, and extremities. CONCLUSION. Our experimental results suggest that this and possibly other iron oxide preparations are alternatives to compounds containing macromolecular gadolinium and could be useful for clinical MR angiography. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,CTR MGH NMR,PHARMACEUT PROGRAM,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NCI NIH HHS [1RO1 CA59649-01, 5RO1 CA 54886-01] NR 10 TC 88 Z9 88 U1 0 U2 1 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 JAN PY 1994 VL 162 IS 1 BP 209 EP 213 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MQ207 UT WOS:A1994MQ20700044 PM 8273667 ER PT J AU SARANTOS, P CHAKRABARTI, R COPELAND, EM SOUBA, WW AF SARANTOS, P CHAKRABARTI, R COPELAND, EM SOUBA, WW TI DEXAMETHASONE INCREASES JEJUNAL GLUTAMINE-SYNTHETASE EXPRESSION VIA TRANSLATIONAL REGULATION SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 34th Annual Meeting of the Society-for-Surgery-of-the-Alimentary-Tract CY MAY 17-19, 1993 CL BOSTON, MA SP SOC SURG ALIMENTARY TRACT ID MESSENGER-RNAS; METABOLISM; IDENTIFICATION; ENDOTOXEMIA; TRANSPORT; SEPSIS AB Glutamine provides energy and precursors for nucleotide biosynthesis for the gut mucosa, and it is essential for intestinal metabolism and function. During stress states, glutamine uptake of circulating and luminal glutamine may be diminished, but the ability of the gut mucosa to synthesize glutamine de novo in response to this decreased delivery remains undefined. Since the glucocorticoids play an important role in regulating interorgan glutamine metabolism during catabolic states, we hypothesized that these hormones induce the expression of gut mucosal glutamine synthetase (GS), the enzyme that catalyzes the intracellular biosynthesis of glutamine. Adult rats were treated with dexamethasone (DEX, 0.5 mg/kg intraperitoneally) or saline (controls). At various times after treatment (4, 12, 24, 48, and 72 hours), jejunal mucosal GS-specific activity was assayed, and total RNA was extracted. GS transcripts were detected by Northern blot analysis, using a radiolabeled rat CS cDNA probe. Transcripts were quantitated by phospho-imaging and normalized to beta-actin. An anti-GS polyclonal antibody was used to quantitate GS protein concentrations by Western blot analysis. The relative quantities of GS translated were measured using a cell-free protein-synthesizing system (reticulocyte lysate assay). Data were analyzed using analysis of variance and were considered statistically significant for p < 0.05. DEX increased GS activity by 45% 12 hours after administration. Western blot analysis revealed an increase in the concentration of the GS protein in the jejunum of DEX-treated animals. Northern blot analysis demonstrated no significant change in CS mRNA levels after DEX treatment, indicating the possibility of posttranscriptional regulation. In vitro translational experiments demonstrated that the quantity of CS translated was increased by 25% after the administration of DEX. These data suggest that glucocorticoids may increase jejunal mucosal GS levels by accelerating protein translation. This adaptive response could provide glutamine for the gut mucosa during stress, when exogenous glutamine supplies may be rate limiting. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. UNIV FLORIDA,COLL MED,DEPT SURG,SURG METAB NUTR LABS,GAINESVILLE,FL. FU PHS HHS [T32] NR 23 TC 12 Z9 12 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD JAN PY 1994 VL 167 IS 1 BP 8 EP 13 DI 10.1016/0002-9610(94)90047-7 PG 6 WC Surgery SC Surgery GA MV407 UT WOS:A1994MV40700002 PM 7906101 ER PT J AU WATKINS, KT COPELAND, EM SOUBA, WW AF WATKINS, KT COPELAND, EM SOUBA, WW TI INDUCTION OF HEPATIC SYSTEM Y+-MEDIATED L-ARGININE TRANSPORT BY PROSTAGLANDIN E(2) SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 34th Annual Meeting of the Society-for-Surgery-of-the-Alimentary-Tract CY MAY 17-19, 1993 CL BOSTON, MA SP SOC SURG ALIMENTARY TRACT ID TUMOR NECROSIS FACTOR; GENE-EXPRESSION; PLASMA-MEMBRANE; ENDOTOXIN; INTERLEUKIN-1; METABOLISM; GLUTAMINE; CELLS; REGENERATION; MODULATION AB The in vivo effects of prostaglandin E(2) (PGE(2)) on L-arginine transport in rat liver were studied using hepatocyte plasma membrane vesicles (HPMVs). Adult rats were treated with a single intraperitoneal injection of PGE(2), and HPMVs were prepared by Percoll density gradient centrifugation at varying time points after PGE(2) administration. The activity of the sodium (Na+)-independent amino acid transport system y(+) (arginine) was evaluated by uptake of tritium-labeled L-arginine using a rapid mixing/filtration technique. Arginine uptake was Naf-independent and consisted of saturable and nonsaturable components. Saturable arginine transport was increased 50% compared with controls 1 hour after PGE(2) administration, at which time it reached peak effect. By P hours after PGE(2) treatment, arginine uptake had returned to control levels. Nonsaturable uptake (diffusion) was unaltered by PGE(2) treatment. Kinetic analysis showed a twofold increase in the V-max for system y(+) with no change in the K-m, consistent with an increase in the number of functional y(+) carriers in the plasma membrane. These data indicate that PGE(2) stimulates hepatic arginine transport in vivo and suggest that prostaglandins play an important role in regulating arginine availability to the liver during critical illness. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. UNIV FLORIDA,COLL MED,SURG METAB NUTR LABS,GAINESVILLE,FL. HARVARD UNIV,SCH MED,BOSTON,MA. FU NCI NIH HHS [T32-CA09605-03, CA 45327] NR 28 TC 8 Z9 9 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD JAN PY 1994 VL 167 IS 1 BP 128 EP 134 DI 10.1016/0002-9610(94)90063-9 PG 7 WC Surgery SC Surgery GA MV407 UT WOS:A1994MV40700018 PM 8311123 ER PT J AU EUBANKS, PJ SAWICKI, MP SAMARA, GJ GATTI, R NAKAMURA, Y TSAO, D JOHNSON, C HURWITZ, M WAN, YJY PASSARO, E AF EUBANKS, PJ SAWICKI, MP SAMARA, GJ GATTI, R NAKAMURA, Y TSAO, D JOHNSON, C HURWITZ, M WAN, YJY PASSARO, E TI PUTATIVE TUMOR-SUPPRESSOR GENE ON CHROMOSOME-11 IS IMPORTANT IN SPORADIC ENDOCRINE TUMOR-FORMATION SO AMERICAN JOURNAL OF SURGERY LA English DT Article ID NEOPLASIA TYPE-1; PARATHYROID TUMORS; SMALL REGION; GASTRINOMA; ALLELES; CANCER; HETEROZYGOSITY; IDENTIFICATION; LOCALIZATION; ASSOCIATION AB Endocrine tumors arising sporadically or as a manifestation of the multiple endocrine neoplasia type I syndrome (MEN I) have been shown to have mutations on chromosome 11. These mutations can be detected at the molecular level by loss of heterozygosity (LOH) for DNA markers from chromosome 11. This study represents one of the largest collections of sporadic endocrine tumors in which LOH was systematically assessed on chromosome 11 for the loci flanking the proposed MEN I region. DNA was isolated from 39 endocrine tumors and probed with ? DNA probes spanning the region of chromosome 11q13 from the loci PYGM to INT-2. Eleven tumors demonstrated LOH at any two loci in this region. The remaining 28 tumors showed no LOH or were noninformative at these loci. Thus, nearly 30% of these tumors showed LOH in the region (from PYGM to INT-2) that is thought to contain the MEN I gene(s). Previous studies of sporadic endocrine tumors have suggested that these tumors may arise via the same mechanism as tumors of the MEN I syndrome. Namely, these sporadic tumors are thought to result from mutations leading to genetic loss on the long arm of chromosome 11, thereby inactivating a possible tumor-suppressor gene (or genes). These findings strongly support the hypothesis that sporadic pancreatic endocrine tumors share a similar etiology of tumorigenesis with tumors of the MEN I syndrome, which principally involves deletion of a tumor-suppressor element (or elements). C1 UNIV CALIF LOS ANGELES, VET ADM WADSWORTH MED CTR W112, HARBOR MED CTR, DEPT SURG, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, HARBOR MED CTR, DEPT PATHOL, LOS ANGELES, CA USA. W LOS ANGELES VAMC, DEPT SURG, LOS ANGELES, CA USA. W LOS ANGELES VAMC, DEPT PATHOL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. ALBERTA CHILDRENS PROV GEN HOSP, DEPT GENET, CALGARY DIV BIOCHEM, CALGARY, AB, CANADA. CANC INST, TOKYO, TOKYO, JAPAN. NR 29 TC 59 Z9 59 U1 0 U2 1 PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC PI BRIDGEWATER PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD JAN PY 1994 VL 167 IS 1 BP 180 EP 185 DI 10.1016/0002-9610(94)90071-X PG 6 WC Surgery SC Surgery GA MV407 UT WOS:A1994MV40700026 PM 7906100 ER PT J AU CLEMENT, PB YOUNG, RH HANNA, W SCULLY, RE AF CLEMENT, PB YOUNG, RH HANNA, W SCULLY, RE TI SCLEROSING PERITONITIS ASSOCIATED WITH LUTEINIZED THECOMAS OF THE OVARY - A CLINICOPATHOLOGICAL ANALYSIS OF 6 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE OVARY; SCLEROSING PERITONITIS; LUTEINIZED THECOMA; LUTEIN CELLS ID LEIOMYOMATOSIS PERITONEALIS DISSEMINATA; FEMALE GENITAL-TRACT; STROMAL TUMORS; ABDOMINAL COCOON; LEVEEN SHUNT; DIALYSIS; FIBROMATOSIS; ASCITES; MESENTERITIS; PROPRANOLOL AB Six cases of a distinctive ovarian lesion associated with sclerosing peritonitis were found in patients 13 to 76 years of age. Five patients presented with abdominal swelling; on examination, three were found to have unilateral or bilateral pelvic masses, one had ascites and evidence of small bowel obstruction, and one had ascites alone. The sixth patient presented with small bowel obstruction. At operation, 1 to 9 L of ascitic fluid were found in five patients. Five patients with bilateral ovarian enlargement underwent bilateral oophorectomy or, in one case, bilateral ovarian wedge resection. The sixth patient had unilateral ovarian enlargement treated by unilateral oophorectomy. All had fibrotic thickening of the peritoneum, most prominently involving the omentum and small bowel, four at initial operation and two at a second operation performed shortly thereafter. One or more episodes of small bowel obstruction subsequently occurred in three of the five patients with follow-up. One woman died of pulmonary embolism 2 months after her initial operation; four were alive without clinical evidence of disease 8 months to 6 years postoperatively. Gross examination revealed unilateral (one case) or bilateral (two cases), predominantly solid ovarian tumors 12 to 31 cm in maximum dimension in three cases and slight enlargement and nodularity of both ovaries in the other three cases. Microscopic examination of the ovaries revealed a cellular proliferation of spindle cells with focal differentiation into nests of luteinized or partially luteinized cells; one case also had occasional foci of sex cord elements. The process was confined to the ovarian cor-tex in the three cases with slight ovarian enlargement. Residual ovarian follicles were entrapped by the proliferation in three cases, but were prominent in only one of them. Additional features included brisk mitotic activity, predominantly in the spindle cells, in three cases, and striking edema in the three cases with significant ovarian enlargement. The ovarian lesions were interpreted as luteinized thecomas, although a closely related hyperplasia with luteinization, instead of early neoplasia, cannot be excluded in the three cases with only slight ovarian enlargement (and in one, prominent entrapment of follicles). The peritoneal process consisted of a variably cellular proliferation of fibroblasts and myofibroblasts separated by collagen, fibrin, and occasional chronic inflammatory cells. These cases and two similar cases from the literature suggest a unique association between some luteinized thecomas (or a closely related proliferative lesion of the ovary) and sclerosing peritonitis, although the relation between the ovarian and peritoneal processes is presently enigmatic. C1 UNIV BRITISH COLUMBIA,VANCOUVER V6T 1W5,BC,CANADA. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV TORONTO,WOMENS COLL HOSP,DEPT PATHOL,TORONTO M5S 1A1,ONTARIO,CANADA. RP CLEMENT, PB (reprint author), VANCOUVER GEN HOSP,DEPT PATHOL,VANCOUVER V5Z 1M9,BC,CANADA. NR 70 TC 52 Z9 54 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD JAN PY 1994 VL 18 IS 1 BP 1 EP 13 DI 10.1097/00000478-199401000-00001 PG 13 WC Pathology; Surgery SC Pathology; Surgery GA MN376 UT WOS:A1994MN37600001 PM 8279621 ER PT J AU SCHOFIELD, DE FLETCHER, JA GRIER, HE YUNIS, EJ AF SCHOFIELD, DE FLETCHER, JA GRIER, HE YUNIS, EJ TI FIBROSARCOMA IN INFANTS AND CHILDREN - APPLICATION OF NEW TECHNIQUES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE FIBROSARCOMA; FIBROMATOSIS; CHROMOSOMAL ABERRATION; FLUORESCENCE IN-SITU HYBRIDIZATION ID FIBRO-SARCOMA; CONGENITAL FIBROSARCOMA; SYNOVIAL SARCOMA; CHROMOSOMES; TUMORS AB Fibrosarcomas occurring in infants and young children are intriguing tumors. Although biologically more benign than their counterparts occurring in old patients, they are histologically similar. Microscopically, they fit in one end of a spectrum of fibrous proliferations occurring in the pediatric population. Prompted by recent karyotypic reports of nonrandom gains of chromosomes 8, 11, 17, and 20 in infantile fibrosarcomas, we retrospectively analyzed 12 infantile fibrosarcomas utilizing fluorescence in-situ hybridization (FISH) with chromosome 8-, 11-, 17-, and 20-specific probes. Parallel studies were performed on fibrosarcomas occurring in older children and young adults and also on cellular fibromatoses, myofibromatoses, and fibromatoses. Gains of chromosomes 8, 11, 17, and 20 (in various combinations) were observed in 11 of 12 fibrosarcomas occurring in infants < 2 years of age. Extra copies of chromosomes 17 and 20 were observed in a fibrosarcoma occurring in a 5-year-old child but no abnormalities were detected by FISH in four additional fibrosarcomas occurring in patients aged 6-17 years. One of three cellular fibromatoses was characterized by extra copies of chromosome 8, 11, 17, and 20. Similar findings were not observed in any of the noncellular fibromatoses or in myofibromatoses. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. CHILDRENS HOSP,DEPT PATHOL,PITTSBURGH,PA 15213. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP SCHOFIELD, DE (reprint author), CHILDRENS HOSP MED CTR,DEPT PATHOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [1K11CA01498-03] NR 29 TC 90 Z9 92 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD JAN PY 1994 VL 18 IS 1 BP 14 EP 24 DI 10.1097/00000478-199401000-00002 PG 11 WC Pathology; Surgery SC Pathology; Surgery GA MN376 UT WOS:A1994MN37600002 PM 8279625 ER PT J AU ALBERT, MM RUSNAK, J LUTHER, MF GRAYBILL, JR AF ALBERT, MM RUSNAK, J LUTHER, MF GRAYBILL, JR TI TREATMENT OF MURINE CRYPTOSPORIDIOSIS WITH ANTICRYPTOSPORIDIAL IMMUNE RAT BILE SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID BOVINE COLOSTRUM; GIARDIA-MURIS; MONOCLONAL-ANTIBODIES; NEONATAL MICE; NUDE-MICE; PARVUM; IMMUNOCOMPETENT; NEUTRALIZATION; SPOROZOITES; PROTOZOAN AB Persistent cryptosporidiosis was established in nu/nu BALB/c mice by oral inoculation with Cryptosporidium parvum oocysts. The model was used to determine the impact of anticryptosporidial immune rat bile on the resolution of the disease. Presence of C. parvum-specific IgA in the immune rat bile was determined by enzyme-linked immunosorbent assay. Infection of mice was verified by stool analysis for oocysts and by hematoxylin and eosin-stained intestinal sections from control mice (infected but untreated). Efficacy of treatment was determined in control and treated mice by analysis of identical, hematoxylin and eosin-stained sections of the small intestine and cecum. Semiquantitative comparisons were made by determining the percent of crypts infected with Cryptosporidium organisms. The scores of treated mice were significantly lower then controls. Microscopic analysis of intestinal sections showed less villus atrophy, crypt hyperplasia, and fewer organisms per crypt in the immune bile-treated mice than in controls. These results support a role for humoral immunity in the eradication of cryptosporidiosis. C1 WILFORD HALL USAF MED CTR,DEPT INFECT DIS,LACKLAND AFB,TX 78236. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. RP ALBERT, MM (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT RES,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 35 TC 6 Z9 7 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD JAN PY 1994 VL 50 IS 1 BP 112 EP 119 PG 8 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA MW296 UT WOS:A1994MW29600017 PM 8304566 ER PT J AU MORRIS, EA TREADWELL, BV AF MORRIS, EA TREADWELL, BV TI EFFECT OF INTERLEUKIN-1 ON ARTICULAR-CARTILAGE FROM YOUNG AND AGED HORSES AND COMPARISON WITH METABOLISM OF OSTEOARTHRITIC CARTILAGE SO AMERICAN JOURNAL OF VETERINARY RESEARCH LA English DT Article ID NECROSIS-FACTOR-ALPHA; PROTEOGLYCAN SYNTHESIS; NEUTRAL PROTEASE; JOINT EFFUSIONS; CHONDROCYTES; INHIBITION; DEGRADATION; COLLAGENASE; SECRETION; INVITRO AB The effect of interleukin 1 (IL-1) on equine articular cartilage was investigated, using a cartilage explant culture system. Measurement of ([S]O4)-S-34 incorporation revealed synthesis of matrix proteoglycan by cartilage to be decreased 45, 59.7, and 37.5% after 1, 3, and 5 days, respectively, in culture in the presence of 5 U of IL-1/ml. There was no change in proteoglycan degradation as determined by measurement of ([S]O4)-S-34 release into the culture medium. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of cartilage-conditioned medium indicated that exposure of cartilage to IL-1 caused a decrease in total protein synthesis by 45, 68, and 87% after 1, 3, and 5 days, respectively, in culture while selectively inducing synthesis of the 57-kd neutral metalloproteinase stromelysin (matrix metalloproteinase-3) in young and adult horses. Identification of stromelysin was confirmed by functional characterization and immunoprecipitation. Baseline total protein synthesis, as well as specific synthesis of stromelysin in cartilage from adult and aged horses, was markedly less than that of young horses. The IL-1-induced reduction in total protein synthesis may not be a characteristic of equine articular cartilage from affected joints of horses with naturally acquired osteoarthritis as indicated by an overall increase in protein synthesis by osteoarthritic explants. Introduction of IL-1 into an equine articular cartilage explant culture system resulted in decrease of matrix component synthesis and increase in specific degradative enzyme synthesis and activity. Articular cartilage from aged horses had markedly less overall metabolic activity, compared with cartilage from young horses. Articular cartilage from affected joints of horses with naturally acquired osteoarthritis did not have metabolic alterations identical to those of IL-1-stimulated normal articular cartilage from the same individual, necessitating reevaluation of the validity of the IL-1-induced model of osteoarthritis. Osteoarthritis is a common, naturally acquired disease of horses, and tissue from animals of all ages and stages of osteoarthritis is available. The equine model of osteoarthritis may afford an important means of studying the alterations in articular cartilage metabolism as a function of age and disease severity. C1 TUFTS UNIV,SCH VET MED,DEPT MED,N GRAFTON,MA 01536. MASSACHUSETTS GEN HOSP,ORTHOPAED RES LABS,BOSTON,MA 02114. NR 40 TC 41 Z9 42 U1 0 U2 1 PU AMER VETERINARY MEDICAL ASSOC PI SCHAUMBURG PA 1931 N MEACHAM RD SUITE 100, SCHAUMBURG, IL 60173-4360 SN 0002-9645 J9 AM J VET RES JI Am. J. Vet. Res. PD JAN PY 1994 VL 55 IS 1 BP 138 EP 146 PG 9 WC Veterinary Sciences SC Veterinary Sciences GA MP547 UT WOS:A1994MP54700022 PM 8141486 ER PT B AU EFIRD, JT PARDO, F AF EFIRD, JT PARDO, F GP AMER STAT ASSOC TI A non-parametric two-sample survival test based on a single occupancy fermi-dirac model for the discrete range distribution SO AMERICAN STATISTICAL ASSOCIATION 1994 PROCEEDINGS OF THE BIOPHARMACEUTICAL SECTION LA English DT Proceedings Paper CT Spring Meeting of the Eastern-North-American-Region of the Biometric-Society CY APR 09-13, 1994 CL CLEVELAND, OH SP Biometric Soc, E N Amer Reg, Amer Stat Assoc, Sect Stat & Environm C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CYCLOTRON LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 BN 1-883276-05-5 PY 1994 BP 166 EP 170 PG 5 WC Pharmacology & Pharmacy; Statistics & Probability SC Pharmacology & Pharmacy; Mathematics GA BE02M UT WOS:A1994BE02M00029 ER PT B AU SMITH, ME FEILD, TC AF SMITH, ME FEILD, TC GP AMER STAT ASSOC TI Veterans and VA system users classified by federal poverty guidelines and thresholds and the VA means test SO AMERICAN STATISTICAL ASSOCIATION 1994 PROCEEDINGS OF THE GOVERNMENT STATISTICS SECTION LA English DT Proceedings Paper CT Annual Meeting of the American-Statistical-Association, Government-Statistics-Section CY AUG 13-18, 1994 CL TORONTO, CANADA SP Amer Stat Assoc, Govt Stat Sect DE POVERTY; HEALTH CARE REFORM C1 US DEPT VET AFFAIRS,WASHINGTON,DC 20420. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 BN 1-883276-11-X PY 1994 BP 28 EP 33 PG 6 WC Social Sciences, Mathematical Methods; Statistics & Probability SC Mathematical Methods In Social Sciences; Mathematics GA BD50Y UT WOS:A1994BD50Y00010 ER PT J AU SHORTEN, GD GOUDSOUZIAN, NG ALI, HH AF SHORTEN, GD GOUDSOUZIAN, NG ALI, HH TI HISTAMINE-RELEASE FOLLOWING ATRACURIUM IN THE ELDERLY - REPLY SO ANAESTHESIA LA English DT Letter RP SHORTEN, GD (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0003-2409 J9 ANAESTHESIA JI Anaesthesia PD JAN PY 1994 VL 49 IS 1 BP 74 EP 75 DI 10.1111/j.1365-2044.1994.tb03322.x PG 2 WC Anesthesiology SC Anesthesiology GA MT091 UT WOS:A1994MT09100022 ER PT S AU ANTONIADES, HN AF ANTONIADES, HN BE Maragoudakis, ME Gullino, PM Lelkes, PI TI CHRONIC CELLULAR INJURY AND HUMAN PROLIFERATIVE DISORDERS SO ANGIOGENESIS: MOLECULAR BIOLOGY, CLINICAL ASPECTS SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES A, LIFE SCIENCES LA English DT Proceedings Paper CT NATO Advanced Study Institute on Angiogenesis: Molecular Biology, Clinical Aspects CY JUN 16-27, 1993 CL RHODES, GREECE SP NATO C1 HARVARD UNIV,SCH PUBL HLTH,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0258-1213 BN 0-306-44713-4 J9 NATO ADV SCI INST SE PY 1994 VL 263 BP 233 EP 238 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BB56B UT WOS:A1994BB56B00025 ER PT J AU URENA, P ABOUSAMRA, AB JUPPNER, H KONG, XF LEE, K BRINGHURST, FR SEGRE, GV AF URENA, P ABOUSAMRA, AB JUPPNER, H KONG, XF LEE, K BRINGHURST, FR SEGRE, GV TI MODE OF ACTION OF THE PARATHYROID-HORMONE (PTH) AND THE PTH-RELATED PEPTIDE (PTHRP) IN CLASSICAL PTH-TARGET ORGANS SO ANNALES D ENDOCRINOLOGIE LA French DT Article DE PTH; PTHRP; RECEPTOR; CLONING ID EXPRESSION CLONING; HUMORAL HYPERCALCEMIA; PHOSPHATE-TRANSPORT; MOLECULAR-CLONING; PLASMA-MEMBRANE; MESSENGER-RNAS; FREE CALCIUM; CYCLIC-AMP; RECEPTOR; RAT AB Calcium and phosphorus metabolism is mainly regulated by PTH through its actions on kidney and bone. PTHrP, which is associated with the hypercalcemia of malignancy syndrome, binds to and activates the same receptor that PTH does. cDNA clones of PTH/PTHrP receptors from rat osteosarcoma (ROS 17/2.8) and opossum kidney (OK) cells are highly homologous and are members of a novel G protein-linked receptor family that includes calcitonin, glucagon, GLP-1, GHRH, VIP, and secretin receptors. Analysis of the protein sequence predicts a receptor with 7 transmembrane domains, a 155 amino acids (aa) extracellular (EC) N-terminal, and 130aa intracellular C-terminal domaina. The extracellular domain has 6 conserved cysteines and 4 potential glycosylation sites. When transfected in COS cells, both receptors are able to bind PTH and PTHrP active fragments with equal affinity. Likewise, agonists activate both adenylate cyclase and phospholipase C efficiently. The N-terminal EC domain and the first EC loop seem to determine the receptor binding capacity with the agonists. Activation of adenylate cyclase and phospholipase C might involve multiple sites between the 3rd helix and the C-terminal tail. Partial characterization of the rat PTH/PTHrP receptor gene demonstrates the existence of at least 15 exons. The first six transmembrane domains are encoded by separated exons. The PTH/PTHrP receptor mRNA is expressed mainly in kidney and bone, and also is widely expressed in many tissues, but not all. A major 2.3-2.5 kb transcript is observed in all these tissues. Nevertheless, 2 larger transcripts are observed in kidney and liver, and multiple smaller mRNA species are observed in kidney, skin, and testis. Whether the presence of multiple mRNA species represent the product of multiple transcriptional start sites, alternative polyadenylation site, alternative mRNA splicing, and/or mRNAs that are encoded by multiple genes is unknown. In conclusion, the cloning of the PTH/PTHrP receptors reveals that PTH and PTHrP can stimulate both adenylate cyclase and phospholipase C. These properties and the existence of multiple transcripts widely expressed in many tissues might explain the diversity of PTH and PTHrP actions. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. HOP NECKER ENFANTS MALAD,DEPT NEPHROL,F-75015 PARIS,FRANCE. RP URENA, P (reprint author), HOP NECKER ENFANTS MALAD,INSERM,U90,161 RUE SEVRES,F-75015 PARIS,FRANCE. NR 48 TC 5 Z9 5 U1 0 U2 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0003-4266 J9 ANN ENDOCRINOL-PARIS JI Ann Endocrinol. PY 1994 VL 55 IS 5 BP 133 EP 141 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PR611 UT WOS:A1994PR61100003 PM 7857077 ER PT J AU HYMAN, BT PENNEY, JB BLACKSTONE, CD YOUNG, AB AF HYMAN, BT PENNEY, JB BLACKSTONE, CD YOUNG, AB TI LOCALIZATION OF NON-N-METHYL-D-ASPARTATE GLUTAMATE RECEPTORS IN NORMAL AND ALZHEIMER HIPPOCAMPAL-FORMATION SO ANNALS OF NEUROLOGY LA English DT Article ID CENTRAL-NERVOUS-SYSTEM; AMINO-ACID RECEPTORS; BINDING-SITES; NEUROFIBRILLARY TANGLES; CORTICAL-NEURONS; RAT-BRAIN; DISEASE; AMPA; NEUROTRANSMITTER; PERMEABILITY AB The hippocampi and adjacent temporal cortices of 24 human brains were examined with antibodies to the GluR1, GluR2/3, and GluR4 subunits of the D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-preferring glutamate receptor. GluR1 immunoreactivity was most dense in the dentate gyrus, with lower densities in other hippocampal and cortical regions. GluR2/3 immunoreactivity was the most intense of the three antibodies, with high levels throughout most hippocampal subfields; where it was localized to cell bodies, proximal axons, and dendrites. GluR4 immunoreactivity was very sparse in all regions. In Alzheimer's disease brains, the general pattern of staining was similar to that seen in control brains. GluR1 and GluR4 immunoreactivity was seen in some but not all neuritic plaques. All three antibodies recognized some neurons undergoing neurofibrillary degeneration. C1 JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROSCI, BALTIMORE, MD 21205 USA. RP HYMAN, BT (reprint author), MASSACHUSETTS GEN HOSP, DEPT NEUROL, NEUROL RES LABS, WARREN 4, BOSTON, MA 02114 USA. FU NIA NIH HHS [AG08487, AG08671]; NIGMS NIH HHS [GM07309] NR 38 TC 24 Z9 24 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0364-5134 EI 1531-8249 J9 ANN NEUROL JI Ann. Neurol. PD JAN PY 1994 VL 35 IS 1 BP 31 EP 37 DI 10.1002/ana.410350106 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MQ911 UT WOS:A1994MQ91100004 PM 8285589 ER PT J AU CANELLOS, GP AF CANELLOS, GP TI CRITICAL-REVIEW OF THE ROLE OF HEMATOPOIETIC GROWTH-FACTORS IN DOSE INTENSIFICATION AND OUTCOME IN THE TREATMENT OF NON-HODGKINS-LYMPHOMA SO ANNALS OF ONCOLOGY LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CANELLOS, GP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 1994 VL 5 SU 2 BP S121 EP S122 PG 2 WC Oncology SC Oncology GA MZ486 UT WOS:A1994MZ48600022 ER PT J AU ROHATINER, AZS FREEDMAN, A NADLER, L LIM, J LISTER, TA AF ROHATINER, AZS FREEDMAN, A NADLER, L LIM, J LISTER, TA TI MYELOABLATIVE THERAPY WITH AUTOLOGOUS BONE-MARROW TRANSPLANTATION AS CONSOLIDATION THERAPY FOR FOLLICULAR LYMPHOMA SO ANNALS OF ONCOLOGY LA English DT Article DE AUTOLOGOUS BONE MARROW TRANSPLANTATION; MYELOABLATIVE THERAPY ID NON-HODGKINS-LYMPHOMA; SINGLE-AGENT CHEMOTHERAPY; NATIONAL-CANCER-INSTITUTE; MALIGNANT-LYMPHOMA; PROGNOSTIC FACTORS; POOR-PROGNOSIS; DOSE THERAPY; GRADE; TRANSFORMATION; COMBINATION AB Since June 1985, 121 patients with follicular lymphoma aged 24-61 years (median 43) have received myeloablative therapy (cyclophosphamide: 60 mg/kg x 2, + total body irradiation: 200 cGy X 6) with autologous bone marrow transplantation (CY + TBI + ABMT) as consolidation of 2nd or subsequent remission. The marrow mononuclear cell fraction was treated in vitro with anti-CD20 alone and baby rabbit complement at St. Bartholomew's Hospital (SBH) and with the addition of anti-B5 and anti-CD10 at the Dana Farber Cancer Institute (DFCI) prior to reinfusion. There were 4 treatment related deaths, (nonengraftment 1, haemorrhage 1, systemic fungal infection 1, veno-occlusive disease 1). The median time for neutrophil recovery (>0.5 X 10(9)/1) was 26 days (range 10 to 59 days), and for platelets (>20 X 10(9)/1), 30 days (range 12 to 73 days). One patient did not engraft and 7 have had delayed recovery of red cells and platelets (>3 months). Two other patients have subsequently developed acute myelogenous leukaemia and 5, evidence of myelodysplasia. Seventy-one patients continue in unmaintained remission between 3 months and 7 years, with a median follow up of 2.5 years. Forty-three have developed recurrent lymphoma; 98 remain alive. Freedom from progression was the same, irrespective of whether patients received CY + TBI + ABMT whilst in a complete or partial remission and did not depend on the specific remission in which treatment was given (2nd: 90 patients vs. >2nd: 31 patients). In comparison with an age-matched, remission-matched historical control group (treated at SBH prior to 1985), the freedom from progression curve for patients receiving CY + TBI + ABMT in 2nd remission is significantly better than that of patients receiving conventional therapy (p = 0.001). The survival curves have not diverged significantly. These preliminary results are encouraging - it remains to be established whether further modifications to the treatment will improve the results. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ROHATINER, AZS (reprint author), ST BARTHOLOMEWS HOSP,ICRF,DEPT MED ONCOL,LONDON ECIA,ENGLAND. NR 25 TC 2 Z9 2 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 1994 VL 5 SU 2 BP S143 EP S146 PG 4 WC Oncology SC Oncology GA MZ486 UT WOS:A1994MZ48600026 ER PT J AU SHAMBERGER, RC MACKLIS, RM SALLAN, SE AF SHAMBERGER, RC MACKLIS, RM SALLAN, SE TI RECENT EXPERIENCE WITH WILMS-TUMOR - 1978-1991 SO ANNALS OF SURGICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 46th Annual Cancer Symposium of the Society-of-Surgical-Oncology CY MAR 18-21, 1993 CL LOS ANGELES, CA SP SOC SURG ONCOL DE WILMS TUMOR; ADJUVANT CHEMOTHERAPY; CLEAR CELL SARCOMA OF KIDNEY; RHABDOID SARCOMA OF KIDNEY; RADIOTHERAPY ID PROGNOSTIC FACTORS; RADIATION-THERAPY; METASTASES; CHILDREN; DIAGNOSIS; KIDNEY; 2ND AB Background: The treatment of Wilms' tumor has undergone major advances in the past four decades. Current therapy is based on both the stage and pathology of the tumor. We have reviewed our recent experience with this tumor to assess the results of treatment on protocols that generally avoid the use of doxorubicin. Methods: Between January 1978 and December 1991 we treated 114 children with renal tumors. Ninety-one (80%) had favorable histology Wilms' tumor and 23 (20%), unfavorable histology tumors (13 anaplastic Wilms' tumors, four clear cell tumors of the kidney, and six sarcomatous tumors with rhabdoid elements). Chemotherapy was divided into two eras: 1978-1982 (vincristine and actinomycin-D) and 1983-1991 [vincristine and actinomycin-D for all patients, and cyclophosphamide for those with favorable histology and metastatic disease (n = 13) and all patients with anaplastic histology (n = 13)]. Four patients with clear cell or rhabdoid/sarcomatous tumor, three of whom are disease-free, were treated with a five-drug regimen (vincristine, doxorubin, cyclophosphamide, platinum, and VP-16). Approximately two thirds of the patients received megavoltage radiotherapy to the tumor bed. Mean abdominal radiation doses from 1978 to 1982 were slightly higher than those used from 1983 to 1991 (2,597 +/- 782 cGy vs. 2,039 +/- 524 cGy, respectively). Results: No isolated local failures were observed in any favorable histology patient who received radiotherapy. Among the 91 patients with favorable histology, there was no statistically significant difference in event-free survival irrespective of stage. Outcome for patients with anaplastic or clear cell variants was not different from that for those patients with favorable histology, but there were only small numbers in these groups for comparison. Only children with a rhabdoid/sarcomatous variant demonstrated survival that was different from all others (p = 0.00). Our previously reported patients with stage I tumors (<550 g) (n = 11) who were treated by nephrectomy only continue to have an excellent outcome (survival 100%). Conclusions: Wilms' tumors remain highly curable. Some unfavorable histology tumors require intensive therapy. Others such as our stage I tumors may be best observed without adjuvant therapy to avoid the toxicity of treatment. C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP SHAMBERGER, RC (reprint author), CHILDRENS HOSP MED CTR,JOINT CTR RADIAT THERAPY,DEPT SURG,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 28 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1068-9265 J9 ANN SURG ONCOL JI Ann. Surg. Oncol. PD JAN PY 1994 VL 1 IS 1 BP 59 EP 65 DI 10.1007/BF02303542 PG 7 WC Oncology; Surgery SC Oncology; Surgery GA NM328 UT WOS:A1994NM32800009 PM 7834430 ER PT J AU CHARLTON, B AUCHINCLOSS, H FATHMAN, CG AF CHARLTON, B AUCHINCLOSS, H FATHMAN, CG TI MECHANISMS OF TRANSPLANTATION TOLERANCE SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE THYMUS; DELETION; ANERGY; SUPPRESSION; CYTOKINE ID NATURAL SUPPRESSOR CELLS; TOTAL-LYMPHOID IRRADIATION; MAJOR HISTOCOMPATIBILITY COMPLEX; CARDIAC ALLOGRAFT SURVIVAL; BONE-MARROW CHIMERAS; CLASS-II MHC; ANTIGEN-PRESENTING CELLS; PANCREATIC BETA-CELLS; VERSUS-HOST-DISEASE; MATURE T-CELLS AB Transplantation tolerance, the long-term acceptance of grafted tissue in the absence of continuous immunosuppression, remains an elusive goal in humans, but it has been achieved in animal models using numerous approaches. The mechanisms behind graft acceptance vary according to the means used to create the state of acceptance. Several major mechanisms can now be recognized. While thymic deletion of T cells appears to be a mainstay of self-tolerance, its role in transplantation tolerance now seems to be less significant. In contrast, extrathymic mechanisms of transplantation tolerance seem to be major factors in long-term graft acceptance. If donor antigens are presented in a nonimmunogenic manner on the graft, e.g. due to modification of graft tissue by culture, peripheral T cells of the recipient may ignore the graft. Alternatively, nonstimulatory presentation of donor antigens on graft tissue can induce a state of unresponsiveness in recipient T cells, i.e. anergy, rather than activating them to destroy the graft. Suppression mechanisms also operate to control graft rejection and may be specific or nonspecific in nature. Specific suppression mechanisms might act in an idiotype or antigen-specific fashion, and evidence is accumulating that this may be mediated through the elaboration of cytokines. Donor antigen-specific T cells may be activated to produce ''protective'' cytokines which then regulate the generation of destructive T cells. Future therapies will be aimed at affecting graft acceptance through these peripheral mechanisms. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. RP CHARLTON, B (reprint author), STANFORD UNIV,SCH MED,DEPT MED,DIV RHEUMATOL & IMMUNOL,STANFORD,CA 94305, USA. NR 216 TC 118 Z9 119 U1 0 U2 2 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1994 VL 12 BP 707 EP 734 DI 10.1146/annurev.immunol.12.1.707 PG 28 WC Immunology SC Immunology GA NF487 UT WOS:A1994NF48700022 PM 8011295 ER PT J AU GERARD, C GERARD, NP AF GERARD, C GERARD, NP TI C5A ANAPHYLATOXIN AND ITS 7 TRANSMEMBRANE-SEGMENT RECEPTOR SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE INFLAMMATION; COMPLEMENT C5A ANAPHYLATOXIN; CHEMOTAXIS; G-PROTEIN COUPLED RECEPTORS; 7 TRANSMEMBRANE-SEGMENT RECEPTORS ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; COLONY-STIMULATING FACTOR; RESPIRATORY-DISTRESS SYNDROME; NEUTROPHIL CHEMOTACTIC FACTORS; RABBIT PERITONEAL NEUTROPHILS; ISCHEMIA-REPERFUSION INJURY; PROTEIN-COUPLED RECEPTORS; WHEAT-GERM-AGGLUTININ; LIGAND-BINDING SITE; DEPLETED HUMAN-SKIN AB The molecular cloning of the C5a receptor places this molecule in the superfamily of G-protein coupled receptors. This superfamily is characterized by the presence of signature motifs including seven hydrophobic domains which span the cell membrane and impart a predicted serpentine topology to the receptor proteins. The identification of other members of this family, including receptors for the chemokines IL-8 and Mip-1/Rantes, thrombin, formylpeptide, and platelet activating factor, provide new tools for understanding structure-function relationships relevant to the inflammatory process. This review focuses on the recent biological studies concerning the ligand C5a and its cellular receptor, the structure/activity relationships so far discerned, signal transduction mechanisms, progress toward identification of receptor antagonists, and some likely directions for future studies. Where appropriate, relevant work on related seven transmembrane segment receptors is discussed. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. RP GERARD, C (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PEDIAT,INA SUE PERLMUTTER LAB,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL 36162, HL 41587] NR 219 TC 353 Z9 358 U1 1 U2 8 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1994 VL 12 BP 775 EP 808 DI 10.1146/annurev.immunol.12.1.775 PG 34 WC Immunology SC Immunology GA NF487 UT WOS:A1994NF48700024 PM 8011297 ER PT J AU KING, GL SHIBA, T OLIVER, J INOGUCHI, T BURSELL, SE AF KING, GL SHIBA, T OLIVER, J INOGUCHI, T BURSELL, SE TI CELLULAR AND MOLECULAR ABNORMALITIES IN THE VASCULAR ENDOTHELIUM OF DIABETES-MELLITUS SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE ENDOTHELIAL CELLS; HYPERGLYCEMIA; DIACYLGLYCEROL/PROTEIN KINASE C; POLYOL; GLYCOSYLATION ID GLOMERULAR BASEMENT-MEMBRANE; GROWTH FACTOR-BETA; PROTEIN-KINASE-C; MESANGIAL CELLS; HIGH GLUCOSE; PERICYTES; COMPLICATIONS; RETINOPATHY; METABOLISM; MATRIX AB Diabetic vascular complications affect both micro- and macrovasculature, primarily in the retina, renal glomeruli, and multiple sites in the macrovessels. This review presents a summary of the abnormal function found in vivo and in cultured vascular cells exposed to elevated levels of glucose. We also discuss the various biochemical hypotheses that have been proposed to explain the adverse effects of hyperglycemia on vascular cells. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02215. RP KING, GL (reprint author), BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,DIV RES,BOSTON,MA 02215, USA. FU NEI NIH HHS [EY05110, EY09178] NR 40 TC 103 Z9 111 U1 1 U2 1 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1994 VL 45 BP 179 EP 188 DI 10.1146/annurev.med.45.1.179 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA NF168 UT WOS:A1994NF16800015 PM 8198375 ER PT J AU CONN, PM CROWLEY, WF AF CONN, PM CROWLEY, WF TI GONADOTROPIN-RELEASING-HORMONE AND ITS ANALOGS SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE GONADS; OVARY; TESTES; PITUITARY; LUTEINIZING HORMONE (LH); FOLLICLE STIMULATING HORMONE (FSH) ID POLYCYSTIC OVARIAN DISEASE; INOSITOL PHOSPHATE PRODUCTION; LUTEINIZING-HORMONE; HYPOTHALAMIC AMENORRHEA; PROSTATE-CANCER; LH-SECRETION; GNRH; AGONIST; DESENSITIZATION; INDUCTION AB GnRH and its analogues have led to exciting new avenues of therapy in virtually every subspecialty of internal medicine as well as in gynecology, pediatrics, and urology. Since their discovery in 1971, it has been demonstrated that GnRH and its analogues enable medical professionals to influence the hypothalamic-pituitary-gonadal axis in two distinct classes of therapeutic applications. The first provides natural sequence GnRH in a pulsatile fashion via portable infusion pumps to mimic the normal physiology of hypothalamic GnRH secretion and restores reproductive potential to infertile men and women with disorders of endogenous GnRH secretion. The second mode uses long-acting GnRH agonists administered in a depot delivery to produce a paradoxical desensitization of pituitary gonadotropin secretion which, in turn, results in a complete ablation of the reproductive axis. This biochemical castration induced by GnRH agonist administration is a safe, effective, complete, and reversible method of removing the overlay of gonadal steroids from a variety of diseases which they are known to exacerbate. These diseases include endometriosis and uterine fibroids in women, prostate cancer in men, and precocious puberty in both sexes. This review examines the physiologic and pharmacologic principles underlying the advances produced by these agents, the mechanism of action of GnRH and its analogues at the cellular level, and the individual therapeutic applications to which these analogues have been applied. Because virtually every subspecialty of medicine will be touched by the GnRH analogues, this review provides an overview and background of their use. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP CONN, PM (reprint author), UNIV IOWA,COLL MED,DEPT PHARMACOL,BOWEN SCI BLDG,IOWA CITY,IA 52242, USA. FU NICHD NIH HHS [U01 HD044417, HD 15080, HD19899, HD24697, P30 HD028138, R01 HD015788, U54 HD028138, U54 HD029164] NR 48 TC 242 Z9 243 U1 0 U2 13 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1994 VL 45 BP 391 EP 405 PG 15 WC Medicine, General & Internal SC General & Internal Medicine GA NF168 UT WOS:A1994NF16800031 PM 8198390 ER PT J AU ZIEGLER, TR GATZEN, C WILMORE, DW AF ZIEGLER, TR GATZEN, C WILMORE, DW TI STRATEGIES FOR ATTENUATING PROTEIN-CATABOLIC RESPONSES IN THE CRITICALLY ILL SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE NUTRITION; CATABOLIC ILLNESS; GROWTH FACTORS; GLUTAMINE; MUSCLE ID HUMAN GROWTH-HORMONE; TOTAL PARENTERAL-NUTRITION; DOUBLE-BLIND; INTRAVENOUS NUTRITION; METABOLIC EFFICACY; NITROGEN-BALANCE; BURNED PATIENTS; FREE GLUTAMINE; INSULIN; MUSCLE AB Specialized enteral and parenteral nutrition are now a standard components of care in critically ill patients. This adjunctive therapy corrects and prevents nutrient deficiencies, attenuates the loss of body protein, and improves clinical outcomes in malnourished patients. Several novel strategies designed to improve the metabolic and clinical effects of specialized nutrition are under vigorous clinical investigation. These new approaches include increased emphasis on enteral feeding to maintain intestinal absorptive, immune, and barrier function; adminstration of conditionally essential amino acids (glutamine, arginine); use of specialized lipid products and antioxidants; and administration of growth factors such as human growth hormone. Randomized, controlled clinical trials will define the clinical and metabolic efficacy and cost-effectiveness of these therapies in specialized nutrition support. C1 ST MARYS HOSP,DEPT SURG,LONDON W2 1NY,ENGLAND. BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,SURG METAB & NUTR LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,JOSLIN DIABET CTR,SCH MED,BOSTON,MA 02215. RP ZIEGLER, TR (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 73 TC 53 Z9 56 U1 1 U2 1 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1994 VL 45 BP 459 EP 480 PG 22 WC Medicine, General & Internal SC General & Internal Medicine GA NF168 UT WOS:A1994NF16800036 PM 8198396 ER PT J AU GUSTAFSON, ML DONAHOE, PK AF GUSTAFSON, ML DONAHOE, PK TI MALE SEX DETERMINATION - CURRENT CONCEPTS OF MALE SEXUAL-DIFFERENTIATION SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE TESTIS-DETERMINING FACTOR; SRY; MULLERIAN INHIBITING SUBSTANCE; TESTOSTERONE; 5-ALPHA-REDUCTASE; ANDROGEN RECEPTOR ID MULLERIAN INHIBITING SUBSTANCE; HUMAN ANDROGEN RECEPTOR; PSEUDOVAGINAL PERINEOSCROTAL HYPOSPADIAS; MIXED GONADAL-DYSGENESIS; H-Y-ANTIGEN; MALE PSEUDOHERMAPHRODITISM; DIHYDROTESTOSTERONE FORMATION; DETERMINING REGION; DETERMINING GENE; FETAL TISSUES AB In order for an infant to develop as a phenotypically complete male or female, a cascade of complex molecular and morphological events must occur at the appropriate time and in the correct sequence during ontogeny. The male embryo's genetic sex is determined by its chromosomal constituents, the most important of which is the sex-determining gene, or testis-determining factor (TDF), on the Y chromosome. Male gonadal sex, or testis formation, is subsequently thought to be determined by this gene and by other secondary pathways. The male gonad, in turn, normally produces hormones such as testosterone and Mullerian inhibiting substance (MIS) that regulate differentiation of the internal and external genitalia, thus determining phenotypic sex. When an abnormality develops in any of the above three processes, an intersex infant with ambiguous genitalia results from the incongruent genetic, gonadal, and phenotypic sex. Clinically, such 46XY males with intersex abnormalities present challenges for gender assignment, timely surgical intervention, and appropriate hormonal therapy. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP GUSTAFSON, ML (reprint author), MASSACHUSETTS GEN HOSP,DIV PEDIAT SURG,BOSTON,MA 02114, USA. NR 71 TC 29 Z9 29 U1 0 U2 3 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1994 VL 45 BP 505 EP 524 PG 20 WC Medicine, General & Internal SC General & Internal Medicine GA NF168 UT WOS:A1994NF16800039 PM 8198399 ER PT J AU COLLINS, LA WENNERSTEN, CB FERRARO, MJ MOELLERING, RC ELIOPOULOS, GM AF COLLINS, LA WENNERSTEN, CB FERRARO, MJ MOELLERING, RC ELIOPOULOS, GM TI COMPARATIVE ACTIVITIES OF PIPERACILLIN AND TAZOBACTAM AGAINST CLINICAL ISOLATES OF LEGIONELLA SPP SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID AMOXYCILLIN CLAVULANIC ACID; COMPARATIVE INVITRO ACTIVITY; ANTI-MICROBIAL AGENTS; PNEUMOPHILA PNEUMONIA; ANTIMICROBIAL AGENTS; SUSCEPTIBILITY AB We evaluated the in vitro activity of piperacillin alone or in combination with the beta-lactamase inhibitor tazobactam against clinical isolates of Legionella species. At an inoculum of approximately 10(4) CFU, tazobactam, piperacillin, and the 8:1 combination had equivalent activities against Legionella spp. At an approximately 10-fold higher inoculum, the following results were obtained, expressed as MICs for 50 and 90% of strains tested (MIC range): piperacillin, 4 and 16 (0.25 to 32) mug/ml; tazobactam, 0.5 and 1 (0.125 to 2) mug/ml; and piperacillin-tazobactam (expressed in terms of MIC of piperacillin) 0.5 and 1 (0.03 to 2) mug/ml. Tazobactam alone and the combination with piperacillin were more active than piperacillin alone at the higher inoculum. C1 DEACONESS HOSP,DEPT MED,185 PILGRIM RD,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 16 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JAN PY 1994 VL 38 IS 1 BP 144 EP 146 PG 3 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA MP524 UT WOS:A1994MP52400025 PM 8141570 ER PT J AU EBERT, SC CRAIG, WA AF EBERT, SC CRAIG, WA TI RETAIN INTERMITTENT DOSING OF CARBAPENEMS - REPLY SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Letter ID IMIPENEM C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. RP EBERT, SC (reprint author), UNIV WISCONSIN,MERITER HOSP,SCH PHARM,DEPT PHARM,MADISON,WI 53715, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JAN PY 1994 VL 38 IS 1 BP 159 EP 160 PG 2 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA MP524 UT WOS:A1994MP52400030 ER PT J AU FOSSEY, MD HAMNER, MB AF FOSSEY, MD HAMNER, MB TI CLONAZEPAM-RELATED SEXUAL DYSFUNCTION IN MALE VETERANS WITH PTSD SO ANXIETY LA English DT Note DE ALPRAZOLAM; ANTIDEPRESSANTS; ANXIETY; BENZODIAZEPINES; DIAZEPAM; LORAZEPAM ID POSTTRAUMATIC-STRESS-DISORDER; PANIC DISORDER; SOCIAL PHOBIA; ALPRAZOLAM; AGORAPHOBIA; THERAPY AB Medication-induced sexual dysfunction can significantly interfere with patients' quality of life and lead to poor compliance. This retrospective study examined the records of 100 male veterans with post-traumatic stress disorder (PTSD) selected in alphabetical order from an active treatment file of 230 patients. Forty-two patients had received clonazepam (mean maximum dose: 3.4 +/- 1.6 mg/day) at some point during their treatment. Of these, 18 (42.9%) complained of significant sexual dysfunction (primarily erectile dysfunction). Eighty-four patients received diazepam (mean maximum dose: 52.1 +/- 29.7 mg/day), nine received alprazolam (mean maximum dose: 5.2 +/- 2.8 mg/day) and eight received lorazepam (mean maximum dose: 3.8 +/- 2.4 mg/day). None of these patients complained of sexual dysfunction during treatment with these three other benzodiazepines. Our findings suggest that benzodiazepines, particularly clonazepam in the current study, can be a cause of sexual dysfunction in many male patients. Prospective studies comparing the overall clinical utility of various benzodiazepines are indicated in this and other clinic populations. (C) 1995 Wiley-Liss, Inc. C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. RP FOSSEY, MD (reprint author), RALPH H JOHNSON VA MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. NR 28 TC 18 Z9 18 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1070-9797 J9 ANXIETY JI Anxiety PY 1994 VL 1 IS 5 BP 233 EP 236 PG 4 WC Psychiatry; Psychology SC Psychiatry; Psychology GA RK515 UT WOS:A1994RK51500007 PM 9160580 ER PT J AU LIPSITZ, SR LAIRD, NM BRENNAN, TA AF LIPSITZ, SR LAIRD, NM BRENNAN, TA TI SIMPLE MOMENT ESTIMATES OF THE KAPPA-COEFFICIENT AND ITS VARIANCE SO APPLIED STATISTICS-JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES C LA English DT Article DE ESTIMATING EQUATION; EXCHANGEABILITY; UNBALANCED DATA ID CORRELATED BINARY REGRESSION; NOMINAL SCALE AGREEMENT; OBSERVERS AB Estimating equations are used to develop simple non-iterative estimates of the kappa-coefficient that can be used when there are more than two random raters and/or unbalanced data (each subject is not judged by every rater). We show that there is a simple way to estimate the variance of any estimate of the kappa-coefficient that is a solution to an estimating equation. Two non-iterative estimates that are shown to be solutions to estimating equations are Fleiss's estimate and Schouten's estimate. Also, assuming that the underlying data are beta-binomial, we compare the asymptotic relative efficiency of the non-iterative estimators Of kappa relative to the iterative maximum likelihood estimator (MLE) of kappa from the beta-binomial distribution. Fleiss's estimator was found to have high efficiency. Finally, simulations are used to compare the finite sample performance of these estimators as well as the MLE from the beta-binomial distribution. In the simulations, the Newton-Raphson algorithm for the MLE from the beta-binomial model did not always converge in small samples, which also supports the use of a non-iterative estimate in small samples. The estimators are also compared by using a psychiatric data set given by Fleiss. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. LIMBURGS UNIV CENTRUM,B-3610 DIEPENBEEK,BELGIUM. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. RP LIPSITZ, SR (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,44 BINNEY ST,BOSTON,MA 02115, USA. NR 13 TC 18 Z9 18 U1 0 U2 1 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0035-9254 J9 APPL STAT-J ROY ST C JI Appl. Stat.-J. R. Stat. Soc. PY 1994 VL 43 IS 2 BP 309 EP 323 DI 10.2307/2986022 PG 15 WC Statistics & Probability SC Mathematics GA NG145 UT WOS:A1994NG14500002 ER PT J AU SAH, RL CHEN, AC GRODZINSKY, AJ TRIPPEL, SB AF SAH, RL CHEN, AC GRODZINSKY, AJ TRIPPEL, SB TI DIFFERENTIAL-EFFECTS OF BFGF AND IGF-I ON MATRIX METABOLISM IN CALF AND ADULT BOVINE CARTILAGE EXPLANTS SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID FIBROBLAST GROWTH-FACTOR; ARTICULAR-CARTILAGE; FACTOR-BETA; PROTEOGLYCAN BIOSYNTHESIS; TERMINAL DIFFERENTIATION; PLATE CHONDROCYTES; COLONY FORMATION; ORGAN-CULTURES; SOFT AGAR; SERUM C1 UNIV CALIF SAN DIEGO,INST BIOMED ENGN,SAN DIEGO,CA 92103. UNIV CALIF SAN DIEGO,DEPT APPL MECH & ENGN SCI,SAN DIEGO,CA 92103. MIT,DEPT ELECT & MECH ENGN,CONTINUUM ELECTRMECH GRP,CAMBRIDGE,MA 02139. HARVARD UNIV,HARVARD MIT DIV HLTH SCI & TECHNOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,ORTHOPAED RES LABS,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. FU NIAMS NIH HHS [AR31068, AR33236] NR 47 TC 152 Z9 156 U1 0 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN PY 1994 VL 308 IS 1 BP 137 EP 147 DI 10.1006/abbi.1994.1020 PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MW719 UT WOS:A1994MW71900020 PM 8311446 ER PT J AU OTTO, MW BRUDER, GE FAVA, M DELIS, DC QUITKIN, FM ROSENBAUM, JF AF OTTO, MW BRUDER, GE FAVA, M DELIS, DC QUITKIN, FM ROSENBAUM, JF TI NORMS FOR DEPRESSED-PATIENTS FOR THE CALIFORNIA VERBAL-LEARNING TEST - ASSOCIATIONS WITH DEPRESSION SEVERITY AND SELF-REPORT OF COGNITIVE DIFFICULTIES SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY LA English DT Article ID MEMORY; IMPAIRMENT AB This study provides norms for depressed subjects for a widely used test of verbal memory, the California Verbal Learning Test (CVLT). Subjects were 156 outpatients with major depression tested during a drug washout period. Mean CVLT memory scores for these patients were generally between one-half and one standard deviation below age- and sex-corrected norms for nondepressed populations. Severity of depression in the patients was not associated with memory performance, but was associated with self-report of cognitive difficulties. A table of age-, sex-, and education-specific norms for the CVLT is provided. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. NEW YORK STATE PSYCHIAT INST & HOSP,NEW YORK,NY 10032. HARVARD UNIV,SCH MED,BOSTON,MA 02115. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. SAN DIEGO VET AFFAIRS MED CTR,SAN DIEGO,CA. UNIV CALIF SAN DIEGO,SCH MED,LA JOLLA,CA 92093. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC 815,BOSTON,MA 02114, USA. NR 18 TC 34 Z9 34 U1 1 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6177 J9 ARCH CLIN NEUROPSYCH JI Arch. Clin. Neuropsychol. PD JAN-FEB PY 1994 VL 9 IS 1 BP 81 EP 88 DI 10.1016/0887-6177(94)90016-7 PG 8 WC Psychology, Clinical; Psychology SC Psychology GA MQ862 UT WOS:A1994MQ86200007 PM 14589514 ER PT J AU RAUCH, SL JENIKE, MA ALPERT, NM BAER, L BREITER, HCR SAVAGE, CR FISCHMAN, AJ AF RAUCH, SL JENIKE, MA ALPERT, NM BAER, L BREITER, HCR SAVAGE, CR FISCHMAN, AJ TI REGIONAL CEREBRAL BLOOD-FLOW MEASURED DURING SYMPTOM PROVOCATION IN OBSESSIVE-COMPULSIVE DISORDER USING OXYGEN 15-LABELED CARBON-DIOXIDE AND POSITRON EMISSION TOMOGRAPHY SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID GLUCOSE METABOLIC RATES; DEPRESSION; ANXIETY AB Background: The study was designed to determine the mediating neuroanatomy of obsessive-compulsive disorder (OCD). Methods: The short half-life tracer oxygen 15-labeled carbon dioxide was used to allow for repeated positron emission tomographic determinations of regional cerebral blood flow on each of eight patients with OCD during a resting and a provoked (symptomatic) state. Results: Individually tailored provocative stimuli were successful in provoking OCD symptoms, in comparison with paired innocuous stimuli, as measured by self-report on OCD analogue scales (P=.002). Omnibus subtraction images demonstrated a statistically significant increase in relative regional cerebral blood now during the OCD symptomatic state vs the resting state in right caudate nucleus (P<.006), left anterior cingulate cortex (P<.045), and bilateral orbitofrontal cortex (P<.008); increases in the left thalamus approached but did not reach statistical significance (P=.07). Conclusions: These findings are consistent with results of previous functional neuroimaging studies and contemporary neurocircuitry models of OCD. The data further implicate orbitofrontal cortex, caudate nucleus, and anterior cigulate cortex in the pathophysiology of OCD and in mediating OCD symptoms. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV NUCL MED,POSITRON EMISS TOMOG LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [5T32CA09362-11] NR 26 TC 622 Z9 628 U1 3 U2 25 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 JAN PY 1994 VL 51 IS 1 BP 62 EP 70 PG 9 WC Psychiatry SC Psychiatry GA MR516 UT WOS:A1994MR51600007 PM 8279930 ER PT J AU SARANTOS, P ABOUHAMZE, A CHAKRABARTI, R HASSELGREN, PO BUCHANAN, T BILLIAR, T MCMANUS, AT SOUBA, WW AF SARANTOS, P ABOUHAMZE, A CHAKRABARTI, R HASSELGREN, PO BUCHANAN, T BILLIAR, T MCMANUS, AT SOUBA, WW TI GLUCOCORTICOIDS REGULATE INTESTINAL GLUTAMINE-SYNTHETASE GENE-EXPRESSION IN ENDOTOXEMIA SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 13th Annual Meeting of the Surgical-Infection-Society CY APR 29, 1993 CL BALTIMORE, MD SP SURG INFECT SOC ID CYTOKINE MODULATION; SKELETAL-MUSCLE; METABOLISM; TRANSPORT; RAT; MONOLAYERS; MEMBRANE; RECEPTOR; SEPSIS; CACO-2 AB Purpose: Although glutamine is required to maintain gut mucosal metabolism and function, intestinal glutamine uptake from the gut lumen and from the bloodstream is decreased during sepsis. We hypothesized that endogenous mucosal glutamine biosynthesis is increased during endotoxemia, and we attempted to define the ''stress'' mediators that regulate the activity of small intestinal glutamine synthetase (GS), the principal enzyme of de novo glutamine biosynthesis in the gut. Methods: Adult rats received Escherichia coli lipopolysaccharide (LPS) (7.5 mg/kg intraperitoneally), RU 38486 (a glucocorticoid antagonist; 10 mg/kg by gavage) 2 hours prior to LPS administration, antibody to tumor necrosis factor (TNF) (4 mg/kg intraperitoneally) prior to LPS administration, or ketorolac tromethamine (a prostaglandin synthesis inhibitor; 1 mg/kg intraperitoneally) followed by LPS administration. Mucosal GS activity was assayed 12 hours after LPS administration. In a separate set of studies, cultured intestinal mucosal cells (Caco-2) were exposed to LPS, interleukin 1 (IL-1), IL-6, TNF-alpha, interferon-gamma, prostaglandin E(2), or dexamethasone. Twelve hours later, GS activity was assayed and messenger RNA was extracted. The GS transcripts were labeled with a GS complementary DNA probe radiolabeled with phosphorus 32, were quantitated by phosphoimaging, and were normalized to beta-actin. Results: In vivo LPS treatment increased mucosal GS activity by 250%. Pretreatment with antibody to TNF or ketorolac did not inhibit the LPS-induced increase in mucosal GS, whereas pretreatment with RU 38486 attenuated the increase in gut GS activity by 60%. Lipopolysaccharide, IL-I, IL-6, TNF-alpha, gamma-interferon, and prostaglandin E(2) did not increase GS activity in Caco-2 cells, whereas dexamethasone increased GS activity and messenger RNA 2.5-fold and threefold, respectively. These data indicate that cytokines and prostaglandins (prostaglandin E(2)) do not regulate mucosal GS expression during endotoxemia. Glucocorticoids, however, stimulate GS gene expression directly. Conclusions: This hormonally mediated response may support de novo mucosal GS during septic states when uptake of glutamine from the lumen and blood is decreased. C1 MASSACHUSETTS GEN HOSP,HARVARD MED SCH,BOSTON,MA. RP SARANTOS, P (reprint author), UNIV FLORIDA,COLL MED,DEPT SURG,GAINESVILLE,FL, USA. FU NCI NIH HHS [CA 45327, T32-CA09605-03] NR 26 TC 17 Z9 17 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD JAN PY 1994 VL 129 IS 1 BP 59 EP 65 PG 7 WC Surgery SC Surgery GA MQ943 UT WOS:A1994MQ94300008 PM 7904150 ER PT J AU MARASCO, WA SZILVAY, AM KALLAND, KH HELLAND, DG REYES, HM WALTER, RJ AF MARASCO, WA SZILVAY, AM KALLAND, KH HELLAND, DG REYES, HM WALTER, RJ TI SPATIAL ASSOCIATION OF HIV-1 TAT PROTEIN AND THE NUCLEOLAR TRANSPORT PROTEIN B23 IN STABLY TRANSFECTED JURKAT T-CELLS SO ARCHIVES OF VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; LONG TERMINAL REPEAT; NUCLEAR MATRIX; MESSENGER-RNA; FUNCTIONAL-CHARACTERIZATION; SEQUENCE REQUIREMENTS; ELECTRON-MICROSCOPY; NUCLEOTIDE-SEQUENCE; GENE-EXPRESSION; AIDS VIRUS AB The human immunodeficiency virus (HIV-1) encodes a transactivator protein, the product of the tat gene (tat), which is essential for virus replication In this study, immunogold electron microscopy was used in a stably transfected Jurkat T-cell line that constitutively expresses HIV-I tat protein to determine the subcellular and intranuclear distribution of tat protein. Two nucleocytoplasmic shuttle proteins C23/nucleolin and B23 and a third nucleolar antigen that was detected by monoclonal antibody MAb 1277 were also examined. In addition, spatial association of C23 and B23 with tat protein at several subcellular locations was examined in dual-labeling experiments. The results showed that tat protein was found in both the cytoplasm and nucleus but was especially prominent within the dense fibrillar and granular components of the nucleolus. There was little labeling of tat protein in the fibrillar centers where MAb 1277 antigen was localized at a comparatively high level. The subcellular and intranucleolar distribution of tat protein was virtually identical to the pattern seen with C23 and B23. Although the intranuclear distributions of C23, B23 and tnt protein were very similar, C23 and tat protein were seldom spatially associated. In contrast, B23 and tat protein were frequently spatially associated in the nucleolus and in several other subcellular locations including the cytoplasm, nucleoplasm, at the nuclear envelope and plasma membrane. While a physical association was not directly demonstrated in this study, the spatial association between B23 and tat protein strongly suggest that such an association may exist. C1 UNIV BERGEN, NATL CTR RES VIROL, BERGEN, NORWAY. UNIV BERGEN, CTR BIOTECHNOL, BERGEN, NORWAY. HEKTOEN INST MED RES, DEPT SURG, CHICAGO, IL 60612 USA. RP MARASCO, WA (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV HUMAN RETROVIROL, 44 BINNEY ST, BOSTON, MA 02115 USA. RI Kalland, Karl-Henning/B-9445-2017 OI Kalland, Karl-Henning/0000-0003-4486-2334 FU NCI NIH HHS [KO8-CA01507] NR 57 TC 33 Z9 33 U1 0 U2 2 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1994 VL 139 IS 1-2 BP 133 EP 154 DI 10.1007/BF01309460 PG 22 WC Virology SC Virology GA PU982 UT WOS:A1994PU98200010 PM 7826206 ER PT S AU KAZEMI, H SOTOARAPE, I AF KAZEMI, H SOTOARAPE, I BE ORegan, RG Nolan, P McQueen, DS Paterson, DJ TI CENTRAL GLUTAMATE AND SUBSTANCE-P IN THE HYPOXIC VENTILATORY RESPONSE SO ARTERIAL CHEMORECEPTORS: CELL TO SYSTEM SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 12th International Meeting of the International-Society-of-Arterial-Chemoreception on Chemoreceptors and Chemoreflexes in Health and Disease CY AUG 09-13, 1993 CL DUBLIN, IRELAND SP INT SOC ARTERIAL CHEMORECEPT C1 MASSACHUSETTS GEN HOSP,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44824-6 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1994 VL 360 BP 281 EP 284 PG 4 WC Cardiac & Cardiovascular Systems; Endocrinology & Metabolism; Physiology SC Cardiovascular System & Cardiology; Endocrinology & Metabolism; Physiology GA BB74U UT WOS:A1994BB74U00046 PM 7532903 ER PT J AU SCHAUB, RG BREE, MP HAYES, LL RUDD, MA RABBANI, L LOSCALZO, J CLINTON, SK AF SCHAUB, RG BREE, MP HAYES, LL RUDD, MA RABBANI, L LOSCALZO, J CLINTON, SK TI RECOMBINANT HUMAN MACROPHAGE-COLONY-STIMULATING FACTOR REDUCES PLASMA-CHOLESTEROL AND CARRAGEENAN GRANULOMA FOAM CELL-FORMATION IN WATANABE HERITABLE HYPERLIPIDEMIC RABBITS SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Article DE FOAM CELLS; RECOMBINANT HUMAN MACROPHAGE COLONY-STIMULATING FACTOR; CHOLESTEROL; WHHL RABBITS; RECOMBINANT PROTEINS; MACROPHAGES ID FACTOR M-CSF; CORONARY ATHEROSCLEROSIS; LYMPHOCYTES-T; GROWTH-FACTOR; MONOCYTE; LESIONS; HYPERCHOLESTEROLEMIA; LIPOPROTEINS; EXPRESSION; GENERATION AB Previous studies have demonstrated that shortterm administration of recombinant human macrophage colony-stimulating factor (rhM-CSF) reduces plasma cholesterol in rabbits, nonhuman primates, and human subjects. This study extended the dose schedule of rhM-CSF to 8 weeks of continuous intravenous infusion (CIVI) in the Watanabe heritable hyperlipidemic (WHHL) rabbit and expanded the scope to include an assessment of macrophage-derived foam cell development. Ten male WHHL rabbits were injected subcutaneously with 1% carrageenan to promote formation of a macrophage-rich foam cell granuloma. Rabbits were infused with either vehicle or rhM-CSF at 100 mu g/kg per day (weeks 1 through 5) followed by 300 mu g/kg per day (weeks 6 through 8). rhM-CSF (100 mu g/kg per day) decreased total plasma cholesterol by 45% at 2 weeks compared with controls. The gradual return of plasma cholesterol toward control concentrations over the subsequent 3 weeks correlated with the appearance of circulating antibodies specific to rhM-CSF. Granuloma weights at harvest (8 weeks after infusion) were significantly lower (2.8+/-0.7 g, mean+/-SEM) in rhM-CSF-treated rabbits relative to controls (7.1+/-1.5 g, P<.05). Granulomas from rabbits treated with rhM-CSF contained lower concentrations of cholesterol (2.0+/-0.7 versus 6.1+/-1.5 mu g/mg, P<.03) and cholesteryl ester (0.7+/-0.4 versus 3.9+/-1.2 mu g/mg, P<.03) than controls. Histological evaluation revealed that granulomas from the rhM-CSF-treated rabbits were more fibrous and contained fewer foam cells than those from controls. Immunohistochemical localization of endogenous macrophage colony-stimulating factor (M-CSF) in granuloma tissue from vehicle-treated rabbits revealed a diffuse, faint staining pattern. Granuloma tissue from rhM-CSF-treated rabbits exhibited staining for M-CSF that was more intense than in tissue from control rabbits. This study showed that the CIVI of rhM-CSF produced a significant reduction in plasma cholesterol and granuloma foam cell formation in WHHL rabbits. The increase in immunoreactive M-CSF in granulomas from rhM-CSF-treated rabbits suggested that M-CSF may have enhanced the viability of macrophages and modulated their function in a manner that stimulated the processing of cholesterol and its mobilization from the granuloma. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP SCHAUB, RG (reprint author), GENET INST INC,87 CAMBRIDGE PK DR,CAMBRIDGE,MA 02140, USA. NR 32 TC 25 Z9 26 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD JAN PY 1994 VL 14 IS 1 BP 70 EP 76 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MQ804 UT WOS:A1994MQ80400011 PM 8274480 ER PT J AU POLISSON, RP DOOLEY, MA DAWSON, DV PISETSKY, DS AF POLISSON, RP DOOLEY, MA DAWSON, DV PISETSKY, DS TI INTERLEUKIN-2 RECEPTOR LEVELS IN THE SERA OF RHEUMATOID-ARTHRITIS PATIENTS TREATED WITH METHOTREXATE SO ARTHRITIS AND RHEUMATISM LA English DT Article ID T-CELL LEUKEMIA; DISEASE-ACTIVITY; ACTIVATION; IL-2; TAC AB Objective. To evaluate the association of the level of soluble serum interleukin-2 receptor (sIL-2R) with disease activity and response to therapy in patients with rheumatoid arthritis (RA). Methods. The sIL-2R levels of 148 patients with refractory RA were determined by enzyme-linked immunosorbent assay. This parameter was correlated with other clinical observations obtained during a prospective, randomized, placebo-controlled trial of methotrexate, sponsored by the Cooperative Systematic Studies of Rheumatic Diseases consortium. Using statistical modeling, the usefulness of sIL-2R as a measure of disease activity and a predictor of outcome was evaluated. Results. The mean sIL-2R level in all RA patients was markedly elevated compared with that in normal control subjects, and decreased significantly during the trial. There was no correlation of the sIL-2R level and the joint pain/tenderness count either at study entry or study end. There was a significant correlation of the sIL-2R level and the erythrocyte sedimentation rate, both at study entry and study end. A multiple linear regression model showed that treatment with methotrexate, but not the sIL-2R level or the change in sIL-2R level, predicted a change in joint count. A stepwise multiple logistic regression model defined no significant predictive information for outcome for the level of sIL-2R at study entry. Conclusion. After controlling for the simultaneous effects of other important clinical variables, the level of sIL-2R does not appear to predict the response to methotrexate in patients with refractory RA. Further analysis of cohorts of patients with earlier RA needs to be performed. C1 DUKE UNIV,MED CTR,DEPT MED,DIV RHEUMATOL & IMMUNOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT COMMUNITY & FAMILY MED,DIV BIOMETRY & MED INFORMAT,DURHAM,NC 27710. RP POLISSON, RP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,ARTHRITIS UNIT,BULFINCH 1,BOSTON,MA 02114, USA. NR 23 TC 21 Z9 21 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 JAN PY 1994 VL 37 IS 1 BP 50 EP 56 DI 10.1002/art.1780370108 PG 7 WC Rheumatology SC Rheumatology GA MR523 UT WOS:A1994MR52300007 PM 8129764 ER PT J AU SAKAS, DE CROWELL, RM ZERVAS, NT AF SAKAS, DE CROWELL, RM ZERVAS, NT TI EFFECTS OF LECITHIN-EMULSIFIED PERFLUOROCHEMICAL COMPOUNDS IN ISCHEMIC BRAIN INJURY SO ARTIFICIAL CELLS BLOOD SUBSTITUTES AND IMMOBILIZATION BIOTECHNOLOGY LA English DT Article DE PERFLUOROCARBON; FLUOROMETHYLOADAMANTANE; CEREBRAL INFARCTION; CEREBRAL ISCHEMIA; CEREBRAL PROTECTION ID OXYGENATED FLUOROCARBON EMULSION; CEREBRAL-ISCHEMIA; ARTIFICIAL BLOOD; POLOXAMER-188; PERFUSION; VISCOSITY; FIBRIN AB A lecithin-emulsified ''Pluronic F-68''-free perfluorochemical compound, named F-1,3-DMA, was tested as a new agent in the prevention of central nervous tissue ischemia. A permanent ischemia leading to cerebral infarction was induced after microsurgical exposure and occlusion of the internal carotid, anterior, and middle cerebral arteries in the rabbit. Following arterial occlusion, F-1,3-DMA was administered intravenously, in a solution rendered isotonic to plasma, over a 30 minute period. The F-1,8-DMA was well tolerated. Hemodynamic, cardiovascular and metabolic parameters were not affected by the infusion of F-1,3-DMA. Although PO2 remained virtually unchanged, animals treated with F-1,3-DMA (n=9), had smaller infarct volume by 61 percent as compared to the control (n=8) group (P < 0.04, Student's t-test). Histopathology did not reveal any F-1.3-DMA related damage in the noninfarcted brain. These results suggest that F-1,8-DMA has nervous tissue ischemia protective properties possibly because of microflow effects although O2 transport to ''local'' tissue may be enhanced as well. We believe that further research is necessary in order to make clinical trials of F-1,3-DMA possible. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,NEUROSURG SERV,BOSTON,MA 02114. NR 14 TC 6 Z9 6 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1073-1199 J9 ARTIF CELL BLOOD SUB JI Artif. Cells Blood Substit. Immobil. Biotechnol. PY 1994 VL 22 IS 1 BP 83 EP 89 DI 10.3109/10731199409117401 PG 7 WC Biotechnology & Applied Microbiology; Engineering, Biomedical; Materials Science, Biomaterials SC Biotechnology & Applied Microbiology; Engineering; Materials Science GA NQ114 UT WOS:A1994NQ11400007 PM 8055099 ER PT J AU WOLF, GL AF WOLF, GL TI TECHNICAL IMPROVEMENTS IN THE STAGING OF CANCER - THE ROLE OF IMAGING AND CONTRAST AGENTS SO ARTIFICIAL CELLS BLOOD SUBSTITUTES AND IMMOBILIZATION BIOTECHNOLOGY LA English DT Article; Proceedings Paper CT Vth International Symposium on Blood Substitutes CY MAR 17-20, 1993 CL SAN DIEGO, CA ID BLOOD-FLOW; INDICATOR; TUMORS; DTPA AB Despite advances in cancer diagnosis, there has been little impact upon outcome. This may be a consequence of the exceptional heterogeneity in cancers, especially their cell types, perfusion, oxygenation, and metabolic circumstances. Better therapeutic plans could require better characterization of individual tumors in individual patients. For some tumors, tissue characterization by sophisticated histologic analysis of biopsy samples may improve staging. However, noninvasive staging is more acceptable to patients and may be more comfortably repeated in the course of monitoring therapeutic regimens. Several imaging applications may serve these goals. First, new contrast agents may allow accurate cancer detection in regional lymph nodes. High resolution CT with perfluorocarbon lymphography is in the clinical trial stage. This could presage minimally invasive ablation of cancer in lymph nodes, as well. Second, new agents will better define local and metastatic cancers, also impacting standard and minimally invasive treatments. Finally, imaging methods may be able to measure perfusion and metabolism in small volumes in vivo, as well as estimate important local pharmacokinetics of therapeutics. RP WOLF, GL (reprint author), MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,149 13TH ST,BOSTON,MA 02129, USA. NR 12 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1073-1199 J9 ARTIF CELL BLOOD SUB JI Artif. Cells Blood Substit. Immobil. Biotechnol. PY 1994 VL 22 IS 2 BP 285 EP 294 DI 10.3109/10731199409117421 PG 10 WC Biotechnology & Applied Microbiology; Engineering, Biomedical; Materials Science, Biomaterials SC Biotechnology & Applied Microbiology; Engineering; Materials Science GA NQ115 UT WOS:A1994NQ11500016 PM 7522085 ER PT J AU TEICHER, BA HOLDEN, SA DUPUIS, NP KUSOMOTO, T LIU, M LIU, F MENON, K AF TEICHER, BA HOLDEN, SA DUPUIS, NP KUSOMOTO, T LIU, M LIU, F MENON, K TI OXYGENATION OF THE RAT-9L GLIOSARCOMA AND THE RAT-13672 MAMMARY-CARCINOMA WITH VARIOUS DOSES OF A HEMOGLOBIN SOLUTION SO ARTIFICIAL CELLS BLOOD SUBSTITUTES AND IMMOBILIZATION BIOTECHNOLOGY LA English DT Article; Proceedings Paper CT Vth International Symposium on Blood Substitutes CY MAR 17-20, 1993 CL SAN DIEGO, CA ID CHEMOTHERAPEUTIC ALKYLATING-AGENTS; RADIATION-THERAPY; TUMORS AB Tumor oxygen tensions were measured using a computer controlled pO(2) microelectrode in two preclinical solid tumor models, the rat 9L gliosarcoma and the rat 13672 mammary carcinoma. Tumor oxygenation profiles were determined under four conditions: 1) normal air breathing, 2) carbogen (95% O-2/5% CO2) breathing, 3) after intravenous administration of a solution of ultrapurified polymerized bovine hemoglobin with normal air breathing and 4) after intravenous administration of a solution of ultrapurified polymerized bovine hemoglobin with carbogen breathing. Both tumors had severely hypoxic regions under normal air breathing conditions. Although carbogen breathing increased the oxygenation of the better oxygenated portions of the tumor, it did not impact on the severely hypoxic tumor regions. Administration of the hemoglobin solution was effective in increasing the oxygenation throughout both tumors under normal air breathing conditions. The addition of carbogen breathing to administration of the hemoglobin solution eliminated severe hypoxia in the 9L gliosarcoma and markedly reduced the severely hypoxic regions of the 13672 mammary carcinoma. C1 HARVARD UNIV,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [P01-CA19589] NR 13 TC 15 Z9 15 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1073-1199 J9 ARTIF CELL BLOOD SUB JI Artif. Cells Blood Substit. Immobil. Biotechnol. PY 1994 VL 22 IS 3 BP 827 EP 833 DI 10.3109/10731199409117917 PG 7 WC Biotechnology & Applied Microbiology; Engineering, Biomedical; Materials Science, Biomaterials SC Biotechnology & Applied Microbiology; Engineering; Materials Science GA NZ321 UT WOS:A1994NZ32100051 PM 7994406 ER PT J AU TEICHER, BA AF TEICHER, BA TI COMBINATION OF PERFLUOROCHEMICAL EMULSIONS AND CARBOGEN BREATHING WITH CANCER-CHEMOTHERAPY SO ARTIFICIAL CELLS BLOOD SUBSTITUTES AND IMMOBILIZATION BIOTECHNOLOGY LA English DT Article; Proceedings Paper CT Vth International Symposium on Blood Substitutes CY MAR 17-20, 1993 CL SAN DIEGO, CA ID MELPHALAN ANTITUMOR-ACTIVITY; FLUOSOL-DA; RADIATION-THERAPY; CYTO-TOXICITY; BLOOD-FLOW; OXYGEN DISTRIBUTION; MAMMARY-CARCINOMA; SOLID TUMORS; RIF-1 TUMOR; X-RAYS AB Over the past ten years several laboratories have explored the use of perfluorochemical emulsions (PFCE) and carbogen (95% O-2/5% CO2; C) or oxygen breathing as an adjuvant to radiation therapy and/or chemotherapy in solid tumor model systems. The rationale for the use of PFCE and C or oxygen breathing in this therapeutic setting is that solid tumor masses contain areas of hypoxia which are therapeutically resistant. Since x-rays and many chemotherapeutic agents require oxygen to be maximally cytotoxic and most normal tissues are well-oxygenated, the additional oxygen put in circulation by the PFCE/C should not increase the normal tissue toxicities produced by the various therapies. Several anticancer agents are dependent on oxygen to be cytotoxic, these drugs such as the iron-chelating peptide bleomycin are enhanced in antitumor activity by the coadministration of a PFCE/C. The antitumor alkylating agents especially cyclophosphamide, BCNU and melphalan show increased tumor cell killing without a concomitant increase in bone marrow toxicity when administered with PFCE/C. Enhanced activity was also observed when topoisomerase II inhibitors such as adriamycin and etoposide were co-administered with PFCE/C. Positive effects, although smaller, were observed when antimetabolites such as 5-fluorouracil and methotrexate were coadministered with PFCE/C. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 42 TC 7 Z9 8 U1 1 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1073-1199 J9 ARTIF CELL BLOOD SUB JI Artif. Cells Blood Substit. Immobil. Biotechnol. PY 1994 VL 22 IS 4 BP 1109 EP 1120 DI 10.3109/10731199409138806 PG 12 WC Biotechnology & Applied Microbiology; Engineering, Biomedical; Materials Science, Biomaterials SC Biotechnology & Applied Microbiology; Engineering; Materials Science GA PF510 UT WOS:A1994PF51000015 PM 7849913 ER PT J AU TEICHER, BA SCHWARTZ, GN DUPUIS, NP KUSOMOTO, T LIU, M LIU, F NORTHEY, D AF TEICHER, BA SCHWARTZ, GN DUPUIS, NP KUSOMOTO, T LIU, M LIU, F NORTHEY, D TI OXYGENATION OF HUMAN TUMOR XENOGRAFTS IN NUDE-MICE BY A PERFLUOROCHEMICAL, EMULSION AND CARBOGEN BREATHING SO ARTIFICIAL CELLS BLOOD SUBSTITUTES AND IMMOBILIZATION BIOTECHNOLOGY LA English DT Article; Proceedings Paper CT Vth International Symposium on Blood Substitutes CY MAR 17-20, 1993 CL SAN DIEGO, CA ID RADIATION-THERAPY; CELLS AB Human solid tumors (prostate carcinomas PC-3 and DU-145, breast carcinoma MX-1, cervical carcinoma ME-180, small cell lung carcinoma SW2, and glioblastoma T98G) were grown as xenografts in nude mice. Using the Eppendorf pO(2) histograph microelectrode system, the oxygen profiles of the turners were determined while the animals breathed air or carbogen (95% O-2/5% CO2), and after administration of the perfluorochemical emulsion Oxygent-CA (8 ml/kg) under air breathing and carbogen breathing conditions. Under normal air breathing with or without Oxygent-CA administration the mean Oxygen tensions were between 4.9 and 9.3 mmHg and each tumor had severely hypoxic regions where the pO(2) was less than 5 mmHg. The severely hypoxic regions comprised 41-71% of the oxygen tension measurements under normal air breathing conditions. Carbogen breathing alone increased the mean oxygen tensions to 10.9-23.9 mmHg. Administration of Oxygent-CA and carbogen breathing increased the mean oxygen tensions over the levels of carbogen breathing alone to varying degrees. The highest mean oxygen tensions were 40.8 mmHg in the T98G glioblastoma and 24.5 mmHg in the ME-180 cervical carcinoma. Investigation of the use of Oxygent-CA/carbogen to increase the oxygenation of clinical tumors is warranted. C1 HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [P01-CA19589] NR 17 TC 7 Z9 7 U1 1 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1073-1199 J9 ARTIF CELL BLOOD SUB JI Artif. Cells Blood Substit. Immobil. Biotechnol. PY 1994 VL 22 IS 4 BP 1369 EP 1375 DI 10.3109/10731199409138839 PG 7 WC Biotechnology & Applied Microbiology; Engineering, Biomedical; Materials Science, Biomaterials SC Biotechnology & Applied Microbiology; Engineering; Materials Science GA PF510 UT WOS:A1994PF51000048 PM 7849946 ER PT S AU HATTORI, M YAMATO, E FUKUDA, M PETRUZZELLI, M WEAVERE, A MACMURRAY, A LANDER, ES CHAPMAN, VM AF HATTORI, M YAMATO, E FUKUDA, M PETRUZZELLI, M WEAVERE, A MACMURRAY, A LANDER, ES CHAPMAN, VM BE Zouali, M TI TYPE-I (INSULIN-DEPENDENT) AND TYPE-II (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS IN BC1[(NODXMUS-SPRETUS)F1XNOD] MICE SO AUTOIMMUNITY: EXPERIMENTAL ASPECTS SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES H, CELL BIOLOGY LA English DT Proceedings Paper CT NATO Advanced Research Workshop on Fundamental and Experimental Aspects of Autoimmunity CY MAY 22-26, 1993 CL MARATEA, ITALY SP NATO C1 JOSLIN DIABET FDN INC,CTR DIABET,IMMUNOL & IMMUNOGENET SECT,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN 33 PA HEIDELBERGER PLATZ 3, W-1000 BERLIN 33, GERMANY SN 1010-8793 BN 3-540-57642-8 J9 NATO ADV SCI INST SE PY 1994 VL 80 BP 275 EP 297 PG 23 WC Immunology SC Immunology GA BA51C UT WOS:A1994BA51C00022 ER PT J AU KAGAN, BL SOKOLOV, Y AF KAGAN, BL SOKOLOV, Y TI USE OF LIPID BILAYER-MEMBRANES TO DETECT PORE FORMATION BY TOXINS SO BACTERIAL PATHOGENESIS, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID FRAGMENTED SARCOPLASMIC-RETICULUM; PLANAR PHOSPHOLIPID-BILAYERS; DIPHTHERIA-TOXIN; ELECTRICAL-PROPERTIES; CHANNELS; INSERTION; MECHANISM; FUSION C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,SCH MED,BRAIN RES INST,LOS ANGELES,CA 90024. PURDUE UNIV,LAB ANIM PROGRAM,W LAFAYETTE,IN 47907. RP KAGAN, BL (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024, USA. FU NIMH NIH HHS [MH43433] NR 26 TC 12 Z9 12 U1 1 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1994 VL 235 BP 691 EP 705 PG 15 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88R UT WOS:A1994BA88R00056 PM 7520122 ER PT S AU BHATIA, SN TONER, M TOMPKINS, RG YARMUSH, ML AF BHATIA, SN TONER, M TOMPKINS, RG YARMUSH, ML BE Kelly, RM Wittrup, KD Karkare, S TI SELECTIVE ADHESION OF HEPATOCYTES ON PATTERNED SURFACES SO BIOCHEMICAL ENGINEERING VIII SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Biochemical Engineering VIII CY JUL 11-16, 1993 CL PRINCETON, NJ SP Engn Fdn, Natl Sci Fdn, New York Acad Sci ID POTENTIAL BIOARTIFICIAL LIVER; CULTURED RAT HEPATOCYTES; HOLLOW FIBER BIOREACTOR; SANDWICH CONFIGURATION; BILIRUBIN CONJUGATION; HEPATIC-FAILURE; CELL-ADHESION; COLLAGEN; MICROCARRIERS; TECHNOLOGY C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02114. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08855. FU NIDDK NIH HHS [DK-41709, DK-43371] NR 44 TC 32 Z9 36 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-914-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 745 BP 187 EP 209 PG 23 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Science & Technology - Other Topics GA BD11Y UT WOS:A1994BD11Y00015 PM 7832508 ER PT S AU STRONG, L YARMUSH, DM YARMUSH, ML AF STRONG, L YARMUSH, DM YARMUSH, ML BE Kelly, RM Wittrup, KD Karkare, S TI ANTIBODY-TARGETED PHOTOLYSIS - PHOTOPHYSICAL, BIOCHEMICAL, AND PHARMACOKINETIC PROPERTIES OF ANTIBACTERIAL CONJUGATES SO BIOCHEMICAL ENGINEERING VIII SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Biochemical Engineering VIII CY JUL 11-16, 1993 CL PRINCETON, NJ SP Engn Fdn, Natl Sci Fdn, New York Acad Sci ID MONOCLONAL-ANTIBODY; LASER PHOTORADIATION; SINGLET OXYGEN; HEMATOPORPHYRIN; TUMORS; CELLS; PHOTODESTRUCTION; IRRADIATION; RADIATION; CARCINOMA C1 RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA 02114. NR 44 TC 6 Z9 6 U1 1 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-914-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 745 BP 297 EP 320 PG 24 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Science & Technology - Other Topics GA BD11Y UT WOS:A1994BD11Y00026 PM 7530432 ER PT J AU MCINTYRE, GD SCOTT, CF RITZ, J BLATTLER, WA LAMBERT, JM AF MCINTYRE, GD SCOTT, CF RITZ, J BLATTLER, WA LAMBERT, JM TI PREPARATION AND CHARACTERIZATION OF INTERLEUKIN-2-GELONIN CONJUGATES MADE USING DIFFERENT CROSS-LINKING REAGENTS SO BIOCONJUGATE CHEMISTRY LA English DT Article ID RIBOSOME-INACTIVATING PROTEINS; DIPHTHERIA-TOXIN FRAGMENT; T-CELL LINES; RICIN-A; ESCHERICHIA-COLI; EUKARYOTIC RIBOSOMES; GALACTOSE-BINDING; LYMPHOID-CELLS; BLOCKED RICIN; GROWTH-FACTOR AB Conjugates of IL-2 with the ribosome-inactivating protein gelonin were prepared using heterobifunctional reagents to link the proteins via disulfide, acid-labile, and noncleavable linkers. In each case, one protein was modified using 2-iminothiolane. The sulfhydryl groups so introduced were then reacted either with 2-nitro-5-dithiobenzoate groups or with iodoacetamido groups which had been introduced into the second protein. In the case of the acid-labile linkage, a reagent which forms a labile bond upon reaction with amino groups, 4-(iodoacetamido)-l-cyclohexene-1,2-dicarboxylic acid anhydride (its synthesis is described in this paper) was used to modify the toxin. The conjugates were separated from nonconjugated proteins by gel filtration on Sephadex G100 (SF). Each was analyzed with respect to its ribosome-inactivating activity, its ability to bind to the IL-2 receptor, and its in vitro cytotoxicity. The ribosome-inactivating activity of gelonin was unaffected by modification with 2-iminothiolane and was retained in conjugates prepared using this ragent. Modification of the toxin with 4-(iodoacetamido)-1-cyclohexene-1,2-dicarboxylic acid anhydride to form the acid-labile link drastically reduced the activity of the toxin. However, the activity of the toxin was recovered following acid treatment to release the native protein. Conjugates containing each type of linkage exhibited both specific binding and selective cytotoxicity toward cells expressing the IL-2 receptor. The most potent of these toxins, that containing the disulfide linkage, exhibited a cytotoxicity which was 2 orders of magnitude greater than that of unconjugated gelonin. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. OI Ritz, Jerome/0000-0001-5526-4669 NR 63 TC 24 Z9 24 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD JAN-FEB PY 1994 VL 5 IS 1 BP 88 EP 97 DI 10.1021/bc00025a012 PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA MW637 UT WOS:A1994MW63700012 PM 8199239 ER PT J AU SCHROEDER, MM HANDELSMAN, L TORRES, L DORFMAN, D RINALDI, P JACOBSON, J WIENER, J RITTER, W AF SCHROEDER, MM HANDELSMAN, L TORRES, L DORFMAN, D RINALDI, P JACOBSON, J WIENER, J RITTER, W TI EARLY AND LATE COGNITIVE EVENT-RELATED POTENTIALS MARK STAGES OF HIV-1 INFECTION IN THE DRUG-USER RISK GROUP SO BIOLOGICAL PSYCHIATRY LA English DT Article DE EVENT-RELATED POTENTIALS; HIV-1 INFECTION; AIDS; DEMENTIA; ADC ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS DEMENTIA COMPLEX; ELECTROPHYSIOLOGICAL DIFFERENCES; DISCRIMINATION TASKS; MISMATCH NEGATIVITY; PARKINSONS-DISEASE; BRAIN; MANIFESTATIONS; P300; SCHIZOPHRENIA AB HIV-1 (Human immunodeficiency virus) infection of the brain causes delays in auditory event-related potential (ERP) components. We recorded auditory ERPs from 38 former parenteral drug users (PDUs) at three stages of HIV-1 infection: seronegative; seropositive; stage II; and seropositive, stage IV. There were five response conditions: Go Nogo, Count, Simple Response, Simple Count, and Ignore. P3 peak latencies were significantly delayed and P3 amplitudes were significantly reduced for all seropositives, including asymptomatics, when compared to PDU seronegative controls. In contrast, the P1 and N1 peak latency measures were delayed only for seropositives with acquired immunodeficiency syndrome (AIDS) qualifying illnesses. There was a significant negative correlation between the CD4 count and the latency of P1, N1, and the MMN. Also, increased P1 and N1 amplitudes correlated with indices of disease progression (Choice RT and CD4 counts, respectively). The results extend previous findings by clarifying the pattern of auditory ERP markers of disease progression. Early, as well as late, brain involvement caused by HIV-1 is marked by delays and decreased amplitudes in cognitive components. In addition, late brain involvement is marked by delays and increased amplitudes in specific, automatic, and/or obligatory components. C1 VET AFFAIRS MED CTR,NEUROL SERV,BRONX,NY. VET AFFAIRS MED CTR,INFECT DIS SERV,BRONX,NY. MT SINAI SCH MED,NEW YORK,NY. ALBERT EINSTEIN COLL MED,DEPT NEUROL,BRONX,NY. ALBERT EINSTEIN COLL MED,DEPT NEUROSCI,BRONX,NY. CUNY,LEHMAN COLL,DEPT PSYCHOL,NEW YORK,NY. RP SCHROEDER, MM (reprint author), BRONX VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 65 TC 24 Z9 24 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD JAN 1 PY 1994 VL 35 IS 1 BP 54 EP 69 DI 10.1016/0006-3223(94)91168-1 PG 16 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MW336 UT WOS:A1994MW33600010 PM 8167205 ER PT S AU HYMAN, BT STRICKLAND, DK REBECK, GW AF HYMAN, BT STRICKLAND, DK REBECK, GW BE Borth, W Feinman, RD Gonias, SL Quigley, JP Strickland, DK TI ALPHA(2)-MACROGLOBULIN RECEPTOR LOW-DENSITY-LIPOPROTEIN RECEPTOR-RELATED PROTEIN - RELATIONSHIP TO APOLIPOPROTEIN-E AND ROLE IN ALZHEIMER-DISEASE SENILE PLAQUES SO BIOLOGY OF ALPHA2-MACROGLOBULIN, ITS RECEPTOR, AND RELATED PROTEINS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Biology of Alpha-Macroglobulin, Its Receptor, and Related Proteins CY OCT 11-14, 1993 CL WOODS HOLE, MA SP NEW YORK ACAD SCI ID IDENTIFICATION; FREQUENCY; INHIBITOR; SUGGESTS; LINKAGE; ALLELE; BRAIN C1 AMER RED CROSS,HOLLAND LABS,ROCKVILLE,MD 20855. RP HYMAN, BT (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. FU NIA NIH HHS [AG05598, AG08487]; NIGMS NIH HHS [GM42581] NR 24 TC 7 Z9 7 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-886-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 737 BP 88 EP 95 DI 10.1111/j.1749-6632.1994.tb44303.x PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics GA BB35Z UT WOS:A1994BB35Z00007 PM 7944156 ER PT J AU COLON, JM SANTORO, N GOLDSMITH, LT WHITCOMB, R MUSKET, D WEISS, G AF COLON, JM SANTORO, N GOLDSMITH, LT WHITCOMB, R MUSKET, D WEISS, G TI RELAXIN SECRETION INTO HUMAN SEMEN IS INDEPENDENT OF GONADOTROPIN STIMULATION SO BIOLOGY OF REPRODUCTION LA English DT Article ID HUMAN SEMINAL PLASMA; PORCINE RELAXIN; CORPUS-LUTEUM; GENE; EXPRESSION; PREGNANCY; INDUCTION; PROSTATE; MOTILITY; PRODUCT AB To investigate the control of relaxin (Rlx) secretion in men, we studied seminal plasma Rlx concentrations after physiologic and supraphysiologic gonadal stimulation. In the first experiment, 14 men with idiopathic hypogonadotropic hypogonadism provided semen samples at various time points before and during therapy with pulsatile GnRH. These data were compared to seminal plasma Rlx values in 5 normal men. In a second experiment, pharmacologic doses of hCG were administered in a fashion similar to that previously shown to have stimulated Rlx secretion from the CL of women. In men with idiopathic hypogonadotropic hypogonadism, no relationship was detected by Linear regression analysis between seminal plasma Rlx and testosterone, testicular volume, ejaculate volume, or the appearance of sperm in the ejaculate. Rlx concentrations varied considerably between subjects (6-120 ng/ml) but remained fairly consistent within the same individual over time. Supraphysiologic gonadal stimulation with hCG similarly failed to alter seminal plasma Rlx (n = 5, mean +/- SEM; 48 +/- 9 ng/ml, 42 +/- 7 ng/ml, and 56 +/- 9 ng/ml on Days 1, 3, and 6, respectively; p > 0.05) in normal men despite dramatic increases in serum testosterone (763 +/- 25 ng/dl, 1702 +/- 136 ng/dl, and 1494 +/- 97 ng/dl on Days 1, 3, and 6, respectively; p < 0.05 vs. Day 1). Taken together, these data suggest that Rlx in men is secreted independently from direct gonadotropin control. C1 MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINE UNIT,BOSTON,MA 02114. RP COLON, JM (reprint author), UMDNJ,NEW JERSEY MED SCH,DEPT OBSTET & GYNECOL,185 S ORANGE AVE MSB-E506,NEWARK,NJ 07103, USA. FU FDA HHS [FD-U-000523-1]; NICHD NIH HHS [HD-15788, HD-22338] NR 32 TC 4 Z9 4 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD JAN PY 1994 VL 50 IS 1 BP 187 EP 192 DI 10.1095/biolreprod50.1.187 PG 6 WC Reproductive Biology SC Reproductive Biology GA MM738 UT WOS:A1994MM73800024 PM 8312442 ER PT J AU YOUNIS, AI TONER, M ALBERTINI, D BIGGERS, JD AF YOUNIS, AI TONER, M ALBERTINI, D BIGGERS, JD TI CRYOBEHAVIOR OF NONHUMAN PRIMATE OOCYTES SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,NERPRC,DIV REPROD BIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,SURG RES LAB,BOSTON,MA 02114. TUFTS UNIV,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,LHRRB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1994 VL 50 SU 1 BP 188 EP 188 PG 1 WC Reproductive Biology SC Reproductive Biology GA NR591 UT WOS:A1994NR59100540 ER PT J AU NIHEI, K KOWALL, NW MCKEE, AC SASAKI, H AF NIHEI, K KOWALL, NW MCKEE, AC SASAKI, H TI NPY IMMUNOREACTIVE NEURONS ARE INVOLVED IN THE DEGENERATION OF AMYOTROPHIC-LATERAL-SCLEROSIS SO BIOMEDICAL RESEARCH-TOKYO LA English DT Article; Proceedings Paper CT 15th Gut Hormone Conference CY OCT 19-22, 1993 CL SHIZUOKA, JAPAN ID ALZHEIMERS-TYPE DEMENTIA; METHYL-D-ASPARTATE; RAT SPINAL-CORD; HUNTINGTONS-DISEASE; NEUROPEPTIDE-Y; NEUROCHEMICAL CHARACTERIZATION; CEREBRAL-CORTEX; KAINIC ACID; ANTISERA; LESIONS AB We studied neuropeptide Y (NPY) immunoreactivity in the brain of amyotrophic lateral sclerosis (ALS) patients and performed a quantitative histochemical study to further define patterns of neuronal degeneration in ALS. The density of NPY fibers in ALS motor cortex is decreased but not in other cortical regions. Although the densities of NPY neurons in the cortex and infracortical white matter are preserved even in high grade cases, the neurons are shrunken and atrophic with pruned dendrites. The degeneration pattern of NPY immunoreactive neurons in ALS motor cortex is closely similar to that of NADPH-diaphorase, and is different from that of parvalbumin immunoreactive cortical interneurons which shows severe depletion in ALS motor cortex. Distinctive patterns of local circuit neuron involvement may be a reflection of the neuronal degeneration mechanism of ALS brain which is quite different from both those of Alzheimer's and Huntington's diseases. C1 VET ADM MED CTR,CTR GERIATR RES EDUC CLIN,BEDFORD,MA 01730. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP NIHEI, K (reprint author), YAMAGATA UNIV,SCH MED,DEPT INTERNAL MED 3,YAMAGATA 99023,JAPAN. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 17 TC 0 Z9 0 U1 0 U2 0 PU BIOMED RES FOUND PI TOKYO PA KANDA PO BOX 182 CHIYODAKU, TOKYO 101-91, JAPAN SN 0388-6107 J9 BIOMED RES-TOKYO JI Biomed. Res. PY 1994 VL 15 SU 2 BP 209 EP 212 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QW117 UT WOS:A1994QW11700036 ER PT J AU GELBER, RD AF GELBER, RD TI BREAST-CANCER AND ADJUVANT TREATMENT SO BIOMEDICINE & PHARMACOTHERAPY LA English DT Note RP GELBER, RD (reprint author), DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0753-3322 J9 BIOMED PHARMACOTHER JI Biomed. Pharmacother. PY 1994 VL 48 IS 8-9 BP 409 EP 409 DI 10.1016/0753-3322(94)90067-1 PG 1 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA PM868 UT WOS:A1994PM86800022 ER PT J AU BYRD, TF AF BYRD, TF TI CYTOKINES AND LEGIONELLOSIS SO BIOTHERAPY LA English DT Article DE FERRITIN; INTERFERON GAMMA; IRON; LACTOFERRIN; MONOCYTE; TRANSFERRIN ID COLONY-STIMULATING FACTOR; RECOMBINANT INTERFERON-GAMMA; HUMAN-MONOCYTES INHIBIT; INTRACELLULAR MULTIPLICATION; LEGIONNAIRES-DISEASE; MONONUCLEAR PHAGOCYTES; PNEUMOPHILA; IRON; MACROPHAGES; TRANSFERRIN AB Recent studies have led to an enhanced understanding of the role of cell-mediated immunity and cytokines in Legionnaires' disease. In particular, the effect of interferon gamma on human mononuclear phagocyte iron metabolism and the role of iron availability in Legionella pneumophila intracellular multiplication in human monocytes has been elucidated. With this knowledge it is now possible to develop treatment strategies for Legionnaires' disease using interferon gamma and/or agents affecting human mononuclear phagocyte iron metabolism. RP BYRD, TF (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,WILSHIRE & SAWTELLE,BLDG 500,ROOM 4469,W111F,LOS ANGELES,CA 90073, USA. NR 21 TC 7 Z9 7 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0921-299X J9 BIOTHERAPY JI Biotherapy PY 1994 VL 7 IS 3-4 BP 179 EP 186 DI 10.1007/BF01878484 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA PQ405 UT WOS:A1994PQ40500005 PM 7865349 ER PT J AU HIRAYAMA, F KATAYAMA, N NEBEN, S DONALDSON, D NICKBARG, EB CLARK, SC OGAWA, M AF HIRAYAMA, F KATAYAMA, N NEBEN, S DONALDSON, D NICKBARG, EB CLARK, SC OGAWA, M TI SYNERGISTIC INTERACTION BETWEEN INTERLEUKIN-12 AND STEEL FACTOR IN SUPPORT OF PROLIFERATION OF MURINE LYMPHOHEMATOPOIETIC PROGENITORS IN CULTURE SO BLOOD LA English DT Article ID CELL STIMULATORY FACTOR; MULTIPOTENTIAL HEMATOPOIETIC PROGENITORS; LYMPHOCYTE MATURATION FACTOR; INTERLEUKIN-3-DEPENDENT PROLIFERATION; FACTOR NKSF; C-KIT; ENHANCEMENT; COLONIES; IDENTIFICATION; IMMUNOGLOBULIN C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. GENET INST INC,CAMBRIDGE,MA. FU NIDDK NIH HHS [DK32294] NR 31 TC 80 Z9 82 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 JAN 1 PY 1994 VL 83 IS 1 BP 92 EP 98 PG 7 WC Hematology SC Hematology GA MQ098 UT WOS:A1994MQ09800013 PM 7506084 ER PT J AU PIGNATA, C SANGHERA, JS COSSETTE, L PELECH, SL RITZ, J AF PIGNATA, C SANGHERA, JS COSSETTE, L PELECH, SL RITZ, J TI INTERLEUKIN-12 INDUCES TYROSINE PHOSPHORYLATION AND ACTIVATION OF 44-KD MITOGEN-ACTIVATED PROTEIN-KINASE IN HUMAN T-CELLS SO BLOOD LA English DT Article ID MICROTUBULE-ASSOCIATED PROTEIN-2; LYMPHOCYTE MATURATION FACTOR; COLONY-STIMULATING FACTOR; SIGNAL-REGULATED KINASES; MAP KINASE; HETERODIMERIC CYTOKINE; IL-12 RECEPTOR; GROWTH-FACTORS; PURIFICATION; TRANSDUCTION C1 UNIV BRITISH COLUMBIA,BIOMED RES CTR,VANCOUVER V6T 1W5,BC,CANADA. KINETEK BIOTECHNOL CORP,RICHMOND,BC,CANADA. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. UNIV BRITISH COLUMBIA,DEPT MED,VANCOUVER V6T 1W5,BC,CANADA. RI Pignata, Claudio/O-2466-2013; Ritz, Jerome/C-7929-2009 OI Pignata, Claudio/0000-0003-1568-9843; Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA41619] NR 35 TC 48 Z9 48 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 JAN 1 PY 1994 VL 83 IS 1 BP 184 EP 190 PG 7 WC Hematology SC Hematology GA MQ098 UT WOS:A1994MQ09800024 PM 7903874 ER PT J AU OGAWA, M SHIH, JP KATAYAMA, N AF OGAWA, M SHIH, JP KATAYAMA, N TI ENRICHMENT FOR PRIMITIVE HEMATOPOIETIC PROGENITORS OF MARROW-CELLS FROM 5-FLUOROURACIL-TREATED MICE AND NORMAL MICE SO BLOOD CELLS LA English DT Article; Proceedings Paper CT Symposium on Frontiers in Stem Cell Biology CY MAY 14-16, 1993 CL SANTA FE, NM DE PRIMITIVE HEMATOPOIETIC PROGENITORS; 5-FLUOROURACIL; C-KIT ID HEMATOPOIETIC STEM-CELLS; C-KIT; BONE-MARROW; SEPARATION; EXPRESSION; RECONSTITUTION; PURIFICATION; FLUORESCENCE; COLONIES AB Study of the mechanisms regulating stem cells would be significantly facilitated if a purified population of stem cells were available. During the last 4 years, our laboratory has been engaged in enrichment of murine marrow cells for primitive hemopoietic progenitors. We primarily used marrow cells from mice treated with 150 mg/kg of 5-fluorouracil (5-FU), and our assay for the primitive progenitors was formation of multilineage colonies supported by a combination of interleukin-3 (IL-3) and IL-6. First, we found that post-5-FU marrow cells with a density of 1.0631-1.0770 g/cm(3), negative for lineage-specific markers and positive for Ly-6A/E are routinely enriched for multipotential progenitors by approximately 800-fold. We then observed that J11d.2 and c-kit are additional useful markers for further enrichment of the primitive hemopoietic progenitors. Cell cycle-dormant primitive progenitors are primarily in the J11d.2(+) fraction, whereas more mature progenitors are J11d.2(-). The primitive progenitors express relatively low levels of c-kit, while more mature, actively cycling progenitors express high levels of c-kit. Combinations of these markers may be useful in enrichment of marrow cells of normal mice for primitive hemopoietic progenitors. C1 MED UNIV S CAROLINA,DEPT MED,DIV EXPTL HEMATOL,CHARLESTON,SC 29425. RP OGAWA, M (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. FU NIDDK NIH HHS [DK32294] NR 21 TC 12 Z9 13 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 1 BP 7 EP 13 PG 7 WC Hematology SC Hematology GA NX139 UT WOS:A1994NX13900002 PM 7994063 ER PT J AU KINASHI, T SPRINGER, TA AF KINASHI, T SPRINGER, TA TI ADHESION MOLECULES IN HEMATOPOIETIC-CELLS SO BLOOD CELLS LA English DT Article; Proceedings Paper CT Symposium on Frontiers in Stem Cell Biology CY MAY 14-16, 1993 CL SANTA FE, NM DE ADHESION MOLECULES; VERY LATE ANTIGEN-4; VASCULAR CELL ADHESION MOLECULE-1; MYELOID CELLS; STROMAL CELLS ID BONE-MARROW CULTURES; C-KIT; MAST-CELLS; B-LYMPHOCYTE; SI-LOCUS; GROWTH; DIFFERENTIATION; RECEPTOR; LIGAND; EXPRESSION AB Interaction with stromal cells is known to be crucial for growth and differentiation of hematopoietic cells. To characterize adhesion molecules involved in this interaction, we examined adhesion of a panel of lymphoid, myeloid, and mast cell lines with stromal cells. We found that very late antigen-4 (VLA-4) and vascular cell adhesion molecule 1 (VCAM-1) were major adhesion molecules in lymphoid and myeloid cells, whereas myeloma cells adhered to stromal cells through hyaluronate. We investigated regulation of VLA-4 during differentiation of myeloid cells using a neutrophil precursor cell line, L-G3. Differentiation of neutrophils induced by granulocyte colony-stimulating factor was accompanied with down-regulation of VLA-4. Induced L-G3 cells adhered to stromal cells in proportion to the expression of VLA-4. Mast cells used two mechanisms to adhere to fibroblasts and stromal cells. They adhered to fibronectin through VLA-5 when stimulated with steel factor and also directly to membrane-anchored steel factor through c-kit. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. FU NIDDK NIH HHS [DK45104] NR 36 TC 67 Z9 68 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 1 BP 25 EP 44 PG 20 WC Hematology SC Hematology GA NX139 UT WOS:A1994NX13900004 PM 7527678 ER PT J AU HIRAYAMA, F OGAWA, M AF HIRAYAMA, F OGAWA, M TI CYTOKINE REGULATION OF EARLY B-LYMPHOPOIESIS ASSESSED IN CULTURE SO BLOOD CELLS LA English DT Article DE B LYMPHOPOIESIS; STEEL FACTOR; INTERLEUKIN-6; GRANULOCYTE COLONY-STIMULATING FACTOR ID CELLS; PROGENITORS AB Lymphohemopoietic progenitors that are capable of expressing B-cell and myeloid lineages may be cultured from bone marrow cells of adult mice by using a two-step methylcellulose culture system, In this system, the primary colonies expressing myeloid lineages are plated in secondary culture for B-lymphoid colony formation, We have observed that combinations of two factors based on steel factor (SLF), such as SLF plus interleukin (IL)-6, SLF plus granulocyte colony-stimulating factor (G-CSF), and SLF plus IL-11 support the differentiation and proliferation of B-cell progenitors from the lymphohemopoietic progenitors, Surprisingly, IL-3 failed to support B lymphopoiesis either alone or in combination with other factors, In addition, when added to permissive culture conditions, IL-3 and IL-1 independently inhibited the B-cell potential of the primary colonies, The inhibitory effects of IL-3 and IL-1 observed in this in vitro system may be significant in the selection of cytokine combinations for in vitro expansion of hemopoietic stem cells. C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. NR 5 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 2-3 BP 341 EP 347 PG 7 WC Hematology SC Hematology GA PZ375 UT WOS:A1994PZ37500020 PM 7538338 ER PT J AU EMERY, DW SABLINSKI, T ARN, JS LEGUERN, C SACHS, DH AF EMERY, DW SABLINSKI, T ARN, JS LEGUERN, C SACHS, DH TI BONE-MARROW CULTURE AND TRANSDUCTION OF STEM-CELLS IN A MINIATURE SWINE MODEL SO BLOOD CELLS LA English DT Article DE TRANSPLANTATION; MAJOR HISTOCOMPATIBILITY COMPLEX; RETROVIRAL TRANSDUCTION; HEMATOPOIETIC STEM CELL; SWINE ID MEDIATED GENE-TRANSFER; BLOOD-CELLS; CORD-BLOOD; EXPRESSION; TRANSPLANTATION; TOLERANCE; CDNA AB Recombinant retroviral vectors, engineered to express the beta-chain gene of swine major histocompatibility complex class II DR, were developed for the genetic modification of swine hematopoietic stem cells (HSC). The expression of these vectors in swine bone marrow has been studied both in culture and after bone marrow transplantation. In addition, myeloid progenitor colony assays were performed on swine umbilical cord blood as part of a study to identify alternative sources of HSC for somatic gene transfer, revealing the presence of both granulocyte macrophage colony forming-units (CFU-GM) and CFU-Mix at frequencies comparable to those found in juvenile swine bone marrow. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. FU NHLBI NIH HHS [HL46532]; NIAID NIH HHS [AI33053] NR 12 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 2-3 BP 498 EP 503 PG 6 WC Hematology SC Hematology GA PZ375 UT WOS:A1994PZ37500038 PM 7749117 ER PT J AU DALEY, GQ AF DALEY, GQ TI GENETIC EVENTS IN CML - FROM TRANSLOCATION TO TRANSPLANTATION SO BONE MARROW TRANSPLANTATION LA English DT Article; Proceedings Paper CT 2nd International Symposium on Autografting for Chronic Myeloid Leukaemia CY JUN 26-27, 1994 CL GENOVA, ITALY ID CHRONIC MYELOGENOUS LEUKEMIA; ABL; MICE; BCR; INDUCTION RP DALEY, GQ (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114, USA. NR 11 TC 1 Z9 1 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PY 1994 VL 14 SU 3 BP S5 EP S9 PG 5 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA QA018 UT WOS:A1994QA01800002 PM 7697009 ER PT S AU CHIAPPELLI, F MANFRINI, E FRANCESCHI, C COSSARIZZA, A BLACK, KL AF CHIAPPELLI, F MANFRINI, E FRANCESCHI, C COSSARIZZA, A BLACK, KL BE deKloet, ER Azmitia, EC Landfield, PW TI STEROID REGULATION OF CYTOKINES - RELEVANCE FOR TH1-TO-TH2 SHIFT SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci ID HUMAN T-CELLS; ALZHEIMERS-DISEASE; GLUCOCORTICOID RECEPTORS; LYMPHOKINE PRODUCTION; HUMAN-LYMPHOCYTES; ANOREXIA-NERVOSA; BRAIN-TUMORS; DEHYDROEPIANDROSTERONE; HELPER; INVITRO C1 UNIV CALIF LOS ANGELES, SCH MED, BRAIN & DENT RES INST, DEPT NEUROBIOL, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, HUMAN IMMUNOL & PSYCHONEUROIMMUNOL LAB, LOS ANGELES, CA 90073 USA. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES, SCH DENT, BRAIN & DENT RES INST, LOS ANGELES, CA 90024 USA. OI Cossarizza, Andrea/0000-0002-5381-1558 FU NIAID NIH HHS [AI07126]; NIDA NIH HHS [DA07683] NR 92 TC 33 Z9 33 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 204 EP 215 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00017 PM 7825877 ER PT S AU CHIAPPELLI, F MANFRINI, E GWIRTSMAN, H GARCIA, C PHAM, L LEE, P FROST, P AF CHIAPPELLI, F MANFRINI, E GWIRTSMAN, H GARCIA, C PHAM, L LEE, P FROST, P BE deKloet, ER Azmitia, EC Landfield, PW TI STEROID RECEPTOR-MEDIATED MODULATION OF CD4+CD62L+ CELL HOMING - IMPLICATIONS FOR DRUG-ABUSERS SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci ID PRODUCTS; ADHESION C1 UNIV CALIF LOS ANGELES, SCH MED, BRAIN RES INST, DEPT NEUROBIOL, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, HUMAN IMMUNOL & PSYCHOEUROIMMUNOL LAB, LOS ANGELES, CA 90073 USA. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES, SCH DENT, DENT RES INST, HUMAN ORAL & MOLEC IMMUNOL LAB, LOS ANGELES, CA 90024 USA. OI Frost, Patrick/0000-0003-3348-5983 FU NIAID NIH HHS [AI07126]; NIDA NIH HHS [DA07683] NR 11 TC 5 Z9 5 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 421 EP 425 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00043 PM 7529973 ER PT S AU CAVINESS, VC TAKAHASHI, T MIYAMA, S TSAI, LH AF CAVINESS, VC TAKAHASHI, T MIYAMA, S TSAI, LH BE Lou, HC Greisen, G Larsen, JF TI CYTOGENESIS IN THE DEVELOPING MOUSE NEOCORTEX SO BRAIN LESIONS IN THE NEWBORN: HYPOXIC AND HAEMODYNAMIC PATHOGENESIS SE ALFRED BENZON SYMPOSIUM SERIES LA English DT Proceedings Paper CT 37th Benzon Symposium on Brain Lesions in the Newborn: Hypoxic and Haemodynamic Pathogenesis CY AUG 15-19, 1993 CL ROYAL DANISH ACAD SCI & LETT, COPENHAGEN, DENMARK SP ROYAL DANISH ACAD SCI & LETT, BENZON FDN HO ROYAL DANISH ACAD SCI & LETT C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MUNKSGAARD PI COPENHAGEN K PA 35 NORRE SOGADE POSTBOX 2148, DK-1016 COPENHAGEN K, DENMARK SN 0105-3639 BN 87-16-11231-8 J9 ALFRED BENZON SYMP S PY 1994 VL 37 BP 25 EP 42 PG 18 WC Clinical Neurology; Neurosciences; Pediatrics SC Neurosciences & Neurology; Pediatrics GA BA54U UT WOS:A1994BA54U00002 ER PT J AU DALKARA, T MOSKOWITZ, MA AF DALKARA, T MOSKOWITZ, MA TI THE COMPLEX ROLE OF NITRIC-OXIDE IN THE PATHOPHYSIOLOGY OF FOCAL CEREBRAL-ISCHEMIA SO BRAIN PATHOLOGY LA English DT Article ID L-ARGININE; CELLS AB Nitrogen monoxide (NO) has recently emerged as an important mediator of cellular and molecular events which impacts the pathophysiology of cerebral ischemia. Although tempting to ask whether NO is ''good or bad'' for cerebral ischemia, the question underestimates the complexities of NO chemistry and physiology as well as oversimplifies the pathophysiology of focal cerebral ischemia. Important vascular and neuronal actions of NO have been defined which both enhance tissue survival and mediate cellular injury and death, and these will be reviewed. Strategies which modify NO synthesis and/or metabolism may someday assume therapeutic importance, but not until the tissue compartments generating NO, the activities of the enzymes that are inducibly and constitutively expressed, and the redox state of NO during the stages of ischemic injury, are defined with greater precision. Our knowledge of these processes is rudimentary. This review will summarize the evidence from animal models which supports an emerging role for NO in ischemic pathophysiology. Important aspects of NO synthesis and inhibitors of this process will also be discussed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROSURG & NUEROL,STROKE RES LAB,BOSTON,MA 02114. RI Moskowitz, Michael/D-9916-2011 NR 6 TC 156 Z9 162 U1 1 U2 2 PU INT SOC NEUROPATHOLOGY PI ZURICH PA ISN JOURNAL PO BOX, CH-8033 ZURICH, SWITZERLAND SN 1015-6305 J9 BRAIN PATHOL JI Brain Pathol. PD JAN PY 1994 VL 4 IS 1 BP 49 EP 57 PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA MU866 UT WOS:A1994MU86600006 PM 7517769 ER PT J AU LEUNIG, M GOETZ, AE GAMARRA, F ZETTERER, G MESSMER, K JAIN, RK AF LEUNIG, M GOETZ, AE GAMARRA, F ZETTERER, G MESSMER, K JAIN, RK TI PHOTODYNAMIC THERAPY-INDUCED ALTERATIONS IN INTERSTITIAL FLUID PRESSURE, VOLUME AND WATER-CONTENT OF AN AMELANOTIC MELANOMA IN THE HAMSTER SO BRITISH JOURNAL OF CANCER LA English DT Note AB The effect of photodynamic therapy (PDT) on interstitial fluid pressure (IFP), tumour volume and water content was measured in melanomas grown in hamsters. Unlike control tumours, treated rumours exhibited a 40-60% increase in volume at 1, 3 and 6 h post PDT. IFP also increased al 1 and 3 h after PDT, but decreased to 50% of control value after 24 h, presumably as a result of PDT-induced microcirculatory impairment. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL, STEELE LAB, BOSTON, MA 02114 USA. UNIV MUNICH, KLINIKUM GROSSHADERN, INST ANAESTHESIOL, D-81366 MUNICH, GERMANY. RP LEUNIG, M (reprint author), UNIV MUNICH, KLINIKUM GROSSHADERN, INST SURG RES, MARCHIONINISTR 15, D-81366 MUNICH, GERMANY. RI Leunig, Michael/E-7951-2017 OI Leunig, Michael/0000-0002-2036-5416 FU NCI NIH HHS [CA-56591] NR 26 TC 34 Z9 35 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD JAN PY 1994 VL 69 IS 1 BP 101 EP 103 DI 10.1038/bjc.1994.15 PG 3 WC Oncology SC Oncology GA MQ287 UT WOS:A1994MQ28700015 PM 8286189 ER PT J AU KAPLAN, SS OGILVY, CS CROWELL, RM AF KAPLAN, SS OGILVY, CS CROWELL, RM TI INCIDENTALLY DISCOVERED ARTERIOVENOUS MALFORMATION OF THE ANTERIOR FOSSA DURA SO BRITISH JOURNAL OF NEUROSURGERY LA English DT Note DE DURAL ARTERIOVENOUS MALFORMATION; OPHTHALMIC ARTERY; ANTERIOR CRANIAL FOSSA; INCIDENTAL ID CRANIAL FOSSA; HEMORRHAGE AB Dural arteriovenous malformations (AVMs) are rare vascular abnormalities that most frequently involve the cavernous, transverse or sigmoid sinus. Anterior cranial fossa dural AVMs are uncommon. We report the clinical, radiological and surgical features of an incidentally discovered anterior fossa dural AVM. The literature regarding the anatomy and clinical presentation of this lesion is reviewed. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,FRUIT ST,BOSTON,MA 02114. NR 27 TC 5 Z9 6 U1 0 U2 0 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXON, ENGLAND OX14 3UE SN 0268-8697 J9 BRIT J NEUROSURG JI Br. J. Neurosurg. PY 1994 VL 8 IS 6 BP 755 EP 759 DI 10.3109/02688699409101194 PG 5 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA QC709 UT WOS:A1994QC70900017 PM 7718176 ER PT S AU LIPTON, SA AF LIPTON, SA BE Disterhoft, JF Gispen, WH Traber, J Khachaturian, ZS TI AIDS-RELATED DEMENTIA AND CALCIUM HOMEOSTASIS SO CALCIUM HYPOTHESIS OF AGING AND DEMENTIA SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Calcium Hypothesis of Aging and Dementia CY DEC 15-17, 1993 CL NIH, BETHESDA, MD SP Alzheimers Assoc, Farbenfabriken Bayer GMBH, Fischer Fdn, French Fdn, NIA, NIH HO NIH ID HUMAN-IMMUNODEFICIENCY-VIRUS; METHYL-D-ASPARTATE; PLATELET-ACTIVATING-FACTOR; TUMOR-NECROSIS-FACTOR; RECEPTOR-MEDIATED NEUROTOXICITY; VASOACTIVE-INTESTINAL-PEPTIDE; PRIMARY CORTICAL CULTURES; AMINO-ACID NEUROTOXICITY; HIV-1 ENVELOPE PROTEIN; RETINAL GANGLION-CELLS C1 CHILDRENS HOSP,DEPT NEUROL,MOLEC & CELLULAR NEUROSCI LAB,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,PROGRAM NEUROSCI,BOSTON,MA 02115. FU NEI NIH HHS [EY05477, EY09024]; NICHD NIH HHS [HD29587] NR 125 TC 49 Z9 50 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-879-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 747 BP 205 EP 224 PG 20 WC Cell Biology; Geriatrics & Gerontology; Multidisciplinary Sciences; Clinical Neurology; Neurosciences SC Cell Biology; Geriatrics & Gerontology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD12A UT WOS:A1994BD12A00014 PM 7847672 ER PT J AU INSKIP, PD EBY, NL COOKFAIR, D FREEDMAN, RS RICHARDSON, GS WACTAWSKIWENDE, J HOOVER, RN BOICE, JD AF INSKIP, PD EBY, NL COOKFAIR, D FREEDMAN, RS RICHARDSON, GS WACTAWSKIWENDE, J HOOVER, RN BOICE, JD TI SERUM ESTROGEN AND ANDROGEN LEVELS FOLLOWING TREATMENT FOR CERVICAL-CANCER SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID POST-MENOPAUSAL WOMEN; POSTMENOPAUSAL WOMEN; ENDOMETRIAL CANCER; BREAST-CANCER; CARDIOVASCULAR-DISEASE; ENDOCRINE FUNCTION; CIGARETTE-SMOKING; STEROID LEVELS; OVARIAN; RISK AB Endogenous sex hormones seem to influence the risk of several common and debilitating diseases. With a view toward better understanding the effects of surgical removal of the ovaries and high-dose pelvic radiotherapy on plasma sex hormone levels, we measured estrogen and androgen concentrations cross-sectionally among 147 women who had been treated for cervical cancer 0.3-18.5 years previously. Pelvic radiotherapy (mean dose to ovaries, 50 Gy) and bilateral ovariectomy were associated with similarly reduced hormone concentrations relative to levels among nonirradiated women with intact ovaries, most of whom had had early-stage disease and were treated by hysterectomy. There was little evidence that radiotherapy in addition to ovariectomy further lowered concentrations below levels associated with ovariectomy alone, such as might be expected if radiation was suppressing adrenal endocrine function. Among women age 50 years or older at the time of blood drawing, the removal or irradiation of the ovaries was associated with approximately 45% lower concentrations of estradiol (mean ratio [MR], 0.55; 95% confidence interval [CI], 0.32-0.95) and testosterone (MR, 0.57; 95% CI, 0.32-0.99), and 25-30% lower concentrations of estrone (MR, 0.69; 95% CI, 0.44-1.09) and androstenedione (MR, 0.76; 95% CI, 0.47-1.23), relative to the hysterectomy-only group. Among women younger than 50, ovariectomy and radiotherapy, alone or in combination, were associated with 83% lower estradiol concentrations (MR, 0.17; 95% CI, 0.09-0.31), 46% lower estrone concentrations (MR, 0.54; 95% CI, 0.37-0.81), 23% lower androstenedione concentrations (MR, 0.77; 95% CI, 0.57-1.04), and 14% lower testosterone levels (MR, 0.86; 95% CI, 0.64-1.15). A possible mechanism for the reductions among postmenopausal women involves effects on androgen-producing cells in the ovary, which retain secretory function after menopause. C1 NCI, DIV CANC ETIOL, EPIDEMIOL & BIOSTAT PROGRAM, BETHESDA, MD 20892 USA. GERMAN CANC RES CTR, INST EPIDEMIOL & BIOMETRY, W-6900 HEIDELBERG, GERMANY. SUNY BUFFALO, SCH MED, DEPT SOCIAL & PREVENT MED, BUFFALO, NY 14260 USA. SUNY BUFFALO, SCH MED, DEPT GYNECOL & OBSTET, BUFFALO, NY USA. UNIV TEXAS, MD ANDERSON CANC CTR, DEPT GYNECOL, HOUSTON, TX 77030 USA. MASSACHUSETTS GEN HOSP, VINCENT GYNECOL SERV, BOSTON, MA USA. NR 59 TC 6 Z9 6 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 EI 1538-7755 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1994 VL 3 IS 1 BP 37 EP 45 PG 9 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA MR391 UT WOS:A1994MR39100008 PM 8118384 ER PT J AU HUNCHAREK, M AF HUNCHAREK, M TI ASBESTOS AND CANCER - EPIDEMIOLOGIC AND PUBLIC-HEALTH CONTROVERSIES SO CANCER INVESTIGATION LA English DT Article ID MALIGNANT MESOTHELIOMA; PLEURAL MESOTHELIOMA; CHRYSOTILE ASBESTOS; EXPOSURE; MORTALITY; WORKERS; TREMOLITE; LUNG; CARCINOGENICITY; TEXTILE RP HUNCHAREK, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114, USA. NR 41 TC 14 Z9 14 U1 0 U2 3 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1994 VL 12 IS 2 BP 214 EP 222 DI 10.3109/07357909409024876 PG 9 WC Oncology SC Oncology GA NE508 UT WOS:A1994NE50800011 PM 8131096 ER PT J AU STEVENSON, MA POLLOCK, SS COLEMAN, CN CALDERWOOD, SK AF STEVENSON, MA POLLOCK, SS COLEMAN, CN CALDERWOOD, SK TI X-IRRADIATION, PHORBOL ESTERS, AND H2O2 STIMULATE MITOGEN-ACTIVATED PROTEIN-KINASE ACTIVITY IN NIH-3T3 CELLS THROUGH THE FORMATION OF REACTIVE OXYGEN INTERMEDIATES SO CANCER RESEARCH LA English DT Note ID C-FOS PROMOTER; IONIZING-RADIATION; TRANSCRIPTION FACTOR; TERNARY COMPLEX; KAPPA-B; GENE; INVOLVEMENT; EXPRESSION; INDUCTION; ELEMENT AB Extracellular signal-regulated kinases (ERKs), also known as mitogen-activated protein (MAP) kinases, are rapidly phosphorylated and activated in response to a number of external factors which promote growth and differentiation (T. G. Boulton, S. H. Nye, D. J. Robbins, N. Y. Ip, E. Radziejewska, S. D. Morgenbesser, R. A. DePinho, N. Panayotatos, M. H. Cobb, and G. D. Yancopoulos, Cell, 65: 663-675,1991; S. L. Pelech and S. S. Jasbinder, Science (Washington DC), 257: 1355-1356, 1992; G. Thomas, Cell, 68: 3-6, 1992). We have identified two novel stimulators of MAP kinase activity, ionizing radiation and H2O2. Both radiation and H2O2, as well as the known agonist 12-O-tetradecanoylphorbol 13-acetate activate MAP kinase through the production of reactive oxygen intermediates. Our results demonstrate a direct link between the MAP kinase signal transduction pathway and reactive oxygen species and provide a unifying mechanism for activation of early- and late-response genes by inducers of oxidative stress. C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. RP HARVARD UNIV, SCH MED, JOINT CTR RADIAT THERAPY, 50 BINNEY ST, BOSTON, MA 02115 USA. NR 21 TC 224 Z9 227 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 EI 1538-7445 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1994 VL 54 IS 1 BP 12 EP 15 PG 4 WC Oncology SC Oncology GA MQ280 UT WOS:A1994MQ28000005 PM 8261431 ER PT J AU EDELMAN, JM CHAN, BMC UNIYAL, S ONODERA, H WANG, DZ STJOHN, NF DAMJANOVICH, L LATZER, DB FINBERG, RW BERGELSON, JM AF EDELMAN, JM CHAN, BMC UNIYAL, S ONODERA, H WANG, DZ STJOHN, NF DAMJANOVICH, L LATZER, DB FINBERG, RW BERGELSON, JM TI THE MOUSE VLA-2 HOMOLOG SUPPORTS COLLAGEN AND LAMININ ADHESION BUT NOT VIRUS BINDING SO CELL ADHESION AND COMMUNICATION LA English DT Article DE MURINE INTEGRIN; ECHOVIRUS; VLA-2 COLLAGEN BINDING; LAMININ BINDING ID INTEGRIN VLA-2; EXTRACELLULAR-MATRIX; VONWILLEBRAND-FACTOR; SEQUENCE-ANALYSIS; ALPHA-2 SUBUNIT; CELL-ADHESION; RECEPTOR; DOMAIN; EXPRESSION; ANTIBODY AB Human VLA-2 (alpha(2) beta(1)) mediates cellular adhesion to collagen and laminin and cell attachment by the human pathogen echovirus 1. We report here the cloning, sequencing and functional expression of the mouse VLA-2 alpha subunit homologue. This integrin subunit is closely related to its human counterpart, with 84% amino acid identity between the human and murine proteins. Conserved structural features include an identical number of amino acids, the presence of an I domain, and identity in the number and position of N-linked glycosylation sites and putative divalent cation binding regions. Murine and human alpha(2) show 30% amino acid divergence within the cytoplasmic tail, a difference that can be detected with antisera directed against the C-terminal peptides. Functionally, mouse alpha(2) was capable of mediating cell attachment to collagen and laminin, and responded to both intra- and extracellular signals with changes in its ligand affinity. In contrast, unlike its human homologue, mouse alpha(2) did not promote binding of echovirus I. Comparison of the primary structure of the homologues leads us to predict that echovirus 1 may bind in the region of the first two thirds of the human alpha(2) 1 domain, where the sequences are most divergent, whereas more conserved flanking regions, and the conserved terminal one third of the I domain, may be involved in adhesion to collagen and laminin. C1 WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. UNIV GUELPH,DEPT CHEM & BIOCHEM,GUELPH N1G 2W1,ON,CANADA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. RI Finberg, Robert/E-3323-2010 FU NCI NIH HHS [CA 19144]; NHLBI NIH HHS [HL 39023]; NIAID NIH HHS [AI 31628] NR 33 TC 11 Z9 12 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1061-5385 J9 CELL ADHES COMMUN JI Cell Adhes. Commun. PY 1994 VL 2 IS 2 BP 131 EP 143 DI 10.3109/15419069409004432 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NV065 UT WOS:A1994NV06500004 PM 8081889 ER PT J AU BERGELSON, JM STJOHN, NF KAWAGUCHI, S PASQUALINI, R BERDICHEVSKY, F HEMLER, ME FINBERG, RW AF BERGELSON, JM STJOHN, NF KAWAGUCHI, S PASQUALINI, R BERDICHEVSKY, F HEMLER, ME FINBERG, RW TI THE I-DOMAIN IS ESSENTIAL FOR ECHOVIRUS-1 INTERACTION WITH VLA-2 SO CELL ADHESION AND COMMUNICATION LA English DT Article DE INTEGRIN; LIGAND INTERACTIONS; VIRUS RECEPTOR; PICORNAVIRUS ID LIGAND-BINDING; EXTRACELLULAR-MATRIX; VITRONECTIN RECEPTOR; MONOCLONAL-ANTIBODY; PLATELET INTEGRIN; ALPHA-2 SUBUNIT; CELL-ADHESION; COLLAGEN; IDENTIFICATION; SITE AB VLA-2, the alpha 2 beta 1 integrin, mediates cell adhesion to collagen and laminin, and is the receptor for the human pathogen echovirus 1. Because of its similarity to domains present in other proteins that interact with collagen, a 191 amino acid region within the alpha 2 subunit (the I domain) has been proposed as a potential site for ligand interactions. Although the alpha 2 subunits of human and murine VLA-2 are 84% identical, human alpha 2 promotes virus binding whereas murine alpha 2 does not. We used murine/human chimeric alpha 2 molecules to identify regions of the human molecule essential for virus binding. Virus bound efficiently to a chimeric protein in which the human I domain was inserted into murine alpha 2, indicating that the human I domain is responsible for specific virus interactions. Monoclonal antibodies that inhibited virus attachment all recognized epitopes within the human I domain, further suggesting that virus interacts with this portion of the molecule. Similarly, antibodies that prevented VLA-2-mediated cell adhesion to collagen also mapped to the I domain. These results indicate that the I domain plays a role in VLA-2 interactions both with virus and with extracellular matrix ligands. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. RP BERGELSON, JM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,JIMMY FUND 409,44 BINNEY ST,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU NIAID NIH HHS [AI31628]; NIGMS NIH HHS [GM38903] NR 34 TC 40 Z9 40 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1061-5385 J9 CELL ADHES COMMUN JI Cell Adhes. Commun. PY 1994 VL 2 IS 5 BP 455 EP 464 DI 10.3109/15419069409004455 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PP745 UT WOS:A1994PP74500007 PM 7842258 ER PT B AU BRUCE, JL PRICE, BD CALDERWOOD, SK AF BRUCE, JL PRICE, BD CALDERWOOD, SK BE Hu, VW TI ACTIVATION OF THE HEAT-SHOCK TRANSCRIPTION FACTOR DURING G1 SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,STRESS PROT GRP,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 155 EP 161 PG 7 GA BA55Y UT WOS:A1994BA55Y00017 ER PT B AU PARDEE, AB DOU, QP KEYOMARSI, K AF PARDEE, AB DOU, QP KEYOMARSI, K BE Hu, VW TI MOLECULES OF DEREGULATED CELL-CYCLE CONTROL IN CANCER SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 303 EP 309 PG 7 GA BA55Y UT WOS:A1994BA55Y00035 ER PT B AU ZOU, ZQ ANISOWICZ, A RAFIDI, K SAGER, R AF ZOU, ZQ ANISOWICZ, A RAFIDI, K SAGER, R BE Hu, VW TI DOWN-REGULATION OF CANDIDATE TUMOR-SUPPRESSOR GENES IN BREAST-CANCER SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC GENET,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 319 EP 322 PG 4 GA BA55Y UT WOS:A1994BA55Y00037 ER PT B AU MOSKOWITZ, MA WAEBER, C AF MOSKOWITZ, MA WAEBER, C BE Municio, AM MirasPortugal, MT TI THE 5-HT(1D) RECEPTOR SUBTYPE AND MIGRAINE HEADACHE SO CELL SIGNAL TRANSDUCTION, SECOND MESSENGERS, AND PROTEIN PHOSPHORYLATION IN HEALTH AND DISEASE LA English DT Proceedings Paper CT International Symposium on Cell Signal Transduction, Second-Messengers, and Protein Phosphorylation in Health and Disease CY JUL 05-09, 1993 CL EL ESCORIAL, SPAIN RP MOSKOWITZ, MA (reprint author), MASSACHUSETTS GEN HOSP,STROKE RES LAB,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44814-9 PY 1994 BP 199 EP 204 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BB81T UT WOS:A1994BB81T00019 ER PT J AU FAMULARO, R FENTON, T KINSCHERFF, R AYOUB, C BARNUM, R AF FAMULARO, R FENTON, T KINSCHERFF, R AYOUB, C BARNUM, R TI MATERNAL AND CHILD POSTTRAUMATIC-STRESS-DISORDER IN CASES OF CHILD MALTREATMENT SO CHILD ABUSE & NEGLECT LA English DT Article DE CHILD ABUSE AND NEGLECT; CHILD MALTREATMENT; POSTTRAUMATIC STRESS DISORDER; PTSD; DOMESTIC VIOLENCE ID POST-TRAUMATIC STRESS; SEXUAL ABUSE; POPULATION; VICTIMS AB The purpose of this study was to examine the rates of posttraumatic stress disorder (PTSD) among a sample of severely maltreated children and their mothers, and to investigate the age of onset of documented maltreatment in these children. The sample consisted of 109 pairs of women and their children who were before a juvenile/family court due to maltreatment of sufficient severity to warrant removal of the child from parental custody. Children were examined using the PTSD Section of the Diagnostic Interview for Children and Adolescents, Revised 6th Version (DICA-6-R). The PTSD Module of the Structured Clinical Interview for DSM-III-R (SCID) was administered to all mothers. Clinical psychiatric interviews were also administered to all children and mothers. From the sample of 109 cases, 15.6% of the mothers met SCID criteria for a current presentation of PTSD, while 36.7% had a past history of PTSD. Of the 109 evaluated children, 35.8% met current DICA criteria for PTSD. Posttraumatic stress disorder is significantly overrepresented in the children of mothers diagnosed with PTSD (p = .00 1). The average age of maltreatment onset was 46.4 months among the children diagnosed as PTSD, and was 61.3 months in the group of seriously maltreated children who did not develop PTSD (p = .039). The onset of maltreatment is significantly earlier among children whose mothers meet PTSD criteria than among other maltreated children (p = .025). Intergenerational transmission of violence and developmental effects of traumatic experiences upon the young child are discussed. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MASSACHUSETTS DEPT MENT HLTH,BOSTON JUVENILE COURT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HARVARD GRAD SCH EDUC,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSSETTS DEPT MENT HLTH,BOSTON JUVENILE COURT,BOSTON,MA 02115. RP FAMULARO, R (reprint author), FRANCISCAN CHILDRENS HOSP,MASSACHUSETTS DEPT MENT HLTH,DEPT PEDIAT,BOSTON JUVENILE COURT CLIN,BOSTON,MA 02108, USA. FU NCI NIH HHS [90-CA-1408] NR 35 TC 64 Z9 66 U1 1 U2 7 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PD JAN PY 1994 VL 18 IS 1 BP 27 EP 36 DI 10.1016/0145-2134(94)90093-0 PG 10 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA MQ185 UT WOS:A1994MQ18500004 PM 8124596 ER PT J AU ROWAN, AB FOY, DW RODRIGUEZ, N RYAN, S AF ROWAN, AB FOY, DW RODRIGUEZ, N RYAN, S TI POSTTRAUMATIC-STRESS-DISORDER IN A CLINICAL-SAMPLE OF ADULTS SEXUALLY ABUSED AS CHILDREN SO CHILD ABUSE & NEGLECT LA English DT Article DE PTSD; CHILD SEXUAL ABUSE; EXPOSURE LEVELS ID POST-TRAUMATIC STRESS; CHILDHOOD; IMPACT; INCEST; SCALE; PTSD AB Forty-seven help-seeking, adult survivors of childhood sexual abuse (CSA) were assessed to examine the relationship between the level of CSA exposure and the subsequent development of posttraumatic stress disorder. CSA exposure was operationalized to include the overall level of exposure, frequency and duration of the abuse, age of onset, use of force, perceived life threat, and the occurrence of penetration. Participants were administered standardized measures of PTSD, including the Structured Clinical Interview of DSM-III-R (SCID). On the SCID, 69% of the survivors met full DSM-III-R criteria for PTSD. Significant correlations were found between several overall exposure measures and PTSD diagnostic status and the intensity of PTSD symptomatology. Similar relationships were identified with the duration and frequency of the abuse, the age of onset, and the use of force. This study is important in that it utilized standardized measures of PTSD and found a significant incidence of PTSD among adult CSA survivors. C1 FULLER THEOL SEMINARY,GRAD SCH PSYCHOL,180 N OAKLAND AVE,PASADENA,CA 91101. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,BRENTWOOD,CA. NR 33 TC 103 Z9 103 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PD JAN PY 1994 VL 18 IS 1 BP 51 EP 61 DI 10.1016/0145-2134(94)90095-7 PG 11 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA MQ185 UT WOS:A1994MQ18500006 PM 8124598 ER PT J AU COHEN, M ADAMS, PC PARRY, G XIONG, J CHAMBERLAIN, D WIECZOREK, I FOX, KAA CHESEBRO, JH STRAIN, J KELLER, C KELLY, A LANCASTER, G ALI, J KRONMAL, R FUSTER, V AF COHEN, M ADAMS, PC PARRY, G XIONG, J CHAMBERLAIN, D WIECZOREK, I FOX, KAA CHESEBRO, JH STRAIN, J KELLER, C KELLY, A LANCASTER, G ALI, J KRONMAL, R FUSTER, V TI COMBINATION ANTITHROMBOTIC THERAPY IN UNSTABLE REST ANGINA AND NON-Q-WAVE INFARCTION IN NONPRIOR ASPIRIN USERS - PRIMARY END-POINTS ANALYSIS FROM THE ATACS TRIAL SO CIRCULATION LA English DT Article DE ISCHEMIA; ASPIRIN; ANTICOAGULANTS ID CANINE CORONARY-ARTERIES; SUBSTITUTE HEART-VALVES; MYOCARDIAL-INFARCTION; OPERATIVE MORTALITY; PECTORIS; HEPARIN; DISEASE; DEATH; REVASCULARIZATION; PATHOGENESIS AB Background The purpose of this study was to compare combination antithrombotic therapy with aspirin plus anticoagulation versus aspirin alone, when added to conventional antianginal therapy in patients with unstable rest angina or non-Q-wave myocardial infarction who were nonprior aspirin users. Methods and Results Two hundred fourteen patients were randomized; 109 were randomized to receive aspirin alone (162.5 mg daily) and 105 to receive a combination of aspirin plus anticoagulation, ie, aspirin 162.5 mg daily plus heparin (activated partial thromboplastin time, two times control) followed by aspirin 162.5 mg daily plus warfarin (international normalized ratio, 2 to 3). Trial therapy was begun by 9.5+/-8.8 hours of qualifying pain and was continued for 12 weeks. Primary end points were recurrent angina with ECG changes, myocardial infarction, and/or death. Analysis by intention to treat of primary events at 12 weeks was performed. At 14 days, there was a significant reduction in total ischemic events in the combination group versus aspirin alone (10.5% versus 27%, P=.004). An efficacy analysis of primary events at 12 weeks also revealed a large reduction in total ischemic events in the combination group versus aspirin alone (13% versus 25%, P=.06). Bleeding complications were slightly more common with combination therapy. Conclusions In nonprior aspirin users, combination antithrombotic therapy with aspirin plus anticoagulation significantly reduces recurrent ischemic events in the early phase of unstable angina. C1 ROYAL VICTORIA INFIRM,DEPT CARDIOL,NEWCASTLE TYNE,TYNE & WEAR,ENGLAND. ROYAL SUSSEX CTY HOSP,DEPT CARDIOL,BRIGHTON,E SUSSEX,ENGLAND. UNIV EDINBURGH,CARDIOVASC RES UNIT,EDINBURGH,MIDLOTHIAN,SCOTLAND. MAYO CLIN,ROCHESTER,MN. BETH ISRAEL HOSP,DIV CARDIOL,NEW YORK,NY. CITY HOSP ELMHURST,DIV CARDIOL,ELMHURST,NY. MT SINAI HOSP,DIV CARDIOL,NEW YORK,NY 10029. STAT & EPIDEMIOL RES CORP,SEATTLE,WA. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RP COHEN, M (reprint author), HAHNEMANN UNIV,DEPT MED,LIKOFF CARDIOVASC INST,MS-119,BROAD & VINE ST,PHILADELPHIA,PA 19102, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 29 TC 303 Z9 308 U1 0 U2 7 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JAN PY 1994 VL 89 IS 1 BP 81 EP 88 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MQ584 UT WOS:A1994MQ58400012 PM 8281698 ER PT J AU PANDOLFI, F BOYLE, LA TRENTIN, L OLIVA, A KURNICK, JT AF PANDOLFI, F BOYLE, LA TRENTIN, L OLIVA, A KURNICK, JT TI T-CELL RECEPTOR GENE REARRANGEMENTS AND CYTOTOXIC ACTIVITIES OF CLONES ISOLATED FROM TUMOR-INFILTRATING LYMPHOCYTES (TIL) FROM MELANOMA PATIENTS SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE TUMOR-INFILTRATING LYMPHOCYTES; HUMAN MELANOMA; CYTOTOXICITY; T CELL RECEPTOR ID AUTOLOGOUS MELANOMA; EXPRESSION; INTERLEUKIN-2; SPECIFICITY; GENERATION; LINES; RECOGNITION; PHENOTYPE; EXPANSION; DOMINANCE AB The lymphocytes which infiltrate tumours and are grown in vitro to be used in adoptive immunotherapy are often characterized by dominant rearrangement of their T cell receptor (TCR) genes. To investigate the frequency and function of cells contributing to the 'dominant' rearrangement, we have cloned two bulk cell lines of TIL derived from melanoma patients (TIL-1 and TIL-5). These IL-2-propagated TIL cell lines had a CD8(+) phenotype and exerted strong cytotoxic activity against autologous melanoma cells, but not against the natural killer (NK)-sensitive K-562 cell line or LAK targets such as Daudi cells. We derived 40 clones from TIL-1 and 23 from TIL-5. Air tested clones were CD3(+), CD4(-), CD8(+) and expressed the alpha/beta TCR. From TIL-1, 27 of 40 clones, and 13/19 of the TIL-5 clones lysed autologous tumour cells. In contrast to the NK-negative bulk cultures, K-562 killing was detected in 21 of the TIL-1 clones and 17 pf the TIL-5 clones. TIL-1 contained eight clones and TIL-5 two clones with lytic capacity against neither autologous tumour cells nor the K562 cell line, although these clones possessed lytic potential as evidenced in a lectin-mediated lysis assay. LAK activity was not detected in most clones. Cytotoxic activity against autologous tumour could be inhibited by preincubation with anti-CD3 or anti-HLA class I MoAbs. Of the 34 TIL-1 clones analysed, 15 shared a rearranged TCR beta EcoRI restriction fragment of approximately 9.5 kb with the bulk culture. Clones sharing the EcoRI 10.5-kb dominant band present in TIL-5 bulk culture were also isolated. When the pattern of TCR beta rearrangement was compared with the cytotoxic functions, the following conclusions could be drawn: (i) clones contributing to the dominant band had heterogeneous functions. Most killed autologous tumour cells, but clones with no cytotoxic activity or even with no proliferative capacity in response to autologous tumour cells were also detected among those contributing to the dominant rearrangement; (ii) some clones that share an apparently identical rearranged band different from the 'dominant' rearrangement, may demonstrate the same cytotoxic function. In addition, our data suggest that many of the clones that share the dominant rearrangement originated from diverse progenitors. The high frequency of clonally diverse anti-tumour reactive TIL is likely to be a reflection of the in vivo selection of the TCR repertoire at the site of tumour. Further study of the TCR gene rearrangements should help to clarify how selection at this level can benefit future immunotherapeutic approaches. C1 UNIV ROMA LA SAPIENZA,CHAIR CLIN IMMUNOL & ALLERGY,ROME,ITALY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. CATHOLIC UNIV ROME,CHAIR METODOL CLIN,ROME,ITALY. RI TRENTIN, LIVIO/J-7676-2016 OI TRENTIN, LIVIO/0000-0003-1222-6149 FU NCI NIH HHS [CA 44324]; NIAMS NIH HHS [AR 39993] NR 29 TC 5 Z9 5 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD JAN PY 1994 VL 95 IS 1 BP 141 EP 147 PG 7 WC Immunology SC Immunology GA MQ997 UT WOS:A1994MQ99700024 PM 8287599 ER PT J AU NEWTON, TF LEUCHTER, AF MILLER, EN WEINER, H AF NEWTON, TF LEUCHTER, AF MILLER, EN WEINER, H TI QUANTITATIVE EEG IN PATIENTS WITH AIDS AND ASYMPTOMATIC HIV-INFECTION SO CLINICAL ELECTROENCEPHALOGRAPHY LA English DT Article DE AIDS; HIV INFECTION; QUANTITATIVE EEG ID IMMUNODEFICIENCY-VIRUS-INFECTION; EARLY NEUROLOGIC ABNORMALITIES; DEMENTIA COMPLEX; NEUROPSYCHOLOGICAL PERFORMANCE; ELECTROENCEPHALOGRAPHY; DIAGNOSIS; COHERENCE; COHORT; MACS; MEN C1 UNIV CALIF LOS ANGELES, NEUROPSYCHIAT INST & HOSP, DEPT BIOBEHAV, LOS ANGELES, CA USA. RP NEWTON, TF (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, DEPT PSYCHIAT W116AC, WILSHIRE & SAWTELLE BLVD, LOS ANGELES, CA 90073 USA. OI newton, thomas/0000-0002-3198-5901 FU NIAID NIH HHS [N01 AI 72631]; NIMH NIH HHS [5T32 MH 119200-2] NR 22 TC 11 Z9 12 U1 0 U2 0 PU EEG & CLINICAL NEUROSCIENCE SOC (E C N S) PI WHEATON PA 805 W LIBERTY DR, PO BOX 725, WHEATON, IL 60187 USA SN 0009-9155 J9 CLIN ELECTROENCEPHAL JI Clin. Electroencephalogr. PD JAN PY 1994 VL 25 IS 1 BP 18 EP 25 PG 8 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA MQ846 UT WOS:A1994MQ84600004 PM 8174287 ER PT J AU BELL, DS BELL, KM CHENEY, PR AF BELL, DS BELL, KM CHENEY, PR TI PRIMARY JUVENILE FIBROMYALGIA SYNDROME AND CHRONIC FATIGUE SYNDROME IN ADOLESCENTS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID FIBROSITIS SYNDROME; SLEEP; DEFINITION; DIAGNOSIS AB Chronic fatigue syndrome (CFS) and primary juvenile fibromyalgia syndrome (PJFS) are illnesses with a similar pattern of symptoms of unknown etiology. Twenty-seven children for whom CFS was diagnosed were evaluated for fibromyalgia by the presence of widespread pain and multiple tender points. Eight children (29.6%) fulfilled criteria for fibromyalgia. Those children who met fibromyalgia criteria had a statistically greater degree of subjective muscle pain, sleep disturbance, and neurological symptoms than did those who did not meet the fibromyalgia criteria. There was no statistical difference between groups in degree of fatigue, headache, sore throat, abdominal pain, depression, lymph node pain, concentration difficulty, eye pain, and joint pain. CFS in children and PJFS appear to be overlapping clinical entities and may be indistinguishable by current diagnostic criteria. C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,DEPT INTERNAL MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP BELL, DS (reprint author), CAMBRIDGE HOSP,DEPT PEDIAT,1493 CAMBRIDGE ST,CAMBRIDGE,MA 02139, USA. NR 29 TC 23 Z9 24 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S21 EP S23 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400008 PM 8148447 ER PT J AU GOLDEN, J FRIM, DM CHAPMAN, PH VONSATTEL, JP AF GOLDEN, J FRIM, DM CHAPMAN, PH VONSATTEL, JP TI MARKED TISSUE EOSINOPHILIA WITHIN ORGANIZING CHRONIC SUBDURAL-HEMATOMA MEMBRANES SO CLINICAL NEUROPATHOLOGY LA English DT Article DE HEAD TRAUMA; SURGICAL PATHOLOGY; SUBDURAL HEMATOMA; EOSINOPHIL AB Chronic subdural hematoma (CSDH) with membranes is a common problem in neurosurgery. Despite its frequency, the pathogenesis of this lesion is poorly understood. We conducted a systematic pathologic review, with clinical correlation, of all CSDH presenting to our institution over a two-year period which had undergone pathological examination. Surprisingly, we found marked tissue eosinophilia in most CSDH membranes in the process of organization. Eosinophils were not evident in fresh hemorrhage or in older membranes which were completely organized. These results demonstrated that eosinophils are frequently present in large numbers in the early phases of chronic subdural membrane (CSM) formation but not associated with chronic, organized membranes. No specific clinical cause for tissue eosinophilia was identified in the cases reviewed. Though the significance of these observations remains unclear, recognition of eosinophilia as a pathological feature of organizing CSM is important in order to avoid confusion with other diagnoses. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. RP GOLDEN, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,NEUROPATHOL SERV,WARREN 3,FRUIT ST,BOSTON,MA 02114, USA. NR 22 TC 13 Z9 13 U1 0 U2 0 PU DUSTRI-VERLAG DR KARL FEISTLE PI MUNCHEN-DEISENHOFEN PA BAHNHOFSTRABE 9 POSTFACH 49, W-8024 MUNCHEN-DEISENHOFEN, GERMANY SN 0722-5091 J9 CLIN NEUROPATHOL JI Clin. Neuropathol. PD JAN-FEB PY 1994 VL 13 IS 1 BP 12 EP 16 PG 5 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA MV184 UT WOS:A1994MV18400002 PM 8033456 ER PT J AU WARNER, J LESSELL, S AF WARNER, J LESSELL, S TI NEUROOPHTHALMOLOGY OF MULTIPLE-SCLEROSIS SO CLINICAL NEUROSCIENCE LA English DT Article DE INTERNUCLEAR OPHTHALMOPLEGIA; NYSTAGMUS; OPTIC NEURITIS; RETINAL VASCULITIS ID VISUAL-EVOKED-POTENTIALS; ACUTE OPTIC NEURITIS; ACQUIRED PENDULAR NYSTAGMUS; FOLLOW-UP; CONTRAST SENSITIVITY; UHTHOFFS SYMPTOM; TREATMENT TRIAL; PARS PLANITIS; LONG-TERM; LESIONS AB Neuro-ophthalmic manifestations are important in multiple sclerosis. Optic neuritis is a frequent harbinger of the disease, and is characterized by subacute painful visual loss, with disproportionate loss of color and contrast sensitivity, central or cecocentral scotoma, and an afferent pupillary defect. Visual recovery is the rule, but tests have been developed to detect most cases of recovered optic neuritis. Intraocular inflammation has come to be recognized as a frequent accompaniment of multiple sclerosis. Because of the predilection of multiple sclerosis for the infratentorial white matter, defects in eye movement control are common, particularly internuclear ophthalmoplegias and nystagmus. (C) 1994 Wiley-Liss, Inc. C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. MASSACHUSETTS EYE & EAR INFIRM,NEUROOPHTHALMOL UNIT,BOSTON,MA. RP WARNER, J (reprint author), UNIV UTAH,MORAN EYE CTR,50 N MED DR,SALT LAKE CITY,UT 84132, USA. NR 63 TC 18 Z9 18 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1065-6766 J9 CLIN NEUROSCI JI Clin. Neurosci. PY 1994 VL 2 IS 3-4 BP 180 EP 188 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA QG247 UT WOS:A1994QG24700002 PM 7749886 ER PT J AU RICHARDSON, EP AF RICHARDSON, EP TI PATHOLOGY OF MULTIPLE-SCLEROSIS - SOME NEW DEVELOPMENTS SO CLINICAL NEUROSCIENCE LA English DT Article DE LESIONS; BLOOD-BRAIN BARRIER; DEMYELINATION; DIGODENDROCYTE; MYELIN SHEATH ID LESION DEVELOPMENT; REMYELINATION; BREAKDOWN AB This chapter reviews some of the current investigations regarding the neuropathology of multiple sclerosis (MS). To an increasing degree, immunocytochemical methods are being used to extend the recognition of cellular activities, particularly of the immune system, in the lesions and surrounding tissues. To some extent, these studies are associated with electron-microscope observations. The blood-brain barrier is the site of the first pathologic events, but it is still unclear as to what initially opens the barrier, or how. As regards the demyelinative process itself, the general impression now is that the primary target of the attack by the disease process is the myelin sheath, not its parent cell, the oligodendrocyte. Uncertainty still exists as to the status of oligodendrocytes in MS. Some, but not all, survive. Remyelination regularly occurs early in MS lesions, but it is ineffective. Many neuropathologic questions remain unanswered and require further research. (C) 1994 Wiley-Liss, Inc., C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP RICHARDSON, EP (reprint author), MASSACHUSETTS GEN HOSP,CHARLES S KUBIK LAB NEUROPATHOL,BOSTON,MA 02114, USA. NR 25 TC 3 Z9 3 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 1065-6766 J9 CLIN NEUROSCI JI Clin. Neurosci. PY 1994 VL 2 IS 3-4 BP 253 EP 257 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA QG247 UT WOS:A1994QG24700011 PM 7749895 ER PT J AU CHANDLER, H CLARK, J MURPHY, S MCCARTHY, J PENENBERG, B DANYLCHUK, K ROEHR, B AF CHANDLER, H CLARK, J MURPHY, S MCCARTHY, J PENENBERG, B DANYLCHUK, K ROEHR, B TI RECONSTRUCTION OF MAJOR SEGMENTAL LOSS OF THE PROXIMAL FEMUR IN REVISION TOTAL HIP-ARTHROPLASTY SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID FEMORAL REPLACEMENT; TUMORS; PROSTHESES; RESECTION AB Reconstruction of major proximal femoral segmental defects is one of the most difficult challenges in revision total hip arthroplasty (THA). One technique that has been successful is the use of a modular, long-stemmed prosthesis, cemented to an allograft proximal femur and press-fit to the host bone. Since July 1989, the authors have used this technique in 30 hips (29 patients). The trochanteric slide approach was used in all cases. Sixty pounds of weight bearing was encouraged for six weeks, then full weight bearing as tolerated. The mean follow-up period was 22 months (range, two to 46 months). All but two grafts united to the host bone clinically and radiographically. Complications included five dislocations, one graft-host nonunion, one graft resorption, and one deep infection requiring resection arthroplasty. The latter patient was subsequently reconstructed successfully using the same technique. Although the follow-up period is short, the authors have been encouraged by the early success of these allograft-prosthetic composites. Advantages of this approach include rapid return to weight bearing, physiologic loading of the distal femur, and reconstitution of vital proximal bone stock. RP CHANDLER, H (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WANG AMBULATORY CARE CTR,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 47 TC 47 Z9 47 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD JAN PY 1994 IS 298 BP 67 EP 74 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MQ192 UT WOS:A1994MQ19200011 PM 8118997 ER PT J AU BUECHEL, FF DRUCKER, D JASTY, M JIRANEK, W HARRIS, WH AF BUECHEL, FF DRUCKER, D JASTY, M JIRANEK, W HARRIS, WH TI OSTEOLYSIS AROUND UNCEMENTED ACETABULAR COMPONENTS OF COBALT-CHROME SURFACE REPLACEMENT HIP-ARTHROPLASTY SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID AGGRESSIVE GRANULOMATOUS LESIONS; LOCALIZED BONE-RESORPTION; FEMORAL COMPONENTS; LYSIS; WEAR; POLYETHYLENE; BIOLOGY; CEMENT; FEMUR AB Ten cases of major osteolysis were identified in patients with hemispherical cobalt chrome acetabular components of cementless resurfacing total hip prostheses at follow-up examinations ranging from two to five years. All components were porous coated with cobalt chrome spheres and were stabilized initially with screws. Five patients were women and five were men, with ages ranging from 20 to 59 years. The radiolucent cystic lesions with peripheral rims of reactive bone formation appeared one to five years after the operation. They measured from 1.5 to 6 cm in the largest diameter and were most often found adjacent to the screws used to secure the acetabular components to the skeleton. On the radiographs, none of the components appeared to be loose. Three patients had revision surgery. In two of the three cases, the implants were found to be firmly fixed. There was no clinical or bacteriologic evidence of infection. The polyethylene articulating surface showed signs of wear in all three cases and in one of the three it dislocated from the metal shell. Granulation tissue was found in the regions of osteolysis, and the diseased tissue contained numerous macrophages and giant cells. Lymphocytes and plasma cells were rare. Numerous small particles of phagocytosed polyethylene and metal in the cells were noted in two casts, whereas only polyethylene was found in the third. The cases presented in this report show that major osteolysis can occur around cementless acetabular components of surface replacement arthroplasty, and is most likely related to the contamination of tissue with particles of the implant materials either from wear or corrosion resulting in a foreign-body reaction to the particulate materials. The high incidence of acetabular osteolysis (ten of 25) with the use of this cementless surface replacement arthroplasty suggests that the presence of polyethylene may be the more important of the two. C1 UNIV MED & DENT NEW JERSEY,DEPT ORTHOPAED SURG,NEWARK,NJ. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA. NR 29 TC 29 Z9 29 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD JAN PY 1994 IS 298 BP 202 EP 211 PG 10 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MQ192 UT WOS:A1994MQ19200027 PM 8118977 ER PT J AU ZHU, L ENDERS, GH WU, CL STARZ, MA MOBERG, KH LEES, JA DYSON, N HARLOW, E AF ZHU, L ENDERS, GH WU, CL STARZ, MA MOBERG, KH LEES, JA DYSON, N HARLOW, E TI GROWTH SUPPRESSION BY MEMBERS OF THE RETINOBLASTOMA PROTEIN FAMILY SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID LARGE T-ANTIGEN; TRANSCRIPTION FACTOR E2F; ADENOVIRUS E1A PROTEINS; HUMAN CYCLIN-A; GENE-PRODUCT; CELL-CYCLE; SUSCEPTIBILITY GENE; COMPLEX-FORMATION; VIRAL ONCOPROTEINS; MOLECULAR-CLONING C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MIT,CTR CANC RES,DEPT BIOL,CAMBRIDGE,MA 02139. RP ZHU, L (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129, USA. RI Tang, Amy/L-3226-2016 OI Tang, Amy/0000-0002-5772-2878 NR 67 TC 16 Z9 16 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 75 EP 84 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600010 PM 7587134 ER PT J AU ECKNER, R ARANY, Z EWEN, M SELLERS, W LIVINGSTON, DM AF ECKNER, R ARANY, Z EWEN, M SELLERS, W LIVINGSTON, DM TI THE ADENOVIRUS E1A-ASSOCIATED 300-KD PROTEIN EXHIBITS PROPERTIES OF A TRANSCRIPTIONAL COACTIVATOR AND BELONGS TO AN EVOLUTIONARILY CONSERVED FAMILY SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID CELL-CYCLE; E1A PROTEINS; DNA-BINDING; GENE-PRODUCT; REPRESSION; DROSOPHILA; TRANSFORMATION; ACTIVATION; INHIBITION; EXPRESSION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. DANA FARBER CANC INST,DEPT NEOPLAST DIS MECHANISMS,BOSTON,MA 02115. NR 48 TC 29 Z9 29 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 85 EP 95 PG 11 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600011 PM 7587135 ER PT J AU KOLODNER, RD HALL, NR LIPFORD, J KANE, MF RAO, MRS MORRISON, P WIRTH, L FINAN, PJ BURN, J CHAPMAN, P EARABINO, C MERCHANT, E BISHOP, DT GARBER, J BRONNER, CE BAKER, SM WARREN, G SMITH, LG LINDBLOM, A TANNERGARD, P BOLLAG, RJ GODWIN, AR WARD, DC NORDENSKJOLD, M LISKAY, RM COPELAND, N JENKINS, N LESCOE, MK EWEL, A LEE, S GRIFFITH, J FISHEL, R AF KOLODNER, RD HALL, NR LIPFORD, J KANE, MF RAO, MRS MORRISON, P WIRTH, L FINAN, PJ BURN, J CHAPMAN, P EARABINO, C MERCHANT, E BISHOP, DT GARBER, J BRONNER, CE BAKER, SM WARREN, G SMITH, LG LINDBLOM, A TANNERGARD, P BOLLAG, RJ GODWIN, AR WARD, DC NORDENSKJOLD, M LISKAY, RM COPELAND, N JENKINS, N LESCOE, MK EWEL, A LEE, S GRIFFITH, J FISHEL, R TI HUMAN MISMATCH REPAIR GENES AND THEIR ASSOCIATION WITH HEREDITARY NONPOLYPOSIS COLON-CANCER SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID NONPOLYPOSIS COLORECTAL-CANCER; HETERODUPLEX PLASMID DNA; MUTS-ENCODED PROTEIN; SACCHAROMYCES-CEREVISIAE; ESCHERICHIA-COLI; MICROSATELLITE INSTABILITY; SOMATIC MUTATIONS; MUTATOR PHENOTYPE; NATURAL-HISTORY; CARCINOGENESIS C1 HARVARD UNIV,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA 02115. HARVARD UNIV,DANA FARBER CANC INST,MOLEC BIOL CARE FACIL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. ST JAMES UNIV HOSP,GENET EPIDEMIOL LAB,IMPERIAL CANC RES FUND,LEEDS LS9 7TF,W YORKSHIRE,ENGLAND. GEN INFIRM,DEPT SURG,LEEDS LS1 3EX,W YORKSHIRE,ENGLAND. GEN INFIRM,CTR DIGEST DIS,LEEDS LS1 3EX,W YORKSHIRE,ENGLAND. UNIV NEWCASTLE UPON TYNE,DEPT HUMAN GENET,NEWCASTLE TYNE NE2 4AA,TYNE & WEAR,ENGLAND. OREGON HLTH SCI UNIV,DEPT MOLEC & MED GENET,PORTLAND,OR 97201. YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT MOLEC BIOPHYS,NEW HAVEN,CT 06510. KAROLINSKA HOSP,DEPT MOLEC MED,S-17176 STOCKHOLM,SWEDEN. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,FREDERICK,MD 21702. UNIV VERMONT,SCH MED,DEPT MICROBIOL & MOLEC GENET,BURLINGTON,VT 05405. UNIV N CAROLINA,SCH MED,LINEBERGER CANC RES CTR,CHAPEL HILL,NC 27599. RP KOLODNER, RD (reprint author), HARVARD UNIV,DANA FARBER CANC INST,DIV CELL & MOLEC BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. OI Bishop, Tim/0000-0002-8752-8785 NR 79 TC 14 Z9 14 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 331 EP 338 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600036 PM 7587085 ER PT J AU LOWE, SW BODIS, S BARDEESY, N MCCLATCHEY, A REMINGTON, L RULEY, HE FISHER, DE JACKS, T PELLETIER, J HOUSMAN, DE AF LOWE, SW BODIS, S BARDEESY, N MCCLATCHEY, A REMINGTON, L RULEY, HE FISHER, DE JACKS, T PELLETIER, J HOUSMAN, DE TI APOPTOSIS AND THE PROGNOSTIC-SIGNIFICANCE OF P53 MUTATION SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID WILD-TYPE P53; CHRONIC LYMPHOCYTIC-LEUKEMIA; PROGRAMMED CELL-DEATH; THYMOCYTE APOPTOSIS; DNA FRAGMENTATION; BREAST-CANCER; LUNG-CANCER; GENE; TUMOR; INDUCTION C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. MCGILL UNIV,DEPT BIOCHEM,MONTREAL,PQ H3G 1Y6,CANADA. VANDERBILT UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,NASHVILLE,TN 37232. MIT,HOWARD HUGHES MED INST,CAMBRIDGE,MA 02139. RP LOWE, SW (reprint author), MIT,CTR CANC RES,CAMBRIDGE,MA 02139, USA. FU NCI NIH HHS [5R27CA-17575, CA-14051, R01CA-40602] NR 45 TC 30 Z9 30 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 419 EP 426 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600046 PM 7587096 ER PT J AU SAGER, R SHENG, S ANISOWICZ, A SOTIROPOULOU, G ZOU, Z STENMAN, G SWISSHELM, K CHEN, Z HENDRIX, MJC PEMBERTON, P RAFIDI, K RYAN, K AF SAGER, R SHENG, S ANISOWICZ, A SOTIROPOULOU, G ZOU, Z STENMAN, G SWISSHELM, K CHEN, Z HENDRIX, MJC PEMBERTON, P RAFIDI, K RYAN, K TI RNA GENETICS OF BREAST-CANCER - MASPIN AS PARADIGM SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID MAMMARY EPITHELIAL-CELLS; TUMOR-SUPPRESSOR GENES; DIFFERENTIAL DISPLAY; DOWN-REGULATION; NUCLEOTIDE-SEQUENCE; MESSENGER-RNAS; CLONING; GROWTH; LINES; COMMUNICATION C1 GOTHENBURG UNIV,SAHLGRENSKA HOSP,DEPT PATHOL,CANC GENET LAB,S-41345 GOTHENBURG,SWEDEN. UNIV WASHINGTON,DEPT PATHOL,SEATTLE,WA 98195. ST LOUIS UNIV,CARDINAL GLENNON CHILDRENS HOSP,SCH MED,PEDIAT RES INST,ST LOUIS,MO 63110. LXR BIOTECHNOL INC,RICHMOND,CA 94804. RP SAGER, R (reprint author), DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 40 TC 117 Z9 120 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 537 EP 546 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600059 PM 7587110 ER PT J AU FRIEND, SH IGGO, R ISHIOKA, C FITZGERALD, M HOOVER, I ONEILL, E FREBOURG, T AF FRIEND, SH IGGO, R ISHIOKA, C FITZGERALD, M HOOVER, I ONEILL, E FREBOURG, T TI OVERCOMING COMPLEXITIES IN GENETIC SCREENING FOR CANCER SUSCEPTIBILITY SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID LINE P53 MUTATIONS; GEL-ELECTROPHORESIS; HUMAN DNA C1 MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. SWISS INST EXPTL CANC RES,CH-1066 EPALINGES,SWITZERLAND. CHU ROUEN,UNITE GENET MOLEC,ROUEN,FRANCE. NR 8 TC 2 Z9 2 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 673 EP 676 PG 4 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600076 PM 7587129 ER PT J AU HARLOW, E AF HARLOW, E TI AN INTRODUCTION TO THE PUZZLE SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID MUTATION; CANCER RP HARLOW, E (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129, USA. NR 6 TC 3 Z9 3 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 709 EP 723 PG 15 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600081 ER PT B AU CANNON, SC AF CANNON, SC BE Fuchs, AF Brandt, T Buttner, U Zee, D TI Promiscuous Na channel behavior as a cause of episodic paralysis and myotonia SO CONTEMPORARY OCULAR MOTOR AND VESTIBULAR RESEARCH: A TRIBUTE TO DAVID A. ROBINSON LA English DT Proceedings Paper CT International Meeting on Contemporary Ocular Motor and Vestibular Research - A Tribute to David A Robinson CY 1993 CL EIBSEE, GERMANY C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART 30 PA RUDIGERSTR 14, W-7000 STUTTGART 30, GERMANY BN 3-13-100421-5 PY 1994 BP 26 EP 33 PG 8 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA BD64D UT WOS:A1994BD64D00004 ER PT J AU WU, J AF WU, J TI ON THERAPY WITH ASIAN PATIENTS SO CONTEMPORARY PSYCHOANALYSIS LA English DT Article C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 24 TC 2 Z9 2 U1 0 U2 0 PU WILLIAM ALANSON WHITE INST PI NEW YORK PA 20 WEST 74TH STREET, NEW YORK, NY 10023 SN 0010-7530 J9 CONTEMP PSYCHOANAL JI Contemp. Psychoanal. PD JAN PY 1994 VL 30 IS 1 BP 152 EP 168 PG 17 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA MX629 UT WOS:A1994MX62900010 ER PT J AU SINGH, BN AF SINGH, BN TI ANTIARRHYTHMIC ACTIONS OF CALCIUM-ANTAGONISTS SO CORONARY ARTERY DISEASE LA English DT Review DE ANTIARRHYTHMIC DRUGS; CALCIUM ANTAGONISTS; POSTMYOCARDIAL INFARCTION SURVIVAL ID PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA; CHRONIC ATRIAL-FIBRILLATION; SUSTAINED VENTRICULAR-TACHYCARDIA; ACUTE MYOCARDIAL-INFARCTION; CONGESTIVE-HEART-FAILURE; INTRAVENOUS DILTIAZEM; CARDIAC-ARRHYTHMIAS; TRIGGERED ACTIVITY; ORAL VERAPAMIL; DOUBLE-BLIND C1 W LOS ANGELES VAMC,DEPT CARDIOL,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA. NR 51 TC 0 Z9 0 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-6928 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD JAN PY 1994 VL 5 IS 1 BP 27 EP 36 DI 10.1097/00019501-199401000-00005 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NA049 UT WOS:A1994NA04900005 PM 8136929 ER PT J AU TOMPKINS, RG AF TOMPKINS, RG TI HUMAN RECOMBINANT INTERLEUKIN-1 RECEPTOR ANTAGONIST IN THE TREATMENT OF SEPSIS SYNDROME SO CRITICAL CARE MEDICINE LA English DT Editorial Material DE INTERLEUKIN-1; SEPSIS; CYTOKINES; PATIENT OUTCOME; SYSTEMIC INFLAMMATORY RESPONSE SYNDROME RP TOMPKINS, RG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT SURG,SURG SERV,BOSTON,MA 02114, USA. NR 3 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1994 VL 22 IS 1 BP 3 EP 3 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA RJ947 UT WOS:A1994RJ94700002 PM 8124969 ER PT J AU SALZMAN, AL STRONG, KE WANG, HL WOLLERT, PS VANDERMEER, TJ FINK, MP AF SALZMAN, AL STRONG, KE WANG, HL WOLLERT, PS VANDERMEER, TJ FINK, MP TI INTRALUMINAL BALLOONLESS AIR TONOMETRY - A NEW METHOD FOR DETERMINATION OF GASTROINTESTINAL MUCOSAL CARBON-DIOXIDE TENSION SO CRITICAL CARE MEDICINE LA English DT Article DE TONOMETRY; INTESTINE; ISCHEMIA; STOMACH; PERFUSION; ACIDOSIS; MUCOSA; SHOCK; BLOOD GAS ANALYSIS; MONITORING, PHYSIOLOGICAL; CRITICAL ILLNESS ID CRITICALLY ILL PATIENTS; GASTRIC INTRAMUCOSAL PH; INTRAMURAL PH; TISSUE OXYGENATION; BACTERIAL TRANSLOCATION; INTESTINAL PERMEABILITY; MESENTERIC ISCHEMIA; HEMORRHAGIC-SHOCK; PREDICTIVE VALUE; GUT ISCHEMIA AB Objective: To determine if air introduced directly into the lumen of a hollow viscus can be used instead of fluid in a Silastic balloon to estimate gastrointestinal mucosal PCO2. Design: Prospective, unblinded comparison of two methods of mucosal PCO2 measurement. Setting: Animal surgery suite at a large, university-affiliated medical center. Interventions: Standard, commercially available, tonometric catheters were positioned in the ileum (n = 4) or the stomach and ileum (n = 12) of anesthetized, immature Yorkshire swine. Using gas-tight purse-string sutures, plastic cannulas were inserted into the lumen of the stomach (n = 12) and the lumen of a 10-cm isolated segment of ileum (n = 16). Data were collected after equilibration periods of 30 or 60 mins. Before each equilibration period, the ''air tonometers'' (i.e., the lumens of the stomach and/or the isolated heal segment) were lavaged with 200 mt (stomach) or 20 mL (ileum) of air. In group 1 (n = 4) and group 2 (n = 3), graded degrees of mesenteric hypoperfusion were achieved by mechanical mesenteric occlusion or pericardial tamponade, respectively. In group 3 (n = 8), graded degrees of respiratory acidosis were induced. At various intervals, PCO2 was determined simultaneously in arterial blood, gastric air, saline from the gastric tonometric balloon, ileal air, and saline from the ileal tonometric balloon. Measurements and Main Results: In pigs with ischemia created by mesenteric vascular occlusion (group 1), there was a moderate correlation between PCO2 values in air samples from the ileal lumen and samples of saline from the standard tonometer (r(2) = .61, p < .001). In pigs with mesenteric ischemia secondary to pericardial tamponade (group 2), air and saline tonometry were well-correlated in the stomach (r(2) = .71, p < .001) and ileum (r(2) = .83, p < .001). In pigs with normal mesenteric perfusion (group 3) and PaCO2 >40 torr (5.3 kPa), PaCO2 correlated with heal mucosal PCO2, determined using air (r(2) = .93, p < .001) or saline (r(2) = .91, p < .001) tonometry, or gastric mucosal PCO2, determined using air (r(2) = 1.00, p < .001) or saline (r(2) = .97, p < .001) tonometry. Values obtained by air tonometry were highly correlated with values obtained using standard saline tonometry in the stomach (r(2) = .98, p < .001; bias = -5 +/- 5 torr [-0.65 +/- 0.65 kPal]) or ileum (r(2) = .96, p < .001; bias = 1 +/- 9 torr [0.13 +/- 1.17 kPa]). Conclusions: a) Under stable hemodynamic and respiratory conditions, air tonometry (which, in theory, can be performed using a conventional nasogastric or nasoenteric feeding tube) estimates gastrointestinal mucosal PCO2 as accurately as standard saline tonometry in the stomach or ileum; b) respiratory acidosis leads to tissue hypercarbia, a phenomenon that must be considered when tonometry is used to guide therapy in the clinical setting; c) under stable, nonischemic conditions, gastric or intestinal tonometry can be used to estimate PaCO2. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RESP CARE,BOSTON,MA 02114. FU NIGMS NIH HHS [2 R01 GM37631-07, 5T32GM07035] NR 39 TC 44 Z9 48 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1994 VL 22 IS 1 BP 126 EP 134 PG 9 WC Critical Care Medicine SC General & Internal Medicine GA RJ947 UT WOS:A1994RJ94700024 PM 8124955 ER PT J AU JELLINEK, M AF JELLINEK, M TI THE DARKSIDE - APPEASING OR CONFRONTING - REPLY SO CRITICAL CARE MEDICINE LA English DT Letter RP JELLINEK, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1994 VL 22 IS 1 BP 180 EP 180 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA RJ947 UT WOS:A1994RJ94700036 ER PT J AU KLEIN, GL COBURN, JW AF KLEIN, GL COBURN, JW TI TOTAL PARENTERAL-NUTRITION AND ITS EFFECTS ON BONE METABOLISM SO CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES LA English DT Review DE HORMONE; OSTEOMALACIA; METABOLIC BONE DISEASE; OSTEOPOROSIS; CYTOCHROME P450; OSTEOCALCIN; CALCITONIN; PARATHYROID HORMONE; VITAMIN-D; ALKALINE PHOSPHATASE; ALUMINUM ID VITAMIN-D; PARATHYROID-HORMONE; GLA-PROTEIN; HEMODIALYSIS-PATIENTS; RENAL OSTEODYSTROPHY; SELENIUM DEFICIENCY; CALCIUM-METABOLISM; DIALYSIS PATIENTS; ALUMINUM CONTENT; DRUG-METABOLISM AB Total parenteral nutrition (TPN) may affect bone metabolism in a variety of ways. These may include potential indirect effects such as on gastrointestinal hormone secretion, liver function, especially cytochrome P450 isoenzymes, metabolic biorhythms where established, and the continuous compared with the intermittent supply of nutrients. More substantial evidence exists for the reduction of bone formation, parathyroid hormone secretion, and calcitriol production in TPN patients along with high urinary calcium excretion. This review considers both aluminum loading and vitamin D sensitivity as etiologic factors and suggests that aluminum may have played a primary role in the pathogenesis of these abnormalities in bone and mineral metabolism, but that vitamin D may have potentiated the deleterious actions of aluminum. While the sources of aluminum contamination of TPN solutions have been identified and efforts are under way to reduce its contamination of TPN solutions, the persistence of low bone mass measurement in TPN patients is a problem that has been identified repeatedly, does not have a current explanation, and requires further study. C1 W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. RP KLEIN, GL (reprint author), UNIV TEXAS,MED BRANCH,DEPT PEDIAT,DIV PEDIAT GASTROENTEROL,CHILDRENS HOSP ROOM C353,GALVESTON,TX 77555, USA. OI Klein, Gordon/0000-0002-3011-4186 NR 129 TC 14 Z9 15 U1 1 U2 1 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, JOURNALS CUSTOMER SERVICE, BOCA RATON, FL 33431 SN 1040-8363 J9 CRIT REV CL LAB SCI JI Crit. Rev. Clin. Lab. Sci. PY 1994 VL 31 IS 2 BP 135 EP 167 DI 10.3109/10408369409084675 PG 33 WC Medical Laboratory Technology SC Medical Laboratory Technology GA NV034 UT WOS:A1994NV03400002 PM 7917007 ER PT J AU HASS, R AF HASS, R TI RETRODIFFERENTIATION AND CELL-DEATH SO CRITICAL REVIEWS IN ONCOGENESIS LA English DT Review ID PROTEIN-KINASE-C; NERVE GROWTH-FACTOR; INDUCED MONOCYTIC DIFFERENTIATION; RETINOBLASTOMA GENE-PRODUCT; WEE1 TYROSINE KINASE; HUMAN-LEUKEMIA-CELLS; DNA-BINDING ACTIVITY; PC12 CELLS; MYOGENIC DIFFERENTIATION; REVERSIBLE INDUCTION AB The reversibility of a differentiation program termed dedifferentiation, redifferentiation, or retrodifferentiation opens a spectrum of new possibilities for cellular development. During differentiation and retrodifferentiation, the expression of gene products associated with a differentiated phenotype and cell cycle regulation demonstrate inverse patterns. This effect requires a coordinated network that simultaneously controls cell growth and differentiation. In particular, crosstalk between induction of differentiation and G(0)/G(1) cell cycle exit can be initiated and sustained by activated serine/threonine kinases and tyrosine kinases. Phosphorylation signals an relayed to certain genes or transcription factors such as Fos/Jun, EGR-1, NF-kappa B, MyoD, or the Myc/Max gene family. However, the precise regulation of these transcription factors to confer signals to differentiation associated and cell cycle-regulatory genes remains unclear. Cell cycle exit into a transient G(0)'-arrest cycle or a terminal G(0) phase is determined by a network of phosphorylation signals involving the retinoblastoma protein and a variety of factors such as the E2F family, cyclins, and cyclin-dependent kinases. In this context, a variety of differentiation-induced cell lines, including monocytic, neuronal, or muscle cells, can progress through the G(0)'-arrest cycle, whereby a certain population retains the capacity to retrodifferentiate and reenter the cell cycle. In contrast, the rest of the differentiated population enters the irreversible G(0) phase (terminal commitment) that finally results in programmed cell death. The expression of growth arrest-specific (gas and gadd) genes is associated with the G(0)'-arrest cycle, and other factors, including c-mpc, p53, mdm2, and bcl2/bclx, contribute to the regulation of the cell death program. Although the precise signaling cascade determining retrodifferentiation or cell death remains unclear, a coordinated inter- and intracellular regulation could establish a certain biological balance between these exclusive pathways. Consequently, a retrodifferentiation process may provide a potential for cell type conversion or transdifferentiation, whereby retrodifferentiated cells can be induced to develop via a different pathway according to tissue-specific requirements. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 NR 115 TC 40 Z9 41 U1 0 U2 2 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, STE 1202, NEW YORK, NY 10016-7892 SN 0893-9675 J9 CRIT REV ONCOGENESIS JI Crit. Rev. Oncog. PY 1994 VL 5 IS 4 BP 359 EP 371 PG 13 WC Biochemistry & Molecular Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Oncology; Cell Biology GA QE876 UT WOS:A1994QE87600002 PM 7711113 ER PT J AU MARGOLIS, HC MORENO, EC AF MARGOLIS, HC MORENO, EC TI COMPOSITION AND CARIOGENIC POTENTIAL OF DENTAL PLAQUE FLUID SO CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE LA English DT Article DE PLAQUE FLUID; PLAQUE; CARIES; DEMINERALIZATION; REMINERALIZATION; CALCULUS AB Our understanding of the chemical events that take place at the tooth-plaque interface has improved greatly through studies of the chemical composition and properties of dental plaque fluid. In the absence of fermentable carbohydrate, plaque fluid has been found to be supersaturated with respect to tooth mineral and other calcium phosphate phases, thus exhibiting the potential to support calculus formation and the remineralization of incipient carious lesions. Following the exposure to fermentable carbohydrate, the degree of saturation of plaque fluid decreases rapidly, primarily due to lactic acid production and the lowering of plaque fluid pH. The extent of these chemical changes has been shown to be associated with differences in caries history. Such studies have been facilitated by the recent development of microanalytical techniques. Unfortunately, little is known about the relationship between the observed chemical changes in plaque fluid and the microbial composition of plaque. Limited information is also available on the association of immune factors in plaque fluid with dental disease. RP MARGOLIS, HC (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07009, DE-03187, DE-07493] NR 0 TC 47 Z9 51 U1 1 U2 2 PU INT AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314-3406 SN 1045-4411 J9 CRIT REV ORAL BIOL M JI Crit. Rev. Oral Biol. Med. PY 1994 VL 5 IS 1 BP 1 EP 25 PG 25 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA PM336 UT WOS:A1994PM33600001 PM 7999948 ER PT J AU JACKS, T REMINGTON, L WILLIAMS, BO SCHMITT, EM HALACHMI, S BRONSON, RT WEINBERG, RA AF JACKS, T REMINGTON, L WILLIAMS, BO SCHMITT, EM HALACHMI, S BRONSON, RT WEINBERG, RA TI TUMOR SPECTRUM ANALYSIS IN P53-MUTANT MICE SO CURRENT BIOLOGY LA English DT Article ID WILD-TYPE P53; BINDING PROTEIN; GENE-EXPRESSION; MUTATIONS; TRANSFORMATION; TRANSCRIPTION; DISRUPTION; ONCOGENE; MOUSE; LINE AB Background: The p53 tumor suppressor gene is mutated in a large percentage of human malignancies, including tumors of the colon, breast, lung and brain. Individuals who inherit one mutant allele of p53 are susceptible to a wide range of tumor types. The gene encodes a transcriptional regulator that may function in the cellular response to DNA damage. The construction of mouse strains carrying germline mutations of p53 facilitates analysis of the function of p53 in normal cells and tumorigenesis. Results: In order to study the effects of p53 mutation in vivo, we have constructed a mouse strain carrying a germline disruption of the gene. This mutation removes approximately 40 % of the coding capacity of p53 and completely eliminates synthesis of p53 protein. As observed previously for a different germline mutation of p53, animals homozygous for this p53 deletion mutation are viable but highly predisposed to malignancy. Heterozygous animals also have an increased cancer risk, although the distribution of tumor types in these animals differs from that in homozygous mutants. In most cases, tumorigenesis in heterozygous animals is accompanied by loss of the wild-type p53 allele. Conclusion: We reaffirm that p53 function is not required for normal mouse development and conclude that p53 status can strongly influence tumor latency and tissue distribution. C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02139. DANA FARBER CANC INST,BOSTON,MA 02215. TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02111. TUFTS UNIV,SCH VET MED,BOSTON,MA 02111. MIT,WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. MIT,DEPT BIOL,CAMBRIDGE,MA 02142. RP JACKS, T (reprint author), MIT,CTR CANC RES,CAMBRIDGE,MA 02139, USA. RI Williams, Bart/A-3539-2013 OI Williams, Bart/0000-0002-5261-5301 FU NCI NIH HHS [5R35-CA39826] NR 36 TC 1415 Z9 1426 U1 1 U2 33 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD JAN 1 PY 1994 VL 4 IS 1 BP 1 EP 7 DI 10.1016/S0960-9822(00)00002-6 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY541 UT WOS:A1994MY54100001 PM 7922305 ER PT S AU COLLINS, TL BURAKOFF, SJ AF COLLINS, TL BURAKOFF, SJ BE Tsuchiya, M Yodoi, J Hibi, T Miura, S TI CD4 AND LCK IN T-CELL ACTIVATION SO CURRENT TOPICS IN MUCOSAL IMMUNOLOGY 1993 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT Tokyo International Symposium on Mucosal Immunology 1993 CY AUG 25-27, 1993 CL TOKYO, JAPAN C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81586-4 J9 INT CONGR SER PY 1994 VL 1047 BP 39 EP 47 PG 9 WC Immunology SC Immunology GA BA04H UT WOS:A1994BA04H00005 ER PT S AU PODOLSKY, DK DIGNASS, A CIACCI, C AF PODOLSKY, DK DIGNASS, A CIACCI, C BE Tsuchiya, M Yodoi, J Hibi, T Miura, S TI INTESTINAL EPITHELIAL LAMINA-PROPRIA INTEGRATION - ROLE OF TGF-BETA, IL-2, AND OTHER CYTOKINES IN MODULATING RESTITUTION SO CURRENT TOPICS IN MUCOSAL IMMUNOLOGY 1993 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT Tokyo International Symposium on Mucosal Immunology 1993 CY AUG 25-27, 1993 CL TOKYO, JAPAN C1 MASSACHUSETTS GEN HOSP,DEPT GASTROINTESTINAL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81586-4 J9 INT CONGR SER PY 1994 VL 1047 BP 135 EP 138 PG 4 WC Immunology SC Immunology GA BA04H UT WOS:A1994BA04H00016 ER PT S AU MORIMOTO, C AF MORIMOTO, C BE Tsuchiya, M Yodoi, J Hibi, T Miura, S TI MOLECULAR-BASIS OF CD26 MEDIATED COSTIMULATION IN CD4 SUBSET - ITS IMPLICATION FOR MUCOSAL IMMUNITY SO CURRENT TOPICS IN MUCOSAL IMMUNOLOGY 1993 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT Tokyo International Symposium on Mucosal Immunology 1993 CY AUG 25-27, 1993 CL TOKYO, JAPAN C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81586-4 J9 INT CONGR SER PY 1994 VL 1047 BP 389 EP 391 PG 3 WC Immunology SC Immunology GA BA04H UT WOS:A1994BA04H00065 ER PT J AU HENTATI, A DENG, HX HAINES, J HUNG, WY PERICACKVANCE, MA SIDDIQUE, T AF HENTATI, A DENG, HX HAINES, J HUNG, WY PERICACKVANCE, MA SIDDIQUE, T TI GENERATION OF DENSE LINKAGE MAP OF CHROMOSOME 2Q33 USING BAND SPECIFIC MICRODISSECTION LIBRARY CLONES SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NORTHWESTERN UNIV,SCH LAW,CHICAGO,IL 60611. MASSACHUSETTS GEN HOSP EAST,CHARLESTON,MA 02127. DUKE UNIV,MED CTR,DURHAM,NC 27710. NR 2 TC 1 Z9 1 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 241 EP 241 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500007 ER PT J AU BASSON, CT SOLOMON, SD WEISSMAN, B MACRAE, CA POZNANSKI, AK PRIETO, F DELAFUENTE, SR PEASE, WE LEVIN, SE HOLMES, L SEIDMAN, JG SEIDMAN, CE AF BASSON, CT SOLOMON, SD WEISSMAN, B MACRAE, CA POZNANSKI, AK PRIETO, F DELAFUENTE, SR PEASE, WE LEVIN, SE HOLMES, L SEIDMAN, JG SEIDMAN, CE TI GENETIC-HETEROGENEITY OF HEART-HAND SYNDROMES SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,HOWARD HUGHES MED INST,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. CHILDRENS MEM HOSP,DEPT RADIOL,CHICAGO,IL 60614. HOSP LA FE,E-46009 VALENCIA,SPAIN. HARRISBURG HOSP,HARRISBURG,PA. UNIV WITWATERSRAND,SCH MED,DEPT PEDIAT,JOHANNESBURG,SOUTH AFRICA. MASSACHUSETTS GEN HOSP,EMBRYOL TERATOL UNIT,BOSTON,MA 02114. RI Solomon, Scott/I-5789-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 266 EP 266 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500023 ER PT J AU TROFATTER, JA LONG, KR MURRELL, JR RUTTER, JL STOTLER, CJ TURNER, AN GUSELLA, JF BUCKLER, AJ AF TROFATTER, JA LONG, KR MURRELL, JR RUTTER, JL STOTLER, CJ TURNER, AN GUSELLA, JF BUCKLER, AJ TI MAPPING EXONS TO CHROMOSOME-22 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 293 EP 293 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500073 ER PT J AU LOVETT, M BUCKLER, A CLINES, G DELMASTRO, R GALLARDO, T HILLIARD, C SIMMONS, A STOTLER, C WANG, L WISE, C AF LOVETT, M BUCKLER, A CLINES, G DELMASTRO, R GALLARDO, T HILLIARD, C SIMMONS, A STOTLER, C WANG, L WISE, C TI TRANSCRIPTION MAPPING ACROSS 4 REGIONS OF HUMAN-CHROMOSOME .5. IMPLICATIONS FOR MAPPING THE Y-CHROMOSOME SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. UNIV TEXAS,SW MED CTR,MCDERMOTT CTR HUMAN GROWTH & DEV,DALLAS,TX 75235. MASSACHUSETTS GEN HOSP,MOLEC GENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 397 EP 397 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500207 ER PT J AU TROFATTER, JA LONG, KR MURRELL, JR RUTTER, JL STOTLER, CJ TURNER, AN GUSELLA, JF BUCKLER, AJ AF TROFATTER, JA LONG, KR MURRELL, JR RUTTER, JL STOTLER, CJ TURNER, AN GUSELLA, JF BUCKLER, AJ TI CONSTRUCTION OF A CHROMOSOME 22-ENRICHED EXON LIBRARY AND ITS POTENTIAL FOR GENERATION OF CHROMOSOME-SPECIFIC PHYSICAL AND TRANSCRIPTION MAPS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 399 EP 400 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500215 ER PT J AU GRUNDY, D RUTTER, J RUSTGI, A HOUSEAL, T MENON, A AF GRUNDY, D RUTTER, J RUSTGI, A HOUSEAL, T MENON, A TI IDENTIFICATION OF A PUTATIVE TUMOR-SUPPRESSOR LOCUS IN 14Q24-32 THAT IS INVOLVED IN FORMATION AND PROGRESSION OF SOLID TUMORS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV CINCINNATI,DEPT MOLEC GENET BIOCHEM & MICROBIOL,CINCINNATI,OH 45267. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA. INTEGRATED GENET INC,FRAMINGHAM,MA 01701. NR 0 TC 3 Z9 3 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 66 IS 1 BP 14 EP 15 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA MR937 UT WOS:A1994MR93700015 ER PT J AU VANCE, JM LOEB, DB WHISENANT, E LUI, W NUNES, K STAJICH, JS RIMMLER, J HAINES, J SMITH, D DRABKIN, H PERICAKVANCE, MA AF VANCE, JM LOEB, DB WHISENANT, E LUI, W NUNES, K STAJICH, JS RIMMLER, J HAINES, J SMITH, D DRABKIN, H PERICAKVANCE, MA TI GENETIC-MAPPING OF MICROSATELLITES SPANNING THE VHL REGION OF CHROMOSOME-3P25 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,DURHAM,NC 27706. UNIV COLORADO,BOULDER,CO 80309. WAYNE STATE UNIV,DETROIT,MI 48202. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 47 EP 48 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400034 ER PT J AU BOUFFARD, D BARNHILL, RL MIHM, MC SOBER, AJ AF BOUFFARD, D BARNHILL, RL MIHM, MC SOBER, AJ TI VERY LATE METASTASIS (27 YEARS) OF CUTANEOUS MALIGNANT-MELANOMA ARISING IN A HALO GIANT CONGENITAL NEVUS SO DERMATOLOGY LA English DT Note DE GIANT CONGENITAL NEVUS; MELANOMA; LEUKODERMA; METASTATIC MELANOMA; PROGNOSIS ID RECURRENCE; LEUKODERMA; VITILIGO; RISK AB We report a case of primary cutaneous melanoma with the incidental finding of a lung metastasis 27 years following the original diagnosis. The case is exceptional in that it is a late metastasis of a melanoma that arose in association with a halo giant congenital nevus. The original tumor was a large dermal/subcutaneous nodule composed of very well-differentiated cells reminiscent of type B nevomelanocytes. The metastasis displayed similar histology. This case emphasizes the unpredictable behavior of malignant melanoma. In cases with 'unusual' histology such as this one, the usual prognostic parameters are less helpful in predicting survival. Melanoma should be included in the differential diagnosis of an undiagnosed lesion suspicious for metastasis even if the primary was removed in the remote past. C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DIV DERMATOPATHOL,BOSTON,MA 02115. NR 16 TC 23 Z9 23 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1994 VL 189 IS 2 BP 162 EP 166 PG 5 WC Dermatology SC Dermatology GA NP886 UT WOS:A1994NP88600013 PM 8075446 ER PT J AU FALO, LD SOBER, AJ BARNHILL, RL AF FALO, LD SOBER, AJ BARNHILL, RL TI EVOLUTION OF A NEVUS-SPILUS SO DERMATOLOGY LA English DT Note DE MELANOCYTIC NEVUS; MELANOMA ID SPECKLED LENTIGINOUS-NEVUS; MALIGNANT-MELANOMA AB The evolution of a naevus spilus is documented with serial photographs over a 12-year period, The lesion was remarkable for increasing numbers of macules and papules within the background of the cafe-au-lait macule, Biopsy of a new papule showed lentiginous melanocytic hyperplasia without atypia, We advise photography and periodic follow-up of large, clinically atypical or changing naevi spill. Indications for considering biopsy of naevi spill, irrespective of size, include atypical clinical features or change in one of the hyperpigmented macules or papules, eventuating in an atypical clinical appearance. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT DERMATOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 11 TC 8 Z9 8 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1994 VL 189 IS 4 BP 382 EP 383 PG 2 WC Dermatology SC Dermatology GA PV885 UT WOS:A1994PV88500011 PM 7873825 ER PT J AU MORGAN, BA TABIN, C AF MORGAN, BA TABIN, C TI HOX GENES AND GROWTH - EARLY AND LATE ROLES IN LIMB BUD MORPHOGENESIS SO DEVELOPMENT LA English DT Article DE HOX GENE; LIMB BUD MORPHOGENESIS; AXIS SPECIFICATION; ANTEROPOSTERIOR DETERMINATION ID EXPRESSION AB In recent years, molecular analysis has led to the identification of some of the key genes that control the morphogenesis of the developing embryo. Detailed functional analysis of these genes is rapidly leading to a new level of understanding of how embryonic form is regulated. Understanding the roles that these genes play in development can additionally provide insights into the evolution of morphology. The 5' genes of the vertebrate Hox clusters are expressed in complex patterns during limb morphogenesis. Various models suggest that the Herd genes specify positional identity along the anteroposterior (A-P) axis of the limb. Close examination of the pattern of Hoxd gene expression in the limb suggests that a distinct combination of Hoxd gene expressed in different digit primordia is unlikely to specify each digit independently. The effects of altering the pattern of expression of the Hoxd-11 gene at different times during limb development indicate that the Hoxd genes have separable early and late roles in limb morphogenesis. In their early role, the Hoxd genes are involved in regulating the growth of the undifferentiated limb mesenchyme. Restriction of the expression of successive 5' Hoxd genes to progressively more posterior regions of the bud results in the asymmetric outgrowth of the limb mesenchyme. Later in limb development, Hoxd genes also regulate the maturation of the nascent skeletal elements. The degree of overlap in function between different Hoxd genes may be different in these early and late roles. The combined action of many Hox genes on distinct developmental processes contribute to pattern asymmetry along the A-P axis. C1 HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP MORGAN, BA (reprint author), MASSACHUSETTS GEN HOSP EAST,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129, USA. NR 14 TC 65 Z9 65 U1 0 U2 3 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 PY 1994 SU S BP 181 EP 186 PG 6 WC Developmental Biology SC Developmental Biology GA QK897 UT WOS:A1994QK89700020 PM 7579519 ER PT J AU WABER, DP ISQUITH, PK KAHN, CM ROMERO, I SALLAN, SE TARBELL, NJ AF WABER, DP ISQUITH, PK KAHN, CM ROMERO, I SALLAN, SE TARBELL, NJ TI METACOGNITIVE FACTORS IN THE VISUOSPATIAL SKILLS OF LONG-TERM SURVIVORS OF ACUTE LYMPHOBLASTIC-LEUKEMIA - AN EXPERIMENTAL APPROACH TO THE REY-OSTERRIETH COMPLEX FIGURE TEST SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID CHILDHOOD LEUKEMIA; CHILDREN; PRODUCTIONS; MEMORY; SEX AB Long-term survivors of childhood acute lymphoblastic leukemia (ALL) can exhibit increased difficulty with visuospatial reasoning tasks. The present study was undertaken to ascertain whether this difficulty reflects underlying spatial/visuoperceptual deficits or has a metacognitive basis. Two studies were carried out investigating performance on the Rey-Osterrieth Complex Figure test. In Study 1, 51 survivors performed the task in the standard format. They recalled fewer organizing-scheme components than normative expectation but more incidental features. In Study 2 the encoding phase of the task was manipulated. Thirty-four survivors were randomized to a linear (LIN) or configurational (CON) presentation and memory productions were evaluated. Organization scores for the CON group were above normative expectation, whereas those of the LIN group remained unchanged. Visuospatial reasoning problems in these children have a metacognitive basis and do not represent a fundamental visuoperceptual or spatial deficit. C1 INTER AMER UNIV,SAN JUAN,PR 00917. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIAT ONCOL,BOSTON,MA 02115. RP WABER, DP (reprint author), CHILDRENS HOSP MED CTR,DEPT PSYCHIAT,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 17 TC 16 Z9 16 U1 1 U2 3 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 8756-5641 J9 DEV NEUROPSYCHOL JI Dev. Neuropsychol. PY 1994 VL 10 IS 4 BP 349 EP 367 PG 19 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA QU256 UT WOS:A1994QU25600001 ER PT J AU SOKOL, SM MACARUSO, P GOLLAN, TH AF SOKOL, SM MACARUSO, P GOLLAN, TH TI DEVELOPMENTAL DYSCALCULIA AND COGNITIVE NEUROPSYCHOLOGY SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID LEARNING-DISABLED CHILDREN; OF-PROCESSING DIFFERENCES; BRAIN-DAMAGED SUBJECTS; GERSTMANN SYNDROME; STRATEGY CHOICE; SINGLE-PATIENT; PERFORMANCE; MEMORY; ABILITIES; PATTERNS AB In this article we present a study investigating the cognitive impairments exhibited in developmental dyscalculia, or arithmetic learning disability. We begin by providing a brief review of the literature on the subject, including both single-case and group designs. In our view both approaches, at least as thus far employed, are associated with theoretical and/or methodological shortcomings. We suggest that the cognitive neuropsychological approach may offer a better paradigm for research in this domain. Accordingly we present a recent cognitive neuropsychological model of numeric processing that has been informed by the patterns of impairment evidenced in individuals with acquired brain damage. We then present preliminary results from several developmental dyslexic students who have numeric processing impairments and attempt to demonstrate how their performance patterns conform to the expectations of the model. Finally, in the discussion, we consider certain methodological issues related to this study and suggest possible directions for future research. C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,NEUROLINGUIST LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 89 TC 13 Z9 13 U1 4 U2 5 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 8756-5641 J9 DEV NEUROPSYCHOL JI Dev. Neuropsychol. PY 1994 VL 10 IS 4 BP 413 EP 441 PG 29 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA QU256 UT WOS:A1994QU25600005 ER PT J AU WAKISAKA, M SPIRO, MJ SPIRO, RG AF WAKISAKA, M SPIRO, MJ SPIRO, RG TI SYNTHESIS OF TYPE-VI COLLAGEN BY CULTURED GLOMERULAR CELLS AND COMPARISON OF ITS REGULATION BY GLUCOSE AND OTHER FACTORS WITH THAT OF TYPE-IV COLLAGEN SO DIABETES LA English DT Article ID BASEMENT-MEMBRANE; EXTRACELLULAR-MATRIX; MESANGIAL CELLS; DIABETIC RATS; GROWTH; COMPONENTS; PROTEINS; INSULIN; LOCALIZATION; KIDNEY AB Homogeneous cultures of calf glomerular mesangial and endothelial cells were found to be active in the synthesis of type VI as well as type IV collagen in contrast to the epithelial eels that were devoted primarily to the production of the tatter collagen. Studies with rat mesangial cells indicated that they responded to high glucose (20 mM) in the medium by a significant (P < 00.001) increase in type VI collagen synthesis as measured by the production of the protein and its mRNA level, both of which were closely correlated to each other and to glucose consumption. Similar observations were made with type IV collagen, but the enhanced formation of this protein was not as rapidly apparent as that of type VI and, moreover, could not be as readily reversed on restoration of the glucose to a physiological level (5 mM). Evaluation of a number of other agents indicated that although mannitol had no effect, L-glucose and NaCl significantly stimulated synthesis of both type VI and IV collagens and glucose consumption. Insulin-like growth factor I and aldosterone, on the other hand, also increased glucose consumption but brought about an enhancement of only type IV collagen production, suggesting that the two collagens are independently regulated. This possibility was supported by our observation that pyruvate, which was actively taken up by the cells, selectively stimulated type IV collagen production. Although the details of the regulation of these two major glomerular extracellular matrix components have not yet been defined, it is apparent that mesangial cells in culture reflect the enhanced formation of type VI and type IV collagen, which is evident in the diabetic glomerular lesions. C1 JOSLIN DIABET CTR,ELLIOTT P JOSLIN RES LAB,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. FU NHLBI NIH HHS [HL-31315]; NIDDK NIH HHS [DK-17477] NR 37 TC 67 Z9 70 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 JAN PY 1994 VL 43 IS 1 BP 95 EP 103 DI 10.2337/diabetes.43.1.95 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MP920 UT WOS:A1994MP92000014 PM 8262324 ER PT J AU AXELROD, L CAMUSO, J WILLIAMS, E KLEINMAN, K BRIONES, E SCHOENFELD, D AF AXELROD, L CAMUSO, J WILLIAMS, E KLEINMAN, K BRIONES, E SCHOENFELD, D TI EFFECTS OF A SMALL QUANTITY OF OMEGA-3-FATTY-ACIDS ON CARDIOVASCULAR RISK-FACTORS IN NIDDM - A RANDOMIZED, PROSPECTIVE, DOUBLE-BLIND, CONTROLLED-STUDY SO DIABETES CARE LA English DT Article ID DIABETES-MELLITUS; PLATELET-FUNCTION; FISH OIL; PLASMA-LIPIDS; DIET; LIPOPROTEINS; SUPPLEMENTS; METABOLISM AB OBJECTIVE- To study the effects of a low dose of omega-3 fatty acids on platelet function and other cardiovascular risk factors in patients with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS- We performed a randomized, prospective, double-blind, controlled study of a low dose of 0-3 fatty acids (2.5 g/day) in 20 ambulatory subjects with NIDDM. Subjects ingested five 1-g fish oil capsules each containing 0.5 g 0-3 fatty acids or five 1-g safflower oil capsules per day for 6 weeks followed by a 6-week washout period. RESULTS- Nine subjects completed the study in each group. Both groups exhibited moderate control of glucose levels; modest elevations in baseline total cholesterol, low- density lipoprotein (LDL) cholesterol, and triglyceride (TG) levels; and normal blood pressure values. In the fish oil group, plasma omega-3 fatty acid levels increased significantly. Fish oil significantly reduced the slope of the dose-response curves for collagen-induced platelet aggregation to one-third the value observed with safflower oil. No difference was observed in collagen-induced production of thromboxane A(2) (TXA(2), measured as the stable derivative TXB(2), or in adenosine-5'-diphosphate- (ADP) induced platelet aggregation or TXA(2) generation. Patients with high initial collagen-induced platelet TXA(2) production showed a significantly larger drop after fish oil than safflower oil. Fish oil significantly reduced TG levels by 44 mg/dl and decreased upright systolic blood pressure (sBP) by 8 mmHg compared with safflower oil. Fish oil caused a significant but small increase in HbA(1c) (0.56%) and total cholesterol (20 mg/dl) but had no effect on fasting glucose, high-density lipoprotein cholesterol, or LDL-cholesterol levels. CONCLUSIONS- Small doses of fish oil inhibit platelet aggregation and TX2A(2) production, reduce upright sBP and TG levels, and have only a small effect on glucose and cholesterol levels in patients with moderately controlled NIDDM. Small quantities of omega-3 fatty acids or dietary fish are safe and potentially beneficial in NIDDM patients. C1 MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP AXELROD, L (reprint author), MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114, USA. NR 26 TC 55 Z9 56 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JAN PY 1994 VL 17 IS 1 BP 37 EP 44 DI 10.2337/diacare.17.1.37 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MP563 UT WOS:A1994MP56300006 PM 8112187 ER PT J AU HORIO, F FUKUDA, M KATOH, H PETRUZZELLI, M YANO, N RITTERSHAUS, C BONNERWEIR, S HATTORI, M AF HORIO, F FUKUDA, M KATOH, H PETRUZZELLI, M YANO, N RITTERSHAUS, C BONNERWEIR, S HATTORI, M TI REACTIVE OXYGEN INTERMEDIATES IN AUTOIMMUNE ISLET-CELL DESTRUCTION OF THE NOD MOUSE INDUCED BY PERITONEAL-EXUDATE CELLS (RICH IN MACROPHAGES) BUT NOT T-CELLS SO DIABETOLOGIA LA English DT Article DE NOD MICE; INSULITIS; REACTIVE OXYGEN INTERMEDIATES; SUPEROXIDE DISMUTASE; PERITONEAL MACROPHAG(E)S ID TUMOR NECROSIS FACTOR; FREE-RADICAL OXYGEN; POLY(ADP-RIBOSE) SYNTHETASE; MONOCLONAL-ANTIBODY; BETA-CELLS; SUPEROXIDE-DISMUTASE; PROINSULIN SYNTHESIS; POLYETHYLENE-GLYCOL; DIABETES-MELLITUS; INTERFERON-GAMMA AB The non-obese diabetic (NOD) mouse spontaneously develops autoimmune Type 1 (insulin-dependent) diabetes mellitus. NOD mice exhibit massive infiltrates of T cells and macrophages into pancreatic islets (insulitis) prior to diabetes. The contribution of oxygen free radicals to the development of insulitis in NOD mice was examined by administration of its scavengers, such as superoxide dismutase and catalase. Bovine superoxide dismutase and catalase were each coupled to polyethylene glycol. The treatment with superoxide dismutase-polyethylene glycol reduced the number of islets with insulitis and increased the undamaged islet tissue, as compared with the control group. The treatment with catalase-polyethylene glycol showed a similar tendency which did not reach significance. Using a flow cytometric assay of the oxidation of 2', 7'-dichlorofluorescein, the content of reactive oxygen intermediates in islet cells in the culture system was measured and the effect of peritoneal exudate cells and T cells on their production examined. Peritoneal exudate cells, but not T cells, from NOD mice increased the content of reactive oxygen intermediates in islet cells of either the NOD mouse or the ILI mouse (MHC-identical to NOD); the addition of superoxide dismutase to the culture medium suppressed this increase in NOD or ILI islet cells. The present data support the concept that production of oxygen free radicals mediated by macrophages can damage islet beta cells, directly resulting in autoimmune Type 1 diabetes in NOD mice. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,JOSLIN DIABET CTR,BOSTON,MA 02215. CENT INST EXPTL ANIM,KAWASAKI,KANAGAWA,JAPAN. T CELL SCI,CAMBRIDGE,MA. FU NIADDK NIH HHS [1P30 AM36836]; NIDDK NIH HHS [R01 DK43613] NR 46 TC 53 Z9 53 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JAN PY 1994 VL 37 IS 1 BP 22 EP 31 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ972 UT WOS:A1994MQ97200004 PM 8150225 ER PT S AU AWERBUCH, T AF AWERBUCH, T BE Wilson, ME Levins, R Spielman, A TI EVOLUTION OF MATHEMATICAL-MODELS OF EPIDEMICS SO DISEASE IN EVOLUTION: GLOBAL CHANGES AND EMERGENCE OF INFECTIOUS DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Emerging Diseases Workshop CY NOV 07-10, 1993 CL WOODS HOLE, MA ID MALARIA C1 DANA FARBER CANC INST,BOSTON,MA 02115. RP AWERBUCH, T (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT POPULAT & INT HLTH,665 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 23 TC 3 Z9 3 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-877-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 740 BP 232 EP 241 DI 10.1111/j.1749-6632.1994.tb19873.x PG 10 WC Public, Environmental & Occupational Health; Infectious Diseases; Multidisciplinary Sciences SC Public, Environmental & Occupational Health; Infectious Diseases; Science & Technology - Other Topics GA BD10S UT WOS:A1994BD10S00026 PM 7840452 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Thymus - Hodgkin's disease, nodular sclerosis type SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 12 EP 16 PG 5 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00001 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Hodgkin's disease, lymphocyte-predominant type, nodular SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 17 EP 23 PG 7 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00002 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Hodgkin's disease, lymphocyte-depletion type (diffuse fibrosis variant) SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 24 EP 27 PG 4 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00003 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Anaplastic large-cell lymphoma SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 28 EP 33 PG 6 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00004 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Spleen - Malignant lymphoma and B-cell chronic lymphocytic leukemia SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 34 EP 40 PG 7 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00005 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Lymph node - Malignant lymphoma SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 55 EP 64 PG 10 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00008 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Thyroid - Malignant lymphoma SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 75 EP 81 PG 7 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00011 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Malignant lymphoma, diffuse, large-cell immunoblastic type in a cardiac allograft recipient SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 82 EP 90 PG 9 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00012 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Malignant lymphoma, diffuse small noncleaved cell, pleomorphic (non-Burkitt) variant SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 91 EP 95 PG 5 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00013 ER PT B AU HARRIS, NL AF HARRIS, NL BE Harris, NL Banks, PM Jaffe, ES TI Thymus - Thymoma, malignant, type 1 and well-differentiated thymic carcinoma SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 126 EP 134 PG 9 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00020 ER PT J AU JENKINSON, SG LEVINE, SM AF JENKINSON, SG LEVINE, SM TI LUNG TRANSPLANTATION SO DM DISEASE-A-MONTH LA English DT Article ID OBSTRUCTIVE PULMONARY-DISEASE; TRANS-BRONCHIAL BIOPSIES; HIGH-RESOLUTION CT; HEART-LUNG; OBLITERATIVE BRONCHIOLITIS; BRONCHOALVEOLAR LAVAGE; CHRONIC REJECTION; NATURAL-HISTORY; RECIPIENTS; EMPHYSEMA AB Solid-organ transplantation has flourished during the last decade, with transplantation of heart and lungs becoming available to patients with end-stage cardiac or pulmonary diseases. The first lung transplant was performed in 1963 on a 58-year-old man with bronchogenic carcinoma. He survived for 18 days. During the next two decades, approximately 40 lung transplant procedures were attempted without success. These early attempts at lung transplantation were unsuccessful because of the development of lung rejection anastomotic complications, or infection in the transplant recipients. In the early 1980s, human heart-lung transplantation was successfully performed for the treatment of pulmonary vascular disease. After this procedure, single-lung transplantation for the treatment of end-stage interstitial lung disease and obstructive lung disease was developed. More recently, the technique of double-lund transplantation has come into existence. This article reviews various aspects of lung transplantation, including immunosuppression, lund graft preservation, the various surgical techniques and types of lund transplant procedures available, recipient and donor selection criteria and postoperative care of the transplant recipient. In addition, infectious and noninfectious complications seen in this particular patient population including acute and chronic rejection, will be discussed. C1 AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT,MED INTENS CARE UNIT,SAN ANTONIO,TX. RP JENKINSON, SG (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. NR 78 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 0011-5029 J9 DM-DIS MON JI DM-Dis.-a-Mon. PD JAN PY 1994 VL 40 IS 1 BP 3 EP 38 PG 36 WC Medicine, General & Internal SC General & Internal Medicine GA MR398 UT WOS:A1994MR39800001 ER PT J AU RUPRECHT, RM BRONSON, R AF RUPRECHT, RM BRONSON, R TI CHEMOPREVENTION OF RETROVIRAL INFECTION - SUCCESS IS DETERMINED BY VIRUS INOCULUM STRENGTH AND CELLULAR-IMMUNITY SO DNA AND CELL BIOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; MIXED LYMPHOCYTE-REACTION; POSTEXPOSURE CHEMOPROPHYLAXIS; PROPHYLACTIC ZIDOVUDINE; INTERFERON-ALPHA; SYNDROME AIDS; 3'-AZIDO-3'-DEOXYTHYMIDINE; HIV-1; CD4+; FAILURE AB We demonstrated earlier that post-exposure prophylaxis with 3'-azido-3'-deoxythymidine (AZT, zidovudine) or with AZT + interferon-alpha (IFN-alpha) prevented viremia and disease in BALB/c mice inoculated with Rauscher murine leukemia virus (RLV). After the 20-day treatment course, most animals were resistant to rechallenge with live virus. Adoptive transfer of T cells from such resistant but not from normal mice into naive recipients provided full protection against virus challenge. From these experiments, we concluded that post-exposure chemoprophylaxis restricted virus replication and allowed the animals to form protective, long-lasting cellular immune responses. Here, the role for cellular immunity during antiviral chemoprophylaxis was tested by comparing treatment success in normal BALB/c mice and in their nude, athymic counterparts. Both were inoculated with equal doses of RLV (10(4) plaque-forming units, pfu). Single-agent AZT or combination therapy with AZT + IFN-alpha, started before or after RLV inoculation, prevented viremia in all normal but not in most nude mice. A significant number of nude mice were completely protected by chemoprevention only when given a 10 times lower virus dose. When normal mice were injected with a 10 times higher virus dose (10(5) pfu), complete protection by chemoprevention was lost. These results demonstrate that the success of chemoprevention depends critically on the virus inoculum. The differential success of chemoprevention in normal and T-cell-deficient mice implies that effective cellular immunity plays an important role in protecting virus-exposed animals against viremia and disease. C1 TUFTS UNIV,SCH VET MED,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP RUPRECHT, RM (reprint author), DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [N01 AI72664, 1RO1-AI32330-02, UO1 AI-24845] NR 34 TC 18 Z9 18 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 JAN PY 1994 VL 13 IS 1 BP 59 EP 66 DI 10.1089/dna.1994.13.59 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA MU600 UT WOS:A1994MU60000007 PM 8286040 ER PT J AU DRINKA, TJK AF DRINKA, TJK TI INTERDISCIPLINARY GERIATRIC TEAMS - APPROACHES TO CONFLICT AS INDICATORS OF POTENTIAL TO MODEL TEAMWORK SO EDUCATIONAL GERONTOLOGY LA English DT Article ID WORK TEAMS AB Interdisciplinary health care teams (IHTs) are essential for the delivery of health care to frail elderly persons. Teaching professionals how to function in health care teams is difficult. Educators often, use linear group development theories for teaching about IHTs. However, distinguishing features of the health care field, such as the diversity of the health professions, the ongoing nature of IHTs, high turnover in health care facilities, and incongruous development of the team and its members, may render linear group theories insufficient as models for IHTs. A team that has moved through its basic developmental phases once or twice may not be an, effective role model for teaching health professionals about IHTs. IHTs develop and function in unpredictable ways and, depending on their cultural depth, may be negative role models for professionals. As a team develops, long-term members should assume leadership roles as teachers of teamwork. Methods for constructively confronting conflict with a focus on integrative problem solving allow team members to move beyond basic group development tasks and to promote continuous reassessment of the team's established norms. Skills in conflict management, problem solving, and assumption of functional leadership are necessary for team members who assume the leadership role of teaching teamwork. In addition, evidence of constructive confrontation may be a good indicator of an IHT's readiness to model teamwork. RP DRINKA, TJK (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON GERIATR RES EDUC & CLIN CTR,MADISON,WI 53705, USA. NR 28 TC 4 Z9 4 U1 1 U2 3 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0360-1277 J9 EDUC GERONTOL JI Educ. Gerontol. PD JAN-FEB PY 1994 VL 20 IS 1 BP 87 EP 103 DI 10.1080/0360127940200107 PG 17 WC Education & Educational Research; Gerontology SC Education & Educational Research; Geriatrics & Gerontology GA MR478 UT WOS:A1994MR47800007 ER PT J AU CLARK, PG DRINKA, TJK AF CLARK, PG DRINKA, TJK TI SPECIAL ISSUE ON CONCEPTUAL FOUNDATIONS FOR INTERDISCIPLINARY EDUCATION IN GERONTOLOGY AND GERIATRICS - INTRODUCTION SO EDUCATIONAL GERONTOLOGY LA English DT Editorial Material C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP CLARK, PG (reprint author), UNIV RHODE ISL,KINGSTON,RI 02881, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0360-1277 J9 EDUC GERONTOL JI Educ. Gerontol. PD JAN-FEB PY 1994 VL 20 IS 1 BP R3 EP R8 PG 6 WC Education & Educational Research; Gerontology SC Education & Educational Research; Geriatrics & Gerontology GA MR478 UT WOS:A1994MR47800001 ER PT S AU ROBINSON, DR XU, LL KNOELL, CT TATENO, S GUO, MY COLVIN, RB OLESIAK, W URAKAZE, M SUGIYAMA, E AURON, PE YEH, ETH AUSTEN, KF SPERLING, RI AF ROBINSON, DR XU, LL KNOELL, CT TATENO, S GUO, MY COLVIN, RB OLESIAK, W URAKAZE, M SUGIYAMA, E AURON, PE YEH, ETH AUSTEN, KF SPERLING, RI BE Galli, C Simopoulos, AP Tremoli, E TI Alleviation of autoimmune disease by omega 3 fatty acids SO EFFECTS OF FATTY ACIDS AND LIPIDS IN HEALTH AND DISEASE SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 1st International Congress of the International-Society-for-the-Study-of-Fatty-Acids-and-Lipids (ISSFAL) CY JUN 30-JUL 03, 1993 CL LUGANO, SWITZERLAND SP INT SOC STUDY FATTY ACIDS & LIPIDS RP MASSACHUSETTS GEN HOSP,MED SERV,ARTHRIT UNIT,BULFINCH 165,BOSTON,MA 02114, USA. NR 0 TC 8 Z9 9 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0084-2230 BN 3-8055-6040-0 J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1994 VL 76 BP 95 EP 102 PG 8 WC Medicine, Research & Experimental; Nutrition & Dietetics SC Research & Experimental Medicine; Nutrition & Dietetics GA BC45J UT WOS:A1994BC45J00021 PM 7856246 ER PT S AU PADANILAM, JT BISCHOF, JC LEE, RC CRAVALHO, EG TOMPKINS, RG YARMUSH, ML TONER, M AF PADANILAM, JT BISCHOF, JC LEE, RC CRAVALHO, EG TOMPKINS, RG YARMUSH, ML TONER, M BE Lee, RC CapelliSchellpfeffer, M Kelley, KM TI EFFECTIVENESS OF POLOXAMER-188 IN ARRESTING CALCEIN LEAKAGE FROM THERMALLY DAMAGED ISOLATED SKELETAL-MUSCLE CELLS SO ELECTRICAL INJURY: A MULTIDISCIPLINARY APPROACH TO THERAPY, PREVENTION, AND REHABILITATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 2nd International Symposium on Electrical Trauma - Electrical Injury: A Multidisciplinary Approach in Therapy, Prevention, and Rehabilitation CY JUN 11-12, 1993 CL CHICAGO, IL SP UNIV CHICAGO, AMER BURN ASSOC, IEEE, ENGINEERS MED & BIOL SOC ID HEMOLYSIS C1 SHRINERS BURNS INST,RES CTR,CAMBRIDGE,MA 02139. MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02114. UNIV CHICAGO,DEPT SURG,CHICAGO,IL 60637. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08855. NR 15 TC 39 Z9 40 U1 1 U2 6 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-864-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 720 BP 111 EP 123 DI 10.1111/j.1749-6632.1994.tb30439.x PG 13 WC Multidisciplinary Sciences; Physiology; Rehabilitation SC Science & Technology - Other Topics; Physiology; Rehabilitation GA BA43Y UT WOS:A1994BA43Y00010 PM 7516633 ER PT J AU MULDER, JE SCHNEYER, AL TAYLOR, AE CROWLEY, WF SLUSS, PM AF MULDER, JE SCHNEYER, AL TAYLOR, AE CROWLEY, WF SLUSS, PM TI THE SPECIES-SPECIFICITY OF THE RECOMBINANT HUMAN AND RAT FOLLICLE-STIMULATING-HORMONE RECEPTOR ARE SIMILAR SO ENDOCRINE LA English DT Article ID PREMATURE OVARIAN FAILURE; RADIORECEPTOR ASSAY; BINDING; FOLLITROPIN; EXPRESSION; TESTIS; PROLACTIN; SERUM AB A readily available source of human FSH (hFSH) receptors has been lacking, and therefore other mammalian receptors such as rat and bovine have been used to study receptor-hFSH interactions and to identify putative modulators of FSH receptor binding. It has been reported that the recently cloned recombinant hFSH receptor exhibits a different species specificity than the native rat (r) FSH receptor, suggesting the presence of evolutionary changes in mammalian FSH receptor binding epitopes and providing a basis for the preferential use of homologous receptors to study FSH bioactivity. The objective of this study was to compare the binding characteristics and species specificity of the recombinant hFSH receptor and recombinant rFSH receptor. The association constants (K-A) of binding of [I-125]hFSH to both types of recombinant receptor, calculated under both steady-state and non-steady state conditions, were within the ranges previously reported for native bovine or rat receptors (10(8)-10(10) M(-1)). Increasing concentrations of unlabelled hFSH, rFSH, ovine (o) FSH, and bovine (b) FSH inhibited [(125)]hFSH binding in a dose dependent and statistically parallel fashion in both receptor assays. The ED(50)'s (ng/ml) for hFSH, rFSH, oFSH and bFSH in the hFSH RRA were 11.8 +/- 1.2, 180.9 +/- 27.0, 122.9 +/- 20.8 and 363.8 +/- 54.3, and in the rFSH RRA were 2.1 +/- 0.14, 3.1 +/- 0.26, 58.4 +/- 3.6 and 74.2 +/- 6.0 respectively. Therefore, there is no absolute difference in species specificity between the recombinant hFSH and rFSH receptor. C1 MASSACHUSETTS GEN HOSP,CTR REPROD ENDOCRINE SCI,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NATL CTR INFERTIL RES,BOSTON,MA 02114. NR 19 TC 7 Z9 7 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0969-711X J9 ENDOCRINE JI Endocrine PD JAN PY 1994 VL 2 IS 1 BP 25 EP 31 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PL769 UT WOS:A1994PL76900003 ER PT J AU HOFMANN, C LORENZ, K BRAITHWAITE, SS COLCA, JR PALAZUK, BJ HOTAMISLIGIL, GS SPIEGELMAN, BM AF HOFMANN, C LORENZ, K BRAITHWAITE, SS COLCA, JR PALAZUK, BJ HOTAMISLIGIL, GS SPIEGELMAN, BM TI ALTERED GENE-EXPRESSION FOR TUMOR-NECROSIS-FACTOR-ALPHA AND ITS RECEPTORS DURING DRUG AND DIETARY MODULATION OF INSULIN-RESISTANCE SO ENDOCRINOLOGY LA English DT Article ID GLUCOSE-TRANSPORT; FACTOR BIOSYNTHESIS; AGENT PIOGLITAZONE; SKELETAL-MUSCLE; CACHECTIN; MICE; CACHEXIA; CLONING; RNA; METABOLISM AB As obesity is a major risk factor for noninsulin-dependent diabetes mellitus, adipose tissue may generate a mediator that influences the activity of insulin on various target tissues. Recent evidence suggests that a cytokine, tumor necrosis factor-alpha (TNF alpha), may serve this role. This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. The effects of moderate weight loss by dietary restriction were also examined. We show here that a marked induction of TNF alpha mRNA occurs in adipose tissues from a mouse model of obesity-linked diabetes (KKA(y)) compared to that in nondiabetic mice (C57). Likewise, RNA transcripts encoding TNF R2 receptors (p75) were significantly increased in fat tissues of the obese diabetic animals. In muscle from these diabetic animals, RNA transcripts encoding both TNF R1 (p55) and R2 were significantly elevated, although R2 transcript abundance was less elevated than in fat. We also observed that the overexpression of mRNA for TNF alpha and both of its receptors could be at least partly normalized by treatment of the diabetic animals with the insulin-sensitizing agent pioglitazone. Treating of the obese diabetic animals by food restriction reduced the expression of mRNA for TNF R2 in muscle, but not fat. These results clearly indicate that gene expression for the TNF systems can be regulated by an insulin-sensitizing drug and reduction of body weight. Such findings support a role for this cytokine in the insulin-resistant diabetic state and show its modulation by therapies that reverse the disorder. C1 LOYOLA UNIV,MED CTR,INST SHOCK TRAUMA,MAYWOOD,IL 60141. UPJOHN CO,METAB DIS RES,KALAMAZOO,MI 49001. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP HOFMANN, C (reprint author), EDWARD HINES VET ADM MED CTR,RES SERV 151,HINES,IL 60141, USA. NR 55 TC 299 Z9 307 U1 2 U2 9 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1994 VL 134 IS 1 BP 264 EP 270 DI 10.1210/en.134.1.264 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ621 UT WOS:A1994MQ62100038 PM 8275942 ER PT J AU LEE, K DEEDS, JD CHIBA, S UNNO, M BOND, AT SEGRE, GV AF LEE, K DEEDS, JD CHIBA, S UNNO, M BOND, AT SEGRE, GV TI PARATHYROID-HORMONE INDUCES SEQUENTIAL C-FOS EXPRESSION IN BONE-CELLS IN-VIVO - IN-SITU LOCALIZATION OF ITS RECEPTOR AND C-FOS MESSENGER RIBONUCLEIC-ACIDS SO ENDOCRINOLOGY LA English DT Article ID RABBIT COSTAL CHONDROCYTES; RAT OSTEO-SARCOMA; ORNITHINE DECARBOXYLASE; ALKALINE-PHOSPHATASE; OSTEOBLASTIC CELLS; EMBRYONIC CHICK; TRANSGENIC MICE; TARGET-CELL; CULTURE; PEPTIDE AB Localization of PTH/PTH-related peptide (PTH/PTHrP) receptor mRNA and PTH induction of c-fos expression were examined in bones of 4-week-old rats by in situ hybridization. Receptor transcripts were most highly expressed by growth plate chondrocytes from lower proliferating to upper hypertrophic cell layers. PTH/PTHrP receptor mRNA also was expressed in osteoblasts as well as in some bone marrow stromal cells. Subcutaneous administration of human PTH-(1-84) (225 mu g/kg) induced rapid, transient, and sequential expression of the protooncogene c-fos mRNA in cells in bone. Osteoblasts and chondrocytes expressing PTH/PTHrP receptor transcripts as well as some stromal cells expressed c-fos mRNA first (15-60 min), followed by transient expression in the majority of stromal cells and in osteoclasts (1-2 h). Delayed and transient induction of c-fos in cells with few or no detectable receptor transcripts suggests that PTH acts indirectly on stromal cells and osteoclasts by either stimulating osteoblasts to secrete a substance(s) that acts locally and/or inducing changes in cell-cell contacts between osteoblasts and adjacent cells. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. CHUGAI PHARMACEUT CO LTD,TOXICOL LABS,MINOWA,NAGANO 39946,JAPAN. FU NIDDK NIH HHS [DK-11794] NR 49 TC 171 Z9 171 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1994 VL 134 IS 1 BP 441 EP 450 DI 10.1210/en.134.1.441 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ621 UT WOS:A1994MQ62100062 PM 8275957 ER PT J AU URENA, P IIDAKLEIN, A KONG, XF JUPPNER, H KRONENBERG, HM ABOUSAMRA, AB SEGRE, GV AF URENA, P IIDAKLEIN, A KONG, XF JUPPNER, H KRONENBERG, HM ABOUSAMRA, AB SEGRE, GV TI REGULATION OF PARATHYROID-HORMONE (PTH)/PTH-RELATED PEPTIDE RECEPTOR MESSENGER-RIBONUCLEIC-ACID BY GLUCOCORTICOIDS AND PTH IN ROS 17/2.8 AND OK CELLS SO ENDOCRINOLOGY LA English DT Article ID OSTEOBLAST-LIKE CELLS; INTRACELLULAR FREE CALCIUM; OSTEOGENIC-SARCOMA CELLS; TUMOR-NECROSIS-FACTOR; OPOSSUM KIDNEY-CELLS; ADENYLATE-CYCLASE; DOWN-REGULATION; OSTEOSARCOMA CELLS; CYCLIC-AMP; CAMP AB To study mechanisms controlling the expression of PTH/PTH-related peptide (PTHrP) receptors in ROS 17/2.8 and OK cells, we investigated the regulation of PTH/PTHrP receptor availability and receptor mRNA levels by glucocorticoids and PTH. Treatment of ROS 17/2.8 cells with dexamethasone (1 mu M) for 2, 4, and 6 days increased specific binding of PTH to 148 +/- 12%, 203 +/- 10%, and 344 +/- 9% (mean +/- SD), respectively, compared to that in untreated control cells. PTH-stimulated cAMP accumulation also increased with dexamethasone treatment (1 mu M) from 230 +/- 15%, 382 +/- 9%, and 820 +/- 9% after 2, 4 and 6 days, respectively, compared to that in untreated cells. Treatment of ROS 17/2.8 cells with [Nle(8),Nle(18),Tyr(34)]bovine PTH-(1-34) amide (NlePTH; 100 nM) alone or together with dexamethasone (1 mu M), however, markedly decreased PTH binding and PTH-stimulated cAMP accumulation. Northern blot analysis showed that dexamethasone dramatically increased steady state levels of PTH/PTHrP receptor mRNA in a time- and dose-dependent manner, which did not occur when NlePTH (100 nM) was added concomitantly to the cultures. As previously reported, daily NlePTH treatment of ROS 17/2.8 cells reduced PTH/PTHrP receptor availability and PTH-stimulated cAMP accumulation markedly within 2 days, which remained at these low levels during continued PTH treatment. In contrast, the identical treatment reduced steady state levels of PTH/PTHrP receptor mRNA in ROS 17/2.8 transiently and to only a slight extent, which then returned to pretreatment levels. Treatment of OK cells with NlePTH (100 nM) for 1, 2, and 4 days decreased PTH binding to 56 +/- 6%, 44 +/- 4%, and 64 +/- 4% (mean +/- SD) and PTH-stimulated cAMP accumulation to 42 +/- 6%, 19 +/- 4%, and 21 +/- 3% (mean +/- SD), respectively, compared to values in untreated control cells. The same treatment, however, had no significant effect on steady state levels of PTH/ PTHrP receptor transcripts. In contrast to its effects in ROS 17/2.8 cells, dexamethasone (1 mu M) treatment of OK cells for 1-4 days did not affect PTH binding, nor did it significantly affect steady state levels of PTH/PTHrP receptor mRNA, although the latter was slightly lowered by dexamethasone treatment. PTH-stimulated cAMP accumulation was unchanged after 1-day treatment with dexamethasone and modestly rose to 142 +/- 4% of the control value by day 4 of glucocorticoid exposure. The concomitant treatment of OK cells with both PTH and dexamethasone may have further diminished the reduced receptor availability induced by PTH alone, but the effects of this concomitant treatment were indistinguishable from those of PTH alone on cAMP accumulation. These data show that the effect of glucocorticoid on PTH/PTHrP receptor availability is cell specific and positively correlates with steady state levels of its mRNA in ROS 17/2.8 cells. Homologous down-regulation of PTH/PTHrP receptors, however, did not occur at the transcriptional level over the duration of these experiments in either ROS 17/2.8 or OK cells; it is likely to involve alternative mechanisms, such as receptor phosphorylation, internalization, and degradation. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. OI Abou-Samra, Abdul/0000-0001-8735-1142 FU NIDDK NIH HHS [DK-11794, DK-45485] NR 32 TC 75 Z9 78 U1 0 U2 3 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1994 VL 134 IS 1 BP 451 EP 456 DI 10.1210/en.134.1.451 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ621 UT WOS:A1994MQ62100063 PM 8275958 ER PT J AU LINDSEY, JC RYAN, LM AF LINDSEY, JC RYAN, LM TI A COMPARISON OF CONTINUOUS-TIME AND DISCRETE-TIME 3-STATE MODELS FOR RODENT TUMORIGENICITY EXPERIMENTS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID SURVIVAL-SACRIFICE EXPERIMENTS; ANIMAL CARCINOGENESIS EXPERIMENTS; ILLNESS-DEATH MODEL; RATES AB The three-state illness-death model provides a useful way to characterize data from a rodent tumorigenicity experiment. Most parametrizations proposed recently in the literature assume discrete time for the death process and either discrete or continuous time for the tumor onset process. We compare these approaches with a third alternative that uses a piecewise continuous model on the hazards for tumor onset and death. Ah three models assume proportional hazards to characterize tumor lethality and the effect of dose on tumor onset and death rate. All of the models can easily be fitted using an Expectation Maximization (EM) algorithm. The piecewise continuous model is particularly appealing in this context because the complete data likelihood corresponds to a standard piecewise exponential model with tumor presence as a time-varying covariate. It can be shown analytically that differences between the parameter estimates given by each model are explained by varying assumptions about when tumor onsets, deaths, and sacrifices occur within intervals. The mixed-time model is seen to be an extension of the grouped data proportional hazards model [Mutat. Res. 24: 267-278 (1981)]. We argue that the continuous-time model is preferable to the discrete- and mixed-time models because it gives reasonable estimates with relatively few intervals while still making full use of the available information. Data from the ED(01) experiment illustrate the results. C1 DANA FARBER CANC INST, DIV BIOSTAT, BOSTON, MA 02115 USA. RP LINDSEY, JC (reprint author), HARVARD UNIV, SCH PUBL HLTH, DEPT BIOSTAT, 677 HUNTINGTON AVE, BOSTON, MA 02115 USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 FU NCI NIH HHS [CA-33041, CA-48061] NR 24 TC 14 Z9 14 U1 0 U2 1 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 9 EP 17 PG 9 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000003 PM 8187731 ER PT J AU SCHECTER, A RYAN, JJ MASUDA, Y BRANDTRAUF, P CONSTABLE, J CAU, HD DAI, LC QUYNH, HT PHUONG, NTN PHIET, PH AF SCHECTER, A RYAN, JJ MASUDA, Y BRANDTRAUF, P CONSTABLE, J CAU, HD DAI, LC QUYNH, HT PHUONG, NTN PHIET, PH TI CHLORINATED AND BROMINATED DIOXINS AND DIBENZOFURANS IN HUMAN TISSUE FOLLOWING EXPOSURE SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID HUMAN ADIPOSE-TISSUE; ELECTRICAL TRANSFORMER INCIDENT; POLYCHLORINATED-BIPHENYLS; VIETNAM VETERANS; CANCER MORTALITY; NEW-YORK; OCCUPATIONAL EXPOSURE; GENERAL-POPULATION; P-DIOXINS; COWS MILK AB With substantial improvements in analytic techniques over the past decade, it has become possible to measure polychlorinated dioxins (PCDDs) and dibenzofurans (PCDFs) in human tissue in a congener-specific fashion down to the low parts per trillion level. This paper reviews findings using these new techniques from a number of recent medical and environmental case studies. These studies include those of workers exposed to a polychlorinated biphenyl (PCB) transformer fire in the United States, German chemical workers exposed to 2,3,7,8-tetrachlorodibenzodioxin (2,3,7,8-TCDD) while cleaning up after an explosion, workers at a municipal incinerator in New York City, a chemist exposed to brominated and chlorinated dioxins, U.S. veterans and also Vietnamese civilians exposed to Agent Orange contaminated with TCDD in Vietnam, and victims of the polychlorinated dibenzofuran and PCB contaminated rice oil (Yusho) incident in Japan. C1 DAIICHI COLL PHARMACEUT SCI, FUKUOKA 815, JAPAN. COLUMBIA UNIV, SCH PUBL HLTH, DIV ENVIRONM SCI, NEW YORK, NY 10032 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, BOSTON, MA 02114 USA. HANOI UNIV, COLL MED, HANOI, VIETNAM. MINIST HLTH, HANOI, VIETNAM. OBSTET & GYNECOL HOSP, HO CHI MINH CITY, VIETNAM. COLL MED HO CHI MINH CITY, HO CHI MINH CITY, VIETNAM. CHO RAY HOSP, HO CHI MINH CITY, VIETNAM. HLTH & WELF CANADA, FOOD DIRECTORATE, OTTAWA K10 9C6, ON, CANADA. RP SCHECTER, A (reprint author), SUNY HLTH SCI CTR SYRACUSE, DEPT PREVENT MED, COLL MED CLIN CAMPUS, 88 ALDRICH AVE, BINGHAMTON, NY 13903 USA. NR 65 TC 19 Z9 20 U1 1 U2 3 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 135 EP 147 PG 13 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000023 PM 8187703 ER PT J AU SCHECTER, A FURST, P FURST, C PAPKE, O BALL, M RYAN, JJ CAU, HD DAI, LC QUYNH, HT CUONG, HQ PHUONG, NTN PHIET, PH BEIM, A CONSTABLE, J STARTIN, J SAMEDY, M YEO, KS AF SCHECTER, A FURST, P FURST, C PAPKE, O BALL, M RYAN, JJ CAU, HD DAI, LC QUYNH, HT CUONG, HQ PHUONG, NTN PHIET, PH BEIM, A CONSTABLE, J STARTIN, J SAMEDY, M YEO, KS TI CHLORINATED DIOXINS AND DIBENZOFURANS IN HUMAN TISSUE FROM GENERAL POPULATIONS - A SELECTIVE REVIEW SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Review ID HUMAN ADIPOSE-TISSUE; EXPOSED VIETNAM VETERANS; HUMAN-MILK; UNITED-STATES; AGENT ORANGE; POLYCHLORINATED DIBENZODIOXINS; BLOOD-SAMPLES; SOVIET-UNION; MALE-RATS; 2,3,7,8-TCDD AB During the past decade a considerable amount of data has been generated concerning polychlorinated dibenzodioxin (PCDD) and polychlorinated dibenzofuran (PCDF) levels in humans from many geographical locations. To organize these data in a useful fashion for environmental purposes and for consideration of human toxicity, selected portions of our data are presented in a somewhat atypical fashion, by percentage contribution of individual congeners to total PCDD/Fs in human tissue, and to the total dioxin equivalents (TEq). This is done to better characterize congener contributions from environmental contamination in various geographical regions at this time and health-related levels. To present the findings in a global perspective, data from widely different locations are presented including the United States, Germany, Vietnam, the former Soviet Union, Thailand, Cambodia, China, South Africa, and Guam. C1 STATE LAB N RHINE WESTPHALIA FOOD PHARMACEUT ENVI, W-4400 MUNSTER, GERMANY. FORSCH GELLSCH MBH, ERGO, W-2000 HAMBURG, GERMANY. HLTH & WELF CANADA, DIV FOOD RES, OTTAWA K1A 0L2, ON, CANADA. COLL MED, NATL COMM STUDY CONSEQUENCES CHEM USED WARTIME 10, HANOI, VIETNAM. OBSTET HOSP, HANOI, VIETNAM. OBSTET HOSP, HO CHI MINH CITY, VIETNAM. CHO RAY HOSP, HO CHI MINH CITY, VIETNAM. BAIKALSK ECOL TOXICOL INST, BAIKALSK 665914, RUSSIA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, BOSTON, MA 02114 USA. MAFF, FOOD SCI LAB, NORWICH NR4 7UQ, ENGLAND. COLL MED DENT & PHARM, PHNOM PENH, CAMBODIA. MINIST HLTH, PHNOM PENH, CAMBODIA. RP SCHECTER, A (reprint author), SUNY HLTH SCI CTR SYRACUSE, COLL MED, DEPT PREVENT MED, 88 ALDRICH AVE, BINGHAMTON, NY 13903 USA. NR 60 TC 73 Z9 78 U1 1 U2 2 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 159 EP 171 PG 13 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000025 PM 8187705 ER PT J AU CASALE, L CARDOZO, C KALB, T LESSER, M AF CASALE, L CARDOZO, C KALB, T LESSER, M TI QUANTITATION OF ENDOPEPTIDASE-24.11 AND ENDOPEPTIDASE-24.15 IN HUMAN BLOOD LEUKOCYTES SO ENZYME & PROTEIN LA English DT Article DE B LYMPHOCYTES; ENDOPEPTIDASE 24.11; ENDOPEPTIDASE 24.15; MONOCYTES; NEUTROPHILS; T LYMPHOCYTES ID LYMPHOBLASTIC-LEUKEMIA ANTIGEN; MEMBRANE-BOUND METALLOENDOPEPTIDASE; ENKEPHALIN-CONTAINING PEPTIDES; NEUTRAL ENDOPEPTIDASE; HUMAN-NEUTROPHILS; SOLUBLE METALLOENDOPEPTIDASE; RAT-BRAIN; ALVEOLAR MACROPHAGES; NATURAL PEPTIDES; LYMPHOID-CELLS AB Endopeptidase 24.11 (EP 24.11; also called neutral endopeptidase, enkephalinase, CALLA, or CD10) and endopeptidase 24.15 (EP 24.15) are widely distributed neutral metalloendopeptidases that degrade a number of bioactive peptides including substance P, bradykinin, neurotensin, and chemotactic peptides. In this study we used sensitive substrates and specific inhibitors to quantitate the levels of these enzymes in purified peripheral human blood leukocytes obtained from healthy blood donors. We found that neutrophils did not contain detectable amounts of EP 24.15. In contrast, T lymphocytes, B lymphocytes, and monocytes contained significant amounts of the enzyme (446 +/- 248,314 +/- 183, and 484 +/- 212 nmol/mg protein/h, respectively). Neutrophils contained significant amounts of EP 24.11 (266 +/- 130 nmol/mg protein/h). Significantly lower levels of the enzyme were found in T lymphocytes, B lymphocytes, and monocytes (94 +/- 31, 87 +/- 38, and 20 +/- 13 nmol/mg protein/h, respectively). These findings suggest that the effects of some bioactive peptides on peripheral blood leukocyte function may be modulated by these enzymes. C1 BRONX VET AFFAIRS MED CTR,PULM SECT,BRONX,NY 10468. MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. MT SINAI SCH MED,DEPT PHARMACOL,NEW YORK,NY 10029. NR 41 TC 5 Z9 5 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1019-6773 J9 ENZYME PROTEIN JI Enzyme Protein PY 1994 VL 48 IS 3 BP 143 EP 148 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TE523 UT WOS:A1994TE52300002 PM 8589801 ER PT J AU TUBIANA, M HOLLAND, R KOPANS, DB KURTZ, JM PETIT, JY RILKE, F SACCHINI, V TORNBERG, S AF TUBIANA, M HOLLAND, R KOPANS, DB KURTZ, JM PETIT, JY RILKE, F SACCHINI, V TORNBERG, S TI MANAGEMENT OF NON-PALPABLE AND SMALL LESIONS FOUND IN MASS BREAST SCREENING SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID DUCTAL CARCINOMA INSITU; INTRADUCTAL CARCINOMA; RADIATION-THERAPY; PREOPERATIVE LOCALIZATION; CONSERVING SURGERY; COST-EFFECTIVENESS; PROGNOSTIC FACTORS; RANDOMIZED TRIAL; NEEDLE-BIOPSY; CANCER C1 UNIV NIJMEGEN,KANKERCTR,NATL EXPERT & TRAINING CTR BREAST CANC SCREENING,NIJMEGEN,NETHERLANDS. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. UNIV GENEVA,HOP CANTONAL,DEPT RADIOL,DIV RADIOONCOL,CH-1211 GENEVA,SWITZERLAND. INST GUSTAVE ROUSSY,DEPT GEN SURG,VILLEJUIF,FRANCE. INST NAZL TUMORI,DEPT SURG,MILAN,ITALY. KAROLINSKA SJUKHUSET,RADIUMHEMMET,CTR ONCOL,STOCKHOLM,SWEDEN. RP TUBIANA, M (reprint author), FAC MED PARIS,CTR ANTOINE BECLERE,RUE ST PERES,F-75006 PARIS,FRANCE. NR 70 TC 28 Z9 31 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 4 BP 538 EP 547 DI 10.1016/0959-8049(94)90435-9 PG 10 WC Oncology SC Oncology GA NL469 UT WOS:A1994NL46900027 PM 8018417 ER PT J AU KLOEN, P JENNINGS, CL GEBHARDT, MC SPRINGFIELD, DS MANKIN, HJ AF KLOEN, P JENNINGS, CL GEBHARDT, MC SPRINGFIELD, DS MANKIN, HJ TI SURAMIN INHIBITS GROWTH AND TRANSFORMING GROWTH-FACTOR-BETA-1 (TGF-BETA-1) BINDING IN OSTEOSARCOMA CELL-LINES SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE SURAMIN; TRANSFORMING GROWTH FACTOR-BETA-1; OSTEOSARCOMA; RECEPTOR; AUTOCRINE GROWTH ID FACTOR-BETA; PROLIFERATION; CARCINOMA; CANCER; LOOP AB Autocrine production of growth factors has been shown to be involved in the multistep process of tumorigenesis. The ability of suramin, a polyanionic anti-parasitic drug, to block growth factor-induced cell proliferation makes it a potential antineoplastic drug. We studied the effects of suramin on seven osteosarcoma cell lines. Using clinically achievable concentrations of suramin (50-400 mu g/ml), we found a time- and dose-dependent inhibition of [H-3]thymidine incorporation. We also showed that suramin is able, dose-dependently, to prevent binding of transforming growth factor (TGF)-beta 1 to its receptors. DNA synthesis inhibition by suramin was attenuated by TGF-beta 1 in some cell lines. Two cell lines that were inhibited by TGF-beta 1 were affected similarly by suramin as cell lines that were stimulated by TGF-beta 1. In conclusion, in five out of seven osteosarcoma cell lines, we showed a correlation between inhibition of growth factor-stimulated mitogenesis and binding of TGF-beta 1 to its receptor. Similar effects in TGF-beta 1-inhibited osteosarcoma cell lines suggest involvement of other mechanisms and/or growth factors. However, suramin proves to be a potent inhibitor of osteosarcoma cell proliferation in vitro. RP KLOEN, P (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,GRAY 6,FRUIT ST,BOSTON,MA 02114, USA. NR 30 TC 29 Z9 30 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 5 BP 678 EP 682 DI 10.1016/0959-8049(94)90544-4 PG 5 WC Oncology SC Oncology GA NP813 UT WOS:A1994NP81300027 PM 8080687 ER PT J AU TEICHER, BA AF TEICHER, BA TI LONIDAMINE - IN-VITRO IN-VIVO CORRELATIONS SO EUROPEAN JOURNAL OF CANCER LA English DT Note ID ASCITES TUMOR-CELLS; ALKYLATING-AGENTS; LUNG-CANCER; ADRIAMYCIN; INVITRO; POTENTIATION; MURINE; INVIVO; CYCLOPHOSPHAMIDE; INHIBITION RP TEICHER, BA (reprint author), CHILDRENS HOSP,DANA FARBER CANC INST,444 BINNEY ST,BOSTON,MA 02115, USA. NR 33 TC 16 Z9 17 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 10 BP 1411 EP 1413 DI 10.1016/0959-8049(94)00265-7 PG 3 WC Oncology SC Oncology GA PP467 UT WOS:A1994PP46700003 PM 7833093 ER PT J AU HALL, NR TAYLOR, GR FINAN, PJ KOLODNER, RD BODMER, WF COTTRELL, SE FRAYLING, I BISHOP, DT AF HALL, NR TAYLOR, GR FINAN, PJ KOLODNER, RD BODMER, WF COTTRELL, SE FRAYLING, I BISHOP, DT TI INTRON SPLICE ACCEPTOR SITE SEQUENCE VARIATION IN THE HEREDITARY NONPOLYPOSIS COLORECTAL-CANCER GENE HMSH2 SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE COLORECTAL CANCER; DNA MUTATION DETECTION; GENETIC SUSCEPTIBILITY; HEREDITARY NONPOLYPOSIS COLORECTAL CANCER; POLYMORPHISM; SPLICE SITE ID FREQUENCY; HOMOLOG; FAMILY; COLON AB Common but weakly penetrant mutations of certain genes may confer an increased susceptibility to colorectal cancer and account for a proportion of 'sporadic' cases. We analysed DNA from 111 colorectal cancer cases and 114 controls for a specific candidate sequence variation in the hereditary non-polyposis colorectal cancer gene hMSH2. The variant sequence was found in a quarter of individuals, and there was no difference between cancer cases and controls, according to age of development of cancer or presence of family history. It thus appears that this particular sequence variation is a polymorphism rather than a mutation which increases cancer susceptibility. C1 ST JAMES UNIV HOSP,IMPERIAL CANC RES FUND,GENET EPIDEMIOL LAB,LEEDS LS9 7TF,W YORKSHIRE,ENGLAND. GEN INFIRM,DEPT SURG,LEEDS LS1 3EX,W YORKSHIRE,ENGLAND. ST JAMES UNIV HOSP,REG DNA LAB,LEEDS LS9 7TF,W YORKSHIRE,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL & MOLEC BIOL,BOSTON,MA 02115. IMPERIAL CANC RES FUND,CANC GENET LAB,LONDON WC2A 3PX,ENGLAND. ST MARKS HOSP,IMPERIAL CANC RES FUND,COLORECTAL CANC UNIT,LONDON EC1V 2PS,ENGLAND. OI Bishop, Tim/0000-0002-8752-8785; Bodmer, Walter/0000-0001-6244-9792 NR 15 TC 16 Z9 16 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1994 VL 30A IS 10 BP 1550 EP 1552 DI 10.1016/0959-8049(94)00326-Z PG 3 WC Oncology SC Oncology GA PP467 UT WOS:A1994PP46700027 PM 7833117 ER PT J AU YOSHIMURA, M PEKARY, AE PANG, XP BERG, L COLE, LA KARDANA, A HERSHMAN, JM AF YOSHIMURA, M PEKARY, AE PANG, XP BERG, L COLE, LA KARDANA, A HERSHMAN, JM TI EFFECT OF PEPTIDE NICKING IN THE HUMAN CHORIONIC-GONADOTROPIN BETA-SUBUNIT ON STIMULATION OF RECOMBINANT HUMAN THYROID-STIMULATING HORMONE RECEPTORS SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Article ID NORMAL PREGNANT-WOMEN; THYROTROPIN; BINDING; CELLS; HETEROGENEITY; HCG; FRAGMENTATION; SERA AB It is now generally accepted that human chorionic gonadotropin (hCG) has thyroid-stimulating activity. Heterologous forms of the hCG molecule occur in the purified preparations extracted from urine of pregnant women and patients with trophoblastic diseases. This work was undertaken to determine the effect of peptide nicking in the hCG-beta subunit on its thyrotropic potency. Using Chinese hamster ovary cells expressing functional human thyroid-stimulating hormone (TSH) receptors, we examined the effect of nicked hCG on cyclic AMP (cAMP) production and receptor binding. The effect of human leukocyte elastase (hLE), a nicking enzyme, on standard hCG also was examined in the cAMP assay and on receptor binding. We studied five hCG preparations extracted from the urine of normal pregnancy (CR-127 and P8) and trophoblastic diseases (C2, C5 and M4). Two preparations (C2, 96% nicked and M4, 100% nicked in the beta 44-49 region) showed about a 1.5-fold potency of standard hCG CR-127, which is also 20% nicked in the same region. Non-nicked hCG (P8) had the weakest potency among all of the samples tested. Treatment of standard hCG with hLE increased the cAMP response about two-fold. Dose-dependent displacement of bovine [I-125]TSH by standard hCG and hLE-digested hCG was observed and was almost identical. We have confirmed the increased in vitro thyrotropic activity of hCG nicked in the beta-intercysteine loop on recombinant human TSH receptors. These data suggest that peptide heterogeneity of the hCG molecule may modulate the in vivo thyrotropic activity of hCG in pregnant women and patients with trophoblastic diseases. C1 W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINOL RES LAB W111D,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. YALE UNIV,SCH MED,DEPT OBSTET & GYNECOL,NEW HAVEN,CT 06510. NR 26 TC 17 Z9 17 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0804-4643 J9 EUR J ENDOCRINOL JI Eur. J. Endocrinol. PD JAN PY 1994 VL 130 IS 1 BP 92 EP 96 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NK507 UT WOS:A1994NK50700012 PM 7510202 ER PT J AU LEY, SC VERBI, W PAPPIN, DJC DRUKER, B DAVIES, AA CRUMPTON, MJ AF LEY, SC VERBI, W PAPPIN, DJC DRUKER, B DAVIES, AA CRUMPTON, MJ TI TYROSINE PHOSPHORYLATION OF ALPHA-TUBULIN IN HUMAN T-LYMPHOCYTES SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE T LYMPHOCYTES; TYROSINE PHOSPHORYLATION; ALPHA TUBULIN ID CELL ANTIGEN RECEPTOR; MICROTUBULE-ASSOCIATED PROTEINS; PHOSPHOINOSITIDE HYDROLYSIS; PHOSPHOLIPASE C-GAMMA-1; SIGNAL TRANSDUCTION; ACTIVATION; KINASE; STIMULATION; RESIDUES; COMPLEX AB N-terminal sequencing of the 55- and 50-kDa polypeptides affinity purified on a phosphotyrosine monoclonal antibody column from activated Jurkat T cells identified alpha and beta tubulin. Two-dimensional gel analysis indicated that a tubulin was directly phosphorylated on tyrosine. beta Tubulin was not detectably tyrosine hosphorylated but was precipitated by anti-phosphotyrosine (PTyr) antibody by virtue of its association with the alpha subunit as a heterodimer. Phosphotyrosyl alpha tubulin was not incorporated into intact microtubules and was all in the unpolymerized soluble fraction. These results suggest that tyrosine phosphorylation of alpha tubulin may inhibit the ability of this subunit to polymerize into microtubules. Stimulation of Jurkat T cells via T cell receptor increased the amount of tubulin precipitated by the anti-PTyr antibody. These data raise the possibility that the polymerization of tubulin heterodimers may be regulated by phosphorylation on tyrosine during T cell activation. C1 IMPERIAL CANC RES FUND,CELL SURFACE BIOCHEM & PROT SEQUENCING LABS,LONDON,ENGLAND. DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA. RP LEY, SC (reprint author), NATL INST MED RES,RIDGEWAY,MILL HILL,LONDON NW7 1AA,ENGLAND. OI Pappin, Darryl/0000-0002-8981-8401 NR 48 TC 43 Z9 44 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 1994 VL 24 IS 1 BP 99 EP 106 DI 10.1002/eji.1830240116 PG 8 WC Immunology SC Immunology GA MT838 UT WOS:A1994MT83800015 PM 7517366 ER PT J AU SHIPLEY, WU AF SHIPLEY, WU TI A PHASE-III TRIAL (RTOG-8610) COMPARING EXTERNAL-REAM IRRADIATION PLUS SHORT-TERM MAXIMAL ANDROGEN BLOCKADE WITH RADIATION-THERAPY ALONE FOR LOCALLY ADVANCED PROSTATE-CANCER SO EUROPEAN UROLOGY LA English DT Article; Proceedings Paper CT 4th International Symposium on Recent Advances in Urological Cancer Diagnosis and Treatment CY JUN 22-24, 1994 CL PARIS, FRANCE DE ADVANCED PROSTATE CANCER; APOPTOSIS; MAXIMAL ANDROGEN BLOCKADE; RADIATION THERAPY RP SHIPLEY, WU (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0302-2838 J9 EUR UROL JI Eur. Urol. PY 1994 VL 26 SU 1 BP 3 EP 3 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA QK607 UT WOS:A1994QK60700002 ER PT J AU SERSHON, PD BARRY, MJ OESTERLING, JE AF SERSHON, PD BARRY, MJ OESTERLING, JE TI SERUM PROSTATE-SPECIFIC ANTIGEN DISCRIMINATES WEAKLY BETWEEN MEN WITH BENIGN PROSTATIC HYPERPLASIA AND PATIENTS WITH ORGAN-CONFINED PROSTATE-CANCER SO EUROPEAN UROLOGY LA English DT Article DE PROSTATE-SPECIFIC ANTIGEN; BENIGN PROSTATIC HYPERPLASIA; PROSTATE CANCER; TUMOR MARKERS; ANTIGENS ID RADICAL PROSTATECTOMY; SIGNAL DETECTABILITY; TREATED PATIENTS; SCREENING-TEST; ADENOCARCINOMA; MARKER; LOCALIZATION; DIAGNOSIS; CARCINOMA; DENSITY AB To determine if serum prostate-specific antigen (PSA) can identify those patients harboring an organ-confined prostate cancer prior to treatment for symptomatic benign prostatic hyperplasia (BPH), we examined retrospectively the preoperative serum PSA level for two groups of men. Group 1 consisted of 187 consecutive patients with a histologic diagnosis of BPH as determined from complete pathologic analysis of the transurethral resection of the prostate (TURF) specimen. Group 2 included 198 consecutive patients with histologically confirmed organ-confined prostate cancer as determined from step-section analysis of the retropubic radical prostatectomy specimen. The median serum PSA value for group 1 was 3.9 ng/ml (range 0.2-55 ng/ml), whereas the median serum PSA level for group 2 was 5.9 ng/ml (range 0.4-58 ng/ml). Although this difference was statistically significant (p < 0.001), the distribution of serum PSA values for group 1 overlapped considerably with the distribution for group 2. For both groups, there was a clustering of PSA values below 10.0 ng/ml(group 1: 90%; group 2: 73%). The area under the receiver operating characteristic curve for log PSA values to discriminate men with BPH from patients with organ-confined prostate cancer was 0.66 (95% confidence interval: 0.60-0.72); a 'perfect' test has an area of 1.0, whereas a test with 'no information value' has an area of 0.5. These findings suggest that serum PSA has only a modest ability to distinguish men with BPH from patients with organ-confined prostate cancer. As a result, some symptomatic BPH patients choosing a non-TURP therapy may harbor a clinically significant prostate cancer despite being evaluated with a serum PSA determination. C1 MAYO CLIN & MAYO FDN,DEPT UROL,ROCHESTER,MN 55905. MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA 02114. FU AHRQ HHS [HS06336] NR 34 TC 38 Z9 39 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0302-2838 J9 EUR UROL JI Eur. Urol. PY 1994 VL 25 IS 4 BP 281 EP 287 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA NN691 UT WOS:A1994NN69100003 PM 7519989 ER PT J AU HAREGEWOIN, A ALEXANDER, E BLACK, PM LOEFFLER, JS AF HAREGEWOIN, A ALEXANDER, E BLACK, PM LOEFFLER, JS TI AUTOCRINE REGULATION OF THE PRODUCTION OF THE GASEOUS MESSENGER NITRIC-OXIDE IN A GLIOBLASTOMA CELL-LINE SO EXPERIMENTAL CELL RESEARCH LA English DT Note ID COLONY-STIMULATING FACTOR; GLUCOCORTICOIDS INHIBIT; INDUCTION; MACROPHAGES; EXPRESSION; SYNTHASE; LIPOPOLYSACCHARIDE; DEXAMETHASONE; MODULATION; CYTOKINES C1 CHILDRENS HOSP, BOSTON, MA USA. DANA FARBER CANC INST, JOINT CTR RADIAT THERAPY, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP HAREGEWOIN, A (reprint author), BRIGHAM & WOMENS HOSP, CTR BRAIN TUMOR, 50 BINNEY ST, BOSTON, MA 02115 USA. NR 26 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER INC PI SAN DIEGO PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4827 EI 1090-2422 J9 EXP CELL RES JI Exp. Cell Res. PD JAN PY 1994 VL 210 IS 1 BP 137 EP 139 DI 10.1006/excr.1994.1020 PG 3 WC Oncology; Cell Biology SC Oncology; Cell Biology GA MP597 UT WOS:A1994MP59700020 PM 8269990 ER PT J AU SCHUMAN, JS ERICKSON, K NATHANSON, JA AF SCHUMAN, JS ERICKSON, K NATHANSON, JA TI NITROVASODILATOR EFFECTS ON INTRAOCULAR-PRESSURE AND OUTFLOW FACILITY IN MONKEYS SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE CYCLIC GMP, NITROVASODILATOR; NITROGLYCERIN; OUTFLOW FACILITY; INTRAOCULAR PRESSURE; HYDRALAZINE ID ATRIAL NATRIURETIC FACTOR; GUANYLATE-CYCLASE; BINDING-SITES; SMOOTH-MUSCLE; LOCALIZATION; TISSUES; RAT; RECEPTORS; HEART; GMP C1 MASSACHUSETTS GEN HOSP,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROPHARMACOL RES LAB,BOSTON,MA 02114. RP SCHUMAN, JS (reprint author), TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,750 WASHINGTON ST,BOX 450,BOSTON,MA 02111, USA. RI Schuman, Joel/K-7304-2012 OI Schuman, Joel/0000-0002-8885-3766 FU NEI NIH HHS [5T32 EY07097-02, EY05077, EY07321] NR 29 TC 90 Z9 92 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JAN PY 1994 VL 58 IS 1 BP 99 EP 105 DI 10.1006/exer.1994.1199 PG 7 WC Ophthalmology SC Ophthalmology GA MX141 UT WOS:A1994MX14100011 PM 8157106 ER PT J AU BROWNELL, AL HANTRAYE, P WULLNER, U HAMBERG, L SHOUP, T ELMALEH, DR FRIM, DM MADRAS, BK BROWNELL, GL ROSEN, BR ISACSON, O AF BROWNELL, AL HANTRAYE, P WULLNER, U HAMBERG, L SHOUP, T ELMALEH, DR FRIM, DM MADRAS, BK BROWNELL, GL ROSEN, BR ISACSON, O TI PET-BASED AND MRI-BASED ASSESSMENT OF GLUCOSE-UTILIZATION, DOPAMINE-RECEPTOR BINDING, AND HEMODYNAMIC-CHANGES AFTER LESIONS TO THE CAUDATE-PUTAMEN IN PRIMATES SO EXPERIMENTAL NEUROLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; HUNTINGTONS-DISEASE; BRAIN DOPAMINE; KAINIC ACID; INTRASTRIATAL INJECTIONS; STRIATAL NEURONS; MODEL; METABOLISM; CHOREA; CLONING C1 MASSACHUSETTS GEN HOSP,PHYS RES LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,NEUROREGENERAT LAB,PROGRAM NEUROSCI,BELMONT,MA 02178. MCLEAN HOSP,BELMONT,MA. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,SOUTHBOROUGH,MA 01772. NEW ENGLAND REG PRIMATE RES CTR,DIV BEHAV BIOL,SOUTHBOROUGH,MA 01772. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. RP BROWNELL, AL (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NMR,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA32873-11]; NINDS NIH HHS [NS30064] NR 57 TC 29 Z9 29 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD JAN PY 1994 VL 125 IS 1 BP 41 EP 51 DI 10.1006/exnr.1994.1004 PG 11 WC Neurosciences SC Neurosciences & Neurology GA MV803 UT WOS:A1994MV80300004 PM 7905836 ER PT J AU STAMENKOVIC, I ARUFFO, A AF STAMENKOVIC, I ARUFFO, A TI HYALURONIC-ACID RECEPTORS SO EXTRACELLULAR MATRIX COMPONENTS SE METHODS IN ENZYMOLOGY LA English DT Review ID LYMPHOCYTE HOMING RECEPTOR; TUMOR-GROWTH INVIVO; T-CELL ACTIVATION; MOLECULAR-CLONING; ADHESION RECEPTOR; CD44 CONFERS; PROTEIN; CDNA; EXPRESSION; SEQUENCE C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02129. BRISTOL MYERS SQUIBB CO,PHARMACEUT RES INST,SEATTLE,WA 98121. RP STAMENKOVIC, I (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA55735] NR 55 TC 15 Z9 17 U1 1 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1994 VL 245 BP 195 EP 216 PG 22 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BC87X UT WOS:A1994BC87X00010 PM 7539092 ER PT J AU TAMESIS, RR MESSMER, EM RICE, BA DUTT, JE FOSTER, CS AF TAMESIS, RR MESSMER, EM RICE, BA DUTT, JE FOSTER, CS TI THE ROLE OF NATURAL-KILLER-CELLS IN THE DEVELOPMENT OF HERPES-SIMPLEX VIRUS TYPE-1 INDUCED STROMAL KERATITIS IN MICE SO EYE LA English DT Article ID DELAYED-TYPE HYPERSENSITIVITY; ANTI-ASIALO GM1; NK CELLS; CORNEAL INFECTION; IMMUNE REGULATION; ANTERIOR-CHAMBER; PASSIVE TRANSFER; NUDE-MICE; INVIVO; TUMOR AB Natural killer (NK) cells and acquired cell-mediated immunity effector cells (delayed type hypersensitivity (DTH) and cytotoxic T lymphocytes (CTL)) have been reported to play a vital role in the defence of the host against tumour and viral infections in locations other than the eve. A vigorous cellular inflammatory response to viral infections of the cornea, however, with the attendant damage to the corneal clarity, has obvious evolutionary disadvantages, and a substantial body of evidence indicates that in animals (e.g. mice) which are highly suceptible to inflammatory destruction of the cornea following corneal encounter with herpes simplex virus, it is the animal's immunological/inflammatory response which is responsible for the corneal damage. We examined the role of natural killer cells in the development of herpes stromal keratitis (HSK) in NK-deficient (C57BL/6J-bgj (beige)) mice and their NK-competent (C57BL/6J (black)) relatives. The beige (NK-deficient) mice were just as resistant to HSK as were the black mice. We also studied the effects of NK cell depletion of BALB/c Igh-1 disparate congenic mice. C.AL-20 (Igh-1d) mice are ordinarily highly susceptible to necrotising HSK. In vivo NK-cell depletion in these mice significantly decreased the incidence and severity of HSK in these animals (p<0.0005). Corneas from untreated C.AL-20 mice contained T cells, macrophages and NK cells. The corneal infiltrate from NK-depleted C.AL-20 mice consisted of T cells and macrophages but no NK cells. These data indicate that NK cells are participants in the development of HSK in the murine model of this disease. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,243 CHARLES ST,BOSTON,MA 02114. FU NEI NIH HHS [EY-06008] NR 57 TC 28 Z9 30 U1 0 U2 0 PU ROYAL COLL OPHTHALMOLOGISTS PI LONDON PA 17 CORNWALL TERRACE, LONDON, ENGLAND NW1 4QW SN 0950-222X J9 EYE JI Eye PY 1994 VL 8 BP 298 EP 306 PN 3 PG 9 WC Ophthalmology SC Ophthalmology GA NY275 UT WOS:A1994NY27500006 PM 7958034 ER PT J AU NISHIO, Y AIELLO, LP KING, GL AF NISHIO, Y AIELLO, LP KING, GL TI GLUCOSE-INDUCED GENES IN BOVINE AORTIC SMOOTH-MUSCLE CELLS IDENTIFIED BY MESSENGER-RNA DIFFERENTIAL DISPLAY SO FASEB JOURNAL LA English DT Note DE GENE REGULATION; ELONGATION FACTOR ID PROTEIN-KINASE-C; ELONGATION FACTOR-II; HUMAN-BREAST-CANCER; GLYCEMIC CONTROL; DIABETIC RATS; CLONING; CDNA; EXPRESSION; MORTALITY; SEQUENCE AB Hyperglycemia is postulated to cause chronic changes in the vasculature of diabetic patients, suggesting structural or genetic alterations. We have characterized the glucose induced alterations of gene expression in cultured bovine aortic smooth muscle cells using the recently developed mRNA differential display method. After five days of incubation with either 5.5 or 22 mM glucose, RNA preparations were isolated from confluent cells and probed with 10 candidate clones identified after screening up to 3000 mRNA species. Among these, three clones (2A, 2C, 3) showed significant changes in expression by Northern blot analysis. Elevated glucose levels decreased the mRNA expression of clones 2A and 3 to 51 +/- 7% (P < .01) and 59 +/- 10% (P < .05) (mean% of control +/- SEM), respectively. Expression of clone 2C was increased in 22 mM glucose condition to 221 +/- 23% (P < .05). Nucleotide sequence analysis showed that clone 3 had 77% homology to the 3'-noncoding region of human elongation factor 2, a member of the GTPase family which is essential for polypeptide synthesis. Clones 2A and 2C do show no homology to known nucleotide sequences. These results indicate that physiologically attainable high glucose conditions can significantly effect gene expression in aortic smooth muscle cells. Furthermore, mRNA differential display can be used in metabolic studies to identify new genes regulated by nutrients such as glucose. C1 HARVARD UNIV,SCH MED,JOSLIN DIABETES CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,JOSLIN DIABET CTR,BEETHAM EYE INST,CAMBRIDGE,MA 02138. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. FU NEI NIH HHS [EY05110]; NIDDK NIH HHS [DK36836] NR 29 TC 88 Z9 89 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 JAN PY 1994 VL 8 IS 1 BP 103 EP 106 PG 4 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA MV282 UT WOS:A1994MV28200015 PM 8299882 ER PT J AU FOITZIK, T BASSI, DG SCHMIDT, J LEWANDROWSKI, KB FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL AF FOITZIK, T BASSI, DG SCHMIDT, J LEWANDROWSKI, KB FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL TI INTRAVENOUS CONTRAST-MEDIUM ACCENTUATES THE SEVERITY OF ACUTE NECROTIZING PANCREATITIS IN THE RAT SO GASTROENTEROLOGY LA English DT Article ID TRYPSINOGEN-ACTIVATION PEPTIDES; COMPUTED-TOMOGRAPHY; NECROSIS; CT; ENHANCEMENT; MECHANISMS; DIAGNOSIS; ISCHEMIA; THERAPY; AGENTS C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 46 TC 90 Z9 95 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 JAN PY 1994 VL 106 IS 1 BP 207 EP 214 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MP419 UT WOS:A1994MP41900026 PM 8276183 ER PT J AU SUMMERGRAD, P AF SUMMERGRAD, P TI MEDICAL PSYCHIATRY UNITS AND THE ROLES OF THE INPATIENT PSYCHIATRIC-SERVICE IN THE GENERAL-HOSPITAL SO GENERAL HOSPITAL PSYCHIATRY LA English DT Article ID IOWA RECORD-LINKAGE; QUALITY ASSURANCE; PHYSICAL ILLNESS; EXCESS MORTALITY; HOMELESS MEN; CARE; DEINSTITUTIONALIZATION; DISORDERS; PATIENT; HEALTH AB The medical-psychiatric unit concept has been the most important influence in the development of general hospital inpatient psychiatry in the last decade. This concept and style of unit organization is reviewed in the context of the history of general hospital inpatient psychiatry. It is suggested that elements of the medical-psychiatry unit model will become more important in the organization of general hospital psychiatric units. Modifications of the medical psychiatry unit concept are suggested to take into account the heterogeneity of many general hospital inpatient services. Implications of these factors are discussed in the context of unit design, models of staff organization, and the formation of networks of care. RP SUMMERGRAD, P (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,INPATIENT PSYCHIAT SERV,BULFINCH 440,BOSTON,MA 02114, USA. NR 87 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD JAN PY 1994 VL 16 IS 1 BP 20 EP 31 DI 10.1016/0163-8343(94)90083-3 PG 12 WC Psychiatry SC Psychiatry GA NL441 UT WOS:A1994NL44100004 PM 8039680 ER PT J AU POWERS, PA SCHERER, SW TSUI, LC GREGG, RG HOGAN, K AF POWERS, PA SCHERER, SW TSUI, LC GREGG, RG HOGAN, K TI LOCALIZATION OF THE GENE ENCODING THE ALPHA(2)/DELTA SUBUNIT (CACNL2A) OF THE HUMAN SKELETAL-MUSCLE VOLTAGE-DEPENDENT CA2+ CHANNEL TO CHROMOSOME 7Q21-Q22 BY SOMATIC-CELL HYBRID ANALYSIS SO GENOMICS LA English DT Note ID CALCIUM-CHANNEL; SEQUENCE C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53705. UNIV WISCONSIN,DEPT PEDIAT,MADISON,WI 53705. UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO M5S 1A8,ON,CANADA. HOSP SICK CHILDREN,RES INST,DEPT GENET,TORONTO M5G 1X8,ON,CANADA. RP POWERS, PA (reprint author), UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV 707,1500 HIGHLAND AVE,MADISON,WI 53705, USA. RI Tsui, Lap-chee/A-1081-2010; Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013 OI Scherer, Stephen /0000-0002-8326-1999 NR 15 TC 17 Z9 17 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 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1994 VL 19 IS 1 BP 192 EP 193 DI 10.1006/geno.1994.1044 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NA601 UT WOS:A1994NA60100043 PM 8188232 ER PT J AU FACCHINETTI, F NERI, I FAVA, M GENAZZANI, AR AF FACCHINETTI, F NERI, I FAVA, M GENAZZANI, AR TI MENSTRUAL-RELATED MOOD CHANGES IN PATIENTS WITH OLIGOMENORRHEA SO GYNECOLOGIC AND OBSTETRIC INVESTIGATION LA English DT Article DE OLIGOMENORRHEA; PREMENSTRUAL SYMPTOMS; ANTICIPATION; HORMONES ID PREMENSTRUAL SYMPTOMS; QUESTIONNAIRE; BELIEFS; WOMEN AB In order to evaluate the role of negative anticipation on self-report of premenstrual symptoms, we studied 13 oligomenorrheic and 12 control women with regular menses. Both hormonal and psychological measures (using the Symptom Rating Test) were obtained once a week for 5-9 weeks. The presence of ovulatory cycles was confirmed by progesterone levels greater than or equal to 3.0 ng/ml. In both groups, there was a significant increase in the total Symptom Rating Test score during the premenstrual phase with respect to the intermenstrual period. As far as specific symptoms were concerned, MANOVA showed significant premenstrual fluctuations in anxiety, depression, somatic symptoms, and inadequacy in both groups. These results suggest that premenstrual discomfort may be unrelated to both cycle length and negative anticipation of one's menses. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. RP FACCHINETTI, F (reprint author), UNIV MODENA,OSTETR GINECOL CLIN,VIA DEL POZZO 71,I-41100 MODENA,ITALY. RI Facchinetti, Fabio/K-9929-2014; Neri, Isabella/P-4506-2016 OI Facchinetti, Fabio/0000-0003-4694-9564; Neri, Isabella/0000-0003-4019-7373 NR 17 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-7346 J9 GYNECOL OBSTET INVES JI Gynecol.Obstet.Invest. PY 1994 VL 38 IS 2 BP 122 EP 126 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA PD060 UT WOS:A1994PD06000012 PM 7959339 ER PT J AU FLEISCHHACKER, DS YOUNG, RH AF FLEISCHHACKER, DS YOUNG, RH TI DYSGERMINOMA OF THE OVARY ASSOCIATED WITH HYPERCALCEMIA SO GYNECOLOGIC ONCOLOGY LA English DT Note ID PARA-NEOPLASTIC HYPERCALCEMIA; HORMONE-RELATED PROTEIN; PARATHYROID-HORMONE; HUMORAL HYPERCALCEMIA; CARCINOMA; ADENOCARCINOMA; PATIENT AB A 19-year-old female presented with a 3-week history of abdominal swelling, polydipsia, and polyuria. Ultrasound examination disclosed a right adnexal mass. Preoperative workup showed that the serum calcium level was elevated to 12.2 mg/dl. Laporotomy disclosed a right ovarian tumor and a right salpingo-oophorectomy was performed. The serum calcium level fell to within the normal range postoperatively. The ovarian tumor was a typical dysgerminoma on both gross and microscopic examination. The majority of ovarian tumors associated with paraneoplastic hypercalcemia in young females are small cell carcinomas of hypercalcemic type. It is important, however, for pathologists to be aware that the dysgerminoma is the second most common ovarian neoplasm associated with hypercalcemia in this age group, as diagnostic confusion between these two tumors may rarely occur on microscopic examination. The literature on ovarian tumors associated with hypercalcemia is briefly reviewed. (C) 1994 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP FLEISCHHACKER, DS (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 33 TC 9 Z9 9 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 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD JAN PY 1994 VL 52 IS 1 BP 87 EP 90 DI 10.1006/gyno.1994.1016 PG 4 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA MW656 UT WOS:A1994MW65600016 PM 8307507 ER PT S AU MUNZENRIDER, JE AF MUNZENRIDER, JE BE Amaldi, U Larsson, B TI PROTON THERAPY WITH THE HARVARD CYCLOTRON SO HADRONTHERAPY IN ONCOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 1st International Symposium on Hadrontherapy CY OCT 18-21, 1993 CL COMO, ITALY C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81918-5 J9 INT CONGR SER PY 1994 VL 1077 BP 83 EP 101 PG 19 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA BC21Q UT WOS:A1994BC21Q00009 ER PT S AU SMITH, A GOITEIN, M DURLACHER, S FLANZ, J LEVINE, A REARDON, P WOODS, S AF SMITH, A GOITEIN, M DURLACHER, S FLANZ, J LEVINE, A REARDON, P WOODS, S BE Amaldi, U Larsson, B TI THE MASSACHUSETTS-GENERAL-HOSPITAL NORTHEAST PROTONTHERAPY CENTER SO HADRONTHERAPY IN ONCOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 1st International Symposium on Hadrontherapy CY OCT 18-21, 1993 CL COMO, ITALY C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81918-5 J9 INT CONGR SER PY 1994 VL 1077 BP 138 EP 144 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA BC21Q UT WOS:A1994BC21Q00015 ER PT J AU VANDERKOLK, BA AF VANDERKOLK, BA TI THE BODY KEEPS THE SCORE - MEMORY AND THE EVOLVING PSYCHOBIOLOGY OF POSTTRAUMATIC STRESS SO HARVARD REVIEW OF PSYCHIATRY LA English DT Review ID POST-TRAUMATIC STRESS; SELF-DESTRUCTIVE BEHAVIOR; URINARY NOREPINEPHRINE; PSYCHOLOGICAL TRAUMA; VIETNAM VETERANS; COMBAT VETERANS; DISORDER; PHENELZINE; PTSD; HIPPOCAMPUS AB Ever since people's responses to overwhelming experiences have been systematically explored, researchers have noted that a trauma is stored in somatic memory and expressed as changes in the biological stress response. Intense emotions at the time of the trauma initiate the long-term conditional responses to reminders of the event, which are associated both with chronic alterations in the physiological stress response and with the amnesias and hypermnesias characteristic of posttraumatic stress disorder (PTSD). Continued physiological hyperarousal and altered stress hormone secretion affect the ongoing evaluation of sensory stimuli as well. Although memory is ordinarily an active and constructive process, in PTSD failure of declarative memory may lead to organization of the trauma on a somatosensory level (as visual images or physical sensations) that is relatively impervious to change. The inability of people with PTSD to integrate traumatic experiences and their tendency, instead, to continuously relive the past are mirrored physiologically and hormonally in the misinterpretation of innocuous stimuli as potential threats. Animal research suggests that intense emotional memories are processed outside of the hippocampally mediated memory system and are difficult to extinguish. Cortical activity can inhibit the expression of these subcortically based emotional memories. The effectiveness of this inhibition depends, in part, on physiological arousal and neurohormonal activity. These formulations have implications for both the psychotherapy and the pharmacotherapy of PTSD. C1 MASSACHUSETTS GEN HOSP,HARVARD MED SCH,TRAUMA CLIN,BOSTON,MA 02114. RP VANDERKOLK, BA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRAUMA CLIN,25 STANIFORD ST,BOSTON,MA 02114, USA. NR 133 TC 391 Z9 395 U1 5 U2 33 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD JAN-FEB PY 1994 VL 1 IS 5 BP 253 EP 265 DI 10.3109/10673229409017088 PG 13 WC Psychiatry SC Psychiatry GA MW401 UT WOS:A1994MW40100001 PM 9384857 ER PT J AU FARAONE, SV BIEDERMAN, J AF FARAONE, SV BIEDERMAN, J TI IS ATTENTION-DEFICIT HYPERACTIVITY DISORDER FAMILIAL SO HARVARD REVIEW OF PSYCHIATRY LA English DT Review ID OBSESSIVE-COMPULSIVE DISORDER; GENETICALLY COMPLEX TRAITS; MINIMAL BRAIN-DYSFUNCTION; LA-TOURETTES SYNDROME; CONDUCT DISORDER; FOLLOW-UP; PSYCHIATRIC STATUS; ANXIETY DISORDERS; RISK-FACTORS; CHILDHOOD HYPERACTIVITY AB Using two sources of data, we review methodologic issues pertinent to family studies of attention deficit hyperactivity disorder to evaluate whether such studies define attention deficit hyperactivity disorder as a familial disorder. We systematically evaluate the relevant literature and provide a detailed overview of the Massachusetts General Hospital family-genetic studies of attention deficit disorder as defined in DSM-III and attention deficit hyperactivity disorder as defined in DSM-III-R. The available literature, and our double-blind, controlled studies indicate that attention deficit disorder and attention deficit hyperactivity disorder are familial. Moreover, the pattern of transmission of comorbid disorders suggests that attention deficit hyperactivity disorder is, from a familial perspective, distinct from anxiety disorders and learning disabilities. In contrast, attention deficit hyperactivity disorder with conduct disorder appears to be a familial subtype, and major depression appears to be a variable expression of the familial predisposition to attention deficit hyperactivity disorder. Although the available literature provides strong evidence for the familial transmission of attention deficit hyperactivity disorder, the mode of transmission requires further clarification. In addition, attention deficit hyperactivity disorder appears to be genetically heterogeneous, indicating that more work is needed to delineate genetically homogeneous subtypes and to describe the range of expression of their underlying genotypes. Family-genetic studies will continue to clarity the etiology and nosology of attention deficit hyperactivity disorder. C1 MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT ACC 725,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. BROCKTON W ROXBURY VET AFFAIRS MED CTR,PSYCHIAT SERV,BROCKTON,MA. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01 MH-41314-01A2] NR 127 TC 63 Z9 64 U1 3 U2 9 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD JAN-FEB PY 1994 VL 1 IS 5 BP 271 EP 287 DI 10.3109/10673229409017090 PG 17 WC Psychiatry SC Psychiatry GA MW401 UT WOS:A1994MW40100003 PM 9384859 ER PT J AU OTTO, MW POLLACK, MH ROSENBAUM, JF SACHS, GS ASHER, RH AF OTTO, MW POLLACK, MH ROSENBAUM, JF SACHS, GS ASHER, RH TI CHILDHOOD HISTORY OF ANXIETY IN ADULTS WITH PANIC DISORDER - ASSOCIATION WITH ANXIETY SENSITIVITY AND COMORBIDITY SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 24th Annual Association-for-Advancement-of-Behavior-Therapy Convention CY NOV 01-04, 1990 CL SAN FRANCISCO, CA SP ASSOC ADV BEHAV THERAPY ID BEHAVIORAL-INHIBITION; AGORAPHOBIA; CHILDREN; SYMPTOMS; PARENTS; HYPOTHESIS; PREDICTORS; ATTACKS; FAMILY; FEAR AB Converging lines of evidence indicate a nonspecific link between childhood anxiety disorders and adult panic disorder. Anxiety sensitivity, defined as the fear of anxiety symptoms, was hypothesized to be a potential mediating variable in this link. This study examined the association among childhood history of anxiety disorders, current anxiety symptoms, and anxiety sensitivity in a sample of 100 patients with panic disorder undergoing treatment. Fifty-five percent of the patients had histories of one or more childhood anxiety disorders. Despite the heterogeneity of symptoms and treatment interventions among these patients, a childhood history of anxiety was associated with comorbid anxiety conditions, agoraphobic avoidance, and anxiety sensitivity scores. Anxiety sensitivity was itself a significant predictor of current severity of illness, but a childhood history of anxiety was not. These findings are consistent with the hypothesis that having an anxiety disorder during childhood is linked with patterns of anxiety and phobic avoidance in adulthood, including the level of anxiety sensitivity in patients with panic disorder. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC-815,15 PARKMAN ST,BOSTON,MA 02114, USA. FU PHS HHS [19600] NR 39 TC 27 Z9 27 U1 1 U2 3 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD JAN-FEB PY 1994 VL 1 IS 5 BP 288 EP 293 DI 10.3109/10673229409017091 PG 6 WC Psychiatry SC Psychiatry GA MW401 UT WOS:A1994MW40100004 PM 9384860 ER PT J AU HYMAN, SE AF HYMAN, SE TI ANOTHER ONE BITES THE DUST - AN INFECTIOUS ORIGIN FOR PEPTIC-ULCERS SO HARVARD REVIEW OF PSYCHIATRY LA English DT Editorial Material ID HELICOBACTER-PYLORI; DUODENAL-ULCER RP HYMAN, SE (reprint author), MASSACHUSETTS GEN HOSP,MOLEC & DEV NEUROSCI LAB,BOSTON,MA 02129, USA. NR 7 TC 8 Z9 8 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD JAN-FEB PY 1994 VL 1 IS 5 BP 294 EP 295 DI 10.3109/10673229409017092 PG 2 WC Psychiatry SC Psychiatry GA MW401 UT WOS:A1994MW40100005 PM 9384861 ER PT J AU LIDDINGTON, R AF LIDDINGTON, R TI X-RAY CRYSTALLOGRAPHY OF PARTIALLY LIGANDED STRUCTURES SO HEMOGLOBINS, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID STATE HUMAN-HEMOGLOBIN; T-STATE; FACTOR REFINEMENT; R-FACTOR; STEREOCHEMISTRY; RESOLUTION; CRYSTALS; BINDING; OXYGEN; DEOXYHEMOGLOBIN RP LIDDINGTON, R (reprint author), CHILDRENS HOSP,DANA FARBER CANC INST,X RAY CRYSTALLOG LAB,BOSTON,MA 02115, USA. NR 36 TC 8 Z9 8 U1 0 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1994 VL 232 BP 15 EP 26 PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88P UT WOS:A1994BA88P00002 PM 8057859 ER PT J AU REID, AE LIANG, TJ AF REID, AE LIANG, TJ TI THE SEARCH FOR THE ULTIMATE SCREENING-TEST FOR HEPATOCELLULAR-CARCINOMA CONTINUES SO HEPATOLOGY LA English DT Note ID ALPHA-FETOPROTEIN; SERUM RP REID, AE (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114, USA. NR 16 TC 1 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD JAN PY 1994 VL 19 IS 1 BP 255 EP 257 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MP425 UT WOS:A1994MP42500036 PM 7506226 ER PT B AU SCHIPANI, E BERGWITZ, C KRONENBERG, HM SEGRE, GV JUPPNER, H AF SCHIPANI, E BERGWITZ, C KRONENBERG, HM SEGRE, GV JUPPNER, H BE Andreoli, M Shields, M TI HUMAN PTH PTHR RECEPTOR - ITS ROLE IN PSEUDOHYPOPARATHYROIDISM TYPE-IB SO HIGHLIGHTS IN MOLECULAR AND CLINICAL ENDOCRINOLOGY SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT 25th National Congress of the Italian-Society-of-Endocrinology CY MAY 22-25, 1994 CL ROME, ITALY RP SCHIPANI, E (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-24-4 J9 FRONT ENDOCRINOL PY 1994 VL 9 BP 93 EP 96 PG 4 WC Cell Biology; Electrochemistry SC Cell Biology; Electrochemistry GA BC27X UT WOS:A1994BC27X00018 ER PT B AU GIORGINO, F SMITH, RJ AF GIORGINO, F SMITH, RJ BE Andreoli, M Shields, M TI INSULIN-LIKE GROWTH FACTOR-I (IGF-I) ACTION AND SIGNAL TRANSDUCTION PATHWAYS IN SKELETAL MUSCLE CELLS SO HIGHLIGHTS IN MOLECULAR AND CLINICAL ENDOCRINOLOGY SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT 25th National Congress of the Italian-Society-of-Endocrinology CY MAY 22-25, 1994 CL ROME, ITALY RP GIORGINO, F (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115, USA. RI Giorgino, Francesco/K-7262-2016 OI Giorgino, Francesco/0000-0001-7372-2678 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-24-4 J9 FRONT ENDOCRINOL PY 1994 VL 9 BP 365 EP 371 PG 7 WC Cell Biology; Electrochemistry SC Cell Biology; Electrochemistry GA BC27X UT WOS:A1994BC27X00069 ER PT J AU WEDDINGTON, WW MCLELLAN, AT AF WEDDINGTON, WW MCLELLAN, AT TI SUBSTANCE-ABUSE TREATMENT SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Letter RP WEDDINGTON, WW (reprint author), VET AFFAIRS MED CTR,DEPT PSYCHIAT,SUBST ABUSE TREATMENT UNIT,PHILADELPHIA,PA 19104, USA. NR 3 TC 0 Z9 0 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD JAN PY 1994 VL 45 IS 1 BP 80 EP 80 PG 1 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA MP418 UT WOS:A1994MP41800020 PM 8125471 ER PT B AU MORIKAWA, E HUANG, ZH ROSENBLATT, S YOSHIDA, T MOSKOWITZ, MA AF MORIKAWA, E HUANG, ZH ROSENBLATT, S YOSHIDA, T MOSKOWITZ, MA BE Bevan, RD Bevan, JA TI THERAPEUTIC POTENTIAL OF L-ARGININE, A PRECURSOR OF NITRIC-OXIDE, IN FOCAL CEREBRAL-ISCHEMIA SO HUMAN BRAIN CIRCULATION: FUNCTIONAL CHANGES IN DISEASE LA English DT Proceedings Paper CT Conference on the Human Brain Circulation: Functional Changes in Disease CY OCT 04-07, 1992 CL BASIN HARBOR, VT SP UNIV VERMONT, DEPT PHARM, TOTMAN LAB HUMAN CEREBROVASC RES C1 MASSACHUSETTS GEN HOSP,HARVARD SCH MED,DEPT NEUROL & NEUROSURG,BOSTON,MA 02114. NR 0 TC 6 Z9 6 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512 BN 0-89603-271-X PY 1994 BP 373 EP 387 PG 15 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA BA82L UT WOS:A1994BA82L00028 ER PT B AU OGILVY, CS KLAASEN, A WELLMAN, T BEVAN, RD BEVAN, JA AF OGILVY, CS KLAASEN, A WELLMAN, T BEVAN, RD BEVAN, JA BE Bevan, RD Bevan, JA TI FEEDING ARTERY RIGIDITY AND HEMODYNAMICS OF CEREBRAL ARTERIOVENOUS-MALFORMATIONS SO HUMAN BRAIN CIRCULATION: FUNCTIONAL CHANGES IN DISEASE LA English DT Proceedings Paper CT Conference on the Human Brain Circulation: Functional Changes in Disease CY OCT 04-07, 1992 CL BASIN HARBOR, VT SP UNIV VERMONT, DEPT PHARM, TOTMAN LAB HUMAN CEREBROVASC RES C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512 BN 0-89603-271-X PY 1994 BP 405 EP 412 PG 8 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA BA82L UT WOS:A1994BA82L00031 ER PT J AU SMITH, MJ ROUSCULP, MD GOLDSMITH, KT CURIEL, DT GARVER, RI AF SMITH, MJ ROUSCULP, MD GOLDSMITH, KT CURIEL, DT GARVER, RI TI SURFACTANT PROTEIN A-DIRECTED TOXIN GENE KILLS LUNG-CANCER CELLS IN-VITRO SO HUMAN GENE THERAPY LA English DT Article ID INSITU HYBRIDIZATION; RETROVIRAL VECTOR; APOPROTEIN; EXPRESSION; EFFICIENCY; MODULATION; CARCINOMA; PROMOTER; THERAPY; INVITRO AB Human surfactant protein A (SPA) expression is considered a marker of respiratory epithelial differentiation. Non-small cell lung cancers (NSCLC) are respiratory epithelial derivatives, and it was previously shown that a minority of these cancers expressed SPA, presumably a consequence of their respiratory epithelial origin. In the studies reported here, SPA-I gene transcriptional regulatory sequences were localized to a 2.75-kb genomic 5'-flanking region fragment obtained by screening a human genomic library. The 2.75-kb fragment was used to direct a luciferase coding sequence transcriptionally within a plasmid construct. In plasmid transduction experiments, the SPA-directed luciferase plasmid produced significant luciferase activity in the SPA-expressing NSCLC cell line, H441, but only background levels in the non-SPA-expressing A549 cells. Because Northern blot analysis of resected NSCLC showed that the majority expressed SPA, an SPA-transcriptional targeting strategy was investigated using chimeric toxin genes comprising the coding sequence for herpes simplex virus thymidine kinase (HSV-TK) under transcriptional control of SPA or SV40 regulatory sequences. As expected, transduction of the constitutive, SV40-directed plasmid followed by ganciclovir treatment reduced numbers of both the A549 and H441 cells. In contrast, the SPA-directed plasmid reduced only the SPA-expressing H441 cells and had no significant effect on the A549 cells. The results of these in vivo experiments suggest the concept of transcriptionally directing toxin genes with SPA can produce targeted toxicity in NSCLC. C1 UAB,SCH MED,DIV PULM & CRIT CARE MED,BIRMINGHAM,AL 35294. UAB,SCH MED,INTERVENT GENET PROGRAM,BIRMINGHAM,AL 35294. UAB,SCH MED,BIRMINGHAM VAMC,BIRMINGHAM,AL 35294. NR 23 TC 48 Z9 48 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD JAN PY 1994 VL 5 IS 1 BP 29 EP 35 DI 10.1089/hum.1994.5.1-29 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA MT853 UT WOS:A1994MT85300005 PM 8155768 ER PT J AU HUMMERICH, H BAXENDALE, S MOTT, R KIRBY, SF MACDONALD, ME GUSELLA, J LEHRACH, H BATES, GP AF HUMMERICH, H BAXENDALE, S MOTT, R KIRBY, SF MACDONALD, ME GUSELLA, J LEHRACH, H BATES, GP TI DISTRIBUTION OF TRINUCLEOTIDE REPEAT SEQUENCES ACROSS A 2-MBP REGION CONTAINING THE HUNTINGTONS-DISEASE GENE SO HUMAN MOLECULAR GENETICS LA English DT Article ID FRAGILE-X-SYNDROME; MYOTONIC-DYSTROPHY; LINKAGE DISEQUILIBRIUM; CANDIDATE REGION; HUMAN GENOME; DNA; RECOMBINATION; CLONING; POLYMORPHISMS; CHROMOSOME-4 AB The recent observation that the mutation underlying a number of genetic diseases including fragile sites, FRAXA and FRAXE (associated with mental retardation), myotonic dystrophy, spinal and bulbar muscular atrophy (Kennedy's disease), Huntington's disease and spinocerebellar ataxia type 1 are caused by the expansion of a trinucleotide repeat sequence will lead to interest in the identification of such sequences in regions related to other diseases. We report here the identification of all ten classes of trinucleotide repeats within a 2 Mbp region of 4p16.3 containing the Huntington's disease (HD) gene. Fifty one triplet repeats were identified and localised on a high resolution restriction map of a cosmid contig covering this region. This included the triplet repeat (CAG)(n), which has subsequently been shown to be expanded in Huntington's disease patients. C1 MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. RP HUMMERICH, H (reprint author), IMPERIAL CANC RES FUND,GENOME ANAL LAB,44 LINCOLNS INN FIELDS,LONDON WC2A 3PX,ENGLAND. RI Bates, Gillian/E-1146-2012 OI Bates, Gillian/0000-0002-4041-6305 NR 63 TC 4 Z9 4 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD JAN PY 1994 VL 3 IS 1 BP 73 EP 78 DI 10.1093/hmg/3.1.73 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA MU617 UT WOS:A1994MU61700015 PM 8162055 ER PT J AU NOVELLETTO, A PERSICHETTI, F SABBADINI, G MANDICH, P BELLONE, E AJMAR, F PERGOLA, M DELSENNO, L MACDONALD, ME GUSELLA, JF FRONTALI, M AF NOVELLETTO, A PERSICHETTI, F SABBADINI, G MANDICH, P BELLONE, E AJMAR, F PERGOLA, M DELSENNO, L MACDONALD, ME GUSELLA, JF FRONTALI, M TI ANALYSIS OF THE TRINUCLEOTIDE REPEAT EXPANSION IN ITALIAN FAMILIES AFFECTED WITH HUNTINGTON DISEASE SO HUMAN MOLECULAR GENETICS LA English DT Article ID LINKAGE; REGION; GENE AB 150 subjects affected with HD and 45 at high risk for the disease were typed for the CAG trinucleotide repeat at the 5' end of IT15. In all of them we find expanded segments showing marked instability upon transmission. Their length distribution matches those previously reported and inversely correlates (- 0.686) with age at onset. Two at risk sibs from a large HD pedigree show expanded segments that overlap the normal distribution and can represent reductions from the HD to the normal range. A case of instability on a normal chromosome is also reported. Finally, an analysis of the CAG repeat as a function of three polymorphic DNA markers at D4S127 and D4S95 loci shows no significant difference in the average repeat length on HD chromosomes grouped according to the cosegregating allele of each marker or to the corresponding haplotype. Despite the marked heterogeneity in repeat length among HD families, haplotypes are not associated with different values around which the repeat length fluctuates. C1 CNR,IST MED SPERIMENTALE,I-00137 ROME,ITALY. UNIV TOR VERGATA,DIPARTIMENTO BIOL,I-00173 ROME,ITALY. UNIV GENOA,IST BIOL & GENET,I-16132 GENOA,ITALY. UNITA SANITARIA LOCALE RM1,ROME,ITALY. UNIV FERRARA,IST CHIM BIOL,I-44100 FERRARA,ITALY. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. OI Novelletto, Andrea/0000-0002-1146-7680 FU NINDS NIH HHS [NINDS NS16367] NR 21 TC 54 Z9 55 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD JAN PY 1994 VL 3 IS 1 BP 93 EP 98 DI 10.1093/hmg/3.1.93 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA MU617 UT WOS:A1994MU61700018 PM 8162059 ER PT J AU DORIA, A WARRAM, JH KROLEWSKI, AS AF DORIA, A WARRAM, JH KROLEWSKI, AS TI MOLECULAR CHARACTERIZATION OF A DDEI MELTING POLYMORPHISM AT THE ANGIOTENSIN I-CONVERTING ENZYME (ACE) LOCUS SO HUMAN MUTATION LA English DT Note ID GENE C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. FU NIDDK NIH HHS [R01 DK41526] NR 8 TC 8 Z9 10 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1994 VL 4 IS 2 BP 155 EP 157 DI 10.1002/humu.1380040211 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA PD334 UT WOS:A1994PD33400010 PM 7981720 ER PT J AU GESSLER, M KONIG, A ARDEN, K GRUNDY, P ORKIN, S SALLAN, S PETERS, C RUYLE, S MANDELL, J LI, F CAVENEE, W BRUNS, G AF GESSLER, M KONIG, A ARDEN, K GRUNDY, P ORKIN, S SALLAN, S PETERS, C RUYLE, S MANDELL, J LI, F CAVENEE, W BRUNS, G TI INFREQUENT MUTATION OF THE WT1 GENE IN 77 WILMS-TUMORS SO HUMAN MUTATION LA English DT Article DE WILMS TUMOR; WT1; ZINC FINGER GENE; TUMOR SUPPRESSOR GENE; NEPHROBLASTOMA; DELETION ANALYSIS; SSCP ANALYSIS; MUTATION SCREENING ID ZINC-FINGER GENE; FAMILIAL PREDISPOSITION; POINT MUTATIONS; CHROMOSOME-11; DELETION; LOCUS; 11P13; HETEROZYGOSITY; POLYMORPHISM; REGION AB Homozygous deletions in Wilms' tumor DNA have been a key step in the identification and isolation of the WT1 gene. Several additional loci are also postulated to contribute to Wilms' tumor formation. To assess the frequency of WT1 alterations we have analyzed the WT1 locus in a panel of 77 Wilms' tumors. Eight tumors showed evidence for large deletions of several hundred or thousand kilobasepairs of DNA, some of which were also cytogenetically detected. Additional intragenic mutations were detected using more sensitive SSCP analyses to scan all 10 WT1 exons. Most of these result in premature stop codons or missense mutations that inactivate the remaining WT1 allele. The overall frequency of WT1 alterations detected with these methods is less than 15%. While some mutations may not be detectable with the methods employed, our results suggest that direct alterations of the WT1 gene are present in only a small fraction of Wilms' tumors. Thus, mutations at other Wilms' tumor loci or disturbance of interactions between these genes likely play an important role in Wilms' tumor development. (C) 1994 Wiley-Liss, Inc. C1 UNIV MARBURG,INST HUMAN GENET,D-35037 MARBURG,GERMANY. UNIV CALIF SAN DIEGO,LUDWIG INST CANC RES,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. CROSS CANC INST,EDMONTON T6G 1Z2,AB,CANADA. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT SURG,DIV UROL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV GENET,BOSTON,MA 02115. OI Peters, Craig/0000-0001-7598-0865 FU NHGRI NIH HHS [HG00186] NR 43 TC 95 Z9 95 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1994 VL 3 IS 3 BP 212 EP 222 DI 10.1002/humu.1380030307 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA ND558 UT WOS:A1994ND55800006 PM 8019557 ER PT J AU DUNCAN, LM TRAVERS, RL KOERNER, FC MIHM, MC SOBER, AJ AF DUNCAN, LM TRAVERS, RL KOERNER, FC MIHM, MC SOBER, AJ TI ESTROGEN AND PROGESTERONE-RECEPTOR ANALYSIS IN PREGNANCY-ASSOCIATED MELANOMA - ABSENCE OF IMMUNOHISTOCHEMICALLY DETECTABLE HORMONE RECEPTORS SO HUMAN PATHOLOGY LA English DT Article DE MELANOMA; ESTROGEN RECEPTOR; PREGNANCY; IMMUNOPEROXIDASE ID MALIGNANT-MELANOMA; CUTANEOUS MELANOMA; TAMOXIFEN; NEVI; CARCINOMAS; ANTIBODIES; PROGNOSIS C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. RP DUNCAN, LM (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,DIV DERMATOPATHOL,WARREN BLDG,ROOM 526,BOSTON,MA 02114, USA. RI Duncan, Lyn/E-9878-2013 NR 37 TC 36 Z9 36 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1994 VL 25 IS 1 BP 36 EP 41 DI 10.1016/0046-8177(94)90168-6 PG 6 WC Pathology SC Pathology GA MW772 UT WOS:A1994MW77200006 PM 8314259 ER PT B AU MEYER, JS TAKASHIMA, S OBARA, K MURAMATSU, K MORTEL, KF AF MEYER, JS TAKASHIMA, S OBARA, K MURAMATSU, K MORTEL, KF BE Omae, T Chalmers, JP Gyarfas, I TI LONGITUDINAL OUTCOME FOLLOWING TREATMENT OF HYPERTENSION AMONG PATIENTS WITH ISCHEMIC VASCULAR DEMENTIA SO HYPERTENSION RESEARCH - CLINICAL AND EXPERIMENTAL, VOL 17, SUPPLEMENT 1, MAY 1994: PROCEEDINGS OF WHO/ISH MEETING ON HYPERTENSION AND CEREBROVASCULAR DISEASE LA English DT Proceedings Paper CT WHO/ISH Meeting on Hypertension and Cerebrovascular Disease CY MAY 25-27, 1993 CL NARA, JAPAN SP WHO, ISH DE CEREBRAL BLOOD FLOW; ISCHEMIC VASCULAR DEMENTIA; LEUKOARAIOSIS; WHITE MATTER; HYPERTENSION C1 BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JAPANESE SOC HYPERTENSION HYPERTENSION RES PUBL OFFICE PI TOYONAKA 565 PA CTR ACAD SOC, OSAKA, 14 FL SENRI LIFE SCI CTR BLDG 4-2 SHENSENRI-HIGASHI-MACHI, TOYONAKA 565 JAPAN PY 1994 BP S89 EP S96 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA BC36J UT WOS:A1994BC36J00015 ER PT B AU MCKENNA, MJ KRISTIANSEN, A HAINES, J AF MCKENNA, MJ KRISTIANSEN, A HAINES, J BE Mogi, G Veldman, JE Kawauchi, H TI ISOLATION AND IDENTIFICATION OF NUCLEIC ACID SEQUENCES FROM CELLOIDIN AND PARAFFIN EMBEDDED HUMAN TEMPORAL BONE SECTIONS SO IMMUNOBIOLOGY IN OTORHINOLARYNGOLOGY: PROGRESS OF A DECADE LA English DT Proceedings Paper CT 4th International Academic Conference on Immunobiology in Otology, Rhinology and Laryngology CY APR 04-07, 1994 CL OITA, JAPAN SP EISAI PHARM CO C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 1 PU KUGLER PUBLICATIONS BV PI AMSTELVEEN PA PO BOX 516, 1180 AM AMSTELVEEN, NETHERLANDS BN 90-6299-114-9 PY 1994 BP 283 EP 288 PG 6 WC Immunology; Otorhinolaryngology SC Immunology; Otorhinolaryngology GA BC13A UT WOS:A1994BC13A00049 ER PT J AU GASSER, DL STERNBERG, NL PIERCE, JC GOLDNERSAUVE, A FENG, H HAQ, AK SPIES, T HUNT, C BUETOW, KH CHAPLIN, DD AF GASSER, DL STERNBERG, NL PIERCE, JC GOLDNERSAUVE, A FENG, H HAQ, AK SPIES, T HUNT, C BUETOW, KH CHAPLIN, DD TI P1 AND COSMID CLONES DEFINE THE ORGANIZATION OF 280 KB OF THE MOUSE H-2-COMPLEX CONTAINING THE CPS-1 AND HSP70 LOCI SO IMMUNOGENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; INDUCED CLEFT-PALATE; CLASS-I GENES; MOLECULAR MAP; REGION; MICE; SUSCEPTIBILITY; INTERVAL; DNA; IDENTIFICATION AB A 280 kilobase (kb) contig was isolated from mouse genomic P1 and cosmid libraries, using as probes human cDNA and genomic DNA fragments that map in the interval between the second component of complement and tumor necrosis factor genes of the HLA complex. The clone contig demonstrates synteny of eleven mouse genes that are homologous to genes initially mapped within the human major histocompatibility complex. These include the mouse homologs of BAT2 (HLA-B-associated transcript 2) through BAT9 and also three HSP70-related genes. Five P1 clones form a contig of 240 kb that spans from BAT9 through BAT3. Twelve cosmid clones are arranged in three contigs that confirm most of the structure of the P1 contig and link the mouse BAT3 homolog to the BAT2 homolog approximately 15 kb farther telomeric. Polymorphic DNA markers within the cloned region were used to map the cleft palate susceptibility-l (Cps-l) locus to the interval between Hsp70.1 and BAT6 (valyl-tRNA synthetase). This refines the location of the Cps-1 locus to a 45 kb region contained in the H2-124 P1 insert. C1 DUPONT MERCK PHARMACEUT CO,GLENOLDEN LABS,GLENOLDEN,PA 19036. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63108. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT INTERNAL MED,ST LOUIS,MO 63110. RP GASSER, DL (reprint author), UNIV PENN,SCH MED,DEPT GENET,422 CURIE BLVD,PHILADELPHIA,PA 19104, USA. OI Chaplin, David/0000-0002-1354-3069 FU NCI NIH HHS [R29 CA50 503]; NIAID NIH HHS [AI 15322]; NIDCR NIH HHS [P50-DE09164] NR 50 TC 23 Z9 23 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JAN PY 1994 VL 39 IS 1 BP 48 EP 55 PG 8 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA MD187 UT WOS:A1994MD18700007 PM 7993390 ER PT J AU BEUTLER, AM WHITTUMHUDSON, JA NANAGARA, R SCHUMACHER, HR HUDSON, AP AF BEUTLER, AM WHITTUMHUDSON, JA NANAGARA, R SCHUMACHER, HR HUDSON, AP TI INTRACELLULAR LOCATION OF INAPPARENTLY INFECTING CHLAMYDIA IN SYNOVIAL TISSUE FROM PATIENTS WITH REITERS-SYNDROME SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT 2nd Molecular Aspects of the Rheumatic Diseases Symposium CY JUN 09-10, 1994 CL UNIV PENN, SCH MED, PHILADELPHIA, PA SP UNIV PENN, SCH MED, PHILADELPHIA VET ADM MED CTR, INST BIOTECHNOL & ADV MOLEC MED HO UNIV PENN, SCH MED DE CHLAMYDIA; REITERS SYNDROME; IN SITU HYBRIDIZATION; SYNOVIA ID INSITU HYBRIDIZATION; REACTIVE ARTHRITIS; TRACHOMATIS; CULTURE; DISEASE; RNA; DNA AB Culture of Chlamydia trachomatis from synovial tissues/fluids from Reiter's syndrome (RS) patients frequently yields negative results. However, we have identified chlamydial RNA at that site in such patients, suggesting that viable organisms may be present. Here we define the cellular location of chlamydia within the synovium via in situ hybridization. Using a chlamydial ribosomal RNA-directed probe, we show that synovial tissue from culture-negative RS patients gives strong hybridization which is often localized to a subsynovial cell layer, rather than to the synovial lining; in some cases, hybridizing cells are dispersed through the synovium. Ah hybridization signal is located within host cells, indicating that infectious extracellular elementary bodies are rare or absent. These data confirm the extensive intracellular presence of inapparent chlamydia in the synovia of RS patients and provide some insight into the usual culture negativity of synovial tissues for the organism. C1 DEPT VET AFFAIRS MED CTR,MED RES SERV,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,CTR ARTHRIT IMMUNOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. JOHNS HOPKINS UNIV,SCH MED,WILMER INST,BALTIMORE,MD 21205. FU NEI NIH HHS [EY-03324]; NIAMS NIH HHS [AR-42541] NR 26 TC 46 Z9 46 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1994 VL 13 IS 2-3 BP 163 EP 171 DI 10.1007/BF02918277 PG 9 WC Immunology SC Immunology GA QN404 UT WOS:A1994QN40400009 PM 7775807 ER PT J AU HAREGEWOIN, A EDWIN, C HOM, RC FINBERG, R AF HAREGEWOIN, A EDWIN, C HOM, RC FINBERG, R TI A 21-MER SYNTHETIC PEPTIDE OF TOXIC-SHOCK-SYNDROME-TOXIN-1, TSST-1[58-78], ACTIVATES T-CELLS BY BINDING TO MHC CLASS-II AND BY AN MHC UNRESTRICTED XENOSTIMULATORY PATHWAY SO IMMUNOLOGICAL INVESTIGATIONS LA English DT Article ID STAPHYLOCOCCAL ENTEROTOXINS; MOLECULES; FRAGMENTS; AFFINITY; INVITRO AB Toxic shock syndrome toxin-1 (TSST-1) is a ''superantigen'' which binds to MHC class II molecules and induces a polyclonal stimulation of T cells. In this communication by using a FACS technique and a 21-mer synthetic peptide from the primary sequence of TSST-1 (KGEKVDLNTKRTKKSQHTSEG), designated TSST-1 (58-78), we demonstrated binding of the peptide only to cells bearing MHC class II. The proliferative effect of TSST-1 (58-78) on human T cells was shown to be inhibited much more by anti-HLA-DR than by anti-HLA class I antibody. Furthermore, human monocytes were able to present TSST-1 (58-78) to a mouse VSV specific T cell clone by a xenostimulatory mechanism. These data indicate this peptide to contain an active site of the TSST-1 holotoxin. RP HAREGEWOIN, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV INFECT DIS,44 BINNEY ST,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU PHS HHS [120382, 2 PO1 DR33506] NR 15 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0882-0139 J9 IMMUNOL INVEST JI Immunol. Invest. PY 1994 VL 23 IS 6-7 BP 413 EP 420 DI 10.3109/08820139409066835 PG 8 WC Immunology SC Immunology GA PN809 UT WOS:A1994PN80900005 PM 7851959 ER PT J AU KELLEY, DM LICHTENSTEIN, A WANG, JY TAYLOR, AN DUBINETT, SM AF KELLEY, DM LICHTENSTEIN, A WANG, JY TAYLOR, AN DUBINETT, SM TI CORTICOTROPIN-RELEASING FACTOR REDUCES LIPOPOLYSACCHARIDE-INDUCED PULMONARY VASCULAR LEAK SO IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY LA English DT Article ID PITUITARY-ADRENAL AXIS; BETA-ENDORPHIN; THERMAL-INJURY; RAT PAWSKIN; HORMONE; MACROPHAGES; EXPRESSION; SECRETION; ADRENOCORTICOTROPIN; INTERLEUKIN-1 AB Previous studies have suggested that corticotropin-releasing factor (CRF) has immunoregulatory effects in addition to its neuroendocrine role. We examined the ability of CRF to inhibit lipopolysaccharide (LPS)-induced pulmonary vascular leak in vivo. Female BALB/C mice were treated with either normal saline (NS) or CRF prior to injection with LPS. Pulmonary vascular leak was inhibited by CRF as assessed by measurement of lung wet-to-dry ratios. The stress-induced increase in serum corticosterone levels in mice injected with LPS alone was not further increased by treatment with CRF. This indicates that the effect of CRF was not mediated centrally by stimulation of endogenous steroid release. Histologic examination of the lungs revealed that leukocyte infiltration was significantly depressed in CRF-treated mice thus confirming the protective effect of CRF. In addition, a modest prolongation of survival was demonstrated in CRF-treated mice following challenge with LPS (p=.08). These data indicate the potential utility of CRF as a modulator of pulmonary vascular leak. C1 UNIV CALIF LOS ANGELES,SCH MED,DIV PULM & CRIT CARE MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DIV ONCOL,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,JONSSON COMPREHENS CANC CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,IMMUNOL PULM LAB,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD RES DIV,LOS ANGELES,CA 90073. NR 35 TC 12 Z9 12 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0892-3973 J9 IMMUNOPHARM IMMUNOT JI Immunopharmacol. Immunotoxicol. PY 1994 VL 16 IS 2 BP 139 EP 148 DI 10.3109/08923979409007086 PG 10 WC Immunology; Pharmacology & Pharmacy; Toxicology SC Immunology; Pharmacology & Pharmacy; Toxicology GA NN361 UT WOS:A1994NN36100002 PM 8077603 ER PT J AU HILLMAN, JD CHEN, AP DUNCAN, M LEE, SW AF HILLMAN, JD CHEN, AP DUNCAN, M LEE, SW TI EVIDENCE THAT L-(+)-LACTATE DEHYDROGENASE-DEFICIENCY IS LETHAL IN STREPTOCOCCUS-MUTANS SO INFECTION AND IMMUNITY LA English DT Article ID BACTERIOCIN; CLONING; INVITRO AB In order to construct an effector strain for the replacement therapy of dental caries, we wished to combine the properties of low-level acid production and high-level colonization potential in a strain of Streptococcus mutans. To this end, we made a deletion in the lactate dehydrogenase (LDH) gene cloned from the bacteriocin-producing S, mutans strain JH1000. However, we were unable to substitute the mutant for the wild-type allele by transformation with linear DNA fragments. The mutated gene, carried on a suicide vector, was shown by Southern analysis to integrate into the JH1000 chromosome to yield transformants carrying both the wild-type gene and mutated LDH gene. Three spontaneous self-recombinants of one heterodiploid strain were isolated by screening 1,500 colonies for a loss of the tetracycline resistance encoded by the gene used to mark the LDH deletion. In all three cases, Southern analysis showed that a loss of tetracycline resistance was accompanied by a loss of the mutated LDH gene, resulting in restoration of the wild-type genotype. However, screening the same number of colonies for self-recombinants that did not make lactic acid during anaerobic grow-th in Todd-Hewitt broth faded to identify clones in which the wild-type allele was lost. A second, simpler screening of more than 80,000 colonies grown aerobically on glucose tetrazolium medium to identify low-level-acid-producing colonies was also unsuccessful. These results are interpreted as indicating that LDH deficiency is lethal in S. mutans under the cultivation conditions used in these experiments. The physiological bases for this hypothesis are described. C1 FORSYTH DENT CTR,DEPT MOLEC GENET,BOSTON,MA 02115. RP HILLMAN, JD (reprint author), UNIV FLORIDA,COLL DENT,DEPT ORAL BIOL,BOX 100-424,GAINESVILLE,FL 32610, USA. FU NIDCR NIH HHS [DEO4529] NR 14 TC 20 Z9 22 U1 1 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 JAN PY 1994 VL 62 IS 1 BP 60 EP 64 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MN488 UT WOS:A1994MN48800009 PM 8262650 ER PT J AU AVERY, RK HOLDEN, JM MADOFF, S ZARTMAN, G BAKER, AS AF AVERY, RK HOLDEN, JM MADOFF, S ZARTMAN, G BAKER, AS TI MYCOPLASMA-HOMINIS WOUND-INFECTION AFTER HIP FUSION SO INFECTIOUS DISEASES IN CLINICAL PRACTICE LA English DT Note ID GENITAL MYCOPLASMAS; SEPTIC ARTHRITIS; POSTPARTUM FEVER; TETRACYCLINE RESISTANCE; UREAPLASMA-UREALYTICUM; COLONIZATION; BACTEREMIA; PATIENT; THERAPY; INVITRO C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MICROBIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. NR 44 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1056-9103 J9 INFECT DIS CLIN PRAC JI Infect. Dis. Clin. Pract. PD JAN-FEB PY 1994 VL 3 IS 1 BP 32 EP 34 DI 10.1097/00019048-199401000-00006 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MV769 UT WOS:A1994MV76900006 ER PT J AU YOSHIKAWA, TT AF YOSHIKAWA, TT TI THE CHALLENGE AND UNIQUE ASPECTS OF TUBERCULOSIS IN OLDER PATIENTS SO INFECTIOUS DISEASES IN CLINICAL PRACTICE LA English DT Article ID IMMUNODEFICIENCY-VIRUS INFECTION; PULMONARY TUBERCULOSIS; MYCOBACTERIUM-TUBERCULOSIS; CLINICAL-FEATURES; ELDERLY PERSONS; SPECIMENS C1 GEORGE WASHINGTON UNIV,DIV AGING STUDIES & SERV,WASHINGTON,DC 20052. RP YOSHIKAWA, TT (reprint author), US DEPT VET AFFAIRS,OFF GERIATR & EXTENDED CARE,MAIL STOP 114,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 31 TC 9 Z9 9 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1056-9103 J9 INFECT DIS CLIN PRAC JI Infect. Dis. Clin. Pract. PD JAN-FEB PY 1994 VL 3 IS 1 BP 62 EP 66 DI 10.1097/00019048-199401000-00020 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MV769 UT WOS:A1994MV76900015 ER PT B AU SCHNEYER, A LAMBERMESSERLIAN, G SLUSS, P ISAACSON, K CROWLEY, WF AF SCHNEYER, A LAMBERMESSERLIAN, G SLUSS, P ISAACSON, K CROWLEY, WF BE Burger, HG Findlay, J Robertson, D DeKretser, D Petraglia, F TI DO ALPHA-INHIBIN PRECURSOR PROTEINS HAVE A ROLE IN GONADAL PHYSIOLOGY SO INHIBIN AND INHIBIN-RELATED PROTEINS SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT International Symposium on Inhibin and Inhibin-Related Proteins CY JUN 17-18, 1993 CL SIENA, ITALY SP ARES SERONO SYMPOSIA RP SCHNEYER, A (reprint author), MASSACHUSETTS GEN HOSP,NATL CTR INFERTIL RES,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-13-9 J9 FRONT ENDOCRINOL PY 1994 VL 3 BP 245 EP 259 PG 15 WC Biochemistry & Molecular Biology; Reproductive Biology SC Biochemistry & Molecular Biology; Reproductive Biology GA BA22Y UT WOS:A1994BA22Y00021 ER PT S AU KRANE, SM AF KRANE, SM BE Greenwald, RA Golub, LM TI CLINICAL IMPORTANCE OF METALLOPROTEINASES AND THEIR INHIBITORS SO INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC POTENTIAL SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Inhibition of Matrix Metalloproteinases - Therapeutic Potential CY JAN 19-22, 1994 CL TAMPA, FL SP New York Acad Sci, Long Island Jewish Med Ctr ID HUMAN FIBROBLAST COLLAGENASE; HUMAN NEUTROPHIL COLLAGENASE; TRANSCRIPTION FACTOR AP-1; MATRIX METALLOPROTEINASES; RHEUMATOID-ARTHRITIS; MESSENGER-RNA; MAMMALIAN COLLAGENASES; CYSTEINE SWITCH; ACTIVE-SITE; II COLLAGEN C1 MASSACHUSETTS GEN HOSP,MED SERV,ARTHRIT UNIT,BOSTON,MA 02114. RP KRANE, SM (reprint author), HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [AR-03564, AR-07258] NR 66 TC 69 Z9 69 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-899-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 732 BP 1 EP 10 DI 10.1111/j.1749-6632.1994.tb24719.x PG 10 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Pharmacology & Pharmacy GA BD10L UT WOS:A1994BD10L00001 PM 7978783 ER PT B AU GELBERMAN, RH EATON, RG URBANIAK, JR AF GELBERMAN, RH EATON, RG URBANIAK, JR BE Schafer, M TI Peripheral nerve compression SO INSTRUCTIONAL COURSE LECTURES, VOL 43, 1994 SE AMERICAN ACADEMY OF ORTHOPAEDIC SURGEONS INSTRUCTIONAL COURSE LECTURES LA English DT Proceedings Paper CT Annual Meeting of the American-Academy-of-Orthopaedic-Surgeons CY FEB, 1993 CL SAN FRANCISCO, CA SP Amer Acad Orthopaed Surgeons C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 18 Z9 19 U1 0 U2 0 PU AMER ACAD ORTHOPAEDIC SURGEONS PI ROSEMONT PA 6300 NORTH RIVER RD, ROSEMONT, IL 60018 BN 0-89203-102-6 J9 AAOS INSTR COURS LEC PY 1994 VL 43 BP 31 EP 53 PG 23 WC Orthopedics SC Orthopedics GA BD14Q UT WOS:A1994BD14Q00006 PM 9097136 ER PT B AU HARRIS, WH AF HARRIS, WH BE Schafer, M TI The case for cemented fixation of the femur in every patient SO INSTRUCTIONAL COURSE LECTURES, VOL 43, 1994 SE AMERICAN ACADEMY OF ORTHOPAEDIC SURGEONS INSTRUCTIONAL COURSE LECTURES LA English DT Proceedings Paper CT Annual Meeting of the American-Academy-of-Orthopaedic-Surgeons CY FEB, 1993 CL SAN FRANCISCO, CA SP Amer Acad Orthopaed Surgeons C1 MASSACHUSETTS GEN HOSP,HIP & IMPLANT UNIT,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER ACAD ORTHOPAEDIC SURGEONS PI ROSEMONT PA 6300 NORTH RIVER RD, ROSEMONT, IL 60018 BN 0-89203-102-6 J9 AAOS INSTR COURS LEC PY 1994 VL 43 BP 367 EP 371 PG 5 WC Orthopedics SC Orthopedics GA BD14Q UT WOS:A1994BD14Q00036 ER PT B AU JASTY, M AF JASTY, M BE Schafer, M TI Cemented fixation of the femur SO INSTRUCTIONAL COURSE LECTURES, VOL 43, 1994 SE AMERICAN ACADEMY OF ORTHOPAEDIC SURGEONS INSTRUCTIONAL COURSE LECTURES LA English DT Proceedings Paper CT Annual Meeting of the American-Academy-of-Orthopaedic-Surgeons CY FEB, 1993 CL SAN FRANCISCO, CA SP Amer Acad Orthopaed Surgeons C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ACAD ORTHOPAEDIC SURGEONS PI ROSEMONT PA 6300 NORTH RIVER RD, ROSEMONT, IL 60018 BN 0-89203-102-6 J9 AAOS INSTR COURS LEC PY 1994 VL 43 BP 373 EP 379 PG 7 WC Orthopedics SC Orthopedics GA BD14Q UT WOS:A1994BD14Q00037 ER PT B AU SPRINGFIELD, DS AF SPRINGFIELD, DS BE Schafer, M TI Staging systems for musculoskeletal neoplasia SO INSTRUCTIONAL COURSE LECTURES, VOL 43, 1994 SE AMERICAN ACADEMY OF ORTHOPAEDIC SURGEONS INSTRUCTIONAL COURSE LECTURES LA English DT Proceedings Paper CT Annual Meeting of the American-Academy-of-Orthopaedic-Surgeons CY FEB, 1993 CL SAN FRANCISCO, CA SP Amer Acad Orthopaed Surgeons C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ACAD ORTHOPAEDIC SURGEONS PI ROSEMONT PA 6300 NORTH RIVER RD, ROSEMONT, IL 60018 BN 0-89203-102-6 J9 AAOS INSTR COURS LEC PY 1994 VL 43 BP 537 EP 542 PG 6 WC Orthopedics SC Orthopedics GA BD14Q UT WOS:A1994BD14Q00054 ER PT J AU RUBIN, RH LIVNI, E BABICH, J ALPERT, NM LIU, YY CLEELAND, R PROSSER, BL THOM, E FISCHMAN, AJ AF RUBIN, RH LIVNI, E BABICH, J ALPERT, NM LIU, YY CLEELAND, R PROSSER, BL THOM, E FISCHMAN, AJ TI TISSUE PHARMACOKINETICS OF FLEROXACIN IN HUMANS AS DETERMINED BY POSITRON EMISSION TOMOGRAPHY SO INTERNATIONAL JOURNAL OF ANTIMICROBIAL AGENTS LA English DT Article DE FLEROXACIN; PHARMACOKINETICS; TISSUE PENETRATION; POSITRON EMISSION TOMOGRAPHY (PET) ID F-18 LABELED FLEROXACIN; CLINICAL PHARMACOKINETICS; SUSCEPTIBILITY; VOLUNTEERS; INFECTIONS; EFFICACY AB The delivery of fleroxacin, a new broad-spectrum fluoroquinolone, to the major organs of the body was studied in 12 normal human volunteers (nine men and three women), utilizing positron emission tomography (PET). Following the infusion of 20 mCi of [F-18]fleroxacin in conjunction with a standard therapeutic dose of 400 mg, images were acquired over 8 h. Beginning the next day, the subjects received unlabeled drug at a dose of 400 mg/day for 3 days, with a repeat PET study on the fifth day. Fleroxacin is distributed widely throughout the body, with the notable exception of the central nervous system, with stable levels achieved within 1 h after completion of the infusion. Especially high peak concentrations (greater than or equal to 18 mu g/g) were achieved in the kidney, liver, lung, myocardium, and spleen. The mean plateau concentrations (2-8 h post-infusion, mu g/g) were: brain, 0.83; myocardium, 4.53; lung, 5.80; liver, 7.31; spleen, 6.00; bowel, 3.53; kidney, 8.85; bone, 2.87; muscle, 4.60; prostate, 4.65; uterus, 3.87; breast, 2.68; and blood, 2.35. Repetitive dosing had no significant effect on the pharmacokinetics of the drug. Since the MIC(90)'s of the family Enterobacteriaceae and Neisseria gonorrhoeae are < 2 mu g/ml, with the great majority of the individual species less than or equal to 1 mu g/ml, these results suggest that a single daily dose of 400 mg of fleroxacin should be effective in the treatment of infections such as urinary tract infection and gonorrhea. C1 HARVARD UNIV,SCH MED,DEPT RADIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DEPT MED,CAMBRIDGE,MA 02138. HOFFMANN LA ROCHE INC,NUTLEY,NJ. HARVARD MIT DIV HLTH SCI & TECHNOL,CTR EXPTL PHARMACOL & THERAPEUT,CAMBRIDGE,MA. RP RUBIN, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 24 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-8579 J9 INT J ANTIMICROB AG JI Int. J. Antimicrob. Agents PY 1994 VL 4 SU 2 BP S15 EP S20 DI 10.1016/0924-8579(94)90017-5 PG 6 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA PC392 UT WOS:A1994PC39200003 PM 18611628 ER PT J AU EPSTEIN, C LYNCH, T SHEFNER, J WEN, P MAXTED, D BRAMAN, V ARINIELLO, P CORAL, F RITZ, J AF EPSTEIN, C LYNCH, T SHEFNER, J WEN, P MAXTED, D BRAMAN, V ARINIELLO, P CORAL, F RITZ, J TI USE OF THE IMMUNOTOXIN N901-BLOCKED RICIN IN PATIENTS WITH SMALL-CELL LUNG-CANCER SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT 3rd International IASLC Workshop on Lung Tumor and Differentiation Antigens CY SEP 08-11, 1993 CL UNIV HOSP ZURICH, ZURICH, SWITZERLAND SP INT ASSOC STUDY LUNG CANC HO UNIV HOSP ZURICH AB In patients with small-cell lung cancer (SCLC), relapse with resistant disease often causes death. N901-blocked ricin (N901-bR), a murine monoclonal antibody (MAb)-blocked ricin immunotoxin, is a potential therapeutic for SCLC. N901-bR targets CD56, presents on SCLC and cells of neuro-ectodermal origin, N901-bR kills up to 5 logs of CD56-positive cells at a concentration of 0.25 nM, while CD56-negative cells require 1000-fold more drug to achieve similar cell kill. We treated 21 patients with relapsed or refractory SCLC with a single 7-day course of N901-bR as a continuous infusion. We determined the MTD and toxicity profile, demonstrated drug binding to tumor cells in biopsies of lung, liver and bone marrow, and determined the time to development of human anti-mouse and anti-ricin antibodies. One patient had a documented PR and 6 patients demonstrated stable disease. Toxicity included transient elevation of liver enzymes, mild thrombocytopenia, hypoalbuminemia, fever, malaise, and evidence of capillary leak syndrome. Toxicities were controllable and reversible. No apparent drug-related central- or peripheral-nervous-system toxicity was noted by serial neurologic examinations, EMGs, and nerve conduction studies. Trials of N901-bR are planned in SCLC patients achieving CR and PR following chemoradiotherapy, and in relapsed/refractory patients. Anti-B4-bR will be added as an immunossuppressant in order to permit delivery of multiple courses of N901-bR. Additional trials will investigate synergy with conventional chemoterapeutics and the use of N901-bR as a sensitizing agent for chemotherapy-resistant tumors. (C) 1994 Wiley-Liss, Inc. C1 IMMUNOGEN INC,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. DANA FARBER CANC INST,BOSTON,MA. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. OI Ritz, Jerome/0000-0001-5526-4669 NR 7 TC 2 Z9 2 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 PY 1994 SU 8 BP 57 EP 59 PG 3 WC Oncology SC Oncology GA NP867 UT WOS:A1994NP86700011 ER PT J AU COLUCCI, RD SCAVONE, JM AUTY, R GLASSNERCOHEN, L AF COLUCCI, RD SCAVONE, JM AUTY, R GLASSNERCOHEN, L TI QUALITY-CONTROL OF EXTEMPORANEOUSLY PREPARED MICRODOSE CAPTOPRIL CAPSULES - WEIGHT VARIATION VERSUS CONTENT UNIFORMITY SO INTERNATIONAL JOURNAL OF CLINICAL PHARMACOLOGY AND THERAPEUTICS LA English DT Article DE MICRODOSE CAPTOPRIL THERAPY; CONGESTIVE HEART FAILURE ID CONGESTIVE HEART-FAILURE; HYPERTENSION AB Microdose (1 mg) captopril therapy is commonly used for the initial dose titration in patients with congestive heart failure. Since this dosage form is not commercially available, it has to be extemporaneously compounded. Quality control of each batch is commonly evaluated using the weight variation technique described in the USP. Despite careful titration with microdose, captopril capsules variability in patient's response has been observed. In order to explain this fluctuation, the actual content of extemporaneously compounded microdose captopril capsules was evaluated using a high pressure liquid chromatographic assay. Microdose captopril capsules were prepared by triturating 25 mg tablets with lactose in a mortar using standard geometric dilution technique and a Sharpe-Dohme hand-operated capsule filling machine. Forty-eight microdose captopril capsules were randomly selected from the compounded batch and were individually assayed for captopril amount. The mean +/- standard deviation (SD) amount of captopril in each capsule was 1.27 g +/- 0.31 mg with a range of 0.84 g to 1.96 mg. The coefficient of variation was 24.5%. Ten captopril capsules were randomly selected from the compounded batch and were individually weighed. The capsules had a mean weight +/- SD of 198.3 g +/- 21.2 mg and a coefficient of variation of 7.3%. Even though the extemporaneously prepared microdose captopril capsules were within acceptable limits for weight variation described in the USP, the actual dose administered to the patients could vary by as much as 24.5%. C1 MASSACHUSETTS GEN HOSP,MASSACHUSETTS COLL PHARM & ALLIED HLTH SCI,BOSTON,MA. BETH ISRAEL HOSP,CHARLES A DANA RES INST,BOSTON,MA 02215. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. RP COLUCCI, RD (reprint author), SCHERING PLOUGH CORP,RES INST,CLIN PHARMACOL CLIN RES,2015 GALLOPING HILL RD K154,4455,KENILWORTH,NJ 07033, USA. FU NCRR NIH HHS [RR-01032] NR 9 TC 2 Z9 2 U1 2 U2 5 PU DUSTRI-VERLAG DR KARL FEISTLE PI MUNCHEN-DEISENHOFEN PA BAHNHOFSTRABE 9 POSTFACH 49, W-8024 MUNCHEN-DEISENHOFEN, GERMANY SN 0946-1965 J9 INT J CLIN PHARM TH JI Int. J. Clin. Pharmacol. Ther. PD JAN PY 1994 VL 32 IS 1 BP 24 EP 25 PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NC058 UT WOS:A1994NC05800005 PM 8199748 ER PT J AU VARDI, DJ BUCHHOLZ, ES AF VARDI, DJ BUCHHOLZ, ES TI GROUP-PSYCHOTHERAPY WITH INNER-CITY GRANDMOTHERS RAISING THEIR GRANDCHILDREN SO INTERNATIONAL JOURNAL OF GROUP PSYCHOTHERAPY LA English DT Article ID TERM GROUP-PSYCHOTHERAPY; GRANDPARENTS; CHILDREN; WOMEN AB A year-long psychotherapy group consisting of two co-therapists and eight grandmothers who were parenting their daughters' children is presented. Three models that correspond to the co-therapists' psychoanalytic developmental orientation were used to describe the group phases of development. A number of themes that emerged at different points in the group's life are delineated. They include: authority, control, sibling rivalry, the generation gap, dealing with schools, illness and mortality, isolation, defensiveness, anger,fear of going crazy, guilt, shame, separation, and abandonment. Transference and countertransference issues are also discussed. C1 MASSACHUSETTS GEN HOSP,TRAUMA CLIN,BOSTON,MA. RP VARDI, DJ (reprint author), NYU,SCH EDUC,DEPT APPL PSYCHOL,PROGRAM SCH PSYCHOL,239 GREENE,5TH FLOOR,NEW YORK,NY 10003, USA. NR 37 TC 4 Z9 4 U1 0 U2 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0020-7284 J9 INT J GROUP PSYCHOTH JI Int. J. Group Psychother. PD JAN PY 1994 VL 44 IS 1 BP 101 EP 122 PG 22 WC Psychology, Clinical SC Psychology GA MR657 UT WOS:A1994MR65700009 PM 8181894 ER PT J AU COLLINSON, AR LAMBERT, JM LIU, Y ODEA, C SHAH, SA RASMUSSEN, RA GOLDMACHER, VS AF COLLINSON, AR LAMBERT, JM LIU, Y ODEA, C SHAH, SA RASMUSSEN, RA GOLDMACHER, VS TI ANTI-CD6-BLOCKED RICIN - AN ANTI-PAN T-CELL IMMUNOTOXIN SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article ID VERSUS-HOST DISEASE; BONE-MARROW TRANSPLANTATION; ANTI-B4-BLOCKED RICIN; CYTO-TOXICITY; PROTEINS; GELONIN; ANTIBODIES; LECTINS; BINDING; PHASE AB We report the development of a potent anti-pan T-cell immunotoxin capable of killing cells in an antigen dependent manner. The immunotoxin is composed of a high affinity anti-CD6 antibody (IgG2a, K(d) = 1.3 x 10(-11) M) conjugated to blocked ricin that is a chemically modified ricin molecule wherein the lectin binding sites of the B-chain have been blocked by covalent attachment of affinity ligands. Conjugation of blocked ricin to the antibody has minimal effect on the apparent affinity of the antibody and no effect on the ribosome-inactivating activity of the ricin A-chain moiety. Anti-CD6-blocked ricin is a specific and highly toxic immunoconjugate killing the antigen-positive Molt-4 cell line with an IC37 of 4 x 10(-12) M after a 24 h exposure of cells to the immunotoxin. Nonspecific cytotoxicity of anti-CD6-blocked ricin for the antigen-negative Namalwa cell line was more than 750-fold lower with an IC37 > 3 x 10(-9) M. The cytotoxicity of anti-CD6-blocked ricin is dependent on the length of the incubation of cells with the conjugate ranging from an IC37 of 1.5 x 10(-11) M leaving a surviving fraction of Molt-4 cells of 0.03 after a 2.5 h exposure to an IC37 Of 5 x 10(-13) M and leaving a surviving fraction of 3 x 10(-6) after a continuous (3 weeks) exposure. Anti-CD6-blocked ricin is also capable of killing CD6 positive cells in human peripheral blood lymphocyte populations. Systemic toxicity of anti-CD6-blocked ricin in mice is similar to the toxicity of other immunotoxins containing blocked ricin that were found to be tolerated well by patients. An application of this immunoconjugate for the prevention and treatment of graft versus host disease or tissue graft rejection is suggested. C1 IMMUNOGEN INC,148 SIDNEY ST,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 31 TC 14 Z9 14 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PD JAN PY 1994 VL 16 IS 1 BP 37 EP 49 DI 10.1016/0192-0561(94)90117-1 PG 13 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA MT114 UT WOS:A1994MT11400005 PM 8150554 ER PT J AU TEICHER, BA HOLDEN, SA HERMAN, TS NORTHEY, D AF TEICHER, BA HOLDEN, SA HERMAN, TS NORTHEY, D TI MODULATION OF [CIS-DIAMINEDICHLOROPLATINUM(II) HYPERTHERMIA] THERAPY BY INHIBITORS OF ARACHIDONIC-ACID METABOLISM SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE CIS-DIAMMINEDICHLOROPLATINUM; HYPERTHERMIA; ARACHIDONIC ACID ID TUMOR-GROWTH DELAY; EXTRACELLULAR-MATRIX; FSAIIC FIBROSARCOMA; RADIATION-THERAPY; INVASIVE ACTIVITY; COLON CANCER; SULINDAC; THROMBOXANE; CELLS; PROSTACYCLIN AB Previous studies have shown that hyperthermia is an effective modulator of cis-diamminedichloroplatinum(II) (CDDP) cytotoxicity. We have examined the potential of inhibitors of the arachidonic acid metabolism to increase the antitumor activity of CDDP and hyperthermia. Sulindac and diflunisal are cyclooxygenase inhibiting non-steroidal anti-inflammatory drugs (NSAIDS) and phenidone is a lipoxygenase inhibitor. Using the FSaIIC in vivo-in vitro excision assay, neither five daily injections of sulindac nor diflunisal added to the killing of FSaIIC cells achieved by one injection of CDDP at normal temperature. When the i.p. injection of CDDP and the NSAIDS were followed immediately by hyperthermia treatment to the tumor bearing limb at 43-degrees-C for 30 min, the cell killing achieved was increased by 2-3-fold by diflunisal over the dose range of CDDP examined but was unaffected by sulindac. Phenidone did not alter the cell killing achieved by CDDP at normal temperature or when the CDDP was followed by local hyperthermia, but use of a combination of sulindac or diflunisal plus phenidone increased the cell killing achieved by 2-10-fold when used with local hyperthermia over the dose range of CDDP tested. In tumor growth delay (TGD) studies, addition of five daily injections of sulindac, diflunisal or phenidone did not increase the TGD achieved by CDDP at normal temperature and neither diflunisal nor phenidone markedly increased the TGD produced by CDDP in conjunction with local hyperthermia, but the administration of sulindac resulted in about a 3-fold increase in TGD as did use of a combination of diflunisal or sulindac plus phenidone. These results indicate that inhibitors of arachidonic acid metabolism can increase the cell killing and the tumor growth delay produced by CDDP plus local hyperthermia. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 43 TC 1 Z9 1 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1994 VL 4 IS 1 BP 17 EP 22 PG 6 WC Oncology SC Oncology GA MN493 UT WOS:A1994MN49300003 PM 21566883 ER PT J AU COLEMAN, CN BEARD, CJ KANTOFF, PW GELMAN, R AF COLEMAN, CN BEARD, CJ KANTOFF, PW GELMAN, R TI RATE OF RELAPSE FOLLOWING TREATMENT FOR LOCALIZED PROSTATE-CANCER - A CRITICAL ANALYSIS OF RETROSPECTIVE REPORTS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Review DE PROSTATE CANCER; RADIATION THERAPY; SURGERY; RELAPSE; RATE OF RELAPSE ID EXTERNAL BEAM RADIATION; RADICAL RETROPUBIC PROSTATECTOMY; SEMINAL-VESICLE INVASION; STAGE-A ADENOCARCINOMA; ANTIGEN LEVELS; METASTATIC DISSEMINATION; DEFINITIVE RADIOTHERAPY; TREATMENT TIME; THERAPY; CARCINOMA AB Purpose: Controversy exists over the optimal treatment for patients with clinically localized prostate cancer. Almost all of the treatment results are from non-randomized trials and interseries comparison is difficult since the apparent success of a treatment, as judged by the actuarial freedom from relapse and survival data, depends on patient selection criteria and post-treatment evaluation, in addition to the efficacy of the therapeutic intervention. In this report the calculation of a hazard function is used to estimate and compare the rate of relapse for the different treatments. Methods and Materials: Clinical reports from major surgery and radiation oncology treatment institutions were analyzed. The actuarial recurrence data were used to calculate the annual rate of recurrence within each series. Results: For all but the lowest volume tumors, patients continue to be at risk of relapse for as long as these series have been followed. Despite the heterogeneity of patient populations, the recurrence rates by stage are similar for patients treated with surgery or irradiation. This result is consistent with pathologic data from prostatectomy specimens which indicate that for lesions > 12 cm(3) (approx. 3 cm in diameter) there is high likelihood of extra-prostatic disease. Conclusion: Treatment outcome for patients with localized prostate cancer may be more dependent on the inherent tumor biology than the particular type of treatment. Accordingly, the expectation and recommendation of a treatment must take into consideration the continued risk of relapse with either radiation therapy or surgery. There are, as yet, insufficient data regarding the impact of screening and earlier diagnosis on the curability of patients with localized prostate cancer. C1 HARVARD UNIV,SCH MED,DEPT MED ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP COLEMAN, CN (reprint author), JOINT CTR RADIAT THERAPY,50 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-42391] NR 100 TC 10 Z9 10 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 1 PY 1994 VL 28 IS 1 BP 303 EP 313 PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA MP353 UT WOS:A1994MP35300038 PM 8270455 ER PT J AU VANDAMME, P SEGERS, P VANCANNEYT, M VANHOVE, K MUTTERS, R HOMMEZ, J DEWHIRST, F PASTER, B KERSTERS, K FALSEN, E DEVRIESE, LA BISGAARD, M HINZ, KH MANNHEIM, W AF VANDAMME, P SEGERS, P VANCANNEYT, M VANHOVE, K MUTTERS, R HOMMEZ, J DEWHIRST, F PASTER, B KERSTERS, K FALSEN, E DEVRIESE, LA BISGAARD, M HINZ, KH MANNHEIM, W TI ORNITHOBACTERIUM-RHINOTRACHEALE GEN-NOV SP-NOV ISOLATED FROM THE AVIAN RESPIRATORY-TRACT SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID FLAVOBACTERIUM-CYTOPHAGA COMPLEX; GRAM-NEGATIVE BACTERIA; FATTY-ACID COMPOSITION; PASTEURELLA-ANATIPESTIFER; DNA HYBRIDIZATION; COMB-NOV; RNA; CAPNOCYTOPHAGA; HEMOPHILUS; DIFFERENTIATION AB The phylogenetic position and various genotypic, chemotaxonomic, and classical phenotypic characteristics of 21 gram-negative avian isolates were studied. These strains constitute a genotypically homogeneous taxon in rRNA superfamily V, as shown by DNA-rRNA hybridization data. Determination of the 16S rRNA sequence of this taxon revealed its detailed position within the ''flavobacter'' subgroup of the ''flavobacter-bacteroides'' phylum as described by Gherna and Woese (R. Gherna and C. R. Woese, Syst. Appl. Microbiol. 15:513-521, 1992). This new taxon is only distantly related to other members of the ''flavobacter-bacteroides'' phylum and is therefore given separate generic status. The DNA-DNA binding values for members of this taxon, for which we propose the name Ornithobacterium rhinotracheale, confirmed that all of the strains are highly interrelated (DNA-DNA binding values greater than 90% were measured). The G + C contents of members of this taxon are between 37 and 39 mol%. An analysis of the cellular proteins and fatty acids and classical phenotypic characteristics allowed us to distinguish O. rhinotracheale from phenotypically similar taxa, such as Riemerella anatipestifer and Capnocytophaga species. The respiratory quinone content (menaquinone 7) and carbohydrate pattern of O. rhinotracheale conform with the respiratory quinone contents and carbohydrate patterns of other members of rRNA superfamily V. C1 STATE UNIV GHENT,FAC DIERGENEESKUNDE,BACTERIOL LAB,B-9000 GHENT,BELGIUM. PHILIPPS UNIV MARBURG KLINIKUM,MARBURG,GERMANY. PROVINCIAAL VERBOND DIERENZIEKTENBESTRIJDING,TORHOUT,BELGIUM. FORSYTH DENT CTR,DEPT MOLEC GENET,BOSTON,MA 02115. GOTHENBURG UNIV,DEPT CLIN BACTERIOL,S-41346 GOTHENBURG,SWEDEN. ROYAL VET & AGR UNIV,FREDERIKSBERG,DENMARK. NATL VET LAB,FREDERIKSBERG,DENMARK. HANNOVER SCH VET MED,GEFLUGEL KLIN,W-3000 HANNOVER 1,GERMANY. RP VANDAMME, P (reprint author), STATE UNIV GHENT,FAC WETENSCHAPPEN,MICROBIOL LAB,KL LEDEGANCKSTR 35,B-9000 GHENT,BELGIUM. RI Vandamme, Peter/B-7967-2009; OI Vandamme, Peter/0000-0002-5581-7937 NR 59 TC 132 Z9 143 U1 1 U2 7 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1994 VL 44 IS 1 BP 24 EP 37 PG 14 WC Microbiology SC Microbiology GA MQ585 UT WOS:A1994MQ58500004 PM 8123560 ER PT J AU LIPTON, SA AF LIPTON, SA TI CA2+, N-METHYL-D-ASPARTATE RECEPTORS, AND AIDS-RELATED NEURONAL INJURY SO INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL 36 SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; PLATELET-ACTIVATING-FACTOR; TUMOR-NECROSIS-FACTOR; CALCIUM-CHANNEL ANTAGONISTS; REDOX MODULATORY SITE; PRIMARY CORTICAL CULTURES; AMINO-ACID NEUROTOXICITY; ENVELOPE PROTEIN GP120; RETINAL GANGLION-CELLS; GUINEA-PIG BRONCHUS C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP LIPTON, SA (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY09024, EY05477]; NICHD NIH HHS [HD29587] NR 132 TC 21 Z9 23 U1 1 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0074-7742 J9 INT REV NEUROBIOL PY 1994 VL 36 BP 1 EP 27 DI 10.1016/S0074-7742(08)60301-3 PG 27 WC Neurosciences SC Neurosciences & Neurology GA BB61T UT WOS:A1994BB61T00001 PM 7822116 ER PT J AU BERLIN, J KING, AC TUTSCH, K FINDLAY, JW KOHLER, P COLLIER, M CLENDENINN, NJ WILDING, G AF BERLIN, J KING, AC TUTSCH, K FINDLAY, JW KOHLER, P COLLIER, M CLENDENINN, NJ WILDING, G TI A PHASE-II STUDY OF VINBLASTINE IN COMBINATION WITH ACRIVASTINE IN PATIENTS WITH ADVANCED RENAL-CELL CARCINOMA SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE RENAL CELL CARCINOMA; ACRIVASTINE; VINBLASTINE; DRUG RESISTANCE; P GLYCOPROTEIN ID MULTIDRUG-RESISTANCE; CONTINUOUS INFUSION; DRUG-RESISTANCE; TRIAL; CYCLOSPORINE; EXPRESSION; MODULATION; VERAPAMIL; ETOPOSIDE; CANCER AB Renal cell carcinoma exhibits chemoresistance attributable in part to the P-glycoprotein drug efflux mechanism. Acrivastine is a hydrophylic antihistamine that has been shown in vitro to reverse this form of resistance. After five patients were treated on a dose-finding study, seventeen patients with metastatic or unresectable renal cell carcinoma were entered into a phase II study of vinblastine in combination with acrivastine. Patients received oral acrivastine at doses of 400 mg every 4 hours for 6 days and a 96-hour continuous infusion of vinblastine at a dose of 1.6 mg/m(2)/24 h. Of 15 evaluable patients, no tumor responses were seen. The regimen was well-tolerated with the majority of toxicities being gastrointestinal and hematologic. Serum levels of acrivastine, its principal metabolite (270C81) and vinblastine were measured during the study. Based on in vitro data, the plasma levels of acrivastine were within a range adequate to block P-glycoprotein activity. High doses of acrivastine were well-tolerated clinically, however, the combination of acrivastine and vinblastine was not active against renal cell carcinoma. C1 UNIV WISCONSIN,CTR COMPREHENS CANC,DEPT HUMAN ONCOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. MERITER HOSP,MADISON,WI. BURROUGHS WELLCOME CO,DEPT CANC THERAPY,RES TRIANGLE PK,NC 27709. NR 17 TC 10 Z9 10 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1994 VL 12 IS 2 BP 137 EP 141 DI 10.1007/BF00874444 PG 5 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA PQ406 UT WOS:A1994PQ40600009 PM 7860231 ER PT J AU WITTE, RS YEAP, BY TRUMP, DL AF WITTE, RS YEAP, BY TRUMP, DL TI TRIMETREXATE IN ADVANCED HORMONE-REFRACTORY PROSTATE-CANCER - AN ECOG PHASE-II TRIAL SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE PROSTATE CARCINOMA; TRIMETREXATE ID METHOTREXATE; CARCINOMA; CHEMOTHERAPY; FLUTAMIDE AB The antitumor activity and toxicity of trimetrexate (TMTX) was evaluated in measurable, hormone-refractory, advanced prostate cancer patients. Patients were required to have an ECOG performance status < 3, bidimensionally measurable disease, serum creatinine less than or equal to 1.5 mg/dL, normal bone marrow function, and adequate hepatic function. Prior non-hormonal systemic therapy, active infection, third space effusions were exclusion criteria. TMTX 12 mg/m(2) daily for five days (8 mg/m(2) for patients with any prior radiation therapy or age greater than or equal to 75 years) was administered every 3 weeks. There were no responses in the 18 eligible patients. Median time to treatment failure and median survival were 6 and 20 weeks, respectively. Myelosuppression was the most frequent toxicity observed and was mild to severe in all but 4 patients. Two patients whom experienced life-threatening reversible leukopenia and grade 4 thrombocytopenia developed in 2 further patients. Non-hematologic toxicity was also reversible and was mild to severe. TMTX at this dose and schedule is inactive in advanced, hormone-refractory prostate cancer. C1 UNIV WISCONSIN,CTR COMPREHENS CANC,MADISON,WI. DANA FARBER CANC INST,BOSTON,MA. FU NCI NIH HHS [CA 21115, CA 21076, CA 23318] NR 16 TC 7 Z9 7 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1994 VL 12 IS 3 BP 255 EP 258 DI 10.1007/BF00873968 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA PX099 UT WOS:A1994PX09900012 PM 7896546 ER PT J AU HENSCHKE, CI STEINER, RM MCLOUD, T WESTCOTT, JL AF HENSCHKE, CI STEINER, RM MCLOUD, T WESTCOTT, JL TI THE PRACTICE OF CHEST RADIOLOGY IN DEPARTMENTS WITH RESIDENCY PROGRAMS SO INVESTIGATIVE RADIOLOGY LA English DT Article DE ORGAN SUBSPECIALIZATION; CHEST RADIOLOGY; DEPARTMENTAL ORGANIZATION ID CORONARY ANGIOGRAPHY; FELLOWSHIP AB OBJECTIVES. The authors assessed to what extent radiology teaching programs employed dedicated chest radiologists and their functions. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT RADIOL,PHILADELPHIA,PA 19107. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HOSP ST RAPHAEL,DEPT RADIOL,NEW HAVEN,CT. RP HENSCHKE, CI (reprint author), NEW YORK HOSP,CORNELL MED CTR,DEPT RADIOL,525 E 68TH ST,NEW YORK,NY 10021, USA. NR 14 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD JAN PY 1994 VL 29 IS 1 BP 48 EP 53 DI 10.1097/00004424-199401000-00007 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NA657 UT WOS:A1994NA65700007 PM 8144337 ER PT J AU CASTRONOVO, FP MCKUSICK, KA STRAUSS, HW AF CASTRONOVO, FP MCKUSICK, KA STRAUSS, HW TI DOSIMETRIC CONSEQUENCES OF RADIOPHARMACEUTICAL INFILTRATIONS SO INVESTIGATIVE RADIOLOGY LA English DT Article DE RADIOPHARMACEUTICAL; INFILTRATION; RAT MODEL; THALLIUM 201 THALLOUS CHLORIDE ID EXTRAVASATION; INJECTION AB RATIONALE AND OBJECTIVES. Little is known about the time-related biologic behavior of radiopharmaceutical misinjections. Such inadvertent tissue infiltration of such injections may not only adversely affect a scheduled test or cause some discomfort, but potentially could produce tissue damage. Radiopharmaceutical infiltrations were assessed in a rat model. METHODS. Particulate and nonparticulate radiopharmaceuticals were injected subcutaneously or intradermally into an anesthetized shaved rat model. The rate of release of the nine infiltrations per radiopharmaceutical per injection type were measured from computer data acquired with a gamma camera up to 24 hours after administration. These data were used for dosimetry determinations. RESULTS. When injected subcutaneously, the particulate radiopharmaceutical, technetium 99m (Tc-99m) albumin microspheres, exhibited essentially no movement, and the soluble agents showed a biexponential release pattern. The rate of release was similar for Tc-99m methylene diphosphonate (Tc-99m MDP) and for Ga-67 citrate (Ga-67), whereas thallous chloride (Tl-201) exhibited the slowest release pattern. The average effective half-lives (T1/2 av-eff) were 78.3 minutes, 76.1 minutes, and 268.4 minutes, respectively. When injected intradermally, the nonparticulates exhibited a triexponential release pattern; MDP showed a more rapid release (T1/2 av-eff, 50 minutes) and Tl-201 showed the slowest (T1/2 av-eff, 491.2 minutes). Absorbed doses were calculated using conventional medical internal radiation dose (MIRD) methodology for small unit density spheres. The absorbed dose was greatest for a Tl-201 infiltration. A Tl-201 infiltrate of 1 mCi per gm of tissue is capable of producing radiation-absorbed doses greater than 500 rads. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. NR 27 TC 5 Z9 6 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD JAN PY 1994 VL 29 IS 1 BP 59 EP 64 DI 10.1097/00004424-199401000-00010 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NA657 UT WOS:A1994NA65700009 PM 8144339 ER PT B AU FOX, L FRIEDOKEN, M STAYER, J AF FOX, L FRIEDOKEN, M STAYER, J GP INT SOC AUGMENTAT & ALTERNAT COMMUN TI DETERMINING INDEPENDENT COMMUNICATION IN AN ADULT WITH SEVERE, NONFLUENT APHASIA AND A VOICE OUTPUT COMMUNICATION AID SO ISAAC '94 CONFERENCE BOOK AND PROCEEDINGS LA English DT Proceedings Paper CT 6th Biennial Conference of the International-Society-for-Augmentative-and-Alternative-Communication (ISAAC 94) CY OCT 09-13, 1994 CL MAASTRICHT, NETHERLANDS SP INT SOC AUGMENTAT & ALTERNAT COMMUN, IRV, INST RES DEV & KNOWLEDGE TRANSFER FIELD REHABIL & HANDICAP, DUTCH COUNCIL DISABLED DE ACQUIRED; LANGUAGE; DISORDER CASE; STUDIES TEACHING; AND OR; INTERVENTION TECHNOLOGY C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. NR 0 TC 0 Z9 0 U1 0 U2 2 PU IRV, INST RES DEV & KNOWLEDGE TRANSF FIELD & REHAB HANDICAP PI HOENSBROEK PA PO BOX 192, 6430 AD HOENSBROEK, NETHERLANDS BN 90-74910-03-3 PY 1994 BP 81 EP 83 PG 3 WC Education, Special; Engineering, Biomedical; Language & Linguistics; Rehabilitation SC Education & Educational Research; Engineering; Linguistics; Rehabilitation GA BC07G UT WOS:A1994BC07G00025 ER PT J AU HUNTER, GJ HAMBERG, LM WEISSKOFF, RM HALPERN, EF BRADY, TJ AF HUNTER, GJ HAMBERG, LM WEISSKOFF, RM HALPERN, EF BRADY, TJ TI MEASUREMENT OF STROKE VOLUME AND CARDIAC-OUTPUT WITHIN A SINGLE-BREATH HOLD WITH ECHO-PLANAR MR-IMAGING SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE HEART, EJECTION FRACTION; HEART, FUNCTION; HEART, MR; HEART, VENTRICLES; HEART, VOLUME; RAPID IMAGING ID VENTRICULAR-FUNCTION; ANGIOGRAPHY; TOMOGRAPHY; NMR AB The measurement of cardiac output and ejection fraction is useful in the treatment of diverse cardiac and cardiopulmonary disease states. Although several techniques are available for accurate measurement of left ventricular parameters, assessment of the right ventricle is less well represented. No single method is overwhelmingly superior, each having different strengths and weaknesses. In the present study, the applicability of an echo-planar magnetic resonance (MR) imaging method in which a complete volumetric measurement of the right and left ventricles may be obtained during 12 heartbeats is demonstrated. This rapidity permits imaging during a 15-second breath hold. The authors show in 12 volunteers that breath-hold echo-planar volume measurements of both ventricles were consistent with results obtained with conventional MR imaging methods. C1 MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BOSTON,MA 02129. RP HUNTER, GJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BLDG 149,13TH ST,CHARLESTOWN NAVY YARD,BOSTON,MA 02129, USA. FU NCI NIH HHS [P01-CA48729] NR 14 TC 18 Z9 19 U1 0 U2 0 PU SOC MAGNETIC RESONANCE IMAGING PI EASTON PA 1991 NORTHAMPTON ST, EASTON, PA 18042-3189 SN 1053-1807 J9 JMRI-J MAGN RESON IM JI JMRI-J. Magn. Reson. Imaging PD JAN-FEB PY 1994 VL 4 IS 1 BP 51 EP 58 DI 10.1002/jmri.1880040112 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NA667 UT WOS:A1994NA66700009 PM 8148556 ER PT J AU WALKER, BD AF WALKER, BD TI THE RATIONALE FOR IMMUNOTHERAPY IN HIV-1 INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS TYPE 1; IMMUNE EFFECTOR MECHANISMS; VACCINE THERAPY ID HUMAN-IMMUNODEFICIENCY-VIRUS; TOXIC LYMPHOCYTES-T; HUMAN MONOCLONAL-ANTIBODY; ENVELOPE GLYCOPROTEIN; CEREBROSPINAL-FLUID; TYPE-1; CELL; AIDS; NEUTRALIZATION; CHIMPANZEES AB Human immunodeficiency virus type 1 (HIV-1) infection causes progressive and ultimately profound immunosuppression. Initially, however, infection is associated with vigorous virus-specific immune responses, including both neutralizing antibodies and cytotoxic T lymphocytes (CTLs). Although the host immune response is ultimately unable to eliminate the virus, experimental data suggest that these immune responses help to inhibit virus replication during the prolonged asymptomatic phase of illness. A number of mechanisms have been proposed to contribute to viral persistence in infected persons, among them direct immunosuppressive effects of the virus; defects in antigen presentation; down-modulation of human leukocyte antigens (HLA); clonal deletion of existing immune responses; sequence variation leading to immune escape; and decreased T-helper cell function. The rationale supporting the use of vaccine therapy in HIV-1 infection is based on the hypothesis that viral persistence is due to an inadequate immune response generated by natural infection and that the immune system can be induced to generate more effective immunoregulatory responses by vaccination. Potential mechanisms by which this might occur include enhanced clearance of circulating virus, enhanced recognition of virus variants, enhanced presentation of viral antigens to the immune system, and increased regional T-cell help. A number of protocols evaluating vaccine therapy in HIV-1 infection are presently under way, the results of which should facilitate rational decisions regarding the use of this approach in HIV-l-infected persons. RP WALKER, BD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INFECT DIS UNIT,55 FRUIT ST,GRAY UNIT 5,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI-30914, AI-28568] NR 53 TC 19 Z9 19 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. PY 1994 VL 7 SU 1 BP S6 EP S13 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NP872 UT WOS:A1994NP87200003 PM 8182510 ER PT J AU OTTO, MW POLLACK, MH AF OTTO, MW POLLACK, MH TI PANIC DISORDER AND HYPOCHONDRIACAL CONCERNS - A REPLY SO JOURNAL OF ANXIETY DISORDERS LA English DT Article ID ANXIETY C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 11 TC 9 Z9 9 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PD JAN-MAR PY 1994 VL 8 IS 1 BP 101 EP 103 DI 10.1016/0887-6185(94)90027-2 PG 3 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA MV822 UT WOS:A1994MV82200009 ER PT J AU ROVIRA, I CHEN, TY WINKLER, M KAWAI, N BLOCH, KD ZAPOL, WM AF ROVIRA, I CHEN, TY WINKLER, M KAWAI, N BLOCH, KD ZAPOL, WM TI EFFECTS OF INHALED NITRIC-OXIDE ON PULMONARY HEMODYNAMICS AND GAS-EXCHANGE IN AN OVINE MODEL OF ARDS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE LAVAGE LUNG INJURY; SHEEP; PULMONARY CIRCULATION; PRESSURE-FLOW RELATIONSHIP; VENOUS ADMIXTURE; GUANOSINE 3',5'-CYCLIC MONOPHOSPHATE ID CYCLIC GUANOSINE-MONOPHOSPHATE; RESPIRATORY-DISTRESS SYNDROME; PRESSURE-FLOW RELATIONSHIP; L-ARGININE; RELAXING FACTOR; CARDIAC-OUTPUT; HYPERTENSION; INVIVO; SHUNT; CIRCULATION AB Inhaling low concentrations of nitric oxide (NO) gas causes selective pulmonary vasodilation of ventilated lung regions. NO activates soluble guanylate cyclase, increasing guanosine 3',5'-cyclic monophosphate (cGMP). Inhibition of NO synthesis enhances hypoxic pulmonary vasoconstriction. Therefore we examined independent and combined effects of NO inhalation and infusion of N-G-nitro-L-arginine methyl ester (L-NAME), an NO synthesis inhibitor, on pulmonary vascular pressure-flow relationships, gas exchange, and plasma cGMP levels in anesthetized and mechanically ventilated sheep with acute lung injury induced by bilateral lavage. After lavage, inhaling 60 ppm by volume of NO decreased pulmonary arterial pressure (PAP) and resistance without any systemic hemodynamic effects, increased arterial PO2, and decreased venous admixture (Qva/QT; all P < 0.05) without altering cardiac output (QT), mixed venous PO2, or O-2 uptake, major determinants of intrapulmonary shunt. During NO inhalation, PAP-left atrial pressure gradient (PAP-LAP) and Qva/QT were reduced (both P < 0.05) independently of QT, which was varied mechanically. L-NAME infusion produced systemic and pulmonary vasoconstriction and increased PAP-LAP gradient across the entire range of QT, whereas Qva/QT was not changed. NO inhalation after L-NAME infusion produced pulmonary vasodilation and decreased Qva/QT to the same degree as NO inhalation alone. Five to 10 min after inhalation of 60 ppm NO, before and after L-NAME infusion, arterial plasma cGMP levels were increased by 80% (both P < 0.05). With NO breathing after L-NAME, we measured a consistent transpulmonary cGMP arteriovenous gradient [31 +/- 8 and 33 +/- 7 (SE) pmol/ml at 5 and 10 min, respectively; both P < 0.05]. NO inhalation before or after L-NAME administration in this acute lung injury model reduced Qva/QT, most likely by increasing cGMP concentration in ventilated lung regions and causing selective pulmonary vasodilation. C1 MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT ANAESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT MED,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-42397] NR 46 TC 54 Z9 54 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 JAN PY 1994 VL 76 IS 1 BP 345 EP 355 PG 11 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA MU486 UT WOS:A1994MU48600048 PM 8175528 ER PT J AU SHARMA, SK BHARGAVA, A PANDE, JN AF SHARMA, SK BHARGAVA, A PANDE, JN TI EFFECT OF PARENTERAL MAGNESIUM-SULFATE ON PULMONARY FUNCTIONS IN BRONCHIAL-ASTHMA SO JOURNAL OF ASTHMA LA English DT Article AB Eighteen patients with bronchial asthma were studied in a single-blind fashion. Each patient received an infusion of magnesium sulfate (MgSO4.7H2O 50% W/V) in a dose equivalent to 10 mmol of elemental magnesium. The airways resistance showed a significant decrease (p < 0.01) while SGaw increased significantly (p < 0.001) with MgSO4 infusion. FEV1 (p < 0.01), FEF25-75% (p < 0.05), and V50 (p < 0.05) also showed statistically significant increase (p < 0.001) with MgSO4 infusion. Significant changes in Raw (p < 0.01) and SGaw (p < 0.01) persisted at 10 and 20 min following MgSO4 infusion. No significant side effects were observed with MgSO4 infusion. It is concluded that modest improvement in airways resistance and specific conductance and only small improvement in maximal expiratory flow rates is consistent with a predominant effect of MgSO4 on large airways in patients with bronchial asthma. RP SHARMA, SK (reprint author), MASSACHUSETTS GEN HOSP,DEPT IMMUNOPATHOL PULM IMMUNOL & MOLEC BIOL,COX 5,BOSTON,MA 02114, USA. NR 0 TC 12 Z9 13 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0277-0903 J9 J ASTHMA JI J. Asthma PY 1994 VL 31 IS 2 BP 109 EP 115 DI 10.3109/02770909409044813 PG 7 WC Allergy; Respiratory System SC Allergy; Respiratory System GA NE683 UT WOS:A1994NE68300005 PM 8175629 ER PT J AU LITWIN, CM CALDERWOOD, SB AF LITWIN, CM CALDERWOOD, SB TI ANALYSIS OF THE COMPLEXITY OF GENE-REGULATION BY FUR IN VIBRIO-CHOLERAE SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; IRON TRANSPORT; TRANSCRIPTIONAL REGULATION; NUCLEOTIDE-SEQUENCE; IDENTIFICATION; PROTEIN; CLONING; OPERON; VIRULENCE; OPERATOR AB Iron concentration influences the expression of a number of genes involved in iron uptake and virulence in bacteria. In Escherichia coli, coordinate regulation of these genes by iron depends on the product of the fur gene, which acts as an iron-responsive, DNA-binding repressor protein. Several genes in Vibrio cholerae are also repressed by iron; and a fur gene, homologous to E. coli fur, has been previously cloned from this organism. The present study was undertaken to define the roles of Fur and iron in regulating gene expression in V. cholerae. V. cholerae strains with a mutation in fur by virtue of suicide plasmid integration into this gene showed derepressed expression of two previously characterized, iron-regulated genes, irgA and viuA, in high concentrations of iron; even in the fur mutants, however, residual two- to threefold regulation by iron persisted. The fur mutant strains constructed by suicide plasmid integration required antibiotic selection to maintain the mutation. To analyze further the effect of Fur and iron on gene regulation in V. cholerae without the need for antibiotic selection, we used in vivo marker exchange to construct a nonrevertible V. cholerae fur mutant. This V. cholerae fur mutant grew significantly less well in Luria-Bertani medium than the wild-type parent but grew slightly better than the wild type under iron-restricted conditions. The V. cholerae fur mutant was unable to utilize a number of carbon sources including glycerol, acetate, succinate, lactate, and fumarate, that supported growth of the wild-type strain on minimal media. We utilized two-dimensional gel electrophoresis of whole-cell protein extracts from the fur mutant and wild-type strains following growth in conditions of either low or high concentrations of iron to identify proteins regulated by iron and/or Fur. Twenty-two proteins were negatively regulated by iron in the wild-type strain but constitutively expressed in the fur mutant, consistent with the model of Fur as an iron-dependent repressor. However, many other proteins were regulated in a different manner by iron and/or Fur. Seventeen proteins were negatively regulated by iron but independent of Fur, suggesting the presence of an additional iron-dependent repressor(s). Six proteins were strongly iron regulated in the fur mutant but hardly expressed at all in the wild-type strain regardless of the iron concentration, suggesting an interaction between Fur and another iron regulatory mechanism. There were 11 proteins that were induced rather than repressed by iron, in four different regulatory classes. Gene regulation in V. cholerae by Fur and iron is much more complex than previously thought and is reminiscent of the Lrp regulon in E. coli. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. OI Litwin, Christine/0000-0002-4311-7714 FU NIAID NIH HHS [AI27329] NR 43 TC 62 Z9 63 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1994 VL 176 IS 1 BP 240 EP 248 PG 9 WC Microbiology SC Microbiology GA MQ381 UT WOS:A1994MQ38100030 PM 8282702 ER PT J AU PIERSON, JL HARRIS, WH AF PIERSON, JL HARRIS, WH TI CEMENTED REVISION FOR FEMORAL OSTEOLYSIS IN CEMENTED ARTHROPLASTIES - RESULTS IN 29 HIPS AFTER A MEAN 8.5-YEAR FOLLOW-UP SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Article ID BONE LYSIS; COMPONENTS AB We reviewed 29 consecutive patients after cemented femoral revision of cemented hip arthroplasties for osteolysis. After an average follow-up of 8.5 years, osteolysis had recurred in only two cases (6.9%) and 25 femoral components (86%) remained well fixed. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 12 TC 15 Z9 16 U1 0 U2 0 PU BRITISH EDITORIAL SOC BONE JOINT SURGERY PI LONDON PA 22 BUCKINGHAM STREET, LONDON, ENGLAND WC2N 6ET SN 0301-620X J9 J BONE JOINT SURG BR JI J. Bone Joint Surg.-Br. Vol. PD JAN PY 1994 VL 76B IS 1 BP 40 EP 44 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MT201 UT WOS:A1994MT20100009 PM 8300679 ER PT J AU JASTY, M BRAGDON, CR LEE, K HANSON, A HARRIS, WH AF JASTY, M BRAGDON, CR LEE, K HANSON, A HARRIS, WH TI SURFACE DAMAGE TO COBALT-CHROME FEMORAL-HEAD PROSTHESES SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Article ID TOTAL HIP-REPLACEMENT; BONE-RESORPTION; WEAR; POLYETHYLENE AB Fifty-four cobalt-chrome alloy femoral heads were retrieved at revision surgery or at post-mortem; 23 came from uncemented, eight from hybrid and 23 from cemented hip arthroplasties. The uncemented and hybrid implants had porous coating, metal backing and modular femoral heads; with one exception none of the cemented implants had any of these. Twenty-five of the 31 heads from uncemented and hybrid arthroplasties, and 11 of the 23 heads from cemented arthroplasties showed surface damage involving more than 25% of the surface. Scanning electron microscopy revealed multidirectional fine scratches 1 mu m to 10 mu m in depth and width which appeared to have been made by fine, hard particles. There was a higher rate of such damage in the uncemented and hybrid arthroplasties than in the cemented implants, suggesting that the abrasive particles were mainly released from the metal, rather than from the cement or polyethylene components of the implants. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP JASTY, M (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,HIP & IMPLANT UNIT,BOSTON,MA 02114, USA. NR 21 TC 77 Z9 78 U1 1 U2 1 PU BRITISH EDITORIAL SOC BONE JOINT SURGERY PI LONDON PA 22 BUCKINGHAM STREET, LONDON, ENGLAND WC2N 6ET SN 0301-620X J9 J BONE JOINT SURG BR JI J. Bone Joint Surg.-Br. Vol. PD JAN PY 1994 VL 76B IS 1 BP 73 EP 77 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MT201 UT WOS:A1994MT20100015 PM 8300686 ER PT J AU MITLAK, BH SCHOENFELD, D NEER, RM AF MITLAK, BH SCHOENFELD, D NEER, RM TI ACCURACY, PRECISION, AND UTILITY OF SPINE AND WHOLE-SKELETON MINERAL MEASUREMENTS BY DXA IN RATS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID OVARIECTOMIZED RATS; BONE MASS; PARATHYROID-HORMONE; TRABECULAR BONE; OSTEOPENIA; ABSORPTIOMETRY; CALCITONIN; CALCIUM; DENSITY AB We evaluated the precision and accuracy of dual-energy x-ray bone densitometry (DXA) in 38 male and female rats aged 1-10 months. The coefficients of variation (CV) estimated from same-day paired measurements of bone mineral content (BMC) were 1.26% at the lumbar spine and 0.690% at the whole skeleton, and the corresponding CV for BMC corrected for projected bone area (i.e., bone mineral density, BMD) were 0.57 and 0.66%. BMC, measured in vivo, correlated closely with the subsequently determined ash weights (spine r(2) = 0.94, whole-skeleton r(2) = 0.97). The long-term CV for BMC measurements, assessed by measuring a frozen animal daily for 4 weeks, were 1.28% for the spine and 1.03% for the whole skeleton; for BMD the corresponding CV were 0.88 and 1.15%. To examine the utility of serial DXA measurements we followed female rats subjected to ovariectomy (OVX) or sham operation at 10 months of age and male rats given daily subcutaneous injections of hPTH-(1-34) or vehicle starting at 10 months of age every 3 weeks for 15 weeks. In the OVX rats a progressive decrease in spine BMC was observed that was most rapid during the first 6 weeks. By 15 weeks the mean spine BMC decreased by 17% in the OVX rats (p < 0.007 versus sham operation). OVX did not affect the accuracy of DXA measurements as assessed by comparison with the ash weight at the end of the 15 week study. PTH treatment increased spine BMC by a mean of 32% and increased whole-skeleton BMC by a mean of 19% within 15 weeks. The long-term in vivo variation was estimated by fitting a model for BMC and BMD in the vehicle-treated male rats and sham-operated female rats, assuming a linear rate of change over the 15 weeks and a different slope and intercept for each animal; the residual root mean squared error was taken as an estimate of variability. Defined in this manner, the long-term variation for BMC measurements in vivo is 5% for the spine and 3% for the whole skeleton; for BMD the corresponding figures are 3 and 2%. This variability is significantly greater than that attributable to instrumental variation and/or same-day repositioning and must be considered when designing experiments requiring serial measurements. C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. RP MITLAK, BH (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BULFINCH 3,BOSTON,MA 02114, USA. NR 27 TC 57 Z9 59 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JAN PY 1994 VL 9 IS 1 BP 119 EP 126 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MW244 UT WOS:A1994MW24400015 PM 8154305 ER PT J AU STRITTMATTER, SM VALENZUELA, D FISHMAN, MC AF STRITTMATTER, SM VALENZUELA, D FISHMAN, MC TI AN AMINO-TERMINAL DOMAIN OF THE GROWTH-ASSOCIATED PROTEIN GAP-43 MEDIATES ITS EFFECTS ON FILOPODIAL FORMATION AND CELL SPREADING SO JOURNAL OF CELL SCIENCE LA English DT Article DE NEURONAL GROWTH CONE; GAP-43 (NEUROMODULIN); GTP-BINDING PROTEIN; SIGNAL TRANSDUCTION; CELL SPREADING; AXONAL GROWTH ID CALMODULIN-BINDING-PROTEIN; PHOSPHOLIPID-METABOLISM; NEURITE RETRACTION; NEURONAL CELLS; CONE MOTILITY; PC12 CELLS; KINASE-C; MEMBRANE; RECEPTOR; IDENTIFICATION AB GAP-43 is a neuronal protein that is believed to be important to neuronal growth and nerve terminal plasticity. It is enriched on the inner surface of growth cone membranes, a localization that may depend upon palmitoylation of Cys3 and Cys4. It is a major substrate for protein kinase C, which phosphorylates Ser41. Isolated GAP-43 can bind to actin and to calmodulin, and can activate the heterotrimeric GTP-binding proteins, G(o) and G(i). A peptide consisting of the GAP-43 sequence 39-55 binds calmodulin, and an amino-terminal GAP-43 (1-10) peptide activates G(o), suggesting that these stretches may be functional domains of the intact protein. When expressed in non-neuronal cells, GAP-43 enhances filopodial extension and has effects upon cell spreading. We have examined the effects of various GAP-43 domains upon this assay, by expression of GAP-43, GAP-43 mutant proteins, and GAP-43-CAT fusion proteins in COS-7 cells. We find that the amino terminus (Met-Leu-Cys-Cys-Met-Arg-Arg-Thr-Lys-Gln) is an important contributor to these effects on cell shape. A GAP-43 protein mutant in Cys3 and Cys4 does not bind to the membrane, and is inactive. Mutants in Arg6 or Lys9 also are inactive, although they remain localized to particulate fractions; Arg7 mutants are active. A chimeric gene consisting of GAP-43 (1-10) fused to chloramphenicol acetyl transferase (CAT) also causes cell shape changes. As for GAP-43, the effects of this fusion protein are abolished by mutations of Cys3, Cys4, Arg6 or Lys9, but not by mutation of Arg7. Therefore, the cell surface activity of transfected GAP-43 depends upon its amino terminus, although other domains may regulate it in this regard. Since the amino-terminal domain includes the peptide stretch known to be capable of activating G(o) and G(i), we examined the effect of GAP-43 on a G(i)-regulated second messenger system, the inhibition of cAMP production in A431 cells. A431 cells stably transfected with GAP-43 spread less well than do controls. In addition, they evidence decreased levels of forskolin-stimulated cAMP, consistent with chronic stimulation of G(i). Stimulation of adenylate cyclase by isoproterenol reverses the GAP-43-induced changes in cell shape. This suggests that G protein stimulation is involved in GAP-43 effects upon cell shape. C1 MASSACHUSETTS GEN HOSP,DEPT BIOL LAB,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP E,SCH MED,DEPT NEUROL,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP E,SCH MED,DEPT MED,BOSTON,MA 02129. OI Strittmatter, Stephen/0000-0001-8188-3092 NR 51 TC 41 Z9 42 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 JAN PY 1994 VL 107 BP 195 EP 204 PN 1 PG 10 WC Cell Biology SC Cell Biology GA MU732 UT WOS:A1994MU73200019 PM 8175908 ER PT J AU KLAUS, S CHOY, L CHAMPIGNY, O CASSARDDOULCIER, AM ROSS, S SPIEGELMAN, B RICQUIER, D AF KLAUS, S CHOY, L CHAMPIGNY, O CASSARDDOULCIER, AM ROSS, S SPIEGELMAN, B RICQUIER, D TI CHARACTERIZATION OF THE NOVEL BROWN ADIPOCYTE CELL-LINE HIB 1B - ADRENERGIC PATHWAYS INVOLVED IN REGULATION OF UNCOUPLING PROTEIN GENE-EXPRESSION SO JOURNAL OF CELL SCIENCE LA English DT Article DE BETA3 ADRENERGIC RECEPTOR; BROWN FAT THERMOGENESIS; HORMONAL REGULATION OF GENE EXPRESSION ID ADIPOSE-TISSUE; BETA-3-ADRENERGIC RECEPTOR; MESSENGER-RNA; MOLECULAR CHARACTERIZATION; LIPOPROTEIN-LIPASE; BETA-ADRENOCEPTOR; PRIMARY CULTURE; AGONIST; THERMOGENIN; UCP AB The HIB 1B cell line, derived from a brown fat tumor of a transgenic mouse, is the first established brown adipocyte cell line capable of expressing the brown fat-specific mitochondrial uncoupling protein (UCP). UCP gene expression, which was virtually undetectable under basic conditions, was stimulated by acute catecholamine or cyclic AMP treatment to levels comparable to primary cultures of brown adipocytes. Elevation of UCP mRNA levels following stimulation was very rapid but transient, decreasing after about 4 hours with a half-life between 9 and 13 hours. Immunoblotting showed the presence of UCP in HIB 1B mitochondria, but expression was much lower than observed in BAT or primary cultures of brown adipocytes. Upon transfection of HIB 1B cells with a reporter gene containing the UCP promoter, the activity of the transgene was regulatable by cAMP and norepinephrine. Investigation of the possible adrenergic receptors involved in UCP stimulation showed that specific beta 3-adrenergic agonists were much less effective than nonspecific beta-adrenergic agonists and that mRNA levels of the atypical, fat-specific beta 3-adrenoceptor were lower than those observed in brown adipocytes differentiated in primary culture. From pharmacological evidence we conclude that beta 3-adrenergic receptors account for approximately 30-40% of catecholamine induced UCP gene stimulation, whereas about 60-70% is stimulated via the classical beta 1/2 adrenergic pathway. We conclude that HIB 1B cells represent a functional system for the study of mechanisms related to brown adipose thermogenesis. C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. UNIV ILLINOIS, DEPT BIOCHEM, CHICAGO, IL 60612 USA. RP KLAUS, S (reprint author), CNRS, CTR RECH ENDOCRINOL MOLEC & DEV, F-92190 MEUDON, FRANCE. NR 41 TC 54 Z9 56 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD JAN PY 1994 VL 107 BP 313 EP 319 PN 1 PG 7 WC Cell Biology SC Cell Biology GA MU732 UT WOS:A1994MU73200029 PM 8175918 ER PT J AU SMITH, DP ENG, C PONDER, BAJ AF SMITH, DP ENG, C PONDER, BAJ TI MUTATIONS OF THE RET PROTOONCOGENE IN THE MULTIPLE ENDOCRINE NEOPLASIA TYPE-2 SYNDROMES AND HIRSCHSPRUNG DISEASE SO JOURNAL OF CELL SCIENCE LA English DT Article DE RET PROTOONCOGENE; RECEPTOR TYROSINE KINASE; INHERITED CANCER SYNDROME; MEN 2; HIRSCHSPRUNG DISEASE ID MEDULLARY-THYROID CARCINOMA; TYROSINE KINASE; TRANSMEMBRANE DOMAIN; TRANSFORMING GENE; POINT MUTATION; II ONCOGENE; LONG ARM; CHROMOSOME-10; PROTOONCOGENE; LINKAGE AB Distinct point mutations in the RET proto-oncogene are the cause of the inherited multiple endocrine neoplasia type 2 syndromes (MEN 2), and the congenital gut disorder Hirschsprung disease. The site and type of these mutations suggests that they have differing effects on the activity of the receptor tyrosine kinase encoded by RET. The normal function of the RET receptor tyrosine kinase has yet to be determined. However, this has been investigated by the inactivation of the RET gene in transgenic mice. The developmental abnormalities apparent in these mice, together with the observation that the major tissues affected in MEN 2 and Hirschsprung disease have a common origin in the embryonal neural crest, suggest that RET encodes a receptor for a developmental regulator involved in the genesis of a variety of neural crest derivatives, and in the organogenesis of the kidney. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,DIV MED ONCOL,BOSTON,MA. RP SMITH, DP (reprint author), UNIV CAMBRIDGE,DEPT PATHOL,CRC,HUMAN CANC GENET RES GRP,CAMBRIDGE,ENGLAND. OI Eng, Charis/0000-0002-3693-5145 NR 69 TC 5 Z9 5 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. PY 1994 SU 18 BP 43 EP 49 PG 7 WC Cell Biology SC Cell Biology GA QK899 UT WOS:A1994QK89900007 ER PT J AU DYSON, N AF DYSON, N TI PRB, P107 AND THE REGULATION OF THE E2F TRANSCRIPTION FACTOR SO JOURNAL OF CELL SCIENCE LA English DT Article DE PRB; P107; E2F TRANSCRIPTION FACTOR; REGULATION ID RETINOBLASTOMA GENE-PRODUCT; ADENOVIRUS E1A PROTEINS; CELL-CYCLE REGULATION; HUMAN MYC PROMOTER; LARGE-T; SUSCEPTIBILITY GENE; MOLECULAR-CLONING; TRANS-ACTIVATION; ANTI-ONCOGENE; DNA-BINDING AB Small DNA tumor viruses, such as adenovirus, encode proteins that deregulate the cell cycle. These proteins are potent transforming agents when tested in standard oncogenic assays. For adenovirus the best characterized viral oncoproteins are the early region 1A (E1A) products. Mutational studies have shown that E1A's oncogenic ability is determined primarily by its ability to bind to certain cellular proteins and interfere with their function. One of these cellular targets for E1A is the product of the retinoblastoma tumor suppressor gene, pRB, pRB is a negative regulator of cell proliferation, and its inactivation has been shown to be an important oncogenic step in the development of many human cancers. In adenovirus-mediated transformation, E1A binds to PRE and inactivates it, thus functionally mimicking the loss of pRB often seen in human tumors. There is now compelling evidence to suggest that pRB regulates transcription at specific phases of the cell cycle by physically associating with key transcription factors. The best characterized target of pRB is the transcription factor E2F. The interaction of pRB and E2F leads to the inhibition of E2F-mediated transactivation. Most of the genes that are known to be controlled by E2F have key roles in the regulation of cell proliferation. During cell cycle progression, phosphorylation of pRB appears to change its conformation and E2F is released. In pathogenic settings E2F transactivation is not regulated by pRB binding. In human tumors with mutations in the retinoblastoma gene, functional pRB is absent and hence can no longer inhibit E2F activity. During adenovirus transformation, E1A binds to pRB and displaces E2F. In both these cases, E2F is released from pRB-mediated regulation at inappropriate times. The activation of these E2F-responsive genes may lead to the stimulation of cell proliferation. While we do not know whether E2F is the only target for pRB action, this work has formed a general picture of how tumor suppressor gene products such as pRB can control specific transcriptional events and act as negative regulators of cell growth. Recent experiments have shown that E2F represents the combined activity of an extensive series of protein complexes. There are at least five genes that encode E2F polypeptides, and probably several more have yet to be identified. The E2F transcription factor is a heterodimer composed of two related polypeptides, one encoded by a member of the E2F gene family and the other by a member of the DP family. Intriguingly DP and E2F genes are also found in Drosophila and these may provide alternative approaches to the investigation of E2F function. In mammalian cells E2F/DP heterodimers are regulated, at least in part, by the formation of many larger complexes. E2F is found in separate complexes with pRB, p107/cyclin A/cdk2 or p107/cyclin E/cdk2, and additional complexes exist that have yet to be fully characterized. These E2F complexes are detected at specific points of the cell cycle and appear to provide different elements of E2F regulation. RP DYSON, N (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC ONCOL LAB,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 87 TC 7 Z9 7 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. PY 1994 SU 18 BP 81 EP 87 PG 7 WC Cell Biology SC Cell Biology GA QK899 UT WOS:A1994QK89900013 ER PT J AU GOLDRING, MB FUKUO, K BIRKHEAD, JR DUDEK, E SANDELL, LJ AF GOLDRING, MB FUKUO, K BIRKHEAD, JR DUDEK, E SANDELL, LJ TI TRANSCRIPTIONAL SUPPRESSION BY INTERLEUKIN-1 AND INTERFERON-GAMMA OF TYPE-II COLLAGEN GENE-EXPRESSION IN HUMAN CHONDROCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE CHONDROCYTE; MESSENGER-RNA STABILITY; TRANSIENT TRANSFECTION; PROMOTER; ENHANCER ID TUMOR-NECROSIS-FACTOR; MESSENGER-RNA LEVELS; GROWTH FACTOR-BETA; CHLORAMPHENICOL ACETYLTRANSFERASE; NUCLEAR FACTOR; 1ST INTRON; REGULATORY SEQUENCES; COSTAL CHONDROCYTES; FIBROBLAST GROWTH; RESPONSE ELEMENT AB Type II collagen is one of the predominant extracellular matrix macromolecules in cartilage responsible for maintenance of integrity of this specialized tissue. We showed previously that interleukin-1 (IL-1) and interferon-gamma (IFN-gamma) are capable of decreasing the levels of alpha 1 (II) procollagen m RNA and suppressing the synthesis of type II collagen in cultured human chondrocytes. Data reported here show that these effects of IL-1 and IFN-gamma on the expression of the human type II collagen gene (COL2A1) are mediated primarily at the transcriptional level. This conclusion is based on three types of experimental evidence: (1) in nuclear run-off assays, preincubation of chondrocytes with either IL-1 or IFN-gamma decreased COL2A1 transcription; (2) experiments with the protein synthesis inhibitor cycloheximide and the transcriptional inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) indicated that the suppression of alpha 1(II) procollagen mRNA by IL-1 could not be ascribed to decreased mRNA stability; and (3) a plasmid (pCAT-B/4.0) containing 4.0 kb of 5'-flanking sequences of COL2A1 (-577/+3428), encompassing the promoter, exon 1 and the putative enhancer sequence in the first intron linked to the chloramphenicol acetyltransferase (CAT) reporter gene, was transfected in human chondrocytes. A high level of expression of pCAT-B/4.0 was observed in human chondrocytes incubated with an insulin-containing serum substitute that is permissive for expression of the COL2A1 gene. Expression of pCAT-B/4.0 in these cells was inhibited by either IL-1 or IFN-gamma. Furthermore, expression of pCAT-B/4.0 was not detected in human dermal fibroblasts. When the putative enhancer fragment in the first intron was removed, the expression in chondrocytes was greatly reduced. These studies demonstrate that expression of COL2A1 is tissue specific and that suppression by either IL-1 or IFN-gamma is mediated primarily at the transcriptional level. (C) 1994 Wiley-Liss, Inc. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,ARTHRIT UNIT,BOSTON,MA 02114. HARVARD UNIV,FAC MED,SCH MED,DIV CELL & DEV BIOL,BOSTON,MA 02114. UNIV WASHINGTON,DEPT ORTHOPAED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT BIOCHEM,SEATTLE,WA 98195. VET ADM MED CTR,SEATTLE,WA 98108. FU NIAMS NIH HHS [AR-07258, AR-03564, AR-34390] NR 76 TC 99 Z9 102 U1 1 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN PY 1994 VL 54 IS 1 BP 85 EP 99 DI 10.1002/jcb.240540110 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MT022 UT WOS:A1994MT02200009 PM 8126089 ER PT J AU KING, GL INOGUCHI, T SHIBA, T PU, X KUNISAKI, M BURSELL, SE AF KING, GL INOGUCHI, T SHIBA, T PU, X KUNISAKI, M BURSELL, SE TI ROLE OF PROTEIN-KINASE-C (PKC) AND ITS ISOFORM BETA-II IN THE DEVELOPMENT OF VASCULAR COMPLICATIONS OF DIABETES-MELLITUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 JOSLIN DIABETES CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 71 EP 71 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400179 ER PT J AU JONES, CLA DEMPSEY, EC KANE, MA AF JONES, CLA DEMPSEY, EC KANE, MA TI ABNORMAL PROTEIN KINASE-C-ALPHA IN HUMAN SMALL-CELL LUNG-CARCINOMA NCI-H345 CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DENVER VAMC,DENVER,CO 80220. UNIV COLORADO,HSC,DENVER,CO 80220. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 75 EP 75 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400191 ER PT J AU RIEDEL, H SHIEH, HL AF RIEDEL, H SHIEH, HL TI A RAPID, PHENOTYPIC SCREEN TO DISSECT PROTEIN-KINASE-C STRUCTURE-FUNCTION AND DRUG-INTERACTION IN YEAST SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. JOSLIN DIABET CTR,MOLEC BIOL SECT,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 79 EP 79 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400206 ER PT J AU BURTON, DR BARBAS, CF BINLEY, JM DITZEL, H HENDRY, M LANE, HC WALKER, R MOORE, JP NARA, PM NORRBY, E THALI, M SODROSKI, J AF BURTON, DR BARBAS, CF BINLEY, JM DITZEL, H HENDRY, M LANE, HC WALKER, R MOORE, JP NARA, PM NORRBY, E THALI, M SODROSKI, J TI RECOMBINANT NEUTRALIZING HUMAN-ANTIBODIES TO HIV-1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 SCRIPPS RES INST, LA JOLLA, CA USA. CALIF INST PUBL HLTH, BERKELEY, CA USA. NIAID, BETHESDA, MD 20892 USA. NCI, FREDERICK, MD 21701 USA. AARON DIAMOND AIDS RES CTR, NEW YORK, NY USA. KAROLINSKA INST, S-10401 STOCKHOLM, SWEDEN. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400581 ER PT J AU SHUSTER, S THOR, AD SMITH, HS MOORE, D STERN, R AF SHUSTER, S THOR, AD SMITH, HS MOORE, D STERN, R TI DEPOSITION OF HYALURONIDASE IS AN INDICATOR FOR FAVORABLE OUTCOME IN BREAST-CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 LAWRENCE LIVERMORE NATL LAB,LIVERMORE,CA 94550. UNIV CALIF SAN FRANCISCO,DEPT PATHOL,SAN FRANCISCO,CA 94143. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. CAL PAC MED CTR,BRUSH CANC RES INST,SAN FRANCISCO,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 244 EP 244 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400792 ER PT J AU HANASAKI, K VARKI, A STAMENKOVIC, I BEVILACQUA, MP AF HANASAKI, K VARKI, A STAMENKOVIC, I BEVILACQUA, MP TI CYTOKINE-INDUCED BETA-GALACTOSIDE ALPHA-2,6-SIALYL-TRANSFERASE IN HUMAN ENDOTHELIAL-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,HOWARD HUGHES MED INST,DEPT PATHOL,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,CTR CANC,GLYCOBIOL PROGRAM,LA JOLLA,CA 92093. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 277 EP 277 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400902 ER PT J AU CARR, MW ROTH, SJ ROSE, SS LUTHER, E SPRINGER, TA AF CARR, MW ROTH, SJ ROSE, SS LUTHER, E SPRINGER, TA TI ISOLATION AND CHARACTERIZATION OF MCP-1 AS A T-CELL CHEMOATTRACTANT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 296 EP 296 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400966 ER PT J AU ELBE, A REISER, H STRUNK, D STINGL, G AF ELBE, A REISER, H STRUNK, D STINGL, G TI FUNCTIONAL EXPRESSION OF THE COSTIMULATORY MOLECULE-B7 ON ACCESSORY CELLS FOR MHC CLASS I-RESTRICTED IMMUNE-RESPONSES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV VIENNA,SCH MED,VIRCC,DIAID,DEPT DERMATOL,A-1010 VIENNA,AUSTRIA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPH BIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 308 EP 308 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25400998 ER PT J AU RYAN, TC CRUIKSHANK, WW BURAKOFF, SJ COLLINS, TL SLECKMANN, BP CENTER, DM AF RYAN, TC CRUIKSHANK, WW BURAKOFF, SJ COLLINS, TL SLECKMANN, BP CENTER, DM TI CD4 MEDIATED T-LYMPHOCYTE CHEMOTAXIS REQUIRES THE PRESENCE BUT NOT THE ENZYMATIC-ACTIVITY OF THE TYROSINE KINASE, P56(1CK) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,BOSTON,MA 02118. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 345 EP 345 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401146 ER PT J AU WAGNER, N ENGEL, P VEGA, M TEDDER, TF AF WAGNER, N ENGEL, P VEGA, M TEDDER, TF TI SIGNAL-TRANSDUCTION THROUGH MHC CLASS-I AND CLASS-II MOLECULES LEADS TO POSITIVE AND NEGATIVE REGULATION OF HOMOTYPIC ADHESION IN HUMAN-LYMPHOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. UNIV AUTONOMA MADRID,HOP PRINCESA,SERV IMMUNOL,E-28006 MADRID,SPAIN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 412 EP 412 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401406 ER PT J AU KANTETI, V PRASAD, S CAI, YC RAAB, M DUCKWORTH, B CANTLEY, LC SHOELSON, SE RUDD, CE AF KANTETI, V PRASAD, S CAI, YC RAAB, M DUCKWORTH, B CANTLEY, LC SHOELSON, SE RUDD, CE TI CD28 ASSOCIATES WITH THE LIPID KINASE, PL3-KINASE VIA A CYTOPLASMIC PYMXM MOTIF SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. JOSLIN DIABET CTR,BOSTON,MA 02115. HARVARD UNIV,DEPT PATHOL,BOSTON,MA 02215. HARVARD UNIV,DEPT PHYSIOL,BOSTON,MA 02215. RI Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 428 EP 428 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401470 ER PT J AU LENSCHOW, DJ FREEMAN, G HODES, R COOKE, M ZENG, Y HATHCOCK, K GRAY, G THISTLETHWAITE, JR GOODNOW, C NADLER, LM BLUESTONE, JA AF LENSCHOW, DJ FREEMAN, G HODES, R COOKE, M ZENG, Y HATHCOCK, K GRAY, G THISTLETHWAITE, JR GOODNOW, C NADLER, LM BLUESTONE, JA TI B7-2, AND NOT B7-1(B7), IS THE PRIMARY COSTIMULATORY MOLECULE FOR T-CELL ACTIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CHICAGO,COMM IMMUNOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT SURG,CHICAGO,IL 60637. NIA,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. STANFORD UNIV,HOWARD HUGHES MED INST,STANFORD,CA 94305. REPLIGEN CORP,CAMBRIDGE,MA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 431 EP 431 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401479 ER PT J AU MILLER, JB SMITH, TH AF MILLER, JB SMITH, TH TI SOMITES, LINEAGES, AND DOMAINS OF MRF PROTEIN EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROMUSC LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 464 EP 464 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401602 ER PT J AU MILLER, JB KACHINSKY, AM AF MILLER, JB KACHINSKY, AM TI MYOGENESIS AND THE INTERMEDIATE FILAMENT PROTEIN, NESTIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROMUSCULAR LAB,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 480 EP 480 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401657 ER PT J AU NEVILLE, C PING, JA ROSENTHAL, N AF NEVILLE, C PING, JA ROSENTHAL, N TI DEVELOPMENTAL REGULATION OF A RAT MYOSIN LIGHT CHAIN-1 TRANSGENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. RI Rosenthal, Nadia/O-7009-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 480 EP 480 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401658 ER PT J AU STAINIER, DYR WEINSTEIN, BM FISHMAN, M AF STAINIER, DYR WEINSTEIN, BM FISHMAN, M TI ZEBRAFISH HEART DEVELOPMENT - A GENETIC APPROACH SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV SCH MED,BOSTON,MA 02129. MASSACHUSSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 483 EP 483 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401668 ER PT J AU BOGDANOVA, N GONG, XH ROSENTHAL, N AF BOGDANOVA, N GONG, XH ROSENTHAL, N TI EXPRESSION OF ZBU1, A HUMAN BRAHMA-RELATED GENE, IN NORMAL AND MALIGNANT-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSSETS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. RI Rosenthal, Nadia/O-7009-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1994 SU 18D BP 526 EP 526 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE254 UT WOS:A1994NE25401838 ER PT J AU IRIKURA, K MAYNARD, KI MOSKOWITZ, MA AF IRIKURA, K MAYNARD, KI MOSKOWITZ, MA TI IMPORTANCE OF NITRIC-OXIDE SYNTHASE INHIBITION TO THE ATTENUATED VASCULAR-RESPONSES INDUCED BY TOPICAL L-NITROARGININE DURING VIBRISSAL STIMULATION SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE NITRIC OXIDE; NITRIC OXIDE SYNTHASE; L-NITROARGININE; CORTICAL BARREL FIELDS; RCBF ID RELAXING FACTOR; L-ARGININE; INVITRO; RELEASE; BRAIN; RAT AB We assessed the regional cerebral blood flow (rCBF) response to vibrissal stimulation before and after nitric oxide synthase (NOS) inhibitors were topically applied through a closed cranial window placed over the cortical barrel fields in anesthetized Sprague-Dawley rats. In the presence of L-nitroarginine (1 mM), both the maximum and total responses became reduced, but only in those animals demonstrating >50% inhibition of NOS activity as determined by the conversion of [H-3]arginine to [H-3]citrulline within homogenates taken from cortical gray matter under the cranial window. The degree of enzyme inhibition depended in part, upon duration after topical application of NOS inhibitor. When >50%, enzyme inhibition correlated with the decrease in maximum and total rCBF response (p < 0.01). These findings emphasize the merits of assessing enzyme activity after administering NOS inhibitors, and suggest that NO generated from parenchymal NOS activity plays an important role in the cerebrovascular response to physiologic somatosensory stimulation under the stated conditions. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NS 10828] NR 16 TC 98 Z9 99 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1994 VL 14 IS 1 BP 45 EP 48 PG 4 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA MW236 UT WOS:A1994MW23600007 PM 7505281 ER PT J AU ROSENBLATT, S IRIKURA, K CADAY, CG FINKLESTEIN, SP MOSKOWITZ, MA AF ROSENBLATT, S IRIKURA, K CADAY, CG FINKLESTEIN, SP MOSKOWITZ, MA TI BASIC FIBROBLAST GROWTH-FACTOR DILATES RAT PIAL ARTERIOLES SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE BASIC FIBROBLAST GROWTH FACTOR; N-G-NITRO-L-ARGININE METHYL ESTER (L-NAME); CRANIAL WINDOW; PIAL ARTERIOLES; VASODILATION ID FACTOR BFGF; BRAIN; NEURONS; FGF; ANGIOGENESIS; DEGENERATION; LOCALIZATION; TRANSECTION; SYSTEM AB Basic fibroblast growth factor (bFGF) is a polypeptide that promotes the survival and differentiation of brain neurons, glia, and endothelial cells. It has been shown recently that intravenously administered bFGF lowers blood pressure by systemic vasodilation; this effect is mediated, in part, by nitric oxide (NO)-dependent mechanisms. In the current study, we directly evaluated the effect of bFGF on pial arterioles of pentobarbital-anesthetized Sprague-Dawley rats (n = 18) using the closed cranial window technique. Basic FGF (5-200 ng/ml) produced dose-dependent vasodilation; maximal vessel diameter (similar to 120% of control) was reached at 100 ng/ml. No vasodilation was found when bFGF was heat inactivated, or preincubated with blocking antibody. Moreover, bFGF-induced vasodilation was attenuated by coadministration of the NO synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME), consistent with an NO-dependent mechanism. These results suggest that bFGF may play an important role in the regulation of cerebrovascular tone and cerebral blood flow. C1 MASSACHUSETTS GEN HOSP,STROKE RES LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,CNS GROWTH FACTOR RES LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. HARVARD MED SCH,BOSTON,MA. RI Moskowitz, Michael/D-9916-2011 FU NIA NIH HHS [AG08207]; NINDS NIH HHS [NS10828] NR 36 TC 74 Z9 80 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1994 VL 14 IS 1 BP 70 EP 74 PG 5 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA MW236 UT WOS:A1994MW23600011 PM 8263060 ER PT J AU RAYMOND, GV HOLMES, LB AF RAYMOND, GV HOLMES, LB TI HEAD CIRCUMFERENCE STANDARDS IN NEONATES SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID FETAL GROWTH; GESTATIONAL-AGE; BIRTH-WEIGHT; INFANTS; SIZE AB Head circumference at birth is an important measure of intrauterine growth, reflecting accurately brain growth and predicting subsequent development. Standards need to reflect the population and the factors that affect intrauterine growth in the population and must be constructed in a manner that is clinically useful and predictive. Many of the present standards used to assess newborn infants are inadequate because of the limitations of sample size and study design. As a result, the current standards are not adequate for premature infants below 30 weeks of gestation and, in newborns from later in gestation, may underreport significant deviations from the mean in certain situations. C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,EMBRYOL TERATOL UNIT,BOSTON,MA 02114. FU NINDS NIH HHS [R01 NS24125, R01 NS26093]; PHS HHS [24125] NR 22 TC 11 Z9 11 U1 0 U2 1 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD JAN PY 1994 VL 9 IS 1 BP 63 EP 66 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA MP947 UT WOS:A1994MP94700016 PM 8151087 ER PT J AU CAI, WY ALEXANDER, JM HEDLEYWHYTE, ET SCHEITHAUER, BW JAMESON, JL ZERVAS, NT KLIBANSKI, A AF CAI, WY ALEXANDER, JM HEDLEYWHYTE, ET SCHEITHAUER, BW JAMESON, JL ZERVAS, NT KLIBANSKI, A TI RAS MUTATIONS IN HUMAN PROLACTINOMAS AND PITUITARY CARCINOMAS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID TUMORS; ONCOGENES; ADENOMAS; DNA; TUMORIGENESIS; ABNORMALITIES; CANCERS; BENIGN; GS AB Pituitary adenomas have been shown to be clonal in origin, indicating that one or more somatic mutations underlie tumor pathogenesis. Mutated oncogenic forms of ras protein have been identified in a number of human neoplasms, including thyroid adenomas and carcinomas. However, the potential role of activated res in the development of specific human pituitary tumor phenotypes has not been determined. Although ras mutations were not found in glycoprotein hormone-secreting or somatotroph adenomas, we recently identified a mutation in the H-ras gene (Gly-Val) at codon 12 in a highly invasive prolactinoma. These data raise the possibility that res mutations might play a role in the pathogenesis of PRL-secreting pituitary tumors and/or may be a marker for tumor invasiveness and malignant transformation. Therefore, we investigated 78 pituitary tumors (59 prolactinomas, 13 invasive prolactinomas, and 6 pituitary carcinomas) for activating point mutation in the three res genes using oligonucleotide-specific hybridization. In contrast to the relatively high frequency of res mutations in many different tumor types, no ras mutations were identified in either prolactinomas or pituitary carcinomas. Our data indicate that res mutations are rare in prolactinomas and pituitary carcinomas. Clin Endocrinol Meteb 78: 89-93, 1994) C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, NEUROENDOCRINE UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT PATHOL, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, THYROID UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT NEUROSURG, BOSTON, MA 02114 USA. MAYO CLIN, DEPT PATHOL, ROCHESTER, MN 55905 USA. OI Jameson, James/0000-0001-9538-4059 FU NIDDK NIH HHS [DK-40947] NR 23 TC 82 Z9 84 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 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1994 VL 78 IS 1 BP 89 EP 93 DI 10.1210/jc.78.1.89 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MR054 UT WOS:A1994MR05400019 PM 8288721 ER PT J AU MEIER, CA BRAVERMAN, LE EBNER, SA VERONIKIS, I DANIELS, GH ROSS, DS DERASKA, DJ DAVIES, TF VALENTINE, M DEGROOT, LJ CURRAN, P MCELLIN, K REYNOLDS, J ROBBINS, J WEINTRAUB, BD AF MEIER, CA BRAVERMAN, LE EBNER, SA VERONIKIS, I DANIELS, GH ROSS, DS DERASKA, DJ DAVIES, TF VALENTINE, M DEGROOT, LJ CURRAN, P MCELLIN, K REYNOLDS, J ROBBINS, J WEINTRAUB, BD TI DIAGNOSTIC USE OF RECOMBINANT HUMAN THYROTROPIN IN PATIENTS WITH THYROID-CARCINOMA (PHASE I/II STUDY) SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID TRIIODOTHYRONINE WITHDRAWAL; SERUM THYROGLOBULIN; CANCER; CELLS AB Current diagnostic studies [radioiodine uptake and serum thyroglobulin (Tg) levels] for residual or metastatic thyroid tissue in patients with differentiated thyroid carcinoma require a hypothyroid status necessary for adequate endogenous TSH stimulation. However, almost all patients have symptoms of clinical hypothyroidism during this period. As shown in the present study, recombinant human TSH (rhTSH) allows stimulation of I-131 uptake and Tg release from residual thyroid tissue in euthyroid patients. To assess safety, dosage, and preliminary efficacy, comparison was made of the stimulation of I-131 uptake and Tg release after rhTSH administration and after T-3 Withdrawal in 19 patients after a recent thyroidectomy for differentiated thyroid carcinoma. Various doses (10-40 U) of rhTSH were injected im for 1-3 days in patients receiving suppressive doses of T-3. Twenty-four hours after the last dose of rhTSH, 1-2 mCi I-131 were administered, followed by a neck and whole body scan 48 h later. After discontinuing T-3 for a median period of 19 days (range, 15-28), endogenous serum TSH levels were markedly elevated, and the patients were given a second dose of I-131 and rescanned 48 h later. The injections of rhTSH were tolerated well. No major adverse effects were reported; nausea was reported in 3 (16%) and vomiting in 1 of the patients treated with high doses. The quality of life, as measured by two psychometric scales, was far better during rhTSH treatment than after T-3 withdrawal. The peak levels of serum TSH (mean +/- so) after a single dose of 10, 20, or 30 U were 127 +/- 19, 309 +/- 156, and 510 +/- 156 mU/L, respectively, and occurred 2-8 h after injection. Twenty-four hours after the injection, TSH levels decreased to 83 +/- 31, 173 +/- 73, and 463 +/- 148 mU/L in these treatment groups, respectively. The quality of the thyroid scans and the number of sites of abnormal I-131 uptake were similar after rhTSH treatment and in the hypothyroid scans in 12 (63%) patients. Two additional sites of uptake in the chest and one in the thyroid bed, not visible on the hypothyroid scans, were identified in 3 (16%) patients after rhTSH. In 1 patient a focus of uptake was better visualized after rhTSH than after withdrawal. In 3 (16%) other patients, 1 lesion in the chest and 2 in the neck were seen only after T-3 withdrawal. The amount of radioiodine uptake in the thyroid bed was lower after rhTSH in 68% of patients; however, the uptake was similar to that measured after T-3 withdrawal when corrected for the increased whole body retention of I-131 during hypothyroidism. Serum Tg levels increased more than 2-fold in response to rhTSH in 73% (11 of 15) of the patients who also had a greater than 2-fold elevation of Tg after T-3 withdrawal. However, the increase was quantitatively lower after rhTSH in 93% (14 of 15) of the patients. In conclusion, rhTSH shows promise in humans as a safe and effective method to stimulate I-131 uptake and Tg secretion without the disadvantages of induced hypothyroidism. A phase III trial is required to definitely demonstrate efficacy. C1 NIDDKD, BETHESDA, MD USA. NIH, DEPT NUCL MED, BETHESDA, MD 20892 USA. UNIV MASSACHUSETTS, MED CTR, DIV ENDOCRINOL & METAB, WORCESTER, MA 01655 USA. MASSACHUSETTS GEN HOSP, THYROID UNIT, BOSTON, MA 02114 USA. MT SINAI SCH MED, DIV ENDOCRINOL & METAB, NEW YORK, NY 10029 USA. UNIV CHICAGO, MED CTR, THYROID STUDY UNIT, CHICAGO, IL 60637 USA. GENZYME CORP, CAMBRIDGE, MA 01239 USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU NIDDK NIH HHS [NIDDK DK-18919] NR 41 TC 199 Z9 203 U1 1 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1994 VL 78 IS 1 BP 188 EP 196 DI 10.1210/jc.78.1.188 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MR054 UT WOS:A1994MR05400037 PM 8288703 ER PT J AU SAMUELS, MH LUTHER, M HENRY, P RIDGWAY, EC AF SAMUELS, MH LUTHER, M HENRY, P RIDGWAY, EC TI EFFECTS OF HYDROCORTISONE ON PULSATILE PITUITARY GLYCOPROTEIN-SECRETION SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; FOLLICLE-STIMULATING-HORMONE; LUTEINIZING-HORMONE; CUSHINGS-SYNDROME; THYROTROPIN SECRETION; THYROID-FUNCTION; ALPHA-SUBUNIT; TSH SECRETION; GONADOTROPIN-SECRETION; PLASMA TESTOSTERONE AB During states of stress, hypothalamic-pituitary-thyroid and hypothalamic-pituitary-gonadal function can be suppressed. One putative mediator of this stress response may be glucocorticoids, which have widespread effects on thyroid and gonadal function. To characterize dynamic pituitary glycoprotein secretion during glucocorticoid administration, 24-h TSH, LH, FSH, and ol-subunit pulses were measured in 10 healthy young subjects on 3 occassions: 1) at baseline, 2) during infusions of 100 mg hydrocortisone (HC) over 24 h, and 3) during infusions of 300 mg HC over 24 h. These HC infusions led to serum cortisol levels similar to the endogenous cortisol levels seen in moderate and severe stress. Both HC infusions had profound rapid effects on TSH levels, decreasing TSH pulse amplitude by 60% and abolishing the nocturnal TSH surge. However, TSH pulse frequency was unaltered. In contrast, HC infusions did not change mean or pulsatile LH, FSH, or alpha-subunit secretion. These results suggest that stress levels of cortisol acutely suppress TSH secretion at the pituitary level, with little effect on the TSH pulse generator. On the other hand, the effects of stress and/or hypercortisolism on the gonadal axis may require higher cortisol levels, more prolonged exposure, or other mediators of the stress response. C1 AUDIE L MURPHY MEM VET ADM MED CTR, RES SERV, SAN ANTONIO, TX 77030 USA. UNIV COLORADO, HLTH SCI CTR, DIV ENDOCRINOL, DENVER, CO 80262 USA. RP SAMUELS, MH (reprint author), OREGON HLTH SCI UNIV, DIV ENDOCRINOL L607, 3181 SW SAM JACKSON PK RD, PORTLAND, OR 97201 USA. FU NCRR NIH HHS [MO1-RR-00051] NR 44 TC 52 Z9 52 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 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1994 VL 78 IS 1 BP 211 EP 215 DI 10.1210/jc.78.1.211 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MR054 UT WOS:A1994MR05400040 PM 8288706 ER PT J AU KANAI, Y LEE, WS YOU, GF BROWN, D HEDIGER, MA AF KANAI, Y LEE, WS YOU, GF BROWN, D HEDIGER, MA TI THE HUMAN KIDNEY LOW-AFFINITY NA+/GLUCOSE COTRANSPORTER SGLT2 - DELINEATION OF THE MAJOR RENAL REABSORPTIVE MECHANISM FOR D-GLUCOSE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE GLUCOSE TRANSPORT; HUMAN KIDNEY; LOW AFFINITY TRANSPORT; GLYCOSURIA; DIABETES ID HUMAN INTESTINAL NA+/GLUCOSE; PROXIMAL TUBULE; SODIUM; TRANSPORT; CELLS; HETEROGENEITY; STOICHIOMETRY; LOCALIZATION; EXPRESSION; VESICLES AB The major reabsorptive mechanism for D-glucose in the kidney is known to involve a low affinity high capacity Na+/glucose cotransporter, which is located in the early proximal convoluted tubule segment S1, and which has a Na+ to glucose coupling ratio of 1:1. Here we provide the first molecular evidence for this renal D-glucose reabsorptive mechanism. We report the characterization of a previously cloned human kidney cDNA that codes for a protein with 59% identity to the high affinity Na+/glucose cotransporter (SGLT1). Using expression studies with Xenopus laevis oocytes we demonstrate that this protein (termed SGLT2) mediates saturable Na+-dependent and phlorizin-sensitive transport of D-glucose and alpha-methyl-D-glucopyranoside (alpha MeGlc) with K-m values of 1.6 mM for alpha MeGle and similar to 250 to 300 mM for Na+, consistent with low affinity Na+/glucose cotransport. In contrast to SGLT1, SGLT2 does not transport D-galactose. By comparing the initial rate of [14C]-alpha MeGIc uptake with the Na+-influx calculated from alpha MeGlc-evoked inward currents, we show that the Naf to glucose coupling ratio of SGLT2. is 1:1. Using combined in situ hybridization and immunocytochemistry with tubule segment specific marker antibodies, we demonstrate an extremely high level of SGLT2 message in proximal tubule S1 segments. This level of expression was also evident on Northern blots and likely confers the high capacity of this glucose transport system. We conclude that SGLT2 has properties characteristic of the renal low affinity high capacity Na+/glucose cotransporter as previously reported for perfused tubule preparations and brush border membrane vesicles. Knowledge of the structural and functional properties of this major renal Na+/glucose reabsorptive mechanism will advance our understanding of the pathophysiology of renal diseases such as familial renal glycosuria and diabetic renal disorders. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV RENAL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02215. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL UNIT,BOSTON,MA 02114. FU NIDDK NIH HHS [DK-42956, DK-43171, DK-43632] NR 41 TC 338 Z9 355 U1 4 U2 22 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1994 VL 93 IS 1 BP 397 EP 404 DI 10.1172/JCI116972 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MY159 UT WOS:A1994MY15900051 PM 8282810 ER PT J AU FISHMAN, JA ROTH, RS ZANZOT, E ENOS, EJ FERRARO, MJ AF FISHMAN, JA ROTH, RS ZANZOT, E ENOS, EJ FERRARO, MJ TI USE OF INDUCED SPUTUM SPECIMENS FOR MICROBIOLOGIC DIAGNOSIS OF INFECTIONS DUE TO ORGANISMS OTHER THAN PNEUMOCYSTIS-CARINII SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; PNEUMONIA; ASPERGILLOSIS; TUBERCULOSIS AB The optimal diagnostic approach to pneumonia provides a rapid microbiologic identification of pulmonary pathogens by the least invasive means. The technique of sputum induction has been useful in the evaluation of patients with Pneumocystis carinii or mycobacterial pneumonia. It is not known whether induced sputum samples are preferable for the detection of pathogens other than P. carinii or mycobacteria. Microbiologic yields were evaluated from identically processed induced and conventional sputum samples collected from 509 consecutive patients. No statistically significant differences were found between the microbiologic yields of induced and spontaneous sputum samples. Bacterial pathogens were isolated in 19.6% of induced and 23.5% of routine specimens. Mycobacteria were cultured from 13.1% of routine and 9.4% of induced specimens. Non-Candida albicans fungi grew from 24% of routine and 20% of induced specimens. The process of sputum induction with aerosolized hypertonic saline did not alter either the purulence or the bacterial quantitation of Gram-stained sputum specimens. Sputum induction has been useful for the cytologic diagnosis of malignancy, for the diagnosis of pneumocystosis and tuberculosis, and in patients unable to spontaneously produce sputum samples. The use of induced sputum samples for the diagnosis of other infections may not be necessary when routine sputum specimens are available. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MICROBIOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. NR 22 TC 27 Z9 29 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1994 VL 32 IS 1 BP 131 EP 134 PG 4 WC Microbiology SC Microbiology GA MP316 UT WOS:A1994MP31600024 PM 8126167 ER PT J AU JORGENSEN, JH FERRARO, MJ MCELMEEL, ML SPARGO, J SWENSON, JM TENOVER, FC AF JORGENSEN, JH FERRARO, MJ MCELMEEL, ML SPARGO, J SWENSON, JM TENOVER, FC TI DETECTION OF PENICILLIN AND EXTENDED-SPECTRUM CEPHALOSPORIN RESISTANCE AMONG STREPTOCOCCUS-PNEUMONIAE CLINICAL ISOLATES BY USE OF THE E-TEST SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID UNITED-STATES; ANTIMICROBIAL RESISTANCE; HAEMOPHILUS-INFLUENZAE; BROTH MICRODILUTION; SUSCEPTIBILITY; MENINGITIS; PNEUMOCOCCI; ANTIBIOTICS; BACTERIA; FAILURE AB Increasing penicillin resistance and the initial recognition of resistance to extended-spectrum cephalosporins among Streptococcus pneumoniae isolates have placed greater emphasis on accurate methods for susceptibility testing of clinical isolates. This study has evaluated the use of the E test (AB Biodisk NA, Piscataway, N.J.) for the detection of penicillin and cefotaxime resistance among 147 pneumococcal clinical isolates in three geographically separate laboratories. These included 42 penicillin-resistant (MIC, greater-than-or-equal-to 2 mug/ml) and 14 cefotaxime-resistant (defined here as an MIC of greater-than-or-equal-to 2 mug/ml) isolates. E test strips were applied to the surface of Mueller-Hinton sheep blood agar plates and incubated at 35-degrees-C in 5% CO2 for 20 to 24 h. E test MICs were compared with MICs determined with lysed horse blood-supplemented Mueller-Hinton broth in a microdilution format as recommended by the National Committee for Clinical Laboratory Standards. Penicillin MICs agreed within one log2 dilution for 136 of 147 (92.5%) isolates, and cefotaxime MICs agreed within one log2 dilution for 142 of 147 (%.6%) isolates. No very major or major interpretive errors occurred with either penicillin or cefotaxime E test MIC results. There were 9.5 and 5.4% minor interpretive category errors with penicillin and cefotaxime E test MICs, respectively. These data indicate that the E test represents a convenient and reliable method for the detection of penicillin or cephalosporin resistance in pneumococci. C1 MASSACHUSETTS GEN HOSP,MICROBIOL LAB,BOSTON,MA 02114. CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,HOSP INFECT PROGRAM,ATLANTA,GA 30333. RP JORGENSEN, JH (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284, USA. NR 26 TC 108 Z9 108 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1994 VL 32 IS 1 BP 159 EP 163 PG 5 WC Microbiology SC Microbiology GA MP316 UT WOS:A1994MP31600030 PM 8126173 ER PT J AU KILBRIDGE, KL KANTOFF, P AF KILBRIDGE, KL KANTOFF, P TI INTRAVESICAL THERAPY FOR SUPERFICIAL BLADDER-CANCER - IS IT A WASH SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID PROGRESSION; RECURRENCE; CARCINOMA; TUMORS; GRADE C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. RP KILBRIDGE, KL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 17 TC 13 Z9 13 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 JAN PY 1994 VL 12 IS 1 BP 1 EP 4 PG 4 WC Oncology SC Oncology GA MQ109 UT WOS:A1994MQ10900001 PM 8270966 ER PT J AU AYASH, LJ ELIAS, A WHEELER, C REICH, E SCHWARTZ, G MAZANEF, R TEPLER, I WARREN, D LYNCH, C GONIN, R SCHNIPPER, L FREI, E ANTMAN, K AF AYASH, LJ ELIAS, A WHEELER, C REICH, E SCHWARTZ, G MAZANEF, R TEPLER, I WARREN, D LYNCH, C GONIN, R SCHNIPPER, L FREI, E ANTMAN, K TI DOUBLE DOSE-INTENSIVE CHEMOTHERAPY WITH AUTOLOGOUS MARROW AND PERIPHERAL-BLOOD PROGENITOR-CELL SUPPORT FOR METASTATIC BREAST-CANCER - A FEASIBILITY STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ALKYLATING-AGENTS; INVITRO; TRANSPORT; CYCLOPHOSPHAMIDE; INTENSIFICATION; TRANSPLANTATION; CARBOPLATIN; COMBINATION; RESISTANCE; MELPHALAN C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP AYASH, LJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [P01-CA-38493] NR 27 TC 132 Z9 133 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 JAN PY 1994 VL 12 IS 1 BP 37 EP 44 PG 8 WC Oncology SC Oncology GA MQ109 UT WOS:A1994MQ10900007 PM 7505807 ER PT J AU FALKSON, G GELMAN, R GLICK, J FALKSON, CI HARRIS, J AF FALKSON, G GELMAN, R GLICK, J FALKSON, CI HARRIS, J TI REINDUCTION WITH THE SAME CYTOSTATIC TREATMENT IN PATIENTS WITH METASTATIC BREAST-CANCER - AN EASTERN-COOPERATIVE-ONCOLOGY-GROUP STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV PENN,CTR CANC,PHILADELPHIA,PA 19104. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. RP FALKSON, G (reprint author), UNIV PRETORIA,DEPT MED ONCOL,POB 667,PRETORIA 0001,SOUTH AFRICA. FU NCI NIH HHS [CA 23318, CA 15488, CA 21692] NR 7 TC 12 Z9 12 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 JAN PY 1994 VL 12 IS 1 BP 45 EP 49 PG 5 WC Oncology SC Oncology GA MQ109 UT WOS:A1994MQ10900008 PM 8270982 ER PT J AU TALCOTT, JA WHALEN, A CLARK, J RIEKER, PP FINBERG, R AF TALCOTT, JA WHALEN, A CLARK, J RIEKER, PP FINBERG, R TI HOME ANTIBIOTIC-THERAPY FOR LOW-RISK CANCER-PATIENTS WITH FEVER AND NEUTROPENIA - A PILOT-STUDY OF 30 PATIENTS BASED ON A VALIDATED PREDICTION RULE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID GRANULOCYTOPENIC PATIENTS; FEBRILE; IDENTIFICATION; COMBINATION C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV CLIN EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP TALCOTT, JA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU NCI NIH HHS [CA01418] NR 18 TC 164 Z9 165 U1 1 U2 3 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 JAN PY 1994 VL 12 IS 1 BP 107 EP 114 PG 8 WC Oncology SC Oncology GA MQ109 UT WOS:A1994MQ10900018 PM 8270967 ER PT J AU DAVAR, G KRAMER, MF GARBER, D ROCA, AL ANDERSEN, JK BEBRIN, W COEN, DM KOSZVNENCHAK, M KNIPE, DM BREAKEFIELD, XO ISACSON, O AF DAVAR, G KRAMER, MF GARBER, D ROCA, AL ANDERSEN, JK BEBRIN, W COEN, DM KOSZVNENCHAK, M KNIPE, DM BREAKEFIELD, XO ISACSON, O TI COMPARATIVE EFFICACY OF EXPRESSION OF GENES DELIVERED TO MOUSE SENSORY NEURONS WITH HERPES-VIRUS VECTORS SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE TRIGEMINAL GANGLION; HERPES SIMPLEX VIRUS; PAIN ID LATENCY-ASSOCIATED TRANSCRIPT; CENTRAL-NERVOUS-SYSTEM; SIMPLEX VIRUS; BETA-GALACTOSIDASE; TRIGEMINAL GANGLION; THYMIDINE KINASE; INFECTED NEURONS; INSITU HYBRIDIZATION; ENOLASE PROMOTER; AXONAL-TRANSPORT AB To achieve gene delivery to sensory neurons of the trigeminal ganglion, thymidine kinase-negative (TK-) herpes simplex viruses (HSV) containing the reporter gene lacZ (the gene for E. coli beta-galactosidase) downstream of viral (in vectors RH116 and tkLTRZ1) or mammalian (in vector NSE-lacZ-tk) promoters were inoculated onto mouse cornea and snout. Trigeminal ganglia were removed 4, 14, 30, and 60 days after inoculation with vectors and histochemically processed with 5-bromo-4-chloro-3 indolyl-beta-galactoside (X-Gal). With vector tk LTRZ 1, large numbers of labeled neurons were observed in rostromedial and central trigeminal ganglion at 4 days after inoculation. A gradual decline in the number of labeled neurons was observed with this vector at subsequent time points. With vectors RH116 and NSE-lacZ-tk, smaller numbers of labeled neurons were seen at 4 days following inoculation than were observed with vector tk LTRZ 1. No labeled neurons could be observed at 14 days after inoculation with vectors RH 1 16 and NSE-lacZ-tk. Immunocytochemistry for E. coli beta-galactosidase and in situ hybridization to HSV latency-associated transcripts revealed labeled neurons in regions of the trigeminal ganglion similar to that observed with X-Gal staining. A comparable distribution of labeled neurons in trigeminal ganglion was also observed after application of the retrograde tracer Fluoro-Gold to mouse cornea and snout. These data provide evidence that retrogradely transported tk- herpes virus vectors can be used to deliver a functional gene to sensory neurons in vivo in an anatomically predictable fashion. (C) 1994 Wiley-Liss, Inc. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MCLEAN HOSP,BELMONT,MA 02178. FU NCCIH NIH HHS [AT24010]; NINDS NIH HHS [1KO8NS01497, NS29178] NR 48 TC 51 Z9 51 U1 1 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JAN 1 PY 1994 VL 339 IS 1 BP 3 EP 11 DI 10.1002/cne.903390103 PG 9 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA ML658 UT WOS:A1994ML65800002 PM 8106660 ER PT J AU TORCHILIN, VP TRUBETSKOY, VS MILSHTEYN, AM CANILLO, J WOLF, GL PAPISOV, MI BOGDANOV, AA NARULA, J KHAW, BA OMELYANENKO, VG AF TORCHILIN, VP TRUBETSKOY, VS MILSHTEYN, AM CANILLO, J WOLF, GL PAPISOV, MI BOGDANOV, AA NARULA, J KHAW, BA OMELYANENKO, VG TI TARGETED DELIVERY OF DIAGNOSTIC AGENTS BY SURFACE-MODIFIED LIPOSOMES SO JOURNAL OF CONTROLLED RELEASE LA English DT Article; Proceedings Paper CT 6th International Symposium on Recent Advances in Drug Delivery Systems CY FEB 21-24, 1993 CL SALT LAKE CITY, UT SP 3M PHARM, BAXTER HEALTHCARE COMP, CIBA GEIGY PHARM DIV, DUPONT MERCK PHARM CO, HOFFMANN LA ROCHE INC, LOHMANN THERAPIE SYST GMBH & CO, PHARMA DELIVERY SYST INC, SAM YANG CO LTD, SHISEIDO RES CTR, SMITHKLINE BEECHAM PHARM, TEKEDA CHEM IND LTD, THERATECH INC, UPJOHN CO, YAMANOUCHI PHARM CO LTD DE LONG-CIRCULATING IMMUNOLIPOSOME; POLYETHYLENE GLYCOL; HEAVY METAL CHELATOR; MYOCARDIAL INFARCTION GAMMA-SCINTIGRAPHY; LYMPH NODE NMR-IMAGING ID GADOLINIUM-LABELED LIPOSOMES; STERICALLY STABILIZED LIPOSOMES; CONTRAST ENHANCEMENT AGENTS; GD-DTPA DERIVATIVES; CIRCULATION TIME; UNILAMELLAR LIPOSOMES; LIVER; INVIVO; IMMUNOLIPOSOMES; CLEARANCE AB Surface-modified LS have been used for the specific delivery of heavy metal-based imaging agents. The liposome surface was modified with PEG, AMmAb, Dext-SA, chelating agent DTPA-PE, and with NGPE-modified chelating polymer: DTPA-NPLL-NGPE. The hypothesis is suggested attempting to explain the phenomenon of long circulation of PEG-coated LS from the point of view of statistical propel-ties of flexible polymer molecule in solution. Direct experiments using fluorescent labels were performed to prove the hypothesis. The calculations performed on the basis of the hypothesis were designed to find the optimal concentration of PEG on the LS surface, and suggested that it not only provides a protective effect but also does not create steric hindrances for the surface-immobilized mAb. As a result, long circulating targeted ILS have been prepared. Intravenously administered In-111-labelled PEG-AMmAb-LS were targeted to the area of experimental myocardial infarction in rabbits under gamma-scintigraphic control. Infarct-to-normal ratios of In-111 radioactivity of about 20 were achieved. PEG-and Dext-modified liposomes with surface-incorporated Gd-labelled DTPA-PE or DTPA-NPLL-NGPE were used for the subcutaneous administration and subsequent NMR-imaging of lymph nodes in rabbits. Two mechanisms of MR-signal enhancement were found for the surface-modified Gd-containing LS: the increase in signal intensity due to the increase in water quantity in the vicinity of Gd atoms because of PEG-associated water; and better lymph node accumulation of Dext-LS via receptor-mediated endocytosis. Surface modification of LS opens the possibilitiy for targeted delivery of heavy metal-based imaging agents. C1 MASSACHUSETTS GEN HOSP EAST,CTR NMR,DEPT RADIOL,BOSTON,MA. NORTHEASTERN UNIV,CTR DRUG TARGETING & ANAL,BOSTON,MA. UNIV UTAH,DEPT PHARMACEUT,SALT LAKE CITY,UT. RP TORCHILIN, VP (reprint author), MASSACHUSETTS GEN HOSP EAST,CTR IMAGING & PHARMACEUT RES,DEPT RADIOL,149,13TH ST,BOSTON,MA 02129, USA. NR 43 TC 40 Z9 43 U1 1 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-3659 J9 J CONTROL RELEASE JI J. Control. Release PD JAN PY 1994 VL 28 IS 1-3 BP 45 EP 58 DI 10.1016/0168-3659(94)90152-X PG 14 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Chemistry; Pharmacology & Pharmacy GA NA912 UT WOS:A1994NA91200005 ER PT J AU STRONG, L LU, XM TOMPKINS, RG YARMUSH, ML AF STRONG, L LU, XM TOMPKINS, RG YARMUSH, ML TI BACTERIAL-CELL KILLING BY ANTIBODY-TARGETED PHOTOLYSIS - ENHANCED EFFECT BY OH RADICAL GENERATION SO JOURNAL OF CONTROLLED RELEASE LA English DT Article; Proceedings Paper CT 6th International Symposium on Recent Advances in Drug Delivery Systems CY FEB 21-24, 1993 CL SALT LAKE CITY, UT SP 3M PHARM, BAXTER HEALTHCARE COMP, CIBA GEIGY PHARM DIV, DUPONT MERCK PHARM CO, HOFFMANN LA ROCHE INC, LOHMANN THERAPIE SYST GMBH & CO, PHARMA DELIVERY SYST INC, SAM YANG CO LTD, SHISEIDO RES CTR, SMITHKLINE BEECHAM PHARM, TEKEDA CHEM IND LTD, THERATECH INC, UPJOHN CO, YAMANOUCHI PHARM CO LTD DE ANTIBODY-TARGETED CELL PHOTOLYSIS; BACTERIAL INFECTION; PHOTOGENERATED FREE-RADICAL TOXIN; TYPE I AND TYPE II PHOTOPROCESS ID NEUTRON-CAPTURE THERAPY; HYDROGEN-PEROXIDE; SINGLET OXYGEN; INVITRO; SUPEROXIDE; CARRIER; TOXIN AB Two structurally distinct immunoconjugates were used for photolysis of bacterial cells. One contained a dextran carbazate (DC) polymer as a linker between the photosensitizer molecules and the Fc oligosaccharide moiety of the monoclonal antibody, while the other linked the photosensitizer molecules and the Fc oligosaccharide by a short ethylenediamine (ED) spacer. The two immunoconjugates exhibited remarkably different photophysical properties and cell killing potential with respect to their abilities to generate singlet oxygen. The DC conjugate exhibited poor singlet oxygen ((1) Delta(g)) yields, yet was shown to produce more efficient cell killing on the basis of (1) Delta(g), dose than did the ED conjugate. In light of the enhanced cell killing capacity of the DC conjugate, a search for other toxic photoproducts was initiated. It was found that the DC conjugate was capable of generating hydroxyl radicals (OH.) upon light illumination. Quantum yields for OH. generation were evaluated. The DC-photosensitizer polymer appeared to initiate a cascade addition reaction presumably by adding peroxides and hydroperoxides to the glucose residues of the dextran carbazate linker. These results suggest that this radical formation could propagate down the DC polymer and account for the superior cell killing exhibited by the DC conjugate. C1 RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02115. SHRINERS BURN INST,BOSTON,MA 02114. NR 31 TC 5 Z9 5 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-3659 J9 J CONTROL RELEASE JI J. Control. Release PD JAN PY 1994 VL 28 IS 1-3 BP 175 EP 186 DI 10.1016/0168-3659(94)90164-3 PG 12 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Chemistry; Pharmacology & Pharmacy GA NA912 UT WOS:A1994NA91200017 ER PT J AU PAPISOV, MI WEISSLEDER, R SCHAFFER, B BOGDANOV, AA BRADY, TJ AF PAPISOV, MI WEISSLEDER, R SCHAFFER, B BOGDANOV, AA BRADY, TJ TI INTRAVENOUS CARRIERS FOR DRUG-DELIVERY TO LYMPH-NODES SO JOURNAL OF CONTROLLED RELEASE LA English DT Article; Proceedings Paper CT 6th International Symposium on Recent Advances in Drug Delivery Systems CY FEB 21-24, 1993 CL SALT LAKE CITY, UT SP 3M PHARM, BAXTER HEALTHCARE COMP, CIBA GEIGY PHARM DIV, DUPONT MERCK PHARM CO, HOFFMANN LA ROCHE INC, LOHMANN THERAPIE SYST GMBH & CO, PHARMA DELIVERY SYST INC, SAM YANG CO LTD, SHISEIDO RES CTR, SMITHKLINE BEECHAM PHARM, TEKEDA CHEM IND LTD, THERATECH INC, UPJOHN CO, YAMANOUCHI PHARM CO LTD C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP PAPISOV, MI (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 1 TC 5 Z9 6 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-3659 J9 J CONTROL RELEASE JI J. Control. Release PD JAN PY 1994 VL 28 IS 1-3 BP 293 EP 294 DI 10.1016/0168-3659(94)90186-4 PG 2 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Chemistry; Pharmacology & Pharmacy GA NA912 UT WOS:A1994NA91200039 ER PT J AU TRUBETSKOY, VS TORCHILIN, VP NARULA, J KHAW, BA AF TRUBETSKOY, VS TORCHILIN, VP NARULA, J KHAW, BA TI TARGETED CONJUGATE BETWEEN ANTIMYOSIN AND RADIOLABELED CHELATING POLYMER - INFLUENCE OF SINGLE-SITE FAB-POLYMER BOND ON THE CONJUGATE PERFORMANCE SO JOURNAL OF CONTROLLED RELEASE LA English DT Article; Proceedings Paper CT 6th International Symposium on Recent Advances in Drug Delivery Systems CY FEB 21-24, 1993 CL SALT LAKE CITY, UT SP 3M PHARM, BAXTER HEALTHCARE COMP, CIBA GEIGY PHARM DIV, DUPONT MERCK PHARM CO, HOFFMANN LA ROCHE INC, LOHMANN THERAPIE SYST GMBH & CO, PHARMA DELIVERY SYST INC, SAM YANG CO LTD, SHISEIDO RES CTR, SMITHKLINE BEECHAM PHARM, TEKEDA CHEM IND LTD, THERATECH INC, UPJOHN CO, YAMANOUCHI PHARM CO LTD C1 NORTHEASTERN UNIV,BOUWE COLL PHARM,CTR DRUG TARGETING & ANAL,BOSTON,MA 02115. RP TRUBETSKOY, VS (reprint author), MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BOSTON,MA 02129, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-3659 J9 J CONTROL RELEASE JI J. Control. Release PD JAN PY 1994 VL 28 IS 1-3 BP 295 EP 296 DI 10.1016/0168-3659(94)90187-2 PG 2 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Chemistry; Pharmacology & Pharmacy GA NA912 UT WOS:A1994NA91200040 ER PT J AU BOGDANOV, A WEISSLEDER, R TSAI, E SCHAFFER, B BOGDANOVA, A NOSSIFF, N PAPISOV, M BRADY, T AF BOGDANOV, A WEISSLEDER, R TSAI, E SCHAFFER, B BOGDANOVA, A NOSSIFF, N PAPISOV, M BRADY, T TI MACROMOLECULAR COMPLEXONE FOR DETECTION OF MICROVASCULATURE BY MAGNETIC-RESONANCE ANGIOGRAPHY SO JOURNAL OF CONTROLLED RELEASE LA English DT Article; Proceedings Paper CT 6th International Symposium on Recent Advances in Drug Delivery Systems CY FEB 21-24, 1993 CL SALT LAKE CITY, UT SP 3M PHARM, BAXTER HEALTHCARE COMP, CIBA GEIGY PHARM DIV, DUPONT MERCK PHARM CO, HOFFMANN LA ROCHE INC, LOHMANN THERAPIE SYST GMBH & CO, PHARMA DELIVERY SYST INC, SAM YANG CO LTD, SHISEIDO RES CTR, SMITHKLINE BEECHAM PHARM, TEKEDA CHEM IND LTD, THERATECH INC, UPJOHN CO, YAMANOUCHI PHARM CO LTD RP BOGDANOV, A (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MGH NMR CTR,DEPT RADIOL,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-3659 J9 J CONTROL RELEASE JI J. Control. Release PD JAN PY 1994 VL 28 IS 1-3 BP 325 EP 326 DI 10.1016/0168-3659(94)90200-3 PG 2 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Chemistry; Pharmacology & Pharmacy GA NA912 UT WOS:A1994NA91200053 ER PT J AU TANIISHII, N WANG, C STASHENKO, P AF TANIISHII, N WANG, C STASHENKO, P TI BONE RESORPTIVE CYTOKINE PRODUCTION IN INFLAMED PULP AND PERIAPICAL LESIONS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 KANAGAWA DENT COLL,YOKOSUKA,JAPAN. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 119 EP 119 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500144 ER PT J AU STASHENKO, P WANG, C WU, Y OSTROFF, G NIEDERMAN, R AF STASHENKO, P WANG, C WU, Y OSTROFF, G NIEDERMAN, R TI INHIBITION OF PERIAPICAL BONE-RESORPTION BY A BIOLOGICAL RESPONSE MODIFIER SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. ALPHA BETA TECHNOL,WORCESTER,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 120 EP 120 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500149 ER PT J AU WANG, CY TANIISHII, N STASHENKO, P AF WANG, CY TANIISHII, N STASHENKO, P TI OSTEOCLAST EXPRESSION OF INTERLEUKIN-1-ALPHA MESSENGER-RNA IN PERIAPICAL LESIONS BY IN-SITU HYBRIDIZATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 120 EP 120 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500145 ER PT J AU NARA, Y KATSUYAMA, S DOGON, IL AF NARA, Y KATSUYAMA, S DOGON, IL TI A COMPARISON OF THE ADHESION OF 2 NEW RESTORATIVE SYSTEMS TO DENTIN WITH WEDGE-SHAPED DEFECT SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIPPON DENT UNIV,NIIGATA,JAPAN. HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 4 Z9 4 U1 1 U2 2 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 130 EP 130 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500232 ER PT J AU SCHLUCKEBIER, SK SCHLESINGER, DH AHERN, JM HAY, DI AF SCHLUCKEBIER, SK SCHLESINGER, DH AHERN, JM HAY, DI TI CHARACTERIZATION OF NOVEL HUMAN SALIVARY ACIDIC PROLINE-RICH PROTEINS (PRPS) SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NYU MED CTR,NEW YORK,NY 10016. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 149 EP 149 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500384 ER PT J AU SPIELMAN, AI LEE, J KHURANA, P SRITHAVAJ, T BIVONA, P HAY, DI AF SPIELMAN, AI LEE, J KHURANA, P SRITHAVAJ, T BIVONA, P HAY, DI TI PURIFICATION OF A HUMAN SUBMANDIBULAR SUBLINGUAL ADHESION-PROMOTING PROTEIN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NYU,COLL DENT,NEW YORK,NY 10003. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 152 EP 152 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500401 ER PT J AU MAIDEN, MFJ SHEEHAN, M TANNER, A AF MAIDEN, MFJ SHEEHAN, M TANNER, A TI ANTIBIOTIC SENSITIVITIES AND PHENOTYPIC CHARACTERS OF BACTEROIDES-FORSYTHUS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 153 EP 153 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500413 ER PT J AU SMITH, DJ KING, WF IMELMANN, C AKITA, H TAUBMAN, MA AF SMITH, DJ KING, WF IMELMANN, C AKITA, H TAUBMAN, MA TI LONGITUDINAL ASSOCIATION OF SALIVARY IGA ANTIBODY AND INITIAL MUTANS STREPTOCOCCAL INFECTION IN CHILDREN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 153 EP 153 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500414 ER PT J AU SMITH, DJ IMELMANN, C KING, W TAUBMAN, MA AF SMITH, DJ IMELMANN, C KING, W TAUBMAN, MA TI CHARACTERISTICS OF SALIVARY IMMUNITY TO CHILDHOOD VACCINES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 1 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 153 EP 153 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500410 ER PT J AU EASTCOTT, JW TAUBMAN, MA SHIMAUCHI, H SMITH, DJ AF EASTCOTT, JW TAUBMAN, MA SHIMAUCHI, H SMITH, DJ TI EFFECT OF ADOPTIVE TRANSFER OF THE CLONE CELLS ON PERIODONTAL BONE LOSS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 159 EP 159 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500461 ER PT J AU DIBART, S SKOBE, Z SNAPP, K SOCRANSKY, SS SMITH, CM AF DIBART, S SKOBE, Z SNAPP, K SOCRANSKY, SS SMITH, CM TI DETECTION OF SUBGINGIVAL SPECIES ON OR IN CREVICULAR EPITHELIAL-CELLS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 161 EP 161 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500474 ER PT J AU SNAPP, KR MEYER, MC AF SNAPP, KR MEYER, MC TI INFLUENCE OF CYTOKINES ON THE ADHESION OF BACTERIA TO EPITHELIUM SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 162 EP 162 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500483 ER PT J AU SOCRANSKY, SS HAFFAJEE, AD DIBART, S SMITH, C MARTIN, L AF SOCRANSKY, SS HAFFAJEE, AD DIBART, S SMITH, C MARTIN, L TI FACTORS AFFECTING MICROBIAL RISK ASSESSMENT AT PERIODONTAL SITES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 188 EP 188 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500692 ER PT J AU AHERN, JM HAY, DI SCHLUCKEBIER, SK SCHLESINGER, DH AF AHERN, JM HAY, DI SCHLUCKEBIER, SK SCHLESINGER, DH TI PHENOTYPING AND QUANTIFICATION OF HUMAN SALIVARY ACIDIC PROLINE-RICH PROTEINS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NYU MED CTR,NEW YORK,NY 10016. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 192 EP 192 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500721 ER PT J AU JAINKITTIVONG, A YEH, CK JOHNSON, DA AF JAINKITTIVONG, A YEH, CK JOHNSON, DA TI SALIVARY HISTATIN LEVELS AND CANDIDA STATUS IN DENTURE PATIENTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 192 EP 192 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500728 ER PT J AU KAWAI, T TAUBMAN, MA SMITH, DJ EASTCOTT, JW AF KAWAI, T TAUBMAN, MA SMITH, DJ EASTCOTT, JW TI ROLE FOR T-LYMPHOCYTE BINDING TO FIBROBLASTS VIA VLA-4 IN MIGRATION TO GINGIVA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 204 EP 204 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500822 ER PT J AU ZHANG, J KASHKET, S VANHOUTE, J AF ZHANG, J KASHKET, S VANHOUTE, J TI PROLONGED ACCUMULATION OF FERMENTABLE SUGARS IN RETAINED FOOD PARTICLES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 206 EP 206 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500835 ER PT J AU SORKIN, BC LINDBERG, K NIEDERMAN, R AF SORKIN, BC LINDBERG, K NIEDERMAN, R TI CADHERIN EXPRESSION IN HUMAN GINGIVAL EPITHELIA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. BIOSURFACE TECHNOL,CAMBRIDGE,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 210 EP 210 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32500869 ER PT J AU BLAKEHASKINS, JC ZHANG, YP SULLIVAN, RJ AF BLAKEHASKINS, JC ZHANG, YP SULLIVAN, RJ TI EFFECT OF MFP DCPD AND NAF/SILICA DENTIFRICES ON THE CARIOGENIC POTENTIAL OF PLAQUE FLUID SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 COLGATE PALMOLIVE CO,CTR TECHNOL,PISCATAWAY,NJ 08854. FORSYTH DENT CTR,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 240 EP 240 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501106 ER PT J AU KELES, A STASHENKO, P AF KELES, A STASHENKO, P TI PHENOTYPIC ANALYSIS OF HUMAN OSTEOBLASTS AND FIBROBLASTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 242 EP 242 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501123 ER PT J AU CAVEDON, K COOKE, S BELCHER, J DEWHIRST, FE PASTER, BJ AF CAVEDON, K COOKE, S BELCHER, J DEWHIRST, FE PASTER, BJ TI IDENTIFICATION OF TREPONEMA SPECIES IN PERIODONTALLY-HEALTHY PLAQUE BY PCR AMPLIFICATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 249 EP 249 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501180 ER PT J AU FRASER, GJ CHAN, ECS SIBOO, R DEWHIRST, FE PASTER, BJ AF FRASER, GJ CHAN, ECS SIBOO, R DEWHIRST, FE PASTER, BJ TI PHYLOGENETIC POSITION OF NEW ORAL TREPONEMES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. MCGILL UNIV,MONTREAL H3A 2T5,QUEBEC,CANADA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 249 EP 249 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501176 ER PT J AU PASTER, BJ BELCHER, JC FRASER, GJ OLSEN, I DEWHIRST, FE AF PASTER, BJ BELCHER, JC FRASER, GJ OLSEN, I DEWHIRST, FE TI PHYLOGENY OF PORPHYROMONAS-CIRCUMDENTARIA, PORPHYROMONAS-SALIVOSA AND RELATED BACTERIA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 249 EP 249 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501181 ER PT J AU PETIT, MDA STASHENKO, P AF PETIT, MDA STASHENKO, P TI SAMPLING AND PROCESSING CONSIDERATIONS FOR IL-1-BETA GCF MEASUREMENTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 ACAD CTR DENT AMSTERDAM,AMSTERDAM,NETHERLANDS. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 258 EP 258 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501254 ER PT J AU TAKEICHI, O TAUBMAN, MA SMITH, DJ HABER, J MORO, I AF TAKEICHI, O TAUBMAN, MA SMITH, DJ HABER, J MORO, I TI ANALYSES OF CYTOKINE MESSAGE OF T-LYMPHOCYTES FROM ADULT PERIODONTITIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. TUFTS UNIV,BOSTON,MA 02111. NIHON UNIV,TOKYO 101,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 258 EP 258 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501255 ER PT J AU GOODSON, JM AF GOODSON, JM TI SYMPOSIUM - CONTROLLED DELIVERY APPLICATIONS IN ORAL-DISEASE THERAPY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 269 EP 269 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501337 ER PT J AU MENGSHOEL, K KASHKET, S DAGOSTINO, R STEPANIANS, M CANCRO, L AF MENGSHOEL, K KASHKET, S DAGOSTINO, R STEPANIANS, M CANCRO, L TI TEST OF A DENTIFRICE IN THE INTRAORAL DELTA-IP MODEL SYSTEM SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. CHESEBROUGH POND USA,TRUMBULL,CT. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 272 EP 272 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501363 ER PT J AU TINER, BD VANSICKELS, JE MCANEAR, JT CASMEDES, HP AF TINER, BD VANSICKELS, JE MCANEAR, JT CASMEDES, HP TI EFFECT OF MAXILLOMANDIBULAR ADVANCEMENT ON OBSTRUCTIVE SLEEP-APNEA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 285 EP 285 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501461 ER PT J AU TAVARES, M AF TAVARES, M TI SYMPOSIUM - FUTURE-DIRECTIONS IN ROOT CARIES RESEARCH SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 290 EP 290 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501505 ER PT J AU ANDERSEN, RN GANESHKUMAR, N KOLENBRANDER, PE AF ANDERSEN, RN GANESHKUMAR, N KOLENBRANDER, PE TI NUCLEOTIDE-SEQUENCE OF COAGGREGATION ADHESIN GENE, SCAA, FROM STREPTOCOCCUS-GORDONII PK488 SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 301 EP 301 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501592 ER PT J AU KIM, ES NICOLAY, O ISRAEL, H LAMSTER, I HEELEY, J HARDGRAVE, K AF KIM, ES NICOLAY, O ISRAEL, H LAMSTER, I HEELEY, J HARDGRAVE, K TI TMJ STRESS INDICATORS IN RABBITS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 COLUMBIA UNIV,NEW YORK,NY 10027. FORSYTH DENT CTR,BOSTON,MA 02115. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 303 EP 303 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501610 ER PT J AU KRESAK, M MORENO, EC HAY, DI AF KRESAK, M MORENO, EC HAY, DI TI ADSORPTION OF PROLINE-RICH SALIVARY PROTEINS PIF-S AND PIF-S(DP) ONTO HYDROXYAPATITE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 303 EP 303 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501605 ER PT J AU MARGOLIS, HC ZHANG, YP MORENO, EC AF MARGOLIS, HC ZHANG, YP MORENO, EC TI KINETICS OF ENAMEL DEMINERALIZATION AT LOW DRIVING FORCES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 303 EP 303 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501604 ER PT J AU MORENO, EC KRESAK, M GAFFAR, A AF MORENO, EC KRESAK, M GAFFAR, A TI ADSORPTION OF PEROXYDIPHOSPHATE ION ONTO HYDROXYAPATITE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. COLGATE PALMOLIVE CO,PISCATAWAY,NJ 08854. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 303 EP 303 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501608 ER PT J AU DRISKO, C COBB, C KILLOY, W LOWENGUTH, R PIHLSTROM, B ENCARNACION, M GOODSON, M AF DRISKO, C COBB, C KILLOY, W LOWENGUTH, R PIHLSTROM, B ENCARNACION, M GOODSON, M TI CLINICAL-RESPONSE TO TETRACYCLINE FIBER PERIODONTAL THERAPY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MISSOURI,COLUMBIA,MO 65201. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. EASTMAN DENT CTR,ROCHESTER,NY 14620. FORSYTH DENT CTR,BOSTON,MA 02115. ALZA CORP,COLUMBIA,MD. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 306 EP 306 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501631 ER PT J AU HAFFAJEE, AD SOCRANSKY, SS DIBART, S AF HAFFAJEE, AD SOCRANSKY, SS DIBART, S TI USE OF MICROBIAL PARAMETERS TO GUIDE PERIODONTAL THERAPY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 306 EP 306 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501629 ER PT J AU PIHLSTROM, B MICHALOWICZ, B COBB, C CATON, J GOODSON, J ENCARNACION, M AF PIHLSTROM, B MICHALOWICZ, B COBB, C CATON, J GOODSON, J ENCARNACION, M TI MAINTENANCE RESPONSE TO TETRACYCLINE PERIODONTAL FIBER THERAPY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MINNESOTA,MINNEAPOLIS,MN 55455. EASTMAN DENT CTR,ROCHESTER,NY 14620. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 306 EP 306 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501635 ER PT J AU LOWENGUTH, R CATON, J CHIN, I DRISKO, C COBB, C MICHALOWICZ, B PHILSTROM, B GOODSON, J AF LOWENGUTH, R CATON, J CHIN, I DRISKO, C COBB, C MICHALOWICZ, B PHILSTROM, B GOODSON, J TI EVALUATION OF VARIOUS TREATMENTS USING CONTROLLED-RELEASE TETRACYCLINE FIBERS - MICROBIOLOGICAL RESPONSE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 EASTMAN DENT CTR,ROCHESTER,NY 14620. FORSYTH DENT CTR,BOSTON,MA 02115. UNIV MISSOURI,ALZA CORP,COLUMBIA,MO 65201. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NR 0 TC 2 Z9 2 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 307 EP 307 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501636 ER PT J AU JAINKITTIVONG, A YEH, CK JOHNSON, DA AF JAINKITTIVONG, A YEH, CK JOHNSON, DA TI SALIVARY FUNCTION AND ORAL CANDIDA STATUS IN HEALTHY DENTURE PATIENTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT DIAGNOST SCI & COMMUNITY DENT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 336 EP 336 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501868 ER PT J AU DOBECK, JM HEELEY, JD SKOBE, Z PROSTAK, K VANHOUTE, H AF DOBECK, JM HEELEY, JD SKOBE, Z PROSTAK, K VANHOUTE, H TI DOUBLE-LABELING OF ODONTOPATHIC BACTERIA IN HUMAN TEETH SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 345 EP 345 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501941 ER PT J AU TANNER, A MAIDEN, MFJ SHULMAN, LH WEBER, HP KENT, RL AF TANNER, A MAIDEN, MFJ SHULMAN, LH WEBER, HP KENT, RL TI MICROBLOTA OF SYMPTOMATIC AND NON-SYMPTOMATIC DENTAL IMPLANTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. HARVARD UNIV,SCH PHYSIOL & PHARMACOL,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 345 EP 345 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501940 ER PT J AU WEISS, EI DOTAN, M METZGER, Z KOLENBRANDER, PE GANESHKUMAR, N AF WEISS, EI DOTAN, M METZGER, Z KOLENBRANDER, PE GANESHKUMAR, N TI ADHERENCE OF F-NUCLEATUM TO MAMMALIAN-CELLS AND TO PERIOPATHOGENIC BACTERIA INVOLVE SIMILAR MECHANISMS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TEL AVIV UNIV,IL-69978 TEL AVIV,ISRAEL. NIDR,BETHESDA,MD 20892. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 347 EP 347 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32501961 ER PT J AU TAVARES, M METERKO, M AF TAVARES, M METERKO, M TI A PATIENT SATISFACTION SURVEY FOR DENTAL IMPLANTS - RESULTS FROM A NATIONWIDE STUDY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 384 EP 384 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502257 ER PT J AU YASKELL, T KASHKET, S AF YASKELL, T KASHKET, S TI REDUCTION OF INTRAORAL DEMINERALIZATION BY SOLUBLE CALCIUM IN SOLID FOOD SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 415 EP 415 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502506 ER PT J AU PROSTAK, K SKOBE, Z AF PROSTAK, K SKOBE, Z TI EFFECTS OF FUROSEMIDE ON ANION TRANSLOCATION THROUGH THE ENAMEL ORGAN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 419 EP 419 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502531 ER PT J AU SMITH, DJ KING, WF TAUBMAN, MA CHANG, CJ AF SMITH, DJ KING, WF TAUBMAN, MA CHANG, CJ TI INHIBITION OF GLUCOSYITRANSFERASE ACTIVITY BY MONOCLONAL-ANTIBODY DIRECTED TO AN ACTIVE-SITE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 425 EP 425 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502586 ER PT J AU TAUBMAN, MA HOLMBERG, C EASTCOTT, JW SMITH, DJ AF TAUBMAN, MA HOLMBERG, C EASTCOTT, JW SMITH, DJ TI IMMUNIZATION OF RATS WITH SYNTHETIC PEPTIDES FROM CATALYTIC AND GLUCAN BINDING REGIONS OF MUTANS STREPTOCOCCAL GTF SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 425 EP 425 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502582 ER PT J AU MILLEMAN, JL PUTT, MS KLEBER, CJ SOPARKAR, PM AF MILLEMAN, JL PUTT, MS KLEBER, CJ SOPARKAR, PM TI EVALUATION OF INTER-EXAMINER RELIABILITY, CONSISTENCY AND SENSITIVITY OF THE MGI SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 INDIANA PURDUE UNIV,FT WAYNE,IN. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 429 EP 429 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502612 ER PT J AU HOUSER, BE ALDER, ME MCANEAR, JT AF HOUSER, BE ALDER, ME MCANEAR, JT TI DENSITY VARIATIONS OF AUTOLOGOUS BONE-GRAFTS IN AUGMENTED MAXILLARY SINUSES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1994 VL 73 SI SI BP 447 EP 447 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MT325 UT WOS:A1994MT32502757 ER PT J AU GUY, SM SMITH, GM BENTLER, PM AF GUY, SM SMITH, GM BENTLER, PM TI CONSEQUENCES OF ADOLESCENT DRUG-USE AND PERSONALITY-FACTORS ON ADULT-DRUG USE SO JOURNAL OF DRUG EDUCATION LA English DT Article ID YOUNG ADULTHOOD; SUBSTANCE USE; PATERNAL DETERMINANTS; MARIHUANA USE; HIGH-SCHOOL; IMPACT; ALCOHOL; MODEL; ENVIRONMENT; INVOLVEMENT AB This study examined the stability of adolescent drug use into young adulthood and explored the possible influence of personality on adolescent and adult drug use. Participants in this longitudinal study (N = 640) completed questionnaires which assessed multiple indicators for latent constructs of tobacco, alcohol, cannabis, and hard drugs, and also for the personality constructs of Socialization. In addition, the effects of obedience and extraversion were examined. Results showed that a general drug use factor in adolescence significantly predicted young adult drug use. A particular effect of adolescent obedience on adult drug use was noted. Within adolescence, obedience, extraversion, and the construct of Socialization were significant predictors of drug use. Early onset of smoking predicted adolescent drug use. The implications of these findings for early drug use education and intervention are discussed. Additional analysis explored the possibility of treating obedience as another indicator of Socialization. This model could not provide as good a fit as the original model. The measure of obedience acted as a better predictor of drug use than an overall factor of Socialization. Gender differences are discussed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP GUY, SM (reprint author), UNIV CALIF LOS ANGELES,DEPT PSYCHOL,405 HILGARD AVE,LOS ANGELES,CA 90024, USA. FU NIDA NIH HHS [DA00017, DA01070] NR 58 TC 34 Z9 34 U1 3 U2 6 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0047-2379 J9 J DRUG EDUC JI J. Drug Educ. PY 1994 VL 24 IS 2 BP 109 EP 132 DI 10.2190/X4WU-BV3X-Q483-Y5BT PG 24 WC Substance Abuse; Education, Scientific Disciplines SC Substance Abuse; Education & Educational Research GA NZ463 UT WOS:A1994NZ46300002 PM 7931922 ER PT J AU LEONG, GB ETH, S SILVA, JA AF LEONG, GB ETH, S SILVA, JA TI TARASOFF DEFENDANTS - SOCIAL-JUSTICE OR ETHICAL DECAY SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; DUTY TO PROTECT; TESTIMONY; JUSTICE; ETHICS; PRIVILEGE; DANGEROUSNESS AB In 1976, the California Supreme Court ruled in Tarasoff v. Regents of the University of California that a duty to protect arises when a psychotherapist's patient poses a serious danger of physical harm to an identifiable third party. Discharging this duty by the issuance of a warning breaches the confidentiality of the psychotherapist-patient relationship. However, the potential benefit to society offsets the possible harm caused by the breach of confidentiality. Until recently, such warnings have served little purpose outside of possibly preventing harm. However, the cumulative effect of three recent California Supreme Court cases has been to permit the use of these confidentiality breaches in criminal proceedings to fulfill prosecutorial goals. Nonetheless, the cost of achieving social justice may be at the expense of other important ethical values for both the psychotherapeutic professions and society in general. C1 W LOS ANGELES VAMC,PSYCHIATRY SERV 116AA,LOS ANGELES,CA 90073. UNIV SO CALIF,SCH MED,LOS ANGELES,CA. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. NR 11 TC 5 Z9 5 U1 0 U2 2 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD JAN PY 1994 VL 39 IS 1 BP 86 EP 93 PG 8 WC Medicine, Legal SC Legal Medicine GA MT466 UT WOS:A1994MT46600009 PM 11644513 ER PT J AU KRAMER, BJ VITALIANO, PP AF KRAMER, BJ VITALIANO, PP TI COPING - A REVIEW OF THE THEORETICAL FRAMEWORKS AND THE MEASURES USED AMONG CAREGIVERS OF INDIVIDUALS WITH DEMENTIA SO JOURNAL OF GERONTOLOGICAL SOCIAL WORK LA English DT Article; Proceedings Paper CT 44th Annual Scientific Meeting of the Gerontological-Society-of-America CY NOV, 1992 CL SAN FRANCISCO, CA SP GERONTOL SOC AMER ID ALZHEIMERS-DISEASE; FAMILY CAREGIVERS; SPOUSE CAREGIVERS; STRESS; STRATEGIES; PREDICTORS; BURDEN; DEPRESSION; APPRAISAL; SUPPORT AB Gerontological social workers are often called upon to evaluate how family members are coping with caring for older adults with dementia. This paper examines the ways in which coping has been conceptualized and measured among caregivers. This review is intended to assist social workers in understanding the issues relevant to the assessment of caregiver coping given current theoretical formulations, to identify some of the gaps in the research conducted to date, and to help practitioners in deciding how to choose a comprehensive measure of coping. This review thereby compares and evaluates the conceptual and theoretical frameworks of 16 studies and examines the psychometric properties of the eight measures they have used to assess the coping of caregivers of older adults with dementia. Conclusions and implications for social work research and practice are discussed. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,GRECC,MADISON,WI. RP KRAMER, BJ (reprint author), UNIV WISCONSIN,SCH SOCIAL WORK,1350 UNIV AVE,MADISON,WI 53706, USA. NR 57 TC 21 Z9 21 U1 0 U2 6 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0163-4372 J9 J GERONTOL SOC WORK JI J. Gerontol. Soc. Work PY 1994 VL 23 IS 1-2 BP 151 EP 174 PG 24 WC Geriatrics & Gerontology; Social Work SC Geriatrics & Gerontology; Social Work GA QW960 UT WOS:A1994QW96000009 ER PT J AU ROHAN, EA BERKMAN, B WALKER, S HOLMES, W AF ROHAN, EA BERKMAN, B WALKER, S HOLMES, W TI THE GERIATRIC ONCOLOGY PATIENT - AGEISM IN SOCIAL-WORK-PRACTICE SO JOURNAL OF GERONTOLOGICAL SOCIAL WORK LA English DT Article ID CANCER AB Elderly oncology patients are at risk of being treated inequitably by health care providers due to ageist attitudes and practices. This study explores whether ageism exists in oncology social work by comparing practice with 305 adult patients under 65 years old to 197 patients 65 and older. The patients received services in three outpatient oncology treatment centers between June 1, 1990 and May 31, 1991. Study focused on social work practice comparing problems addressed, treatment modalities utilized and intensity of treatment. Social workers engaged in significantly more individual treatment, had a higher number of patient-social worker contacts, and engaged in longer duration of treatment with younger than with older patients. Concomitantly, social workers spent less time addressing significant problems related to adjustment to illness with elderly oncology patients. These findings suggest that social workers may not be effectively helping elderly oncology patients cope with important issues of illness and aging. RP ROHAN, EA (reprint author), MASSACHUSETTS GEN HOSP,32 FRUIT ST,BOSTON,MA 02114, USA. NR 24 TC 23 Z9 23 U1 0 U2 5 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0163-4372 J9 J GERONTOL SOC WORK JI J. Gerontol. Soc. Work PY 1994 VL 23 IS 1-2 BP 201 EP 221 PG 21 WC Geriatrics & Gerontology; Social Work SC Geriatrics & Gerontology; Social Work GA QW960 UT WOS:A1994QW96000011 ER PT J AU KUSSIE, PH PARHAMISEREN, B WYSOCKI, LJ MARGOLIES, MN AF KUSSIE, PH PARHAMISEREN, B WYSOCKI, LJ MARGOLIES, MN TI A SINGLE ENGINEERED AMINO-ACID SUBSTITUTION CHANGES ANTIBODY FINE SPECIFICITY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PARA-AZOPHENYLARSONATE FAB-36-71; VARIABLE REGION; 3-DIMENSIONAL STRUCTURE; SOMATIC MUTATION; IMMUNE-RESPONSE; HYDROGEN-BONDS; HEAVY-CHAIN; AFFINITY; BINDING; MOUSE AB During the acquisition of humoral immunity, the process of somatic hypermutation introduces nucleotide substitutions into expressed antibody (Ab) V region genes. Studies employing in vitro mutagenesis have shown that recurrent mutations observed in vivo often enhance the affinity of the target Ab for Ag. Here we show that a single amino acid replacement at position 35 in the H chain of an unmutated Ab with specificity for p-azophenylarsonate (Ars) confers specificity for the structurally related hapten p-azophenylsulfonate (Sulf) while abolishing specificity for Ars. The mutant Ab binds Sulf with an affinity characteristic of Ab produced by memory B cells. The same mutation in the somatically mutated anti-Ars Ab 36-71, for which the Fab crystal structure is known, resulted in a significant shift in fine specificity from Ars to Sulf. Examination of the crystal structure suggests that the specificity change is caused by a decrease in binding site size and/or new hydrogen bond geometry. Because the mutation at position 35 had been observed in somatically mutated Ab elicited by immunization with Ars followed by Sulf, the results confirm that somatic mutation in vivo can alter Ab specificity. The results also support the potential of Ab engineering to alter antigenic specificity. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,JACKSON 14,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NATL JEWISH CTR IMMUNOL & RESP MED,DEPT PEDIAT,DIV BASIC SCI,DENVER,CO 80206. UNIV COLORADO,HLTH SCI CTR,DEPT MICROBIOL & IMMUNOL,DENVER,CO 80208. FU NCI NIH HHS [R01CA24432] NR 40 TC 35 Z9 35 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1994 VL 152 IS 1 BP 146 EP 152 PG 7 WC Immunology SC Immunology GA MN408 UT WOS:A1994MN40800018 PM 8254187 ER PT J AU PETRINI, JHJ DONOVAN, JW DIMARE, C WEAVER, DT AF PETRINI, JHJ DONOVAN, JW DIMARE, C WEAVER, DT TI NORMAL V(D)J CODING JUNCTION FORMATION IN DNA LIGASE-I DEFICIENCY SYNDROMES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID BLOOMS SYNDROME CELLS; SISTER-CHROMATID EXCHANGES; COMBINED IMMUNE-DEFICIENCY; PRE-B CELLS; SCID MUTATION; SYNDROME LYMPHOCYTES; MAMMALIAN-CELLS; RECOMBINATION; GENE; MICE AB Bloom syndrome and a clinically related syndrome represented by the cell line 46BR have been associated with reduction in DNA ligase I activity. In-these syndromes, DNA ligase I deficiency severely impairs the development and function of the immune system. We undertook analysis of DNA ligase I-deficient cells to determine whether the observed immune deficiency is attributable to a perturbation in the process of V(D)j recombination. V(D)J recombination in Bloom syndrome cell lines and 46BR was examined by a transient transfection assay. No effect on the fidelity of coding and signal junction formation in DNA ligase I-deficient cells was observed. The frequency of V(D)J recombination in DNA ligase I-deficient cells was also examined using recombination substrates modified to function in human cells. Similar recombination frequencies were observed in normal and DNA ligase I-deficient cells, demonstrating that the efficiency of the V(D)J recombination process is unaffected by alterations in DNA ligase I activity. Rearranged immunoglobulin loci from Bloom syndrome cell lines and patient material were molecularly cloned by an inverse polymerase chain reaction strategy which should be applicable to a variety of human immunodeficiency syndromes and were indistinguishable from those found in normal bone marrow samples. Our data argue that the immune system defects associated with DNA ligase I deficiency do not result from perturbation of the V(D)J recombination pathway. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,MAYER 718,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [CA52694]; NIAID NIH HHS [AI08308] NR 48 TC 37 Z9 38 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1994 VL 152 IS 1 BP 176 EP 183 PG 8 WC Immunology SC Immunology GA MN408 UT WOS:A1994MN40800021 PM 8254190 ER PT J AU LARRICK, JW HIRATA, M ZHENG, H ZHONG, J BOLIN, D CAVAILLON, JM WARREN, HS WRIGHT, SC AF LARRICK, JW HIRATA, M ZHENG, H ZHONG, J BOLIN, D CAVAILLON, JM WARREN, HS WRIGHT, SC TI A NOVEL GRANULOCYTE-DERIVED PEPTIDE WITH LIPOPOLYSACCHARIDE-NEUTRALIZING ACTIVITY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PERMEABILITY-INCREASING PROTEIN; NECROSIS-FACTOR RELEASE; GRAM-NEGATIVE BACTERIA; L-ARGININE; BINDING-PROTEIN; NITRIC-OXIDE; SEPTIC SHOCK; MURINE MACROPHAGES; RELAXING FACTOR; CYTO-TOXICITY AB Rabbit CAP18 (cationic antimicrobial protein, 18 kDa) is a leukocyte protein identified and purified using as an assay its capacity to bind and inhibit various activities of LPS. Oligonucleotide probes designed from the putative N-terminal protein sequence were used to obtain the corresponding cDNA from a rabbit bone marrow cDNA library. Examination of the cDNA sequence revealed that the protein fragment of the putative N-terminus was actually a 37-amino-acid C-terminal fragment. This fragment, designated CAP18(106-142), inhibits many activities of LPS. In the present studies, synthetic CAP18(106-142) is shown to: 1) bind to erythrocytes coated with diverse strains of LPS; 2) inhibit LPS-induced release of cytokines (TNF, IL-1, IL-6) and nitric oxide from macrophages; 3) inhibit LPS-induced LAL coagulation and 4) protect mice from LPS lethality. CAP18(106-142) may have therapeutic utility for conditions associated with elevated concentrations of LPS. C1 IWATE MED UNIV,SCH MED,DEPT BACTERIOL,MORIOKA,IWATE 020,JAPAN. HOFFMANN LA ROCHE INC,DEPT PROT BIOCHEM,NUTLEY,NJ 07110. MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. INST PASTEUR,UNITE IMMUNOALLERGIE,F-75724 PARIS 15,FRANCE. RP LARRICK, JW (reprint author), PALO ALTO INST MOLEC MED,2462 WYANDOTTE ST,MT VIEW,CA 94043, USA. FU NIGMS NIH HHS [R01-GM47720] NR 61 TC 121 Z9 123 U1 0 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1994 VL 152 IS 1 BP 231 EP 240 PG 10 WC Immunology SC Immunology GA MN408 UT WOS:A1994MN40800027 PM 8254193 ER PT J AU SYKES, M HARTY, MW PEARSON, DA AF SYKES, M HARTY, MW PEARSON, DA TI STRAIN DEPENDENCE OF INTERLEUKIN-2-INDUCED GRAFT-VERSUS-HOST DISEASE PROTECTION - EVIDENCE THAT INTERLEUKIN-2 INHIBITS SELECTED CD4 FUNCTIONS SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE GRAFT-VERSUS-HOST DISEASE; INTERLEUKIN-2; BONE MARROW TRANSPLANTATION; HISTOCOMPATIBILITY ANTIGENS; T-CELLS ID BONE-MARROW TRANSPLANTATION; II H-2 DIFFERENCES; T-CELL SUBSETS; MAJOR HISTOCOMPATIBILITY BARRIERS; MONOCLONAL-ANTIBODIES; L3T4+ CELLS; LEUKEMIA; MICE; ANTIGENS; GVHD AB Treatment of lethally irradiated mice with a short course of high-dose interleukin (IL)-2 markedly inhibits acute and chronic graft-versus-host disease (GVHD), while preserving a graft-versus-leukemia (GVL) effect of allogeneic T-cells. We recently demonstrated that this GVL effect, observed with the EL4 leukemia/lymphoma in the A/J --> B10 strain combination, was mediated by CD8(+) A/J T-cells in a CD4-independent fashion. IL-2 inhibited only the activity of CD4(+) cells, and not that of CD4-independent CD8(+) T-cells in A/J spleen cell inocula. This inhibition of CD4 function was sufficient to markedly inhibit GVHD, thus explaining the dissociation of GVHD and GVL in IL-2-treated mice. We have now performed studies to determine the capacity of IL-2 to inhibit GVHD induced across a variety of different histocompatibility barriers. IL-2 significantly delayed GVHD mortality in three of four additional fully major histocompatibility complex (MHC) plus minor-disparate strain combinations when CD4 C T-cells were given. Numbers of CD8(+) T-cells comparable to those that might contaminate human marrow demonstrated a relatively poor capacity to produce acute GVHD when given without CD4(+) cells in all of three additional strain combinations evaluated. In one of these strain combinations (B10 --> BALB/c), IL-2 protected against acute but not chronic GVHD mortality when CD4(+) cells were given with or without CD8(+) cells. In one fully allogeneic strain combination, BIO --> A/J, IL-2 did not inhibit the GVHD produced by CD4(+) cells given with or without CD8(+) cells. IL-2 was unable to inhibit CD8-mediated GVHD in strain combinations differing at isolated class I MRC loci. In a strain combination differing only at multiple minor histoincompatibility antigen (HA) loci, B10 --> C3H.SW, GVHD was largely CD8-dependent, but IL-2 did not inhibit the small CD4-mediated component of GVHD. Together, these results suggest that IL-2 inhibits a restricted subset of CD4 cells or functions, and that the type of CD4 activities mediating GVHD is determined by the particular histoincompatibilities between donor and host. RP SYKES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR TRANSPLANTAT RES BIOL,SURG SERV,MGH-E,BOSTON,MA 02129, USA. FU NCI NIH HHS [NCI RO1CA55290] NR 42 TC 16 Z9 16 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 JAN PY 1994 VL 15 IS 1 BP 11 EP 21 DI 10.1097/00002371-199401000-00002 PG 11 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA MN046 UT WOS:A1994MN04600002 PM 8110726 ER PT J AU GE, YM EZZELL, RM TOMPKINS, RG WARREN, HS AF GE, YM EZZELL, RM TOMPKINS, RG WARREN, HS TI CELLULAR-DISTRIBUTION OF ENDOTOXIN AFTER INJECTION OF CHEMICALLY PURIFIED LIPOPOLYSACCHARIDE DIFFERS FROM THAT AFTER INJECTION OF LIVE BACTERIA SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HIGH-DENSITY LIPOPROTEIN; SALMONELLA-TYPHIMURIUM LIPOPOLYSACCHARIDES; ESCHERICHIA-COLI; RAT; BINDING; LOCALIZATION; MACROPHAGES; INVIVO; SHOCK; CELLS AB Lipopolysaccharide (LPS) chemically extracted from gram-negative bacteria is often used in animal models to study endotoxemia. Laser confocal microscopy and immunofluorescence staining for comparison of injections of live Escherichia coli O111:B4 bacteria with LPS extracted from the same strain showed that cellular localization and time course in rat organs were markedly different after the two injections. Fluorescent staining and image analysis software allowed quantitative comparison of LPS within tissues at different times and doses. Antigenic LPS was detected in all tissues 1 hour after injection of both bacteria and LPS and was present in liver and spleen over the 28-day study period. Whole bacteria were identified in tissue macrophages for the first 48 h after injection; later, bacterial cell walls were replaced by diffuse antigenic material throughout the cytoplasm. Antigenic LPS was localized within hepatocytes only after injection of chemically purified LPS. Cellular localization of LPS in tissues is dependent on the form injected. Animal models that use purified LPS may not be representative of gram-negative bacteremia. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,5TH FLOOR,149 13TH ST,BOSTON,MA 02129. SHRINERS BURNS INST,DEPT MED,CHILDRENS SERV,DEPT MED,SURG SERV,INFECT DIS UNIT,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. FU NIAID NIH HHS [AI-28943]; NIDDK NIH HHS [DK-43351] NR 34 TC 47 Z9 47 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 JAN PY 1994 VL 169 IS 1 BP 95 EP 104 PG 10 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MP527 UT WOS:A1994MP52700014 PM 8277203 ER PT J AU WOLFSDORF, JI CRIGLER, JF AF WOLFSDORF, JI CRIGLER, JF TI BIOCHEMICAL-EVIDENCE FOR THE REQUIREMENT OF CONTINUOUS GLUCOSE THERAPY IN YOUNG-ADULTS WITH TYPE-1 GLYCOGEN-STORAGE-DISEASE SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article ID UNCOOKED CORNSTARCH; RENAL-DISEASE; HYPOGLYCEMIA; GLUCOSE-6-PHOSPHATASE; RESPONSES; CHILDREN; DEXTROSE; HUMANS AB To determine whether patients with GSD-1 need nocturnal glucose therapy after completing physical growth and development, studies were performed on two consecutive nights. On the first night uncooked cornstarch (UCS) was given at the calculated glucose production rate at 21:00 h and 02:00 h. On the second night UCS was given at 21:00 h but omitted at 02:00 h. Six GSD-1 patients, aged 17.2-20.9 years, previously treated with continuous glucose therapy were studied. Measurements were made of plasma glucose (PG), serum insulin, growth hormone, cortisol, plasma glucagon (n = 4), and blood lactate at 30-60-min intervals. Serum uric acid, cholesterol, and triglycerides were measured at 21:00 h and 07:00 h, and serum FFA at 21:00 h, 02:00 h and 07:00 h on the first night and immediately before treatment for hypoglycaemia on the second night. For five hours after UCS at 21:00h, mean PG, serum insulin and blood lactate concentrations were similar on the two nights. With UCS at 02:00h, mean PG concentrations were greater than or equal to 4.1mmol/L from 02:00 to 07:00h. Without UCS at 02:00h, in all subjects PG concentrations fell to < 2.5 mmol/L after 6.5-8.5 h and mean blood lactate concentration increased to 7.4 +/- 3.0 mmol/L. Young adults with GSD-1 developed hypoglycaemia and hyperlactataemia after a relatively brief period without exogenous glucose and, therefore, need to continue nocturnal glucose therapy to prevent fasting hypoglycaemia. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP WOLFSDORF, JI (reprint author), CHILDRENS HOSP,DEPT MED,DIV ENDOCRINOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NCRR NIH HHS [RR02172] NR 27 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 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1994 VL 17 IS 2 BP 234 EP 241 DI 10.1007/BF00711624 PG 8 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA NU100 UT WOS:A1994NU10000010 PM 7967479 ER PT J AU TOONE, JR APPLEGARTH, DA LEVY, HL AF TOONE, JR APPLEGARTH, DA LEVY, HL TI PRENATAL-DIAGNOSIS OF NONKETOTIC HYPERGLYCINEMIA - EXPERIENCE IN 50 AT-RISK PREGNANCIES SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article; Proceedings Paper CT Symposium: From Genotype to Phenotype, at the 31st Annual Meeting of the Society-for-the-Study-of-Inborn-Errors-of-Metabolism CY SEP 07-10, 1993 CL MANCHESTER, ENGLAND SP SOC STUDY INBORN ERRORS METAB ID NONKETOTIC HYPERGLYCINEMIA C1 MASSACHUSETTS GEN HOSP,JOSEPH P KENNEDY JR LABS NEUROL SERV,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02129. RP TOONE, JR (reprint author), BRITISH COLUMBIA CHILDRENS HOSP,DEPT PATHOL,BIOCHEM DIS LAB,4480 OAK ST,VANCOUVER V6H 3V4,BC,CANADA. NR 4 TC 13 Z9 13 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1994 VL 17 IS 3 BP 342 EP 344 DI 10.1007/BF00711825 PG 3 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA PB070 UT WOS:A1994PB07000024 PM 7807948 ER PT J AU GENTRY, RT BARAONA, E LIEBER, CS AF GENTRY, RT BARAONA, E LIEBER, CS TI GASTRIC FIRST PASS METABOLISM OF ALCOHOL SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Editorial Material ID HUMAN GASTROINTESTINAL-TRACT; DEHYDROGENASE-ACTIVITY; 1ST-PASS METABOLISM; H-2-RECEPTOR ANTAGONISTS; POSTPRANDIAL ABSORPTION; H2-RECEPTOR ANTAGONISTS; ENZYMATIC-PROPERTIES; ETHANOL-METABOLISM; CLASS-IV; RAT C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,NEW YORK,NY. MT SINAI SCH MED,NEW YORK,NY. NR 55 TC 44 Z9 45 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 JAN PY 1994 VL 123 IS 1 BP 21 EP 26 PG 6 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA MZ688 UT WOS:A1994MZ68800013 PM 8288957 ER PT J AU GENTRY, RT BARAONA, E LIEBER, CS AF GENTRY, RT BARAONA, E LIEBER, CS TI REBUTTAL TO ANTAGONIST SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Editorial Material ID ALCOHOL-DEHYDROGENASE; ETHANOL-METABOLISM; RAT; ABSORPTION C1 BRONX VET AFFAIRS MED CTR,NEW YORK,NY. MT SINAI SCH MED,NEW YORK,NY. NR 15 TC 8 Z9 8 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 JAN PY 1994 VL 123 IS 1 BP 32 EP 33 PG 2 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA MZ688 UT WOS:A1994MZ68800016 ER PT J AU HOSTETLER, JS CATANZARO, A STEVENS, DA GRAYBILL, JR SHARKEY, PK LARSEN, RA TUCKER, RM ALHAIDARY, AD RINALDI, MG CLOUD, GA GALGIANI, JN AF HOSTETLER, JS CATANZARO, A STEVENS, DA GRAYBILL, JR SHARKEY, PK LARSEN, RA TUCKER, RM ALHAIDARY, AD RINALDI, MG CLOUD, GA GALGIANI, JN TI TREATMENT OF COCCIDIOIDOMYCOSIS WITH SCH-39304 SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article ID AMBULATORY PERITONEAL-DIALYSIS; FLUCONAZOLE; SCH-39304; THERAPY AB A new oral triazole antifungal, SCH 39304, was administered to 54 patients with progressive infections due to Coccidioides immitis from six collaborating centers. Patients were grouped according to site of infection including chronic pulmonary (25), bone/joint (17) and skin/soft tissue (12). The median age was 40 years; 83% were male, 52% white, 13% HIV-infected and 35% had failed previous therapy. The majority of patients were treated with either 100 mg or 200 mg day(-1). One patient on renal dialysis received 300 mg day(-1). Baseline abnormalities were reassessed for evidence of efficacy every 4 months and expressed in a standardized scoring system. Cumulative overall response rates at 4, 8 and 12 months were 7%, 36% and 66% respectively. Twelve month response rates by disease were 77% (pulmonary), 62% (skin/soft tissue) and 31% (bone/joint). Fifteen patients failed therapy although seven of these were still on treatment when the study was discontinued. Two failed due to toxicity. Possible symptoms or signs of toxicity occurred in 24 (44%) patients and were generally mild. SCH 39304 is an effective and well tolerated therapy for progressive forms of coccidioidomycosis. C1 SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,DEPT MED,DIV INFECT DIS & GEOG MED,STANFORD,CA 94305. CALIF INST MED RES,SAN JOSE,CA 95128. NIAID,MYCOSES STUDY GRP,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DIV PULM MED,SAN DIEGO,CA 92103. AUDIE L MURPHY MEM VET ADM MED CTR,MED LAB,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV SO CALIF,LOS ANGELES CTY MED CTR,LOS ANGELES,CA 90033. WENATCHEE VALLEY CLIN,DIV CLIN RES,WENATCHEE,WA. VET AFFAIRS MED CTR,MED SERV,TUCSON,AZ. UNIV ARIZONA,DEPT MED,TUCSON,AZ. UNIV ALABAMA,CTR COMPREHENS CANC,BIOSTAT UNIT,BIRMINGHAM,AL 35294. FU NIAID NIH HHS [N01-AI-15082] NR 14 TC 9 Z9 9 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1994 VL 32 IS 2 BP 105 EP 114 PG 10 WC Mycology SC Mycology GA NH896 UT WOS:A1994NH89600003 PM 8064541 ER PT J AU FAVA, M BLESS, E OTTO, MW PAVA, JA ROSENBAUM, JF AF FAVA, M BLESS, E OTTO, MW PAVA, JA ROSENBAUM, JF TI DYSFUNCTIONAL ATTITUDES IN MAJOR DEPRESSION - CHANGES WITH PHARMACOTHERAPY SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID COGNITIONS; ANGER AB High levels of dysfunctional attitudes have been associated with greater severity of depression and poorer response to pharmacological treatment. The goal of our study was to examine this relationship and the changes in dysfunctional attitudes after treatment with fluoxetine, a relatively selective serotonin uptake inhibitor. Dysfunctional attitudes were evaluated with both the Cognitions Questionnaire (CQ) and the Dysfunctional Attitudes Scale (DAS) in 115 outpatients diagnosed as having major depressive disorder. After 8 weeks of treatment with fluoxetine, 67 of these patients again completed the DAS and the CQ. Dysfunctional attitudes were associated with depression severity both before and after treatment and decreased linearly with treatment of the depression. Negative thinking and dysfunctional attitudes, as measured by both DAS and CQ, were not predictive of the degree of improvement in depressive symptoms. These findings partly support a state-dependent interpretation of dysfunctional attitudes, and provide evidence of significant reductions in these attitudes after treatment with a serotonin uptake inhibitor. C1 MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,BOSTON,MA 02114. RP FAVA, M (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WACC 815,BOSTON,MA 02114, USA. NR 18 TC 41 Z9 41 U1 0 U2 3 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 JAN PY 1994 VL 182 IS 1 BP 45 EP 49 PG 5 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MQ763 UT WOS:A1994MQ76300008 PM 8277301 ER PT J AU ENOCHS, WS SARNA, T ZECCA, L RILEY, PA SWARTZ, HM AF ENOCHS, WS SARNA, T ZECCA, L RILEY, PA SWARTZ, HM TI THE ROLES OF NEUROMELANIN, BINDING OF METAL-IONS, AND OXIDATIVE CYTOTOXICITY IN THE PATHOGENESIS OF PARKINSONS-DISEASE - A HYPOTHESIS SO JOURNAL OF NEURAL TRANSMISSION-PARKINSONS DISEASE AND DEMENTIA SECTION LA English DT Review DE NEUROMELANIN; MELANINS; METAL IONS; FREE RADICALS; OXYGEN TOXICITY; SUBSTANTIA NIGRA; AGING; PARKINSONS DISEASE; IDIOPATHIC PARALYSIS AGITANS ID ELECTRON-SPIN-RESONANCE; MPTP-INDUCED NEUROTOXICITY; PIGMENTED NERVE-CELLS; X-RAY-MICROANALYSIS; SUBSTANTIA-NIGRA; HYDROGEN-PEROXIDE; SULFHYDRYL COMPOUNDS; FREE-RADICALS; HUMAN-BRAIN; TRANSITION-METALS AB A characteristic feature of both Parkinson's disease (idiopathic paralysis agitans) and normal aging is loss of pigmented neurons in the substantia nigra. This has been found to correlate with the accumulation of neuromelanin and with oxidative stress in this brain region, but a clear association between these factors has not been established. Based on our recent demonstration that neuromelanin is a true melanin, containing bound metal ions in situ, we present a general model for its accumulation in vivo and the hypotheses (1) that it has a cytoprotective function in the sequestration of redox-active metal ions under normal conditions but (2) that it has a cytotoxic role in the pathogenesis of Parkinson's disease. Thus, neuromelanin accumulates normally through the autooxidation of catecholamines and serves tightly to bind redox-active metal ions, processes which would accelerate under conditions of intracellular or extracellular oxidative stress. Based on the known properties of melanin, however, neuromelanin also has the potential for exacerbating oxidative stress, eg by generating H2O2 when it is intact or by releasing redox-active metal ions if it loses its integrity; these reactions also would modulate the reactivity of the neuromelanin. By overwhelming intracellular antioxidative defense mechanisms, such a positive-feedback cycle could turn a condition of chronic or repeated oxidative stress in vulnerable neurons into an acute crisis, leading to cellular death. If the cumulative stress in duration and/or degree is severe enough, neuronal depletion could be sufficient to cause Parkinson's disease during life. One possible trigger for this cascade is suggested by the increased nigral iron contents in postmortem parkinsonian brains and the correlation of this disease with urban living where exposure to heavy metal ions is high: the saturation of neuromelanin with redox-active metal ions. Parkinson's disease therefore may be a form of accelerated aging in the substantia nigra associated with environmental toxins in which neuromelanin has a central, active role. C1 UNIV ILLINOIS, COLL MED, URBANA, IL 61801 USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. JAGIELLONIAN UNIV, KRAKOW, POLAND. CNR, IST TECNOL BIOMED AVANZATE, I-20131 MILAN, ITALY. UNIV LONDON, LONDON, ENGLAND. DARTMOUTH COLL SCH MED, HANOVER, NH USA. NR 151 TC 86 Z9 86 U1 2 U2 12 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0936-3076 J9 J NEURAL TRANSM-PARK JI J. Neural Transm.-Park. Dis. Dement. Sect. PY 1994 VL 7 IS 2 BP 83 EP 100 DI 10.1007/BF02260963 PG 18 WC Clinical Neurology SC Neurosciences & Neurology GA NM281 UT WOS:A1994NM28100001 PM 7710667 ER PT J AU REQUINTINA, PJ OXENKRUG, GF YUWILER, A OXENKRUG, AG AF REQUINTINA, PJ OXENKRUG, GF YUWILER, A OXENKRUG, AG TI SYNERGISTIC SEDATIVE EFFECT OF SELECTIVE MAO-A, BUT NOT MAO-B, INHIBITORS AND MELATONIN IN FROGS SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article; Proceedings Paper CT 5th International Amine Oxidase Workshop - Amine Oxidases: Function and Dysfunction CY AUG 22-25, 1992 CL GALWAY, IRELAND AB Total suppression of righting reflex in frogs (Rana pipiens, 25-35 mg b.w.) was observed after combined administration of melatonin (12.5 mg/kg) and selective inhibitors of MAO-A: clorgyline (2.5 mg/kg) and moclobemide (50 mg/kg) but not MAO-B: selegiline (25 mg/kg) and Ro-19-6327 (50 mg/kg). None of these drugs alone affected the righting reflex. Clorgyline and selegiline selectively inhibited brain MAO-A and MAO-B activity (by more than 90%), resp. Frogs might represent a convenient model to study the selective MAO-A and B type inhibitors since they provide the opportunity to correlate behaviour and biochemical changes induced by MAO inhibitors. C1 BROWN UNIV,SCH MED,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,NEUROCHEM LAB,LOS ANGELES,CA 90073. RP REQUINTINA, PJ (reprint author), VET ADM MED CTR,PSYCHIAT SERV,PINEAL RES LAB,T-20,830 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. OI Oxenkrug, Gregory/0000-0002-7193-9117 NR 10 TC 5 Z9 5 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 1994 IS 41 BP 141 EP 144 PG 4 WC Neurosciences SC Neurosciences & Neurology GA PW142 UT WOS:A1994PW14200021 ER PT J AU OXENKRUG, GF REQUINTINA, PJ CORREA, RM YUWILER, A AF OXENKRUG, GF REQUINTINA, PJ CORREA, RM YUWILER, A TI THE EFFECT OF 6-MONTHS L-DEPRENYL ADMINISTRATION ON PINEAL MAO-A AND MAO-B ACTIVITY AND ON THE CONTENT OF MELATONIN AND RELATED INDOLES IN AGED FEMALE FISHER 344N RATS SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article; Proceedings Paper CT 5th International Amine Oxidase Workshop - Amine Oxidases: Function and Dysfunction CY AUG 22-25, 1992 CL GALWAY, IRELAND ID LIFE AB Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night. Daytime values were unchanged by the treatment. The data suggest that stimulation of pineal melatonin biosynthesis might be one of the consequences of MAO-A inhibition contributing to life span prolongation induced by chronic selegiline treatment. C1 BROWN UNIV,SCH MED,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. W LOS ANGELES VET AFFAIRS MED CTR,NEUROCHEM LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP OXENKRUG, GF (reprint author), VET ADM MED CTR,PSYCHIAT SERV,PINEAL RES LAB,830 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. OI Oxenkrug, Gregory/0000-0002-7193-9117 NR 11 TC 6 Z9 7 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 1994 IS 41 BP 249 EP 252 PG 4 WC Neurosciences SC Neurosciences & Neurology GA PW142 UT WOS:A1994PW14200034 ER PT J AU BASHIR, R MCMANUS, B CUNNINGHAM, C WEISENBURGER, D HOCHBERG, F AF BASHIR, R MCMANUS, B CUNNINGHAM, C WEISENBURGER, D HOCHBERG, F TI DETECTION OF EBER-1 RNA IN PRIMARY BRAIN LYMPHOMAS IN IMMUNOCOMPETENT AND IMMUNOCOMPROMISED PATIENTS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE LYMPHOMA; CENTRAL NERVOUS SYSTEM LYMPHOMA; EPSTEIN-BARR VIRUS; ACQUIRED IMMUNE DEFICIENCY SYNDROME; EBER-1 ID EPSTEIN-BARR-VIRUS; NERVOUS-SYSTEM LYMPHOMA; IMMUNE-DEFICIENCY-SYNDROME; POLYMERASE CHAIN-REACTION; INSITU HYBRIDIZATION; CNS LYMPHOMAS; CELL-LINES; IMMUNODEFICIENCY; AIDS; ASSOCIATION AB Tissue from primary central nervous system lymphoma (PCNSL) which developed in five patients with acquired immune deficiency syndrome (AIDS), nine patients without immunodeficiency, and two Epstein-Barr virus (EBV)-positive control cell lines (B95-8 and Raji) were examined for the presence of EBER-1 RNA. The tissues were hybridized with digoxigenin-labeled sense or anti-sense EBER-1 riboprobes. In all five AIDS-related PCNSLs, strong hybridization signals were found with the EBER-1 anti-sense probe. Signals could be eliminated by preincubation of the tissues with RNase-A. Hybridization with the EBER-1 sense probe showed no signal. All PCNSLs from immunocompetent patients (five paraffin-embedded, four frozen) showed no hybridization signals with EBER-1 sense or antisense probe but good hybridization signals with probes to immunoglobulin kappa or lambda light chain indicating RNA preservation. The paraffin-embedded B95-8-positive control cell-line showed positive hybridization in most cells with the anti-sense EBER-1 probe, and up to one percent of the cells had a weak signal with the sense probe. Most Raji cells showed a uniform signal with the anti-sense EBER-1 probe only. We conclude that, PCNSLs that arise in AIDS patients are associated with latent EBV infections, whereas PCNSLs from immunocompetent patients are not indicating a probable role for EBV in pathogenesis of these tumors. C1 UNIV NEBRASKA,MED CTR,DEPT PATHOL & MICROBIOL,OMAHA,NE. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP BASHIR, R (reprint author), UNIV NEBRASKA,MED CTR,DEPT INTERNAL MED,NEUROL SECT,600 S 42ND ST,OMAHA,NE 68198, USA. NR 28 TC 11 Z9 11 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1994 VL 20 IS 1 BP 47 EP 53 DI 10.1007/BF01057960 PG 7 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA PF373 UT WOS:A1994PF37300005 PM 7807183 ER PT J AU FINE, HA AF FINE, HA TI THE BASIS FOR CURRENT TREATMENT RECOMMENDATIONS FOR MALIGNANT GLIOMAS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE GLIOMA; CHEMOTHERAPY; RADIOTHERAPY ID THERAPY-ONCOLOGY-GROUP; HIGH-GRADE GLIOMAS; RADIATION-THERAPY; BRAIN-TUMORS; GLIOBLASTOMA-MULTIFORME; POSTOPERATIVE TREATMENT; SUCCESSFUL CHEMOTHERAPY; ANAPLASTIC ASTROCYTOMA; ADJUVANT CHEMOTHERAPY; INITIAL MANAGEMENT AB Although primary brain tumors represent an important cause of cancer related mortality in the United States, advances in the treatment of these tumors has been slow and has generally lagged behind that of most systemic tumors. One of the major reasons for this is the paucity of well conducted, prospective radiation and chemotherapy trials. For the brain tumor trials that have been conducted, small patient numbers, heterogeneous patient populations, and non-uniformity of response criteria, have made the current clinical data base difficult to interpret. Data from several prospective, multi-institutional randomized trials have defined a role for radiation therapy in the treatment of malignant gliomas and on-going trials will help define refinements in technique. Although there does appear to be a place for the use of chemotherapy in the treatment of a subgroup of patients with malignant gliomas, its role for the majority of patients remains unclear. Only through better understanding of the biology of these tumors, more effective therapies, and the implementation of better clinical trial design can we hope to make significant progress in the treatment of malignant gliomas. C1 HARVARD UNIV,SCH MED,CTR BRAIN TUMOR,BOSTON,MA. RP FINE, HA (reprint author), BRIGHAM & WOMENS HOSP,DANA FARBER CANC INST,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 70 TC 112 Z9 114 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1994 VL 20 IS 2 BP 111 EP 120 DI 10.1007/BF01052722 PG 10 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA PF783 UT WOS:A1994PF78300004 PM 7807189 ER PT J AU ROBBERECHT, W SAPP, P VIAENE, MK ROSEN, D MCKENNAYASEK, D HAINES, J HORVITZ, R THEYS, P BROWN, R AF ROBBERECHT, W SAPP, P VIAENE, MK ROSEN, D MCKENNAYASEK, D HAINES, J HORVITZ, R THEYS, P BROWN, R TI CU/ZN SUPEROXIDE-DISMUTASE ACTIVITY IN FAMILIAL AND SPORADIC AMYOTROPHIC-LATERAL-SCLEROSIS SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE MOTOR NEURON DISEASE; AMYOTROPHIC LATERAL SCLEROSIS; SUPEROXIDE DISMUTASE; FREE RADICALS ID LINKAGE; DISEASE AB Amyotrophic lateral sclerosis (ALS) is a degenerative motor neuron disease that is inherited as an autosomal dominant trait in similar to 10% of cases. Recently we and others identified several single-base mutations in the Cu/Zn superoxide dismutase (SOD1) gene in patients with familial ALS (FALS). Using single-strand conformational polymorphism, we studied the C to G mutation in exon 2 of the SOD1 gene(resulting in a leucine to valine substitution in position 38) in affected and unaffected members of a large Belgian family with FALS. We measured the SOD1 activity in red blood cell lysates in 14 members of this family, including the only surviving clinically affected patient. SOD1 activity of the family members carrying the mutation was less than half that of members without the mutation. In addition, in 11 patients with sporadic ALS and 11 age- and sex-matched controls, red blood cell SOD1 activity was normal. These studies indicate that SOD1 activity is reduced in these FALS patients but not in sporadic ALS patients. Moreover, this SOD1 enzyme abnormality is detectable years before onset of clinical ALS in carriers of this FALS mutation. C1 UNIV LEUVEN,SCH MED,OCCUPAT HLTH LAB,LOUVAIN,BELGIUM. MASSACHUSETTS GEN HOSP,DAY NEUROMUSCULAR RES LAB,BOSTON,MA. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,MOLEC NEUROGENET LAB,BOSTON,MA 02129. MIT,HOWARD HUGHES MED INST,DEPT BIOL,CAMBRIDGE,MA 02139. RP ROBBERECHT, W (reprint author), UNIV HOSP GASTHUISBERG,DEPT NEUROL,HEREST 49,B-3000 LOUVAIN,BELGIUM. RI Haines, Jonathan/C-3374-2012 FU NINDS NIH HHS [F32 NS09263-01A1, NS31248-01] NR 21 TC 157 Z9 157 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1994 VL 62 IS 1 BP 384 EP 387 PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MM536 UT WOS:A1994MM53600049 PM 8263541 ER PT J AU BEAL, F BROUILLET, E FERRANTE, R KOWALL, N HANTRAYE, P AF BEAL, F BROUILLET, E FERRANTE, R KOWALL, N HANTRAYE, P TI 3-NITROPROPIONIC ACID PRODUCES SELECTIVE STRIATAL LESIONS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. RI Kowall, Neil/G-6364-2012; Brouillet, Emmanuel/B-4784-2014 OI Kowall, Neil/0000-0002-6624-0213; Brouillet, Emmanuel/0000-0001-6322-7403 NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1994 VL 62 SU S BP S28 EP S28 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NQ959 UT WOS:A1994NQ95900108 ER PT J AU HILDEBRANDT, N AF HILDEBRANDT, N TI THE REICHER-WHEELER EFFECT AND MODELS OF DEEP AND PHONOLOGICAL DYSLEXIA SO JOURNAL OF NEUROLINGUISTICS LA English DT Article ID WORD RECOGNITION; ACQUIRED DYSLEXIA; SEMANTIC ERRORS; READING ALOUD; APHASIA; ALEXIA; SOUND; ACTIVATION; LEXICON AB Current accounts of the functional impairment underlying phonological dyslexia (PD) do not postulate any disturbance of accessing the orthographic lexicon. For deep dyslexia (DD), only the right-hemisphere hypothesis involves such a disturbance. However, neither PD nor DD subjects showed the normal word-superiority effects in a Reicher-Wheeler experiment (forced-choice identification of single letters that had been displayed briefly either as single letters or in words or nonwords with a backward mask). Since these word-superiority effects have been argued to lie at the word-specific level, the existing accounts cannot explain the observed results for both PD and DD subjects. Three other accounts are proposed. The most parsimonious account is a degradation hypothesis: as stress is placed on the reading system, reading performance will be seen to degrade gracefully across a number of different tasks and types of stimuli, resulting in symptoms of PD or DD and producing the correlated pattern of performance in oral reading, repetition, lexical decision, and the Reicher-Wheeler task, which was observed for the nine subjects reported here and which is consistent with many previously reported PD and DD subjects. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,BOSTON,MA 02114. NR 71 TC 3 Z9 3 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0911-6044 J9 J NEUROLINGUIST JI J. Neurolinguist. PD JAN PY 1994 VL 8 IS 1 BP 1 EP 18 DI 10.1016/0911-6044(94)90002-7 PG 18 WC Linguistics; Neurosciences; Psychology, Experimental SC Linguistics; Neurosciences & Neurology; Psychology GA NU682 UT WOS:A1994NU68200001 ER PT J AU LOUIS, DN AF LOUIS, DN TI THE P53 GENE AND PROTEIN IN HUMAN BRAIN-TUMORS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Review DE ASTROCYTOMA; BRAIN TUMOR; GLIOBLASTOMA MULTIFORME; P53 ID WILD-TYPE P53; CENTRAL-NERVOUS-SYSTEM; PRIMITIVE NEUROECTODERMAL TUMORS; HUMAN-MALIGNANT ASTROCYTOMA; CELL-CYCLE; SUPPRESSOR GENE; SV40-TRANSFORMED CELLS; GROWTH-REGULATION; BINDING-PROTEIN; MUTANT P53 C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP LOUIS, DN (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,MOLEC NEUROONCOL LAB,WARREN 3,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA57683, CA09144] NR 102 TC 283 Z9 285 U1 0 U2 4 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 JAN PY 1994 VL 53 IS 1 BP 11 EP 21 DI 10.1097/00005072-199401000-00002 PG 11 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA MQ712 UT WOS:A1994MQ71200002 PM 8301315 ER PT J AU SOBEL, RA GREER, JM ISAAC, J FONDREN, G LEES, MB AF SOBEL, RA GREER, JM ISAAC, J FONDREN, G LEES, MB TI IMMUNOLOCALIZATION OF PROTEOLIPID PROTEIN PEPTIDE 103-116 IN MYELIN SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE MYELIN; PROTEOLIPID PROTEIN; IMMUNOELECTRON MICROSCOPY ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; 2',3'-CYCLIC NUCLEOTIDE 3'-PHOSPHODIESTERASE; CENTRAL NERVOUS-SYSTEM; ENCEPHALITOGENIC DETERMINANT; SYNTHETIC PEPTIDE; BASIC-PROTEIN; SJL MICE; MEMBRANE; IDENTIFICATION; TOPOLOGY AB Determination of the topographic orientation of proteolipid protein (PLP) within myelin is part of an overall understanding of the functions of PLP and the roles of its multiple domains in diseases that primarily affect central nervous system (CNS) myelin. As part of an analysis of PLP orientation, two mouse monoclonal antibodies (mAb) and a rabbit antiserum against a synthetic peptide corresponding to PLP residues 103-116 (YKTTICGKGLSATV) were tested for their reactivity on compact CNS myelin. By ELISA, the antibodies react with intact PLP and PLP residues 103-116, but not with other PLP peptides. Ultrathin cryosections of adult rat optic nerve were immunostained and antibody binding was localized using appropriate second antibodies coupled to 1 nm gold particles that were visualized by silver enhancement. Localization of the particles on the major or intermediate dense lines was determined by three independent observers. Using the PLP peptide mAb and the polyclonal antibody, we demonstrated that greater than or equal to 71% of the particles were localized on the major dense line. At least 66% of particles directed against myelin basic protein, which is known to occur on the major dense line, were also found in that location. These semiquantitative morphologic observations suggest that PLP residues 103-116 occur on the cytoplasmic face of the myelin membrane. (C) 1994 Wiley-Liss, Inc. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. STANFORD UNIV,SCH MED,DEPT PATHOL,STANFORD,CA. EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DEPT BIOMED SCI,WALTHAM,MA. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP SOBEL, RA (reprint author), VET AFFAIRS MED CTR,LAB SERV 113,3801 MIRANDA AVE,PALO ALTO,CA 94304, USA. RI Greer, Judith/C-4945-2009 OI Greer, Judith/0000-0003-4440-4309 FU NINDS NIH HHS [NS 13649, NS 16945, NS 26773] NR 33 TC 11 Z9 11 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD JAN 1 PY 1994 VL 37 IS 1 BP 36 EP 43 DI 10.1002/jnr.490370106 PG 8 WC Neurosciences SC Neurosciences & Neurology GA MR524 UT WOS:A1994MR52400004 PM 7511704 ER PT J AU SANDERSON, IR HE, YP AF SANDERSON, IR HE, YP TI NUCLEOTIDE UPTAKE AND METABOLISM BY INTESTINAL EPITHELIAL-CELLS SO JOURNAL OF NUTRITION LA English DT Article; Proceedings Paper CT Roundtable Symposium on Nucleotides and Nutrition CY MAR 28, 1993 CL NEW ORLEANS, LA SP AMER INST NUTR, WYETH AYERST INT INC DE SMALL INTESTINE; PURINE; PYRIMIDINE; NUCLEOTIDES ID TRANSPORT; RAT; NUCLEOSIDES; INFANTS; PURINE; CACO-2; SYSTEM; GROWTH; LINE AB The epithelial cells of the gastrointestinal tract are the first to encounter ingested nucleotides. Enterocytes metabolize or transport nucleotides (often partially metabolized) to other cell types. Nucleotides may also affect enterocyte gene expression. These interactions in intestinal cell lines (Caco-2 and IEC-6 cells) are described. Nucleotides and nucleosides are efficiently taken up by neoplastic cells (Caco-2) and substantially metabolized during absorption by epithelial monolayers. In nonmalignant cells (IEC-B), nucleotide pools are smaller than enterocytes of neoplastic origin (Caco-2). Consequently, cell proliferation in IEC-6 cells is more dependent on an external supply of nucleotides. Cell differentiation was examined by measuring brush border enzyme activities (sucrase, lactase and alkaline phosphatase). Nucleotides enhanced the expression of brush border enzymes in carcinoma cells only when stressed by glutamine deprivation. IEC-6 cells, which are poorly differentiated in optimal media, require basement membrane (Matrigel) for expression of brush border enzymes. Under these conditions, adding nucleotides to the culture medium enhanced enzyme activity. In addition to being substrates for intestinal absorption, nucleotides may affect enterocyte differentiation. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP SANDERSON, IR (reprint author), CHILDRENS HOSP BOSTON,MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02129, USA. FU NICHD NIH HHS [R01-HD-12437]; NIDDK NIH HHS [P01-DK33506] NR 19 TC 42 Z9 47 U1 0 U2 5 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD JAN PY 1994 VL 124 IS 1 SU S BP S131 EP S137 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MR866 UT WOS:A1994MR86600005 PM 8283303 ER PT J AU WALKER, WA AF WALKER, WA TI NUCLEOTIDES AND NUTRITION - ROLE DIETARY-SUPPLEMENT SO JOURNAL OF NUTRITION LA English DT Editorial Material C1 HARVARD UNIV,CHILDRENS HOSP,DEPT PEDIAT,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,CHARLESTON,MA 02129. MASSACHUSETTS GEN HOSP,CHARLESTON,MA 02129. RP WALKER, WA (reprint author), HARVARD UNIV,CHILDRENS HOSP,DEPT PEDIAT,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,CHARLESTON,MA 02129, USA. NR 0 TC 5 Z9 5 U1 0 U2 2 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD JAN PY 1994 VL 124 IS 1 SU S BP S121 EP S123 PG 3 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MR866 UT WOS:A1994MR86600002 PM 8283300 ER PT J AU SANDELL, LJ SUGAI, JV TRIPPEL, SB AF SANDELL, LJ SUGAI, JV TRIPPEL, SB TI EXPRESSION OF COLLAGEN-I, COLLAGEN-II, COLLAGEN-X, AND COLLAGEN-XI AND AGGRECAN MESSENGER-RNAS BY BOVINE GROWTH-PLATE CHONDROCYTES IN-SITU SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article ID ENDOCHONDRAL OSSIFICATION; INSITU HYBRIDIZATION; MESSENGER-RNAS; HYPERTROPHIC CHONDROCYTES; TERMINAL DIFFERENTIATION; ARTICULAR-CARTILAGE; OSSEOUS JUNCTION; EPIPHYSEAL PLATE; GENE-EXPRESSION; BONE-GROWTH AB The cells responsible for skeletal growth are the chondrocytes of the cartilaginous growth plate. These cells differentiate through a series of maturational stages, establishing different zones in the growth plate. Among the major functions of these cells is the production of appropriate extracellular matrix, primarily composed of collagens and proteoglycans. To determine whether matrix synthesis varies with respect to maturational stage and in which cell populations different collagens are expressed, bovine growth plates were analyzed by in situ hybridization to mRNA and by Northern blot hybridization. The most abundant collagen mRNA in the growth plate was type-II collagen. This mRNA was present at relatively low levels in the most immature cells of the growth plate but increased several-fold as cells entered the proliferative stage and remained high through subsequent phases of maturation. Type-XI collagen mRNA and mRNA for the cartilage-characteristic proteoglycan, aggrecan, were codistributed with the type-II collagen mRNA; however, both were present in much smaller quantities. Type-X procollagen mRNA was localized to chondrocytes late in their maturation and was expressed at levels similar to the expression of type-II collagen. In situ hybridization of serial sections revealed that growth plate chondrocytes in their more mature stages contain both type-II and type-X collagen mRNA. Type-I collagen mRNA was not observed in growth plate chondrocytes at any maturational stage; rather, it was localized to a morphologically distinct population of cells attached to calcifying cartilage septa in the region of vascular invasion. These data indicate that the genes for major matrix constituents synthesized by the growth plate in some cases are expressed differentially at different stages of cellular maturation and in other cases are expressed coordinately. The pattern of mRNA expression suggests possible mechanisms of gene regulation. C1 UNIV WASHINGTON,DEPT ORTHOPAED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT BIOCHEM,SEATTLE,WA 98195. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP SANDELL, LJ (reprint author), SEATTLE VET ADM MED CTR,DEPT ORTHOPAED,ORT 112,1660 S COLUMBIAN WAY,SEATTLE,WA 98108, USA. FU NIAMS NIH HHS [AR31068, AR36994] NR 71 TC 55 Z9 59 U1 0 U2 2 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0736-0266 J9 J ORTHOPAED RES JI J. Orthop. Res. PD JAN PY 1994 VL 12 IS 1 BP 1 EP 14 DI 10.1002/jor.1100120102 PG 14 WC Orthopedics SC Orthopedics GA MX659 UT WOS:A1994MX65900001 PM 8113931 ER PT J AU BODE, BP AF BODE, BP TI NOVEL CONTROL OF THE POSITION-DEPENDENT EXPRESSION OF GENES IN HEPATOCYTES - THE GLUT-1 TRANSPORTER SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Editorial Material ID DIGITONIN COLLAGENASE PERFUSION; PERIVENOUS HEPATOCYTES; GLUCOSE-TRANSPORT; RAT-LIVER; CELLS RP BODE, BP (reprint author), MASSACHUSETTS GEN HOSP,DIV SURG ONCOL,BOSTON,MA 02114, USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD JAN-FEB PY 1994 VL 18 IS 1 BP 83 EP 84 DI 10.1177/014860719401800183 PG 2 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MR804 UT WOS:A1994MR80400018 PM 8164312 ER PT J AU ZIEGLER, TR AF ZIEGLER, TR TI GLUTAMINE IS ESSENTIAL FOR EPIDERMAL GROWTH-FACTOR - STIMULATED INTESTINAL-CELL PROLIFERATION SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ZIEGLER, TR (reprint author), JOSLIN DIABET FDN INC,BOSTON,MA 02215, USA. NR 4 TC 2 Z9 2 U1 0 U2 1 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD JAN-FEB PY 1994 VL 18 IS 1 BP 84 EP 86 DI 10.1177/014860719401800184 PG 3 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MR804 UT WOS:A1994MR80400019 PM 8164313 ER PT J AU GUINAN, EC LOPEZ, KD HUHN, RD FELSER, JM NATHAN, DG AF GUINAN, EC LOPEZ, KD HUHN, RD FELSER, JM NATHAN, DG TI EVALUATION OF GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR FOR TREATMENT OF PANCYTOPENIA IN CHILDREN WITH FANCONI-ANEMIA SO JOURNAL OF PEDIATRICS LA English DT Article ID BONE-MARROW TRANSPLANTATION; APLASTIC-ANEMIA; PHASE-I/II; RECOMBINANT; SUSCEPTIBILITY; NEUTROPENIA; FAILURE AB Fanconi anemia is a congenital syndrome characterized by multiple specific physical anomalies, progressive marrow failure, and a predisposition to acute leukemia. We studied the toxicity and efficacy of daily subcutaneous administration of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) in patients with Fanconi anemia and pancytopenia. The toxicity of GM-CSF at the doses and schedule used was minimal. Six of seven patients entered had an increase in the neutrophil count of 7- to 25-fold, which was maintained during the course of study. Despite increases in the reticulocyte count, increases in hemoglobin concentration were rare. No improvement in platelet count was evident in any patient. No patient has evidence of leukemia after up to 19 months of continuous GM-CSF exposure, and all five surviving patients remain responsive to treatment. Although the optimal dose, schedule, and choice of cytokine for patients with marrow failure and Fanconi anemia are not established by this preliminary study, the data indicate that (1) GM-CSF may be able to palliate at least the neutropenia and potentially the neutropenic complications of the disease, (2) this effect can be sustained for more than 1 year, and (3) rapid evolution of acute leukemia is unlikely to be a frequent outcome of such treatment. The clinical impact of GM-CSF or other cytokines in patients with Fanconi anemia and pancytopenia remains to be established by further studies. C1 SANDOZ PHARMACEUT CORP, CYTOKINE DEV UNIT, E HANOVER, NJ USA. HARVARD UNIV, CHILDRENS HOSP, SCH MED, DIV HEMATOL ONCOL, BOSTON, MA 02115 USA. RP GUINAN, EC (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT PEDIAT ONCOL, 44 BINNEY ST, BOSTON, MA 02115 USA. FU NCRR NIH HHS [M01 RR 02172] NR 24 TC 29 Z9 30 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD JAN PY 1994 VL 124 IS 1 BP 144 EP 150 DI 10.1016/S0022-3476(94)70271-3 PG 7 WC Pediatrics SC Pediatrics GA MQ570 UT WOS:A1994MQ57000026 PM 8283365 ER PT J AU HALGREN, E BAUDENA, P HEIT, G CLARKE, M MARINKOVIC, K AF HALGREN, E BAUDENA, P HEIT, G CLARKE, M MARINKOVIC, K TI SPATIOTEMPORAL STAGES IN FACE AND WORD-PROCESSING .1. DEPTH RECORDED POTENTIALS IN THE HUMAN OCCIPITAL AND PARIETAL LOBES SO JOURNAL OF PHYSIOLOGY-PARIS LA English DT Article DE N400; P300; MEMORY; HIPPOCAMPUS; FUSIFORM-G ID EVENT-RELATED POTENTIALS; HUMAN HIPPOCAMPAL-FORMATION; RECOGNITION MEMORY; ENDOGENOUS POTENTIALS; BRAIN POTENTIALS; RHESUS-MONKEY; VISUAL-CORTEX; EVOKED-POTENTIALS; CORTICAL ACTIVITY; LANGUAGE AREA AB Evoked potentials (EPs) were used to help identify the timing, location, and intensity of the information-processing stages applied to faces and words in humans. EP generators were localized using intracranial recordings in 33 patients with depth electrodes implanted in order to direct surgical treatment of drug-resistant epilepsy. While awaiting spontaneous seizure onset, the patients gave their fully informed consent to perform cognitive tasks. Depth recordings were obtained from 1198 sites in the occipital. temporal and parietal cortices, and in the limbic system (amygdala, hippocampal formation and posterior cingulate gyrus). Twenty-three patients received a declarative memory recognition task in which faces of previously unfamiliar young adults without verbalizable distinguishing features were exposed for 300 ms every 3 s; 25 patients received an analogous task using words. For component identification, some patients also received simple auditory (21 patients) or visual (12 patients) discrimination tasks. Eight successive EP stages preceding the behavioral response (at about 600 ms) could be distinguished by latency, and each of 14 anatomical structures was found to participate in 2-8 of these stages. The earliest response, an N75-P105, focal in the most medial and posterior of the leads implanted in the occipital lobe (lingual g), was probably generated in visual cortical areas 17 and 18. These components were not visible in response to words, presumably because words were presented foveally. A focal evoked alpha rhythm to both words and faces was also noted in the lingual g. This was followed by an N130-P180-N240 focal and polarity-inverting in the basal occipitotemporal cortex (fusiform g, probably areas 19 and 37). In most cases, the P180 was evoked only by faces, and not by words, letters or symbols. Although largest in the fusiform g this sequence of potentials (especially the N240) was also observed in the supramarginal g, posterior superior and middle temporal g, posterior cingulate g, and posterior hippocampal formation. The N130, but not later components of this complex, was observed in the anterior hippocampus and amygdala. Faces only also evoked longer-latency potentials up to 600 ms in the right fusiform g. Words only evoked a series of potentials beginning at 190 ms and extending to 600 ms in the fusiform g and near the angular g (especially left). Both words and faces evoked a N150-P200-PN260 in the lingual g, and posterior inferior and middle temporal g. A N310-N430-P630 sequence to words and faces was largest and polarity-inverted in the hippocampal formation and amygdala, but was also probably locally-generated in many sites including the lingual g, lateral occipitotemporal cortex, middle and superior temporal g, temporal pole, supramarginal g, and posterior cingulate g. The P660 had the same distribution as has been noted for the P3b to rare target simple auditory and visual stimuli in 'oddball' tasks, with inversions in the hippocampus. In several sites, the N310 and N430 were smaller to repeated faces, and the P630 was larger. Putative information-processing functions were tentatively assigned to successive EP components based upon their cognitive correlates, as well as the functions and connections of their generating structures. For the N75-P105, this putative function is simple feature detection in primary visual cortex (V1 and V2). The N130-P180-N240 may embody structural face encoding in posterobasal inferotemporal cortex (homologous to V4?), with the results being spread widely to inferotemporal, multimodal and paralimbic cortices. For words, similar visual-form encoding (in fusiform g) or visual-phonemic encoding (in angular g) may occur between 150 and 280 ms. During the N310, faces and words may be multiply encoded for form and identity (inferotemporal), emotional (amygdala), recent declarative mnestic (hippocampal formation), and semantic (supramarginal and superior temporal sulcal supramodal cortices) characteristics. These multiple characteristics may be contextually integrated across inferotemporal, supramodal association, and limbic cortices during the N430, with cognitive closure following in the P630. In sum, visual information arrives at area 17 by about 75 ms, and is structurally-encoded in occipito-temporal cortex during the next 110 ms. By 150-200 ms after stimulus onset, activation has spread to parietal, lateral temporal, and limbic cortices, all of which continue to participate with the more posterior areas for the next 500 ms of event-encoding. Thus, face and word processing is serial in the sense that it can be divided into successive temporal stages, but highly parallel in that (after the initial stages where visual primitives are extracted) multiple anatomical areas with distinct perceptual, mnestic and emotional functions are engaged simultaneously. Consequently, declarative memory and emotional encoding can participate in early stages of perceptual, as well as later stages of cognitive integration. Conversely, occipitotemporal cortex is involved both early in processing (immediately after V1), as well as later, in the N430. That is, most stages of face and word processing appear to take advantage of the rich 'upstream' and 'downstream' anatomical connections in the ventral visual processing stream to link the more strictly perceptual networks with semantic, emotional, and mnestic networks. C1 CTR PAUL BROCA, INSERM, U97, F-75014 PARIS, FRANCE. UNIV CALIF LOS ANGELES, W LOS ANGELES VAMC, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA 90024 USA. STANFORD UNIV, STANFORD, CA 94305 USA. UNIV N TEXAS, DEPT PSYCHOL, DENTON, TX 76203 USA. UNIV CALIF LOS ANGELES, DEPT PSYCHOL, STANFORD, CA 94305 USA. RP HALGREN, E (reprint author), CHRU PONTCHAILLOU, NEUROL CLIN, INSERM, CJF 90-12, F-35033 RENNES, FRANCE. FU NINDS NIH HHS [R01 NS018741] NR 200 TC 278 Z9 280 U1 0 U2 14 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0928-4257 J9 J PHYSIOL-PARIS JI J. Physiol.-Paris PY 1994 VL 88 IS 1 BP 1 EP 50 DI 10.1016/0928-4257(94)90092-2 PG 50 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA NP319 UT WOS:A1994NP31900001 PM 8019524 ER PT J AU HALGREN, E BAUDENA, P HEIT, G CLARKE, M MARINKOVIC, K CHAUVEL, P AF HALGREN, E BAUDENA, P HEIT, G CLARKE, M MARINKOVIC, K CHAUVEL, P TI SPATIOTEMPORAL STAGES IN FACE AND WORD-PROCESSING .2. DEPTH-RECORDED POTENTIALS IN THE HUMAN FRONTAL AND ROLANDIC CORTICES SO JOURNAL OF PHYSIOLOGY-PARIS LA English DT Article DE N400; P300; MEMORY; ORBITOFRONTAL; CINGULATE ID MOVEMENT-RELATED POTENTIALS; HUMAN HIPPOCAMPAL-FORMATION; SUPPLEMENTARY MOTOR AREA; EVENT-RELATED POTENTIALS; VISUAL EVOKED-POTENTIALS; RHESUS-MONKEY; VOLUNTARY MOVEMENTS; ENDOGENOUS POTENTIALS; RECOGNITION MEMORY; BRAIN POTENTIALS AB Evoked potentials (EPs) were recorded directly from 650 frontal and peri-Rolandic sites in 26 subjects during face and/or word recognition, as well as during control tasks (simple auditory and visual discrimination). Electrodes were implanted in order to localize epileptogenic foci resistant to medication, and thus direct their surgical removal. While awaiting spontaneous seizure onset, the patients gave informed consent to perform cognitive tasks during intracerebral EEG recording. The earliest potentials appeared to be related to sensory stimulation, were prominent in lateral prefrontal cortex, and occurred at peak latencies of about 150 and 190 ms. A small triphasic complex beginning slightly later (peak latencies about 200-285-350 ms) appeared to correspond to the scalp N2-P3a-slow wave, associated with non-specific orienting. Multiple components peaking from 280 to 900 ms. and apparently specific to words were occasionally recorded in the left inferior frontal g, pars triangularis (Broca's area). Components peaking at about 430 and 600 ms were recorded in all parts of the prefrontal cortex, but were largest (up to 180 muV) and frequently polarity-inverted in the ventro-lateral prefrontal cortex. These components appeared to represent the N4-P3b, which have been associated with contextual integration and cognitive closure. Finally, a late negativity (650-900 ms) was recorded in precentral and premotor cortices, probably corresponding to a peri-movement readiness potential. In summary, EP components related to early sensory processing were most prominent in lateral prefrontal, to orienting in medial limbic, to word-specific processing in Broca's area, to cognitive integration in ventro-lateral prefrontal, and to response organization in premotor cortices. Thus, multiple frontal areas are involved in multiple stages of face and word processing, in a highly parallel but nonetheless differentiated manner. C1 CTR PAUL BROCA, INSERM, U97, F-75014 PARIS, FRANCE. UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR, CTR EPILEPSY, LOS ANGELES, CA 90024 USA. STANFORD UNIV, DEPT NEUROSURG, STANFORD, CA 94305 USA. UNIV N TEXAS, DEPT PSYCHOL, DENTON, TX 76203 USA. UNIV CALIF LOS ANGELES, DEPT PSYCHOL, STANFORD, CA 94305 USA. RP HALGREN, E (reprint author), CHRU PONTCHAILLOU, NEUROL CLIN, INSERM, CJF 90-12, F-35033 RENNES, FRANCE. FU NINDS NIH HHS [NS18741] NR 154 TC 152 Z9 152 U1 0 U2 6 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0928-4257 J9 J PHYSIOL-PARIS JI J. Physiol.-Paris PY 1994 VL 88 IS 1 BP 51 EP 80 DI 10.1016/0928-4257(94)90093-0 PG 30 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA NP319 UT WOS:A1994NP31900002 PM 8019525 ER PT J AU SORMANTI, M DUNGAN, S RIEKER, PP AF SORMANTI, M DUNGAN, S RIEKER, PP TI PEDIATRIC BONE-MARROW TRANSPLANTATION - PSYCHOSOCIAL ISSUES FOR PARENTS AFTER A CHILDS HOSPITALIZATION SO JOURNAL OF PSYCHOSOCIAL ONCOLOGY LA English DT Article ID QUALITY-OF-LIFE; SURVIVORS; CANCER; ADJUSTMENT; STRESS AB Bone marrow transplantation (BMT), once a highly experimental procedure performed in only a handful of medical centers, has become increasingly common and is now considered to be the treatment of choice for some diseases. Although a growing number of pediatric patients undergo this life-saving procedure, psychosocial research has focused primarily on adult BMT patients. This article presents data from an exploratory study of 73 parents whose children successfully completed the transplant. The study identified the major concerns and needs of this unique population as they coped with life after a child's transplant. The results indicated that although most parents coped adequately, certain problems such as financial strains and fears of relapse remained. C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. RP SORMANTI, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 35 TC 19 Z9 19 U1 0 U2 1 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0734-7332 J9 J PSYCHOSOC ONCOL JI J. Psychosoc. Oncol. PY 1994 VL 12 IS 4 BP 23 EP 42 PG 20 WC Psychology, Social SC Psychology GA QJ143 UT WOS:A1994QJ14300002 ER PT J AU SORMANTI, M AF SORMANTI, M TI FIELDWORK INSTRUCTION IN ONCOLOGY SOCIAL-WORK - SUPERVISORY ISSUES SO JOURNAL OF PSYCHOSOCIAL ONCOLOGY LA English DT Article AB This article reports a study of supervisory issues that are unique to working with social work students who are placed in an oncology setting. The author used focus-group methodology to interview 10 female supervisors from hospitals in the greater Boston area whose mean number of years in oncology was 10.5 years. Three main themes emerged during the interview. One, oncology social work is different from and perhaps more difficult than social work in other settings; thus, supervision of beginners differs from supervision of beginners in other specialties. Two, the problems in oncology are difficult to grapple with; therefore, a certain type of student is required to do the work well. Three, gaps in the curricula of schools of social work have a negative impact on the total learning experience of students in oncology and other medical settings. The group also discussed concerns that students bring to supervision, including somatic reactions, dissynchrony with peers, and countertransference. The author offers recommendations for dealing with the issues raised in the focus group. C1 BOSTON COLL,SCH SOCIAL WORK,CHESTNUT HILL,MA 02167. RP SORMANTI, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 29 TC 9 Z9 9 U1 1 U2 2 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0734-7332 J9 J PSYCHOSOC ONCOL JI J. Psychosoc. Oncol. PY 1994 VL 12 IS 3 BP 73 EP 87 DI 10.1300/J077V12N03_05 PG 15 WC Psychology, Social SC Psychology GA PX994 UT WOS:A1994PX99400005 ER PT J AU BAINES, MG BILLINGSLEY, KA DEFOUGEROLLES, AR DUCLOS, AJ OLNEY, HJ POMERANTZ, DK GENDRON, RL AF BAINES, MG BILLINGSLEY, KA DEFOUGEROLLES, AR DUCLOS, AJ OLNEY, HJ POMERANTZ, DK GENDRON, RL TI EVALUATION OF THE ROLE OF EXOGENOUS PATHOGENS ON THE INCIDENCE OF EMBRYO LOSS DURING EARLY-PREGNANCY IN MICE SO JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Article DE PREGNANT; SPONTANEOUS ABORTION; RESORPTION; PATHOGENS; INFECTION ID SPONTANEOUS-ABORTION; FETAL RESORPTION; CELLS; MECHANISMS; FAILURE AB The mating of CBA/j female mice (H2(k)) by DBA/2j male mice (H2(d)) typically results in an elevated incidence of spontaneous embryo loss thus providing an ideal genetically controlled laboratory model for the study of the factors causing early embryo loss during pregnancy. There is now considerable data on the cells and factors involved in fetal resorption but little is known about the events which activate this process. While the activation of the maternal response to the fetal implant could have endogenous or genetic origins, a role for exogenous factors including microbial pathogens could also be involved. In order to investigate these possibilities, the reproductive success of CBA/j female x DBA/2j male matings in a conventional animal care facility were compared with matings in a specific pathogen free (SPF) animal facility. All animals housed under these conditions were routinely screened by immunoassay and culture, for the presence of a number of viral and bacterial pathogens of mice. The incidence of spontaneous embryo loss in specific pathogen free CBA female mice mated by DBA and other male strains was found to be virtually identical to that of CBA female mice infected with multiple viral pathogens and housed under otherwise identical conditions (non-SPF). However, the numbers of implantation per pregnancy was significantly greater in an SPF facility. Therefore, exposure of mating mice to exogenous viral and bacterial pathogens did not appear to alter the overall incidence of spontaneous embryo resorption. It was concluded that the immunomodulatory effects of infection by common murine pathogens neither augmented nor reduced post-implantation embryo losses. C1 UNIV WESTERN ONTARIO,DEPT PHYSIOL,LONDON N6A 5C1,ONTARIO,CANADA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP BAINES, MG (reprint author), MCGILL UNIV,DEPT MICROBIOL & IMMUNOL,3775 UNIV ST,MONTREAL H3A 2B4,QUEBEC,CANADA. NR 28 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-0378 J9 J REPROD IMMUNOL JI J. Reprod. Immunol. PD JAN PY 1994 VL 26 IS 1 BP 17 EP 30 DI 10.1016/0165-0378(93)00863-O PG 14 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA ND301 UT WOS:A1994ND30100002 PM 8040834 ER PT J AU CAPLAN, D UTMAN, JA AF CAPLAN, D UTMAN, JA TI SELECTIVE ACOUSTIC-PHONETIC IMPAIRMENT AND LEXICAL ACCESS IN AN APHASIC PATIENT SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article ID SPOKEN WORD-RECOGNITION; AUDITORY COMPREHENSION; SPEECH AB The relationship between acoustic-phonetic disturbances and lexical access was explored in an aphasic patient. M.L. had a restricted disturbance of phonemic discrimination that affected the discrimination of voicing contrasts in nonword stimuli. Despite this impairment, her discrimination of voicing contrasts in words and her comprehension of auditorily presented words containing voiced segments was excellent. Performance on lexical decision was unpaired: M.L.'s rejection of nonwords was poor and her reaction times and error rates for word stimuli showed a trend toward being influenced by the lexical status (word or nonword) of the item that would be formed by a change in voicing. The results are consistent with a role for a phonemic code in auditory word recognition, coupled with lexical-to-acoustic/phonetic feedback, but are also compatible with the view that other access codes for the Phonological Input Lexicon are also available. RP CAPLAN, D (reprint author), MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,VINCENT BURNHAM 827,FRUIT ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC00776-01] NR 37 TC 18 Z9 18 U1 0 U2 3 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 JAN PY 1994 VL 95 IS 1 BP 512 EP 517 DI 10.1121/1.408345 PG 6 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA MR055 UT WOS:A1994MR05500053 PM 8120262 ER PT J AU WILENS, TE BIEDERMAN, J AF WILENS, TE BIEDERMAN, J TI SAFETY OF CLONIDINE AND NORTRIPTYLINE - REPLY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP WILENS, TE (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1994 VL 33 IS 1 BP 143 EP 143 DI 10.1097/00004583-199401000-00022 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA MQ579 UT WOS:A1994MQ57900022 ER PT J AU ROELKE, M GARAN, H MCGOVERN, BA RUSKIN, JN AF ROELKE, M GARAN, H MCGOVERN, BA RUSKIN, JN TI ANALYSIS OF THE INITIATION OF SPONTANEOUS MONOMORPHIC VENTRICULAR-TACHYCARDIA BY STORED INTRACARDIAC ELECTROGRAMS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR; ARRHYTHMIAS; SEQUENCE; COMPLEXES; SURVIVAL; TORSADE; POINTES; DEATH AB Objectives. This study was designed to analyze stored intracardiac electrograms generated during spontaneous monomorphic ventricular tachycardia to examine the possible mechanisms responsible for the initiation of ventricular tachycardia in a group of postinfarction patients. Background. Implantable cardioverter-defibrillators capable of storing electrograms during an arrhythmic event provide an intracardiac electrogram analog to Holter ambulatory electrocardiographic monitoring. Such electrograms are of value in arrhythmia diagnosis and in determining the appropriateness of implantable cardioverter-defibrillator therapy and may aid in understanding the initiation of ventricular arrhythmias. Methods. We studied 73 stored electrograms in 22 postinfarction patients with spontaneous monomorphic ventricular tachycardia. Premature depolarizations before tachycardia were classified by morphology and number. Electrogram morphology was compared with the morphology of the baseline rhythm and ventricular tachycardia. Prematurity was assessed by the coupling interval and a calculated prematurity ratio. Results. During baseline rhythm, ectopic activity was present in 30 (41%) of 73 stored episodes. Ventricular tachycardia was preceded by a short-long-short sequence in 14% of episodes and by a rapid ventricular rhythm in 5.5% of episodes. The onset of ventricular tachycardia was marked by single premature depolarizations in 33 episodes (45%), by pairs in 16 (22%) and by multiple complexes in 24 (33%). Morphology was similar to that of the ensuing tachycardia in 35 episodes (48%). The mean coupling interval was 364 ms, and the mean prematurity ratio was 0.56. In all 10 episodes (14%) where the prematurity ratio was <0.40, a short-long-short sequence was responsible. When classified by morphology, the mean prematurity ratio of depolarizations dissimilar to ventricular tachycardia (0.53) was significantly less than that of the morphologically similar group (0.60, p = 0.035). Conclusions. In this select group of postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter-defibrillators, ventricular tachycardia was most often preceded by late-coupled premature depolarizations. Not infrequently, a short-long-short sequence occurred before tachycardia. Premature depolarizations with a morphology different from that of the tachycardia occurred earlier in the cardiac cycle than did those with a morphology similar to that of the tachycardia. These findings may reflect different mechanisms of ventricular tachycardia initiation. C1 MASSACHUSETTS GEN HOSP,CARDIAC ARRHYTHMIA SERV,FRUIT ST,BOSTON,MA 02114. NR 24 TC 65 Z9 66 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 JAN PY 1994 VL 23 IS 1 BP 117 EP 122 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MQ784 UT WOS:A1994MQ78400016 PM 8277069 ER PT J AU RIVERA, JM SIU, SC HANDSCHUMACHER, MD LETHOR, JP GUERRERO, JL VLAHAKES, GJ MITCHELL, JD WEYMAN, AE KING, MEE LEVINE, RA AF RIVERA, JM SIU, SC HANDSCHUMACHER, MD LETHOR, JP GUERRERO, JL VLAHAKES, GJ MITCHELL, JD WEYMAN, AE KING, MEE LEVINE, RA TI 3-DIMENSIONAL RECONSTRUCTION OF VENTRICULAR SEPTAL-DEFECTS - VALIDATION STUDIES AND IN-VIVO FEASIBILITY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID TWO-DIMENSIONAL ECHOCARDIOGRAPHY; TRANSCATHETER CLOSURE; COLOR DOPPLER; REAL-TIME; VOLUME; FLOW; DISPLAY; IMAGES; CHILDREN; ACCURACY AB Objectives. The purpose of this study was to demonstrate the feasibility of in vivo three-dimensional reconstruction of ventricular septal defects and to validate its quantitative accuracy for defect localization in excised hearts (used to permit comparison of three-dimensional and direct measurements without cardiac contraction). Background. Appreciating the three-dimensional spatial relations of ventricular septal defects could be useful in planning surgical and catheter approaches. Currently, however, echocardiography provides only two-dimensional views, requiring mental integration. A recently developed system automatically combines two-dimensional echocardiographic images with their spatial locations to produce a three-dimensional construct. Methods. Surgically created ventricular septal defects of varying size and location were imaged and reconstructed, along with the left and right ventrides, in the beating heart of six dogs to demonstrate the in vivo feasibility of producing a coherent image of the defect that portrays its relation to surrounding structures. Two additional gel-filled excised hearts with defects were completely reconstructed. Quantitative localization of the defects relative to other structures (ventricular apexes and valve insertions) was then validated for seven defects in excised hearts. The right septal margins of the exposed defects were also traced and compared with their reconstructed areas and circumferences. Results. The three-dimensional images provided coherent images and correct spatial appreciation of the defects (two inlet, two trabecular, one outlet and one membranous Gerbode in vivo; one inlet and one apical in excised hearts). The distances between defects and other structures in the excised hearts agreed well with direct measures (y = 1.05x - 0.18, r = 0.98, SEE = 0.30 cm), as did reconstructed areas (y = 1.0x - 0.23, r = 0.98, SEE = 0.21 cm2) and circumferences (y = 0.97x + 0.13, r = 0.97, SEE = 0.3 cm). Conclusions. Three-dimensional reconstruction of ventricular septal defects can be achieved in the beating heart and provides an accurate appreciation of defect size and location that could be of value in planning interventions. C1 MASSACHUSETTS GEN HOSP,NONINVAS CARDIAC LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI rivera, miguel/D-5026-2014 FU NHLBI NIH HHS [HL 38176] NR 57 TC 44 Z9 44 U1 0 U2 3 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 JAN PY 1994 VL 23 IS 1 BP 201 EP 208 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MQ784 UT WOS:A1994MQ78400028 PM 8277082 ER PT J AU LUPTON, JR ROBINSON, MC MORIN, JL AF LUPTON, JR ROBINSON, MC MORIN, JL TI CHOLESTEROL-LOWERING EFFECT OF BARLEY BRAN FLOUR AND OIL SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID SERUM-LIPID RESPONSE; BLOOD-PRESSURE; HYPERCHOLESTEROLEMIC MEN; METABOLISM; GRAIN; CEREALS; PRODUCT; WHEAT; FOODS; DIET AB Objective To compare the effects of adding barley bran flour and a barley oil extract to a fat-modified diet on serum lipids in persons with hypercholesterolemia. Design The basic design of the study was a randomized, 30-day intervention trial: it included a neutral-fiber control group and a 1-week preintervention period for the collection of baseline data. Subjects The subjects were 79 men aad women with hyper cholesterolemia. Subjects had a mean age of 48.2 years, and all completed the study. Intervention All participants were instructed to follow the National Cholesterol Education Program (NCEP) step I diet and were randomly assigned to one of three treatment groups: 20 g added cellulose; 3 g added barley oil extract, or 30 g added barley bran flour. Main outcome measures Total serum cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and very-low-density lipoprotein cholesterol were measured, along with serum triglycerides, before the intervention, at week I, at week 3, and at the end of the intervention. Statistical analyses performed Student's paired t test was used to detect significant changes within each treatment group from baseline to the end of the 30-day intervention. Ln addition, Pearson's correlation coefficients were used to detect significant correlations between the variables measured. Results Addition of barley bran flour significantly (P=.0001) decreased total serum cholesterol (-0.60 mmol/L as did addition of barley oil (-0.50 mmol/L, P=.002) after 30 days of intervention. Similarly, LDL-C decreased 6.5% with addition of barley bran flour (P=.036) and 9.2% with addition of barley oil (P=.003), Total serum cholesterol or LDL-C of the cellulose control group did not decrease significantly over the same period. HDL-C decreased significantly in the cellulose control group and the barley bran flour group (-0.15 mmol/L, P=.012, and -0.15 mmol/L, P=.006, respectively), but not in the barley oil group. Conclusion We conclude that addition of barley bran flour or barley oil enhances the cholesterol-lowering effect of the NCEP step 1 diet in individuals with hypercholesterolemia. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. OLIN E TEAGUE VET ADM MED CTR,TEMPLE,TX 76504. RP LUPTON, JR (reprint author), TEXAS A&M UNIV,FAC NUTR,COLL STN,TX 77843, USA. NR 34 TC 50 Z9 52 U1 0 U2 5 PU AMER DIETETIC ASSN 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 JAN PY 1994 VL 94 IS 1 BP 65 EP 70 DI 10.1016/0002-8223(94)92044-3 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MR351 UT WOS:A1994MR35100016 PM 8270757 ER PT J AU JENDERS, RA ESTEY, G MARTIN, M HAMILTON, G FORDCARLETON, P THOMPSON, BT OLIVER, DE ECCLES, R BARNETT, GO ZIELSTORFF, RD FITZMAURICE, JB AF JENDERS, RA ESTEY, G MARTIN, M HAMILTON, G FORDCARLETON, P THOMPSON, BT OLIVER, DE ECCLES, R BARNETT, GO ZIELSTORFF, RD FITZMAURICE, JB TI INDEXING GUIDELINES - APPLICATIONS IN USE OF PULMONARY-ARTERY CATHETERS AND PRESSURE ULCER PREVENTION SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC ID KNOWLEDGE AB In a busy clinical environment, access to knowledge must be rapid and specific to the clinical query at hand. This requires indices which support easy navigation within a knowledge source. We have developed a computer-based tool for trouble-shooting pulmonary artery waveforms using a graphical index. Preliminary results of domain knowledge tests for a group of clinicians exposed to the system (N = 33) show a mean improvement on a 30-point test of 5.33 (p<0.001) compared to a control group (N = 19) improvement of 0.47 (p = 0.61). Survey of the experimental group (N = 25) showed 84% (p = 0.001) found the system easy to use. We discuss lessons learned in indexing this domain area to computer-based indexing of guidelines for pressure ulcer prevention. RP JENDERS, RA (reprint author), MASSACHUSETTS GEN HOSP,COMP SCI LAB,BOSTON,MA 02114, USA. NR 9 TC 0 Z9 0 U1 0 U2 0 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. PY 1994 SU S BP 802 EP 806 PG 5 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 QF216 UT WOS:A1994QF21600141 ER PT J AU MERZ, RB CIMINO, C BARNETT, GO BLEWETT, DR GNASSI, JA GRUNDMEIER, R HASSAN, L AF MERZ, RB CIMINO, C BARNETT, GO BLEWETT, DR GNASSI, JA GRUNDMEIER, R HASSAN, L TI A PRE-SEARCH ESTIMATION ALGORITHM FOR MEDLINE STRATEGIES WITH QUALIFIERS SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC ID CO-OCCURRENCE DATA; INFORMATION-RETRIEVAL AB Inexperienced users of online medical databases often have difficulty formulating their queries. Systems designed to assist them usually do not estimate how effective the initial search strategy will be before performing an actual search. Consequently, the search may find an overwhelming number of citations, or retrieve nothing at all. We have developed an estimation algorithm to predict the outcome of a MEDLINE search. The portion of the algorithm described here estimates retrieval for strategies containing qualifiers. In test searches, the estimate reduced the trial-and-error of strategy formulation. However, the accuracy of the estimate fell short of expectations. Our results show that pre-search estimation for strategies with qualifiers cannot be performed effectively with only the occurrence data that is presently available. They further imply that automated search intermediaries can benefit from medical knowledge which expresses the relationships that exist between terms. C1 MASSACHUSETTS GEN HOSP,COMP SCI LAB,BOSTON,MA 02114. NR 17 TC 0 Z9 0 U1 0 U2 0 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. PY 1994 SU S BP 910 EP 914 PG 5 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 QF216 UT WOS:A1994QF21600160 ER PT J AU ZIELSTORFF, RD ESTEY, G FITZMAURICE, JB MARTIN, M BARNETT, GO AF ZIELSTORFF, RD ESTEY, G FITZMAURICE, JB MARTIN, M BARNETT, GO TI USER EVALUATION - PA CATHETER WAVE-FORMS TROUBLESHOOTING SYSTEM SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC AB This paper reports on a user satisfaction survey of a system for consultation and education in troubleshooting pulmonary artery catheter waveforms. The twelve-item End-User Computing Satisfaction Questionnaire was used to assess users' rating in four areas. On a scale of 1-5 (with 1 the lowest), the ratings were: Contents, 3.5; Accuracy, 4.5; Format, 4.2; Ease of Use, 4.4, and Timeliness, 4.1. Comparison with ratings in a survey that included a variety of applications and settings is provided. RP ZIELSTORFF, RD (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 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. PY 1994 SU S BP 1008 EP 1008 PG 1 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 QF216 UT WOS:A1994QF21600215 ER PT J AU GNASSI, JA BORMEL, JI BLEWETT, DR KIM, RJ BARNETT, O AF GNASSI, JA BORMEL, JI BLEWETT, DR KIM, RJ BARNETT, O TI A MEDICAL INFORMATION RESOURCE SERVER - ONE-STOP SHOPPING ON THE INTERNET SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC RP GNASSI, JA (reprint author), MASSACHUSETTS GEN HOSP,COMP SCI LAB,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 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. PY 1994 SU S BP 1025 EP 1025 PG 1 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 QF216 UT WOS:A1994QF21600228 ER PT J AU BARNETT, GO LINK, DA FELDMAN, MJ COLEMAN, MA FAMIGLIETTI, KT KIM, RJ RAILA, WF MCARDLE, P AF BARNETT, GO LINK, DA FELDMAN, MJ COLEMAN, MA FAMIGLIETTI, KT KIM, RJ RAILA, WF MCARDLE, P TI CLINICAL-ASSESSMENT - A COMPUTER-BASED AID TO ASSESSING THE CLINICAL PROBLEM-SOLVING ABILITY OF MEDICAL-STUDENTS SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC RP BARNETT, GO (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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. PY 1994 SU S BP 1045 EP 1045 PG 1 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 QF216 UT WOS:A1994QF21600248 ER PT J AU ESTEY, G FORDCARLETON, P THOMPSON, BT JENDERS, RA OLIVER, DE ECCLES, R MARTIN, M ZIELSTORFF, R FITZMAURICE, JB BARNETT, GO AF ESTEY, G FORDCARLETON, P THOMPSON, BT JENDERS, RA OLIVER, DE ECCLES, R MARTIN, M ZIELSTORFF, R FITZMAURICE, JB BARNETT, GO TI THE PA CATHETER WAVE-FORMS TROUBLESHOOTING SYSTEM - A DEMONSTRATION OF SIMPLE GRAPHICAL KNOWLEDGE ACCESS FOR CLINICAL CARE SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article; Proceedings Paper CT 18th Annual Symposium on Computer Applications in Medical Care - Transforming Information, Changing Health Care CY NOV 05-09, 1994 CL WASHINGTON, DC SP AMER MED INFORMAT ASSOC RP ESTEY, G (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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. PY 1994 SU S BP 1052 EP 1052 PG 1 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 QF216 UT WOS:A1994QF21600255 ER PT J AU RABITO, CA PANICO, F RUBIN, R TOLKOFFRUBIN, N TEPLICK, R AF RABITO, CA PANICO, F RUBIN, R TOLKOFFRUBIN, N TEPLICK, R TI NONINVASIVE, REAL-TIME MONITORING OF RENAL-FUNCTION DURING CRITICAL CARE SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE CRITICAL CARE; ACUTE RENAL FAILURE; DIETHYLENE TRIAMINE PENTAACETIC ACID; GFR; CREATININE ID GLOMERULAR-FILTRATION RATE; CADMIUM TELLURIDE DETECTOR; CDTE DETECTOR; FAILURE; MANAGEMENT AB The inadequacy of the current techniques to monitor renal function has been the most important limitation for determining the appropriateness of a particular form of therapy in acute renal failure. The objective of this study was to determine the advantage offered by a new method of accurate, noninvasive, and realtime monitoring of renal function during the critical care of patients. A radiation detector attached to a miniature data logger was used to monitor the clearance of the glomerular filtration agent Tc-99m-diethylene triamine pentaacetic acid from the extracellular space in 20 patients admitted into an intensive care unit. The rate constant for this clearance was calculated online from 5-min epoch lengths of activity versus time. Changes in this constant were compared with changes in plasma creatinine and timed urine output. The results showed that the ambulatory renal monitor could accurately measure rapid changes in renal function during the critical care of patients who are at risk of acute renal failure with a resolution time of 5 to 10 min. The sensitivity and specificity of the technique are also superior to plasma creatinine and urine output because it can detect minimal and transient changes in renal function that otherwise may have gone undetected by these parameters. This unique approach should allow for the immediate institution and/or adjustment of the appropriate therapeutic procedure to preserve or improve the renal function. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT INTERNAL MED,BOSTON,MA 02114. RP RABITO, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114, USA. NR 26 TC 23 Z9 24 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD JAN PY 1994 VL 4 IS 7 BP 1421 EP 1428 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA MU490 UT WOS:A1994MU49000005 PM 8161724 ER PT J AU GERTLER, JP BLANKENSTEIJN, JD BREWSTER, DC MONCURE, AC CAMBRIA, RP LAMURAGLIA, GM DARLING, RC ABBOTT, WM AF GERTLER, JP BLANKENSTEIJN, JD BREWSTER, DC MONCURE, AC CAMBRIA, RP LAMURAGLIA, GM DARLING, RC ABBOTT, WM TI CAROTID ENDARTERECTOMY FOR UNSTABLE AND COMPELLING NEUROLOGIC CONDITIONS - DO RESULTS JUSTIFY AN AGGRESSIVE APPROACH SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 41st Scientific Meeting of the International-Society-for-Cardiovascular-Surgery, North-American-Chapter CY JUN 07-08, 1993 CL WASHINGTON, DC SP INT SOC CARDIOVASC SURG, N AMER CHAPTER ID ARTERY OCCLUSION; CEREBROVASCULAR-DISEASE; SUGGESTED STANDARDS; EMERGENCY-SURGERY; MANAGEMENT; ISCHEMIA; THROMBOENDARTERECTOMY; DEFICITS; WORK AB Purpose: In a retrospective study the outcome of 70 carotid endarterectomies (CEA) in 68 patients with neurologically unstable conditions or anatomically compelling findings on carotid angiography was examined to more accurately identify patients who might benefit from CEA in this setting. Methods: Out of a total of 1734 CEAs performed from 1978 to 1992, five groups of patients were selected: group A, stroke in evolution with tight stenosis (n = 5); group C, crescendo transient ischemic attacks (CTIA) continuing despite heparin (n = 14); group D, CTIA (above criteria) ceasing with heparin (n = 21); and group E, anatomically compelling situation on carotid angiography (n = 13). Data collected included preoperative and postoperative Neurologic Event Severity Score (NESS), CHAT classification, arteriosclerosis risk factors, demographics, and long-term overall and transient ischemic attack/stroke-free survival rates. Results: Risk factors and demographics were similar in all groups. By NESS criteria the conditions of 97.3% of patients in the neurologically unstable groups A to C were improved or stabilized after operation, with one deterioration (2.7%). All patients in group B either stabilized or improved. In group D, one patient's NESS deteriorated, resulting in 3.5% overall morbidity rate and no deaths for groups A to D. Follow-up showed an overall survival rate by Kaplan-Meier analysis equivalent to a matched control population, with 85% alive at 5 years. The cumulative TLA/stroke-free survival rate at 5 years was 75%. Conclusions: In this retrospective series, CEA performed for compelling or unstable neurologic findings carried low morbidity and mortality rates. Early aggressive surgical therapy of neurologically unstable patients may be warranted because our results improved on the anticipated natural history of the conditions studied. Further clarification of proper patient selection is necessary before this principle can be applied broadly. RP GERTLER, JP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR AMBULATORY CARE,DEPT SURG,BOSTON,MA 02114, USA. RI Blankensteijn, Jan/Q-9291-2016 OI Blankensteijn, Jan/0000-0002-2062-8749 NR 50 TC 42 Z9 43 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD JAN PY 1994 VL 19 IS 1 BP 32 EP 42 PG 11 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA MU494 UT WOS:A1994MU49400004 PM 8301736 ER PT J AU LI, ML GARCEA, RL AF LI, ML GARCEA, RL TI IDENTIFICATION OF THE THREONINE PHOSPHORYLATION SITES ON THE POLYOMAVIRUS MAJOR CAPSID PROTEIN VP1 - RELATIONSHIP TO THE ACTIVITY OF MIDDLE T-ANTIGEN SO JOURNAL OF VIROLOGY LA English DT Article ID HOST RANGE; CELL-TRANSFORMATION; MOUSE KIDNEY; VIRUS; RESOLUTION; MUTANTS; GENE; ENCAPSIDATION; VIRIONS AB Phosphorylation of the polyomavirus major capsid protein VP1 nas examined after in vivo P-32 labeling of virus-infected cells. Two phosphorylated peptide fragments of VP1 were identified by protease digestion, high-performance liquid chromatography purification, mass spectrometry, and N-terminal sequencing. The peptides from residues 58 to 78 and residues 153 to 173 were phosphorylated on threonine. Site-directed mutations were introduced at these threonine sites, and mutant viruses were reconstructed. A threonine-to-glycine change at residue 63 (mutant G63) and a threonine-to-alanine change at residue 156 (mutant A156) resulted in viruses defective in phosphorylation of the respective peptides after in vivo labeling. Growth of the mutant G63 virus was similar to that of the wild-type virus, but the mutant A156 was inefficient in assembly of 240S viral particles. Polyomavirus nontransforming host range (hr-t) mutants are defective in VP1 threonine phosphorylation when grown in nonpermissive cells (R. L. Garcea, K. Ballmer-Hofer, and T. L. Benjamin, J. Virol. 54:311-316, 1985). Proteolytic mapping of VP1 peptides after in vivo labeling from hr-t mutant virus infections demonstrated that both residues T-63 and T-156 were affected. These results suggest that the block in virion assembly in hr-t mutant viruses is associated with a defect in phosphorylation of threonine 156. C1 DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA 02115. FU NCI NIH HHS [CA37667, R01 CA037667] NR 31 TC 23 Z9 23 U1 0 U2 1 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 JAN PY 1994 VL 68 IS 1 BP 320 EP 327 PG 8 WC Virology SC Virology GA MW251 UT WOS:A1994MW25100035 PM 8254743 ER PT J AU RIEDEL, H AF RIEDEL, H TI EPIDERMAL GROWTH-FACTOR (EGF) MODULATION OF FELINE SARCOMA-VIRUS FMS TYROSINE KINASE-ACTIVITY, INTERNALIZATION, DEGRADATION, AND TRANSFORMING POTENTIAL IN AN EGF RECEPTOR/V-FMS CHIMERA SO JOURNAL OF VIROLOGY LA English DT Article ID STIMULATING FACTOR-I; NIH 3T3 CELLS; PROTO-ONCOGENE PRODUCT; HUMAN INSULIN-RECEPTOR; HUMAN-FIBROBLASTS; PHORBOL ESTERS; CSF-1 RECEPTOR; GENE-PRODUCT; NUCLEOTIDE-SEQUENCE; SIGNAL TRANSDUCTION AB The feline sarcoma virus oncogene v-fms has significantly contributed to the dissection of peptide growth factor action since it encodes the transmembrane tyrosine kinase gp140(v-fms) a transforming version of colony-stimulating factor 1 receptor, a member of the growth factor receptor tyrosine kinase family. In this study, the functional significance of structural differences between distinct tyrosine kinase types, in particular between cellular receptors and viral transforming proteins of distinct structural types, has been further investigated, and their functional compatibility has been addressed. For this purpose, major functional domains of three structurally distinct tyrosine kinases were combined into two chimeric receptors. The cytoplasmic gp140(v-fms) kinase domain and the kinase domain of Rous sarcoma virus pp60(v-src) were each fused to the extracellular ligand-binding domain of the epidermal growth factor (EGF) receptor to create chimeras EFR and ESR, respectively, which were studied upon stable expression in NIH 3T3 fibroblasts. Both chimeras were faithfully synthesized and routed to the cell surface, where they displayed EGF-specific, low-affinity ligand-binding domains in contrast to the high- and low-affinity EGF-binding sites of normal EGF receptors. While the EFR kinase was EGF controlled for autophosphorylation and substrate phosphorylation in vitro, in vivo, and in digitonin-treated cells, the ESR kinase was not responsive to EGF. While ESR appeared to recycle to the cell surface upon endocytosis, EGF induced efficient EFR internalization and degradation, and phorbol esters stimulated protein kinase C-mediated downmodulation of EFR. Despite its ligand-inducible kinase activity, EFR was partly EGF independent in mediating mitogenesis and cell transformation, while ESR appeared biologically inactive. C1 GENENTECH INC,DEPT DEV BIOL,S SAN FRANCISCO,CA 94080. RP RIEDEL, H (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,DEPT MED,MOLEC BIOL SECT,BOSTON,MA 02115, USA. NR 64 TC 3 Z9 3 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 JAN PY 1994 VL 68 IS 1 BP 411 EP 424 PG 14 WC Virology SC Virology GA MW251 UT WOS:A1994MW25100045 PM 8254751 ER PT J AU MOORE, JP SATTENTAU, QJ WYATT, R SODROSKI, J AF MOORE, JP SATTENTAU, QJ WYATT, R SODROSKI, J TI PROBING THE STRUCTURE OF THE HUMAN-IMMUNODEFICIENCY-VIRUS SURFACE GLYCOPROTEIN GP120 WITH A PANEL OF MONOCLONAL-ANTIBODIES SO JOURNAL OF VIROLOGY LA English DT Article ID CD4 BINDING-SITE; TYPE-1 GP120; ENVELOPE GLYCOPROTEIN; HTLV-III; SOLUBLE CD4; NEUTRALIZING ANTIBODIES; CONFORMATIONAL-CHANGES; RECOMBINANT GP120; VARIABLE REGIONS; AIDS PATIENTS AB We have probed the structures of monomeric and oligomeric gp120 glycoproteins from the W isolate of human immunodeficiency virus type 1 (HIV-1) with a panel of monoclonal antibodies (MAbs); most of these MAbs are directed against continuous epitopes. On native monomeric gp120, most of the first conserved (C1) domain is accessible to MAbs, although some regions of C1 are relatively inaccessible. All of the MAbs directed against the C2, C3, and C5 domains bind preferentially to denatured monomeric gp120, indicating that these regions of gp120 are poorly accessible on the native monomer, although the extreme C terminus in C5 is well exposed. Segments of the V1, V2, and V3 loops are exposed on the surface of monomeric gp120, although the base of the V3 loop is inaccessible. A portion of C4 is also available for MAb binding on monomeric gp120, as is the extreme C terminus in C5. However, on oligomeric gp120-gp41 complexes, only the V2 and V3 loops (and perhaps V1) are well exposed and a segment of the C4 region is partially exposed; continuous epitopes in C1 and C5 that are accessible to antibodies on monomeric gp120 are occluded on the oligomer. Although deletion of the V1, V2, and V3 loops resulted in increased exposure of several discontinuous epitopes overlapping the CD4-binding site, the exposure of most continuous epitopes on the monomeric gp120 glycoprotein was not affected. These results imply a HIV-1 gp120 structure in which the conserved continuous determinants are inaccessible; in some cases, this inaccessibility is due to intramolecular interactions between conserved regions, and in other cases, it is due to intermolecular interactions with other components of the glycoprotein spike. These findings have implications for the design of subunit vaccines based on gp120. C1 CTR IMMUNOL MARSEILLE LUMINY,F-13288 MARSEILLE 09,FRANCE. DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. RP MOORE, JP (reprint author), NYU,SCH MED,AARON DIAMOND AIDS RES CTR,455 1ST AVE,7TH FLOOR,NEW YORK,NY 10016, USA. FU NIAID NIH HHS [1 P30 AI27742-04, AI24755, AI31783] NR 80 TC 243 Z9 243 U1 0 U2 5 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 JAN PY 1994 VL 68 IS 1 BP 469 EP 484 PG 16 WC Virology SC Virology GA MW251 UT WOS:A1994MW25100052 PM 7504741 ER PT J AU GERETY, MB CORNELL, JE MULROW, CD TULEY, M HAZUDA, HP LICHTENSTEIN, M AGUILAR, C KADRI, AA ROSENBERG, J AF GERETY, MB CORNELL, JE MULROW, CD TULEY, M HAZUDA, HP LICHTENSTEIN, M AGUILAR, C KADRI, AA ROSENBERG, J TI THE SICKNESS IMPACT PROFILE FOR NURSING-HOMES (SIP-NH) SO JOURNALS OF GERONTOLOGY LA English DT Article ID HEALTH-STATUS MEASURE; MEXICAN-AMERICANS; VALIDATION; IMPAIRMENT; VALIDITY AB Background. Valid, feasible measures of functional status are needed to evaluate the expanding nursing home population. This study attempts to increase relevance and reduce respondent burden of the Sickness Impact Profile (SIP) for nursing home residents while maintaining internal consistency and validity. Methods. 231 residents from one academic and four community nursing homes, aged greater-than-or-equal-to 60 with a Mini-Mental State Exam score greater-than-or-equal-to 11, were study participants. Nominal group process was used to identify items and/or categories for removal. Candidate items were those that: represented restrictions of the nursing home environment. had weak item-total score correlations, and/or made minimal contribution to category internal consistency. Reduction was constrained by: minimum correlation of r = .90 between SIP and Sickness Impact Profile for Nursing Homes (SIP-NH) scores, coefficients alpha that fell within 95% confidence regions about predicted alpha. Convergent and discriminant validity were evaluated with the Katz Activities of Daily Living, Physical Disability Index, Geriatric Depression Scale, and Folstein Mini-Mental State Exam. Results. The SIP-NH contains 66 items, a 51.5% reduction. Correlations between the SIP-NH and SIP were: total score r = .98, Physical dimension r = .97, and Psychosocial dimension r = .97. Alpha coefficients all fell within the 95% confidence regions. The SIP and the SIP-NH did not differ in correlations with validating instruments. Conclusions. The SIP-NH reduces respondent burden and has acceptable internal consistency and external validity. Potentially useful for discriminatory and predictive purposes, responsiveness to change will require longitudinal evaluation. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIAT & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN EPIDEMIOL,SAN ANTONIO,TX 78284. RP GERETY, MB (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIAT RES EDUC & CLIN,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [NIA UO1AG09117] NR 23 TC 28 Z9 28 U1 5 U2 5 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0022-1422 J9 J GERONTOL JI J. Gerontol. PD JAN PY 1994 VL 49 IS 1 BP M2 EP M8 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA MQ845 UT WOS:A1994MQ84500012 PM 8282976 ER PT J AU SALUSKY, IB RAMIREZ, JA OPPENHEIM, W GALES, B SEGRE, GV GOODMAN, WG AF SALUSKY, IB RAMIREZ, JA OPPENHEIM, W GALES, B SEGRE, GV GOODMAN, WG TI BIOCHEMICAL MARKERS OF RENAL OSTEODYSTROPHY IN PEDIATRIC-PATIENTS UNDERGOING CAPD CCPD SO KIDNEY INTERNATIONAL LA English DT Article ID BONE-DISEASE; CALCIUM-CARBONATE; ALUMINUM LEVELS; CHILDREN; DIALYSIS; FAILURE; HISTOMORPHOMETRY AB Serum intact PTH [1-84] levels were evaluated as a potential non-invasive method for the diagnosis of renal osteodystrophy in children treated with CAPD/CCPD. Sixty-eight bone biopsy samples were obtained from 55 patients, aged 13 +/- 5 (X +/- SD) years, undergoing CAPD/CCPD for 29 +/- 13 months; osteitis fibrosa was present in 34 cases, mild lesions of secondary hyperparathyroidism in six, 15 had adynamic lesions, and 13 were classified as normal histology. Serum calcium levels were higher in patients with adynamic bone or normal bone histology than in those with secondary hyperparathyroidism, whereas serum phosphorus, alkaline phosphatase and PTH levels were greater in patients with osteitis fibrosa. The combination of a serum PTH level >200 pg/ml and a serum calcium value < 10 mg/dl was 85% sensitive and 100%, specific for identifying patients with high-turnover lesions of bone. Serum PTH values <200 pg/ml were 100% sensitive but only 79% specific for patients with adynamic bone; specificity increased to 92%, however, using the combined criteria of a PTH level <150 pg/ml and a serum calcium level >10 mg/dl. Higher serum calcium levels and serum PTH values within or below the normal range characterize patients with the adynamic lesion of renal osteodystrophy. Serum PTH levels of approximately 200 pg/ml are useful for distinguishing patients with low-turnover lesions of renal osteodystrophy from those with secondary hyperparathyroidism. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PEDIAT, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT RADIOL, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT ORTHOPED, LOS ANGELES, CA 90024 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED, ENDOCRINE UNIT, BOSTON, MA 02114 USA. FU NCRR NIH HHS [RR-00865]; NIDDK NIH HHS [DK-35423] NR 28 TC 158 Z9 164 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1994 VL 45 IS 1 BP 253 EP 258 DI 10.1038/ki.1994.31 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA MM730 UT WOS:A1994MM73000031 PM 8127016 ER PT J AU ALALOUSI, S CARLSON, JA BLESSING, K COOK, MG COCHRAN, AJ WEN, DR BARNHILL, RL AF ALALOUSI, S CARLSON, JA BLESSING, K COOK, MG COCHRAN, AJ WEN, DR BARNHILL, RL TI THE IN-VIVO EXPRESSION OF BASIC FIBROBLASTIC GROWTH-FACTOR IN CUTANEOUS MELANOMA - IMPLICATIONS FOR DESMOPLASIA AND ANGIOGENESIS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. UNIV ABERDEEN,ABERDEEN,SCOTLAND. ST GEORGE HOSP,LONDON,ENGLAND. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A43 EP A43 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600252 ER PT J AU BAILEY, EM FERRY, JA HARRIS, NL MIHM, MC JACOBSON, JO DUNCAN, LM AF BAILEY, EM FERRY, JA HARRIS, NL MIHM, MC JACOBSON, JO DUNCAN, LM TI LOW-GRADE B-CELL LYMPHOMA OF MUCOSA-ASSOCIATED LYMPHOID-TISSUE (MALT) TYPE OF SKIN AND SOFT-TISSUE - A STUDY OF 15 PRIMARY AND SECONDARY CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. BRIGHAM & WOMENS HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A44 EP A44 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600256 ER PT J AU CARLSON, JA GOODMAN, ML PILCH, BZ AF CARLSON, JA GOODMAN, ML PILCH, BZ TI ACINIC CELL-CARCINOMA - A STUDY OF 28 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A98 EP A98 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600580 ER PT J AU CENTENO, BA VICKERY, AL DANIELS, GH SZYFELBEIN, WM AF CENTENO, BA VICKERY, AL DANIELS, GH SZYFELBEIN, WM TI FINE-NEEDLE ASPIRATION BIOPSY OF THYROIDS IN PATIENTS WITH PRIOR GRAVES-DISEASE TREATED WITH RADIOACTIVE IODINE - CYTOMORPHOLOGIC FINDINGS AND POTENTIAL PITFALLS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A34 EP A34 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600195 ER PT J AU CRESPO, P GALANOPOULOS, T ANTONIADES, HN OHARA, CJ AF CRESPO, P GALANOPOULOS, T ANTONIADES, HN OHARA, CJ TI PLATELET-DERIVED GROWTH-FACTOR IN PRIMARY HUMAN LUNG CARCINOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 BOSTON UNIV,MALLORY INST PATHOL,BOSTON,MA. CTR BLOOD RES,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A150 EP A150 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600889 ER PT J AU DELAMONTE, SM SHAUGHNESSY, K HUTCHINS, GM AF DELAMONTE, SM SHAUGHNESSY, K HUTCHINS, GM TI CLINICOPATHOLOGICAL CORRELATES OF GESTATIONAL CEREBRAL-HEMORRHAGE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A145 EP A145 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600863 ER PT J AU DELAMONTE, SM MARSHALL, G WELCH, J DOE, EJ REYNOLDS, S HUTCHINS, GM AF DELAMONTE, SM MARSHALL, G WELCH, J DOE, EJ REYNOLDS, S HUTCHINS, GM TI THE NEUROANATOMICAL SUBSTRATE OF SCHIZOPHRENIA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. NEW HAMPSHIRE HOSP,CONCORD,NH. JOHNS HOPKINS MED INST,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A138 EP A138 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600817 ER PT J AU FANBURG, JC ROSENBERG, AE WEAVER, DL LESLIE, KO MANN, KG TRACY, RP AF FANBURG, JC ROSENBERG, AE WEAVER, DL LESLIE, KO MANN, KG TRACY, RP TI THE USE OF MONOCLONAL ANTI-OSTEOCALCIN AND ANTI-OSTEONECTIN ANTIBODIES IN THE DIAGNOSIS OF OSTEOSARCOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV VERMONT,BURLINGTON,VT. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A7 EP A7 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600033 ER PT J AU FLEISCHHACKER, DS YOUNG, RH SCULLY, RE AF FLEISCHHACKER, DS YOUNG, RH SCULLY, RE TI BREAST-CARCINOMA METASTIC TO THE OVARY - A STUDY OF 76 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A88 EP A88 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600518 ER PT J AU GULLEY, ML AMIN, MB BANKS, PM AYALA, AG EBLE, JN SRIGLEY, JR EAGAN, PA RO, JY AF GULLEY, ML AMIN, MB BANKS, PM AYALA, AG EBLE, JN SRIGLEY, JR EAGAN, PA RO, JY TI EPSTEIN-BARR-VIRUS IS DETECTED IN NASOPHARYNGEAL CARCINOMA BUT NOT IN LYMPHOEPITHELIOMA-LIKE CARCINOMA OF THE BLADDER SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX USA. UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX USA. HENRY FORD HOSP, DETROIT, MI 48202 USA. SUNNYBROOK MED CTR, TORONTO M4N 3M5, ON, CANADA. RICHARD L ROUDEBUSH VET AFFAIRS MED CTR, INDIANAPOLIS, IN USA. UNIV TEXAS, MD ANDERSON CANC CTR, HOUSTON, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0023-6837 EI 1530-0307 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A126 EP A126 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600748 ER PT J AU JONES, EC PINS, M DICKERSIN, GR YOUNG, RH AF JONES, EC PINS, M DICKERSIN, GR YOUNG, RH TI METANEPHRIC ADENOMA OF THE KIDNEY - A STUDY OF 6 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 VANCOUVER GEN HOSP,VANCOUVER,BC,CANADA. UNIV BRITISH COLUMBIA,VANCOUVER,BC,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A77 EP A77 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600456 ER PT J AU JONES, MA YOUNG, RH SCULLY, RE AF JONES, MA YOUNG, RH SCULLY, RE TI MALIGNANT MESOTHELIOMA OF THE TUNICA VAGINALIS - A CLINICOPATHOLOGICAL ANALYSIS OF 12 CASES WITH REVIEW OF THE LITERATURE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MAINE MED CTR,PORTLAND,ME 04102. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A78 EP A78 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600457 ER PT J AU KAPLAN, MA HARRIS, NL AF KAPLAN, MA HARRIS, NL TI EXPRESSION OF EPSTEIN-BARR-VIRUS (EBV) GENE-PRODUCTS AND RELATED CELLULAR PROTEINS IN POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDERS (PTLD) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A112 EP A112 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600666 ER PT J AU KUPRYJANCZYK, J BELL, DA BEAUCHAMP, R YANDELL, DW THOR, AD AF KUPRYJANCZYK, J BELL, DA BEAUCHAMP, R YANDELL, DW THOR, AD TI P53 ANALYSIS OF OVARIAN BORDERLINE TUMORS AND STAGE-I CARCINOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A91 EP A91 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600539 ER PT J AU NICKELEIT, V ZAGACHIN, L ANDRES, G NISHIKAWA, K COLVIN, R AF NICKELEIT, V ZAGACHIN, L ANDRES, G NISHIKAWA, K COLVIN, R TI FIBRONECTIN IS SYNTHESIZED IN CRESCENTS IN AUTOIMMUNE GLOMERULONEPHRITIS IN THE RAT SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A160 EP A160 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600949 ER PT J AU NIELSEN, GP ROSENBERG, AE YOUNG, RH SCULLY, RE AF NIELSEN, GP ROSENBERG, AE YOUNG, RH SCULLY, RE TI SMOOTH-MUSCLE TUMORS OF THE VULVA - ANALYSIS OF 18 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A93 EP A93 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600549 ER PT J AU OCONNELL, JX FANBURG, JC BHAN, AK ROSENBERG, AE AF OCONNELL, JX FANBURG, JC BHAN, AK ROSENBERG, AE TI GIANT-CELL TUMOR OF TENDON SHEATH AND PIGMENTED VILLONODULAR SYNOVITIS - AN IMMUNOHISTOCHEMICAL STUDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 VANCOUVER GEN HOSP,VANCOUVER,BC,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A9 EP A9 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600046 ER PT J AU OCONNELL, JX OKEEFE, RP KANAPURAM, SV SPRINGFIELD, D MANKIN, HJ ROSENBERG, AE AF OCONNELL, JX OKEEFE, RP KANAPURAM, SV SPRINGFIELD, D MANKIN, HJ ROSENBERG, AE TI CALCIFIC MYONECROSIS - A CLINICOPATHOLOGICAL STUDY OF A DISTINCTIVE SOFT-TISSUE PSEUDOTUMOR SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 VANCOUVER GEN HOSP,VANCOUVER,BC,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A9 EP A9 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600047 ER PT J AU PINS, MR YOUNG, RH SCULLY, RE AF PINS, MR YOUNG, RH SCULLY, RE TI PRIMARY SQUAMOUS-CELL CARCINOMA OF THE OVARY - A REPORT OF 33 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A94 EP A94 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600556 ER PT J AU SUSTER, S WONG, TY AF SUSTER, S WONG, TY TI POLYMORPHOUS SWEAT GLAND CARCINOMA - CLINICOPATHOLOGICAL STUDY OF 9 CASES OF A DISTINCTIVE LOW-GRADE CUTANEOUS ADNEXAL NEOPLASM SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MT SINAI MED CTR,DEPT PATHOL,MIAMI,FL. UNIV MIAMI,SCH MED,MIAMI,FL. MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A50 EP A50 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600291 ER PT J AU TAHAN, SR STEIN, AL HERSH, A AF TAHAN, SR STEIN, AL HERSH, A TI MODEL PREDICTING RISK FOR METASTASIS IN SQUAMOUS-CELL CARCINOMA OF THE LIP USING LIGHT-MICROSCOPIC MEASURES AND PCNA INDEX SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NEW ENGLAND DEACONESS HOSP,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A101 EP A101 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600597 ER PT J AU WONG, TY SUSTER, S DUNCAN, LM MIHM, MC AF WONG, TY SUSTER, S DUNCAN, LM MIHM, MC TI NEVOID MELANOMA - CLINICOPATHOLOGICAL STUDY OF 7 CASES OF A DISTINCTIVE VARIANT OF LOW-GRADE MELANOMA MIMICKING DERMAL NEVUS AND SPINDLE AND EPITHELIOID CELL NEVUS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MT SINAI MED CTR,DEPT PATHOL,MIAMI,FL. MIAMI SCH MED,MIAMI,FL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A51 EP A51 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600295 ER PT J AU WONG, TY SUSTER, S AF WONG, TY SUSTER, S TI TRICHOLEMMAL CARCINOMA - A CLINICOPATHOLOGICAL STUDY OF 13 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MT SINAI MED CTR,DEPT PATHOL,MIAMI,FL. UNIV MIAMI,SCH MED,MIAMI,FL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A50 EP A50 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600294 ER PT J AU YANG, WI ZUKERBERG, L ARNOLD, A HARRIS, N AF YANG, WI ZUKERBERG, L ARNOLD, A HARRIS, N TI BCL-1 (CYCLIN D1) PROTEIN EXPRESSION IN LOW-GRADE B-CELL LYMPHOMAS AND REACTIVE HYPERPLASIA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1994 VL 70 IS 1 BP A124 EP A124 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MW426 UT WOS:A1994MW42600736 ER PT S AU DOHLMAN, C DOANE, M AF DOHLMAN, C DOANE, M BE Sullivan, DA TI KERATOPROSTHESIS IN END-STAGE DRY EYE SO LACRIMAL GLAND, TEAR FILM, AND DRY EYE SYNDROMES: BASIC SCIENCE AND CLINICAL RELEVANCE SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT International Conference on the Lacrimal Gland, Tear Film and Dry Eye Syndromes: Basic Science and Clinical Relevance CY NOV 14-17, 1992 CL SOUTHAMPTON, BERMUDA RP DOHLMAN, C (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,SCHEPENS EYE RES INST,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44676-6 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1994 VL 350 BP 561 EP 564 PG 4 WC Ophthalmology; Physiology SC Ophthalmology; Physiology GA BA17X UT WOS:A1994BA17X00095 PM 8030536 ER PT S AU TALAL, N AF TALAL, N BE Sullivan, DA TI SJOGRENS-SYNDROME - CLOSE TO CAUSE AND CURE SO LACRIMAL GLAND, TEAR FILM, AND DRY EYE SYNDROMES: BASIC SCIENCE AND CLINICAL RELEVANCE SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT International Conference on the Lacrimal Gland, Tear Film and Dry Eye Syndromes: Basic Science and Clinical Relevance CY NOV 14-17, 1992 CL SOUTHAMPTON, BERMUDA RP TALAL, N (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET HOSP,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [1R01 DE09311-01] NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44676-6 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1994 VL 350 BP 679 EP 682 PG 4 WC Ophthalmology; Physiology SC Ophthalmology; Physiology GA BA17X UT WOS:A1994BA17X00114 PM 8030555 ER PT S AU ZEITELS, SM DAVIS, RK AF ZEITELS, SM DAVIS, RK BE Smee, R Bridger, GP TI CANCER OF THE SUPRAGLOTTIS - ENDOSCOPIC LASER MANAGEMENT SO LARYNGEAL CANCER SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 2nd World Congress on Laryngeal Cancer CY FEB 20-24, 1994 CL SYDNEY, AUSTRALIA SP INST RADIAT ONCOL, PRINCE WALES HOSP, DEPT OTOLARYNGOL, UNIV NEW S WALES DE CANCER; ENDOSCOPY; EPIGLOTTIS; LARYNGOSCOPE; LARYNGOSCOPY; LARYNX; LASER MICROSURGERY; SUPRAGLOTTIS C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON VET AFFAIRS MED CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81810-3 J9 INT CONGR SER PY 1994 VL 1063 BP 444 EP 456 PG 13 WC Oncology; Otorhinolaryngology SC Oncology; Otorhinolaryngology GA BC83P UT WOS:A1994BC83P00074 ER PT J AU ZEITELS, SM KOUFMAN, JA DAVIS, RK VAUGHAN, CW AF ZEITELS, SM KOUFMAN, JA DAVIS, RK VAUGHAN, CW TI ENDOSCOPIC TREATMENT OF SUPRAGLOTTIC AND HYPOPHARYNX CANCER SO LARYNGOSCOPE LA English DT Article ID CLINICAL EXPERIENCE; LASER SURGERY; CO2-LASER; LARYNX; CARCINOMA; NECK AB Transoral excision of supraglottic and hypopharynx cancer as a single modality is effective when lesions are selected for small size and endoscopic accessibility. Excisional biopsy with clear margins of larger supraglottic tumors in combination with postoperative radiotherapy provides an excellent treatment alternative for selected lesions in patients who are not candidates for open surgery. In this preliminary report, 45 cases using this minimally invasive approach are reviewed outlining oncologic rationale and functional advantages. A large bore tubed laryngoscope or the adjustable bivalve supraglottiscope was used along with a carbon dioxide laser in all cases. In 22 of the 45 patients (mostly T1), local en bloc excision of the primary cancer was performed as sole treatment on selected lesions of the supraglottis and hypopharynx. There were no local recurrences, however, 1 patient developed a neck recurrence and was salvaged by neck dissection. Twenty-three of the 45 patients had more extensive primaries (mostly T2, T3) and NO necks. Transoral excisional biopsy was followed by full-course radiation therapy to the primary site and both necks. Ah 23 were followed a minimum of 2 years, and the median follow-up period was 58 months. Clear margins were obtained in 16 of 23, and there were no recurrences in the larynx. Two of 16 did fail in the neck and died despite neck dissection. Seven of 23 patients had positive margins and, despite full-course radiotherapy to the primary site and both necks, 5 of 7 failed locally or regionally. Two of the 7 died of their disease despite open salvage surgery. Therefore, 4 of 23 patients who underwent transoral excision of larger lesions followed by full-course radiotherapy died of recurrent cancer. C1 MASSACHUSETTS EYE & EAR INFIRM,HARVARD MED SCH,BOSTON VET AFFAIRS MED CTR,BOSTON,MA. N CAROLINA BAPTIST HOSP,BOWMAN GRAY SCH MED,WINSTON SALEM,NC. UNIV UTAH,MED CTR,SALT LAKE CITY,UT. UNIV UTAH,SCH MED,SALT LAKE CITY,UT. BOSTON UNIV,SCH MED,BOSTON VET AFFAIRS MED CTR,BOSTON,MA. RP ZEITELS, SM (reprint author), MASSACHUSETTS EYE & EAR INFIRM,HARVARD MED SCH,DEPT OTOL & LARYNGOL,243 CHARLES ST,BOSTON,MA 02130, USA. NR 35 TC 70 Z9 72 U1 0 U2 1 PU LARYNGOSCOPE CO PI ST LOUIS PA 10 S BROADWAY 14TH FLOOR, ST LOUIS, MO 63102-1741 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD JAN PY 1994 VL 104 IS 1 BP 71 EP 78 PN 1 PG 8 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA MQ954 UT WOS:A1994MQ95400012 PM 8295459 ER PT B AU MARTIN, A GREVELINK, J STARR, J FEWKES, J FLOTTE, T ANDERSON, RR DEUTSCH, TF AF MARTIN, A GREVELINK, J STARR, J FEWKES, J FLOTTE, T ANDERSON, RR DEUTSCH, TF BE Anderson, RR Katzir, A TI DETERMINATION OF PROTOPORPHYRIN-IX DISTRIBUTIONS IN SKIN TUMORS AFTER THE APPLICATION OF TOPICAL AMINOLEVULINIC ACID SO LASER SURGERY: ADVANCED CHARACTERIZATION, THERAPEUTICS, AND SYSTEMS IV, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Laser Surgery: Advanced Characterization, Therapeutics, and Systems IV CY JAN 22-25, 1994 CL LOS ANGELES, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1421-2 J9 P SOC PHOTO-OPT INS PY 1994 VL 2128 BP 225 EP 230 DI 10.1117/12.184902 PG 6 WC Optics; Surgery SC Optics; Surgery GA BB54S UT WOS:A1994BB54S00032 ER PT B AU LIN, G GUT, I LEE, S FLOTTE, TJ DOUKAS, AG AF LIN, G GUT, I LEE, S FLOTTE, TJ DOUKAS, AG BE Jacques, SL Katzir, A TI APPROACHES TO MEASURING LINEAR AND NONLINEAR ACOUSTIC PROPERTIES OF BIOLOGICAL-MATERIAL SO LASER-TISSUE INTERACTION V, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Laser-Tissue Interaction V CY JAN 24-27, 1994 CL LOS ANGELES, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1429-8 J9 P SOC PHOTO-OPT INS PY 1994 VL 2134 BP 171 EP 178 PG 8 WC Engineering, Biomedical; Optics SC Engineering; Optics GA BB54R UT WOS:A1994BB54R00020 ER PT B AU DOMANKEVITZ, Y BUA, D CHUNG, J HANEL, E SILVER, G NISHIOKA, NS AF DOMANKEVITZ, Y BUA, D CHUNG, J HANEL, E SILVER, G NISHIOKA, NS BE Jacques, SL Katzir, A TI EFFECT OF SCANNED QUASI CW CO2-LASER IRRADIATION ON TISSUE THERMAL-DAMAGE SO LASER-TISSUE INTERACTION V, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Laser-Tissue Interaction V CY JAN 24-27, 1994 CL LOS ANGELES, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1429-8 J9 P SOC PHOTO-OPT INS PY 1994 VL 2134 BP 288 EP 290 PG 3 WC Engineering, Biomedical; Optics SC Engineering; Optics GA BB54R UT WOS:A1994BB54R00031 ER PT J AU LIN, CP WEAVER, YK BIRNGRUBER, R FUJIMOTO, JG PULIAFITO, CA AF LIN, CP WEAVER, YK BIRNGRUBER, R FUJIMOTO, JG PULIAFITO, CA TI INTRAOCULAR MICROSURGERY WITH A PICOSECOND ND-YAG LASER SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE VITREOUS SURGERY; PHOTODISRUPTION; OPTICAL BREAKDOWN ID OPTICAL-BREAKDOWN; PULSED NEODYMIUM; SURGERY; DAMAGE; CAVITATION; GENERATION; REDUCTION AB We investigated the use of picosecond Nd:YAG laser pulses for intraocular microsurgery. With a pulse duration of 100 picoseconds, only 70 muJ of pulse energy is required to consistently produce optical breakdown in the deep vitreous. This pulse energy is nearly two orders of magnitude less than the typical pulse energies used in conventional (nanosecond) photodisruptors. The reduced pulse energy results in a smaller zone of tissue damage, an important consideration when operating close to the retina or other sensitive ocular structures. Efficient cutting action is achieved by applying multiple pulses at a moderately high repetition rate of 50-200 Hz. An in vitro model was developed to assess axial confinement of picosecond photodisruption. In vivo vitreous membrane surgery was performed in experimental rabbit eyes to demonstrate a potential clinical application of picosecond laser-induced optical breakdown. (C) 1994 Wiley-Liss, Inc. C1 TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,LASER RES LAB,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. RI Birngruber, Reginald/Q-2342-2016 FU NIGMS NIH HHS [5R01 GM35459-06] NR 21 TC 21 Z9 21 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1994 VL 15 IS 1 BP 44 EP 53 DI 10.1002/lsm.1900150107 PG 10 WC Dermatology; Surgery SC Dermatology; Surgery GA PP488 UT WOS:A1994PP48800006 PM 7997047 ER PT J AU INDERFURTH, JHC FERGUSON, RD FRISH, MB BIRNGRUBER, R AF INDERFURTH, JHC FERGUSON, RD FRISH, MB BIRNGRUBER, R TI DYNAMIC REFLECTOMETER FOR CONTROL OF LASER PHOTOCOAGULATION ON THE RETINA SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE ARGON LASER; FEEDBACK CONTROL; LESION INTENSITY; REFLECTANCE AB In retinal laser photocoagulation, constant exposure parameters do not result in identical lesions. This lack of reproducibility increases the rate of complications from over- or undertreatment and inhibits determination of the optimal treatment endpoints for different retinal disorders. To this end, a feedback-controlled photocoagulator could make retinal photocoagulation a safer, more reproducible, and faster procedure. A dynamic confocal reflectometer was integrated into a slit lamp laser delivery system. Real-time reflectance changes on the retinas of pigmented rabbits were obtained by monitoring the increasing back-scattered light of the coagulating beam during argon laser photocoagulation. Reproducible temporal reflectance patterns were measured that correlated with ophthalmoscopically assessed lesion intensity independent of the exposure parameters, the transparency of the optical media, and the focusing conditions. As a step toward the development of a feedback-controlled photocoagulator, the confocal reflectometer has been proven in animal trials closely resembling clinical practice. (C) 1994 Wiley-Liss, Inc. C1 PHYS SCI INC,20 NEW ENGLAND BUSINESS CTR,ANDOVER,MA 01810. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MED LASER CTR LUBECK,D-23562 LUBECK,GERMANY. RI Birngruber, Reginald/Q-2342-2016 FU NEI NIH HHS [I R43 EY08630-02, 2 R44 EY08630-02] NR 19 TC 22 Z9 22 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 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1994 VL 15 IS 1 BP 54 EP 61 DI 10.1002/lsm.1900150108 PG 8 WC Dermatology; Surgery SC Dermatology; Surgery GA PP488 UT WOS:A1994PP48800007 PM 7997048 ER PT B AU WEBB, RH ROGOMENTICH, F AF WEBB, RH ROGOMENTICH, F GP IEEE TI MICROLASER MICROSCOPE SO LEOS '94 - CONFERENCE PROCEEDINGS, VOL 2: IEEE LASERS AND ELECTRO-OPTICS SOCIETY 1994 7TH ANNUAL MEETING LA English DT Proceedings Paper CT 7th Annual Meeting of the IEEE Lasers-and-Electro-Optics-Society CY OCT 31-NOV 03, 1994 CL BOSTON, MA SP IEEE, LASERS & ELECTRO OPT SOC C1 MASSACHUSETTS GEN HOSP,SCHEPENS EYE RES INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU I E E E PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 BN 0-7803-1470-0 J9 IEEE LEOS ANN MTG PY 1994 BP 303 EP 304 PG 2 WC Optics SC Optics GA BC36N UT WOS:A1994BC36N00144 ER PT J AU ROBERTSON, MJ RITZ, J AF ROBERTSON, MJ RITZ, J TI PROGNOSTIC-SIGNIFICANCE OF THE SURFACE-ANTIGENS EXPRESSED BY LEUKEMIC-CELLS SO LEUKEMIA & LYMPHOMA LA English DT Article; Proceedings Paper CT GEIL 94: Immunology and Leukemia CY APR 26, 1991-APR 27, 1994 CL NANCY, FRANCE SP GRP ETUDE IMMUNOL LEUCEMINES, CONSEIL EUROPE, PROGRAMME COMETT, MINIST AFFAIRES SOCIALES SANTE & VILLE FRANCE, MINIST RECH & ENSEIGNMENT SUPERIEUR FRANCE, FOND CONTRE LEUCEMIES, INSERM, CNRS, ASSOC FRANCAISE CYTOMETRE, VILLE NANCY, UNIV NANCY DE IMMUNOPHENOTYPE; SURFACE MARKER ANALYSIS; CELL SURFACE ANTIGENS; ACUTE LEUKEMIA; ALL; AML; CLL; CML; PLI; GLPD; LGL-LEUKEMIA RP ROBERTSON, MJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 NR 0 TC 2 Z9 2 U1 0 U2 0 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 PY 1994 VL 13 SU 1 BP 15 EP 22 DI 10.3109/10428199409052667 PG 8 WC Oncology; Hematology SC Oncology; Hematology GA NK902 UT WOS:A1994NK90200005 PM 8075574 ER PT J AU LIPKOWSKI, AW CARR, DB LANGLADE, A OSGOOD, PF SZYFELBEIN, SK AF LIPKOWSKI, AW CARR, DB LANGLADE, A OSGOOD, PF SZYFELBEIN, SK TI MORPHINE-3-GLUCURONIDE - SILENT REGULATOR OF MORPHINE ACTIONS SO LIFE SCIENCES LA English DT Article DE MORPHINE-3-GLUCURONIDE; OPIOID; ANALGESIA; MORPHINE ID GLUCURONIDATION; ANALGESIA; TOLERANCE; PAIN AB To assess whether stoichiometric manipulation of morphine (M) metabolism can enhance analgesia or slow the development of M tolerance we co-administered M-3- glucuronide (M3G) during single or repeated doses of morphine in rats. Although M3G itself lacked analgesic activity, co-injection of M3G with M increased and prolonged analgesia beyond that seen with M. In addition, diminution of the acute analgesic effect of M after 3 once-daily doses of M did not occur after daily co-injection of M3G and M. Thus the traditional view that tolerance to the effects of M is due solely to effects mediated through opioid receptors must be broadened to include the contributions of enzyme induction or stoichiometric equilibration of M3G in this process. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MGH PAIN CTR,ANALGES PEPTIDE RES UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MGH PAIN CTR,DEPT MED,ANALGES PEPTIDE RES UNIT,BOSTON,MA 02114. POLISH ACAD SCI,MED RES CTR,WARSAW,POLAND. HOP LARIBOISIERE,CTR TRAITEMENT DOULEUR,F-75475 PARIS,FRANCE. NR 20 TC 40 Z9 42 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 55 IS 2 BP 149 EP 154 DI 10.1016/0024-3205(94)90106-6 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA NQ400 UT WOS:A1994NQ40000008 PM 8015358 ER PT J AU BURKE, WJ RAGHU, G STRONG, R AF BURKE, WJ RAGHU, G STRONG, R TI TAXOL PROTECTS AGAINST CALCIUM-MEDIATED DEATH OF DIFFERENTIATED RAT PHEOCHROMOCYTOMA CELLS SO LIFE SCIENCES LA English DT Letter DE TAXOL; CALCIUM-MEDIATED CELL DEATH; PC12 CELLS; NERVE GROWTH FACTOR ID ALZHEIMERS-DISEASE; GLUTAMATE NEUROTOXICITY; DECREASED TRANSPORT; NITRIC-OXIDE; PHOSPHORYLATION; HYDROXYLASE; NERVE; TAU AB Elevated levels of intraneuronal calcium may contribute to neuronal death in both Alzheimer's disease and stroke. In part, this neuronal death may be due to calcium-induced disruption of microtubules and inhibition of axonal transport. Taxol stabilizes microtubules to disaggregation. To determine whether taxol could protect against calcium-mediated neuron eel death, a test system was established using a nerve growth factor-differentiated rat pheochromocytoma cell line (PC12 cells). PC12 cells were cultured with nerve growth factor to induce a neuronal phenotype. After 15 days, the cells were exposed to taxol, the calcium ionophore, A23187, or taxol plus ionophore for up to 24 h. Taxol alone reduced cell survival in a concentration dependent manner. At a concentration of 50 nM survival was reduced to between 63% and 84% of control after 4 h of exposure. The ionophore (1 mu M) variably reduced cell survival to between 10 and 55% at 4h. However, when taxol was added to the ionophore the cell survival was significantly increased by 1.5 to 4-fold. The protective effect of taxol lasted up to 24h. We conclude that taxol has a protective effect on calcium-mediated neurotoxicity. Drugs targeting underlying cellular mechanisms involved in calcium-mediated neuronal death may lead to successful therapy for Alzheimer's disease and stroke. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,SAN ANTONIO,TX 78284. ST LOUIS UNIV,SCH MED,DEPT NEUROL,ST LOUIS,MO. ST LOUIS UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63104. ST LOUIS UNIV,SCH MED,DEPT ANAT,ST LOUIS,MO. VET ADM MED CTR,ST LOUIS,MO 63125. UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,SAN ANTONIO,TX 78284. NR 26 TC 3 Z9 3 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 55 IS 16 BP PL313 EP PL319 PG 7 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA PF351 UT WOS:A1994PF35100012 ER PT J AU MISTEREK, K MASZCZYNSKA, I DOROCIAK, A GUMULKA, SW CARR, DB SZYFELBEIN, SK LIPKOWSKI, AW AF MISTEREK, K MASZCZYNSKA, I DOROCIAK, A GUMULKA, SW CARR, DB SZYFELBEIN, SK LIPKOWSKI, AW TI SPINAL COADMINISTRATION OF PEPTIDE SUBSTANCE-P ANTAGONIST INCREASES ANTINOCICEPTIVE EFFECT OF THE OPIOID PEPTIDE BIPHALIN SO LIFE SCIENCES LA English DT Article ID PRIMARY AFFERENT NEUROTRANSMITTER; MU-OPIATE RECEPTORS; INTRATHECAL INJECTION; EXCITATORY COMPOUNDS; NOCICEPTIVE INPUT; MORPHINE; ANALOGS; MICE; PAIN; RAT AB Intrathecal injection of 0.25 mu g of undecapeptide substance P antagonist (SPA) produced transient antinociception with a peak effect at 5 min. Increasing the SPA dose resulted in neurotoxicity. Intrathecal injection of the opioid peptide biphalin (BIP) produced antinociception for over 3 hrs without neurotoxicity. Coadministration of SPA (at subtoxic doses) increased BIP's antinociceptive effect. Naltrexone reversed analgesia due to BIP alone as well as after BIP+SPA. C1 POLISH ACAD SCI,MED RES CTR,PL-00784 WARSAW,POLAND. MED ACAD WARSAW,DEPT PHARMACODYNAM,PL-00927 WARSAW,POLAND. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 27 TC 37 Z9 37 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 54 IS 14 BP 939 EP 944 DI 10.1016/0024-3205(94)00494-3 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MZ462 UT WOS:A1994MZ46200001 PM 7511201 ER PT J AU CHA, JHJ DURE, LS AF CHA, JHJ DURE, LS TI TRINUCLEOTIDE REPEATS IN NEUROLOGIC DISEASES - AN HYPOTHESIS CONCERNING THE PATHOGENESIS OF HUNTINGTONS-DISEASE, KENNEDYS DISEASE, AND SPINOCEREBELLAR ATAXIA TYPE-I SO LIFE SCIENCES LA English DT Article DE TRINUCLEOTIDE REPEAT; GENETIC ABNORMALITIES; HUNTINGTONS DISEASE; KENNEDYS DISEASE ID ANDROGEN RESISTANCE; RECEPTOR; SPERMINE; ACTIVATION; MUTATIONS; ATROPHY; LINKAGE AB Three neurodegenerative diseases, Huntington's disease (HD), Kennedy's disease (hereditary spinobulbar muscular atrophy, SBMA), and type 1 spinocerebellar ataxia (SCA-1) have been found to share a common genetic defect: an unstable region of repeated CAG trinucleotides which are thought to be translated into a polyglutamine moiety. The unstable repeat regions occur near the N-termini of the predicted proteins for HD and SBMA, but the location of the CAG repeat region is not known for SCA-1. Each disease is notable for a relatively circumscribed region of central nervous system pathology, and the lack of predicted similarity of the abnormal proteins makes a common mechanism related to the function of each protein unlikely. In order to reconcile the similar genetic abnormalities with the disparities in phenotypes, we suggest a common thread with regard to the pathogenesis of neuronal death. We hypothesize that the mechanism of neurotoxicity in these diseases occurs not through the production of abnormal proteins, but by the generation of abnormal posttranslational cleavage products. These products, in part consisting of abnormally large polyglutamine moieties, act to disturb the cellular and mitochondrial milieu such that energy metabolism is impaired, rendering specific regions of the nervous system vulnerable, and resulting in the clinical phenotypes of HD, SBMA, and SCA-1. We offer this interpretation of recent genetic findings from a neurobiologic perspective, in addition to suggesting testable hypotheses concerning potential disease mechanisms. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Dure, Leon/B-3243-2008 FU PHS HHS [K1100983] NR 40 TC 29 Z9 31 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 54 IS 20 BP 1459 EP 1464 DI 10.1016/0024-3205(94)90012-4 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA NF171 UT WOS:A1994NF17100001 PM 8190020 ER PT J AU GOODMAN, BM CARNES, M LENT, SJ AF GOODMAN, BM CARNES, M LENT, SJ TI MODEL SIMULATIONS OF ACTH PULSATILITY SO LIFE SCIENCES LA English DT Article DE ACTH; MODELING; PULSATILITY ID ADRENOCORTICOTROPIN SECRETION; HORMONE AB Using high intensity venous sampling (1-2 min integrated intervals) we have observed rapid (<10 min) large amplitude (up to 80 pg/ml) fluctuations in plasma ACTH concentrations in addition to variations at longer time scales. We developed a mathematical model to assess whether plausible physiological explanations could account for our observations and compared model simulations with time series from two human subjects. Three key features enabled the model to accurately simulate the observed time series. 1) The pattern of instantaneous secretory events comprising a pulse followed a Poisson process during baseline activity and rapidly shifted to a step function pattern during a pulsatile episode. 2) The fraction of secreted ACTH shunted between a fast and slow clearance mechanism varied biphasically between baseline and pulsatile states. 3) A brief rate-sensitive suppression of secretion was invoked when secretory rates increased above a threshold amount. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53792. RP GOODMAN, BM (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCRR NIH HHS [RR-03186]; NIDDK NIH HHS [DK-40759] NR 26 TC 4 Z9 4 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 54 IS 22 BP 1659 EP 1669 DI 10.1016/0024-3205(94)00606-7 PG 11 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA NH399 UT WOS:A1994NH39900003 PM 8177008 ER PT J AU LANGLADE, A CARR, DB SERRIE, A SILBERT, BS SZYFELBEIN, SK LIPKOWSKI, AW AF LANGLADE, A CARR, DB SERRIE, A SILBERT, BS SZYFELBEIN, SK LIPKOWSKI, AW TI ENHANCED POTENCY OF INTRAVENOUS, BUT NOT INTRATHECAL, MORPHINE AND MORPHINE-6-GLUCURONIDE AFTER BURN TRAUMA SO LIFE SCIENCES LA English DT Article DE MORPHINE; MORPHINE-6-GLUCURONIDE; BURN TRAUMA ID RECEPTOR-BINDING; OPIOID RECEPTOR; BETA-ENDORPHIN; SITES; RAT; INFLAMMATION; METABOLITES; AGONIST; PLASMA; INJURY AB We examined the analgesic effect of morphine (M) and its metabolite morphine-6-glucuronide (M6G) in a rat model of acute thermal trauma. M or M6G were given by intrathecal (IT) or intravenous (IV) routes after brief burn or sham burn delivered during inhalational anesthesia. In the sham group, M6G was significantly less potent than M when given IV, yet tended to be more potent than M when given IT. For both drugs, thermal injury increased IV potency, yet decreased (for M) or displayed a trend to decrease (for M6G) IT potency. The increased potency seen with IV but not IT opioid administration may reflect pharmacokinetic (e.g., diminished clearance) and/or pharmacodynamic responses (e.g., activation of peripheral opioid receptors) after thermal injury. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,ANALGES PEPTIDE RES UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED ENDOCRINOL,ANALGES PEPTIDE RES UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. HOP LARIBOISIERE,CTR TRAITEMENT DOULEUR,F-75475 PARIS,FRANCE. ST VINCENTS HOSP,MELBOURNE,VIC,AUSTRALIA. POLISH ACAD SCI,MED RES CTR,WARSAW,POLAND. NR 32 TC 8 Z9 8 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 54 IS 22 BP 1699 EP 1709 DI 10.1016/0024-3205(94)00610-5 PG 11 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA NH399 UT WOS:A1994NH39900007 PM 8177011 ER PT J AU FICHTNER, CG ARORA, RC OCONNOR, FL CRAYTON, JW AF FICHTNER, CG ARORA, RC OCONNOR, FL CRAYTON, JW TI PLATELET PAROXETINE BINDING AND FLUOXETINE PHARMACOTHERAPY IN POSTTRAUMATIC-STRESS-DISORDER - PRELIMINARY-OBSERVATIONS ON A POSSIBLE PREDICTOR OF CLINICAL TREATMENT RESPONSE SO LIFE SCIENCES LA English DT Letter ID PTSD; FLUVOXAMINE; IMIPRAMINE; TRIAL AB Recent open clinical trials have found the selective serotonin reuptake inhibitor (SSRI) fluoxetine to be beneficial in the treatment of posttraumatic stress disorder (PTSD) symptoms. We have reported previously that the binding of a newer SSRI, paroxetine, to blood platelets is decreased in PTSD patients compared to normal control subjects. In the current study, pretreatment platelet paroxetine binding data were analyzed for ten Vietnam combat veterans who were treated clinically with fluoxetine for PTSD, diagnosed on the basis of the Structured Clinical Interview for DSM-III-R. Specific binding of H-3-paroxetine is reported in terms of the dissociation constant (K(d)) and the maximum density of binding sites (B(max)). Based on our previous findings we hypothesized that decreased platelet H-3-paroxetine binding would be associated with positive therapeutic response to subsequent treatment with fluoxetine. Global clinical improvement ratings, conducted blind to the biochemical data, were used to separate patients into five maximal responders and five partial responders. The results indicated that maximal responders had lower pretreatment K(d) values (p=.016) and a trend toward lower pretreatment B(max) values (p=.075) than the partial responders. These preliminary findings may warrant further study of platelet SSRI binding as a possible predictor of SSRI treatment response in PTSD patients. C1 LOYOLA UNIV,STRITCH SCH MED,DEPT PSYCHIAT,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT PHARMACOL,MAYWOOD,IL 60153. US DEPT VET AFFAIRS,EDWARD HINES JR HOSP,PSYCHIAT SERV,BIOL PSYCHIAT SECT 116A7,HINES,IL 60141. RP FICHTNER, CG (reprint author), US DEPT VET AFFAIRS,EDWARD HINES JR HOSP,PSYCHIAT SERV,POSTTRAUMAT STRESS DISORDER SECT,HINES,IL 60141, USA. NR 32 TC 9 Z9 9 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1994 VL 54 IS 3 BP PL39 EP PL44 DI 10.1016/0024-3205(94)00592-3 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MM383 UT WOS:A1994MM38300010 PM 8289574 ER PT S AU KAPLAN, WD AF KAPLAN, WD BE Meyer, JL TI LYMPHOSCINTIGRAPHY - IMPORTANCE TO CANCER-DETECTION AND RADIATION TREATMENT PLANNING SO LYMPHATIC SYSTEM AND CANCER: MECHANISMS AND CLINICAL MANAGEMENT SE FRONTIERS OF RADIATION THERAPY AND ONCOLOGY LA English DT Proceedings Paper CT 28th Annual San Francisco Cancer Symposium CY MAR 06-07, 1993 CL SAN FRANCISCO, CA RP KAPLAN, WD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0071-9676 BN 3-8055-5889-9 J9 FRONT RADIAT THER ON JI Front.Radiat.Ther.Oncol. PY 1994 VL 28 BP 25 EP 36 PG 12 WC Oncology; Physiology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Physiology; Radiology, Nuclear Medicine & Medical Imaging GA BB35T UT WOS:A1994BB35T00003 PM 7982601 ER PT S AU NAKFOOR, BM SHIPLEY, WU ZIETMAN, AL AF NAKFOOR, BM SHIPLEY, WU ZIETMAN, AL BE Meyer, JL TI EARLY-STAGE TESTICULAR SEMINOMA - THE ROLE OF RADIATION-THERAPY FOLLOWING ORCHIECTOMY SO LYMPHATIC SYSTEM AND CANCER: MECHANISMS AND CLINICAL MANAGEMENT SE FRONTIERS OF RADIATION THERAPY AND ONCOLOGY LA English DT Proceedings Paper CT 28th Annual San Francisco Cancer Symposium CY MAR 06-07, 1993 CL SAN FRANCISCO, CA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,GENITOURINARY ONCOL UNIT,BOSTON,MA 02114. RP SHIPLEY, WU (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,GENITOURINARY ONCOL UNIT,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0071-9676 BN 3-8055-5889-9 J9 FRONT RADIAT THER ON JI Front.Radiat.Ther.Oncol. PY 1994 VL 28 BP 183 EP 195 PG 13 WC Oncology; Physiology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Physiology; Radiology, Nuclear Medicine & Medical Imaging GA BB35T UT WOS:A1994BB35T00016 PM 7982596 ER PT J AU BIERER, BE AF BIERER, BE TI CYCLOSPORINE-A, FK506, AND RAPAMYCIN - BINDING TO IMMUNOPHILINS AND BIOLOGICAL ACTION SO LYMPHOCYTE ACTIVATION SE CHEMICAL IMMUNOLOGY LA English DT Review ID CIS-TRANS-ISOMERASE; T-CELL ACTIVATION; P70 S6 KINASE; CALCINEURIN PHOSPHATASE-ACTIVITY; PEPTIDYL-PROLYL ISOMERASE; IMMUNOSUPPRESSIVE MACROLIDES FK-506; LEUKOCYTE CHEMOTACTIC ACTIVITY; CYCLOPHILIN MULTIGENE FAMILY; HUMAN FK506-BINDING PROTEIN; HEAT-SHOCK PROTEIN C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. RP BIERER, BE (reprint author), DANA FARBER CANC INST,DIV PEDIAT ONCOL,DANA 1710A,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI32514] NR 169 TC 38 Z9 39 U1 3 U2 4 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 1015-0145 J9 CHEM IMMUNOL JI Chem.Immunol. PY 1994 VL 59 BP 128 EP 155 PG 28 WC Allergy; Immunology SC Allergy; Immunology GA BB31P UT WOS:A1994BB31P00007 PM 7524531 ER PT J AU CHIAPPELLI, F GARCIA, C MANFRINI, E FROST, P AF CHIAPPELLI, F GARCIA, C MANFRINI, E FROST, P TI MIGRATION OF HUMAN CD4+ LYMPHOCYTES - IMPLICATIONS FOR COCAINE AND ALCOHOL ABUSERS SO LYMPHOLOGY LA English DT Article; Proceedings Paper CT 14th International Congress of Lymphology CY SEP 20-26, 1993 CL WASHINGTON, DC SP INT SOC LYMPHOL, NIH ID NODE HOMING RECEPTOR; T-CELLS; HELPER-INDUCER; SUBSETS; DIFFERENTIATION; ACTIVATION; EXPRESSION; ADHESION; TQ1 AB T lymphocytes migrate across body tissues and organs, and home to sites where infection agents and tumors harbor. Cortisol and other glucocorticoids modulate the migration of helper T cells (CD4+), and particularly of CD4+ cells that expresses the homing receptor LECAM-1. A large proportion of these cells express the naive CD4 phenotype (CD4+CD45RA+), which in part determines their transit through the lymphatic system and the lymph nodes. We discuss implications for cocaine and alcohol abusers, who are at high risk for HIV infection and AIDS. C1 W LOS ANGELES VET AFFAIRS MED CTR,HUMAN IMMUNOL & PSYCHONEUROIMMUNOL LAB,LOS ANGELES,CA 90073. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES,SCH MED,BRI,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90024, USA. NR 29 TC 0 Z9 0 U1 0 U2 0 PU LYMPHOLOGY PI TUCSON PA C/O C L WITTE MD 1501 N CAMPBELL AVE DEPT SURGERY, TUCSON, AZ 85724 SN 0024-7766 J9 LYMPHOLOGY JI Lymphology PY 1994 VL 27 SU S BP 206 EP 211 PG 6 WC Immunology; Physiology SC Immunology; Physiology GA PK086 UT WOS:A1994PK08600055 ER PT J AU CHIAPPELLI, F TIO, DL FROST, P TAYLOR, AN AF CHIAPPELLI, F TIO, DL FROST, P TAYLOR, AN TI DIFFERENTIAL DISTRIBUTION OF THYMOCYTE SUBPOPULATIONS IN PREPUBERTAL MALE FETAL ALCOHOL EXPOSED RATS SO LYMPHOLOGY LA English DT Article; Proceedings Paper CT 14th International Congress of Lymphology CY SEP 20-26, 1993 CL WASHINGTON, DC SP INT SOC LYMPHOL, NIH ID PROLIFERATIVE RESPONSE; ETHANOL INUTERO; CELLS AB We reported significant differences in the response of thymocytes to mitogen stimulation among fetal alcohol exposed (FAE) and control male rats at postnatal day 45. We did not observe these differences in blood lymphocytes at any age tested. Thus, we have begun to test the hypothesis that the migration of thymocytes into peripheral blood is disturbed in FAE rats. We present preliminary flow cytometric analyses that suggest altered expression of the common leukocyte antigen (CD45RC) by thymocytes in prepubertal male FAE Sprague Dawley rats. This difference is not evident in peripheral blood, confirming the hypothesis that FAE disturbs the development of cellular immunity and the ''thymus-blood loop'' of lymphoid cell trafficking. C1 W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,LOS ANGELES,CA 90073. RP CHIAPPELLI, F (reprint author), UNIV CALIF LOS ANGELES,SCH MED,BRI,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90024, USA. NR 9 TC 1 Z9 1 U1 0 U2 0 PU LYMPHOLOGY PI TUCSON PA C/O C L WITTE MD 1501 N CAMPBELL AVE DEPT SURGERY, TUCSON, AZ 85724 SN 0024-7766 J9 LYMPHOLOGY JI Lymphology PY 1994 VL 27 SU S BP 212 EP 214 PG 3 WC Immunology; Physiology SC Immunology; Physiology GA PK086 UT WOS:A1994PK08600056 ER PT J AU WOLF, GL ROGOWSKA, J GAZELLE, GS HALPERN, EF AF WOLF, GL ROGOWSKA, J GAZELLE, GS HALPERN, EF TI METHODS FOR QUANTITATIVE CT LYMPHOGRAPHY SO LYMPHOLOGY LA English DT Article; Proceedings Paper CT 14th International Congress of Lymphology CY SEP 20-26, 1993 CL WASHINGTON, DC SP INT SOC LYMPHOL, NIH RP WOLF, GL (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 4 TC 4 Z9 4 U1 0 U2 0 PU LYMPHOLOGY PI TUCSON PA C/O C L WITTE MD 1501 N CAMPBELL AVE DEPT SURGERY, TUCSON, AZ 85724 SN 0024-7766 J9 LYMPHOLOGY JI Lymphology PY 1994 VL 27 SU S BP 261 EP 264 PG 4 WC Immunology; Physiology SC Immunology; Physiology GA PK086 UT WOS:A1994PK08600068 ER PT J AU KANTOR, HL RZEDZIAN, RR BUXTON, R BERLINER, E BEAULIEU, P ROSEN, B BRADY, TJ PYKETT, IL AF KANTOR, HL RZEDZIAN, RR BUXTON, R BERLINER, E BEAULIEU, P ROSEN, B BRADY, TJ PYKETT, IL TI CONTRAST-INDUCED MYOCARDIAL SIGNAL REDUCTION - EFFECT OF LANTHANIDE CHELATES ON ULTRA-HIGH-SPEED MR-IMAGES SO MAGNETIC RESONANCE IMAGING LA English DT Article DE CONTRAST AGENT; CARDIAC; FLOW ENHANCEMENT; DYSPROSIUM; GADOLINIUM AB The myocardial MR signal reduction associated with an intravenous bolus of Gd-DTPA and Dy-DTPA was studied in a canine model. Imaging was performed with a high speed echo-planar type imaging system (Instascan, Advanced NMR Systems, Inc.). Gated spin-echo images were obtained with TE of 30 ms, which permits image acquisition in approximately 40 ms. The gated TR was dependent on the heart rate, with an average TR of 2.4 s. After 0.1 mmol/kg of contrast was injected, 70 images were acquired, which showed in an 80-image data set a reduction in myocardial signal with a gradual return to normal. After dipyridamole infusion, the signal loss was significantly more pronounced, and earlier than in the control data set. There was no significant difference between Gd-DTPA and Dy-DTPA in these imaging studies despite the theoretical prediction of better Dy signal reduction, possibly due to physiological variability during the course of a study or between studies. The cause of enhanced contrast effect after dipyridamole infusion is discussed, as is the basis for dipyridamole enhancement, and the possible role of contrast enhanced MR imaging in the detection of cardiac disease. RP KANTOR, HL (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114, USA. FU NCI NIH HHS [5P01CA48729-03]; NHLBI NIH HHS [HL34454-03, HL39810-02] NR 0 TC 10 Z9 10 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0730-725X J9 MAGN RESON IMAGING JI Magn. Reson. Imaging PY 1994 VL 12 IS 1 BP 51 EP 59 DI 10.1016/0730-725X(94)92352-3 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ML325 UT WOS:A1994ML32500007 PM 8295508 ER PT J AU LO, EH PAN, Y MATSUMOTO, K KOWALL, NW AF LO, EH PAN, Y MATSUMOTO, K KOWALL, NW TI BLOOD-BRAIN-BARRIER DISRUPTION IN EXPERIMENTAL FOCAL ISCHEMIA - COMPARISON BETWEEN IN-VIVO MRI AND IMMUNOCYTOCHEMISTRY SO MAGNETIC RESONANCE IMAGING LA English DT Article DE BLOOD-BRAIN BARRIER; CEREBRAL ISCHEMIA; CEREBRAL BLOOD FLOW; MRI; GDDTPA; IMMUNOCYTOCHEMISTRY AB The definition of blood-brain barrier (BBB) damage in cerebral ischemia using contrast-enhanced MRI has not been clearly correlated to the spread of edema or other histological measures of barrier disruption. In this study, we used a rabbit model of focal cerebral ischemia to compare GdDTPA-enhanced MRI with spin-echo images of brain injury and immunocytochemical detection of BBB damage and vasogenic edema. After 4 h of transient ischemia followed by 6 h of reperfusion, in vivo T2W and T1W images were obtained in a 1.5 T magnet using a 3-inch surface coil. After MRI, the animals were sacrificed and anti-serum protein (IgG) monoclonal antibodies were used to detect regions of increased BBB permeability to serum proteins. Ischemic neuronal damage was confirmed with cresyl-violet histology. T2W scans showed focal regions of increased signal intensity in the ischemic hemisphere (17.0 +/- 4.1%) that primarily involved the cortex and striatum. T2W scans showed corresponding regions of hypointensity but demonstrated, in general, smaller lesion sizes (10.1 +/- 2.9%). GdDTPA-enhanced images showed variable areas of BBB disruption that included regions of intense leakage as well as lesions that only showed subtle enhancement along the periphery of damaged tissue. It appeared that large and more severe lesions corresponded to peripheral enhancement whereas smaller lesions showed central parenchymal enhancement. The extent of MR contrast enhancement did not correlate well with immunocytochemical images of serum protein leakage. Anti-Ige stains demonstrated widespread regions of BBB damage corresponding with areas of damaged neurons that appeared pyknotic on cresyl-violet sections. Severely damaged neurons also showed cellular IgG uptake. These data suggest that GdDTPA leakage in cerebral ischemia can be variable in a model of focal ischemia with reperfusion and does not precisely correlate with vasogenic edema defined by serum protein extravasation across the BBB. RP LO, EH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR IMAGING & PHARMACEUT RES,MGH E BLDG 149,BOSTON,MA 02129, USA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 42 Z9 44 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0730-725X J9 MAGN RESON IMAGING JI Magn. Reson. Imaging PY 1994 VL 12 IS 3 BP 403 EP 411 DI 10.1016/0730-725X(94)92533-X PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA PE077 UT WOS:A1994PE07700004 PM 8007769 ER PT S AU TAKAYAMA, K QURESHI, N COTTER, RJ AF TAKAYAMA, K QURESHI, N COTTER, RJ BE Fenselau, C TI MASS-SPECTRAL ANALYSIS OF LIPID-A OF GRAM-NEGATIVE BACTERIA SO MASS SPECTROMETRY FOR THE CHARACTERIZATION OF MICROORGANISMS SE ACS SYMPOSIUM SERIES LA English DT Article; Proceedings Paper CT Symposium on Mass Spectrometry for the Characterization of Microorganisms, at the 204th National Meeting of the American-Chemical-Society CY AUG 23-28, 1992 CL WASHINGTON, DC SP AMER CHEM SOC, DIV ANAL CHEM ID LASER DESORPTION; SALMONELLA-TYPHIMURIUM; STRUCTURAL DETERMINATION; SPECTROMETRY; LIPOPOLYSACCHARIDES; FRAGMENTATION; MUTANT AB Positive ion FAB-MS, LD-MS, and PD-MS were utilized to obtain important structural information on the 4'-monophosphoryl lipid A (MPLA) derived from the lipopolysaccharides of Salmonella typhimurium and other Gram-negative bacterial strains which led to the elucidation of its chemical structure. The spectra of MPLA generated by these methods showed peaks corresponding to cationized molecular ions, losses of fatty acyl groups, and cleavage of the disaccharide yielding oxonium ions (FAB-MS and PD-MS), and several two-bond ring cleavages LD-MS and PD-MS). The distribution of the fatty acyl groups on the MPLA molecule was then deduced from its size and fragmentation pattern. We suggest that one could now identify and differentiate certain Gram-negative bacterial strains by performing mass spectral analysis of the isolated MPLA. C1 UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL,BALTIMORE,MD 21205. RP TAKAYAMA, K (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705, USA. NR 22 TC 2 Z9 2 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0097-6156 BN 0-8412-2737-3 J9 ACS SYM SER PY 1994 VL 541 BP 173 EP 184 PG 12 WC Chemistry, Multidisciplinary; Chemistry, Analytical; Microbiology SC Chemistry; Microbiology GA BZ67V UT WOS:A1994BZ67V00012 ER PT J AU TANG, ZQ ZHANG, ZY ZHENG, YS CORBLEY, MJ TONG, TJ AF TANG, ZQ ZHANG, ZY ZHENG, YS CORBLEY, MJ TONG, TJ TI CELL AGING OF HUMAN-DIPLOID FIBROBLASTS IS ASSOCIATED WITH CHANGES IN RESPONSIVENESS TO EPIDERMAL GROWTH-FACTOR AND CHANGES IN HER-2 EXPRESSION SO MECHANISMS OF AGEING AND DEVELOPMENT LA English DT Article DE CELL AGING; EPIDERMAL GROWTH FACTOR; HER-2; SENESCENCE; 2BS FIBROBLASTS ID FACTOR RECEPTOR; NEU ONCOGENE; EGF RECEPTOR; TYROSINE KINASE; WI-38 CELLS; PROTEIN; GENE; PHOSPHORYLATION; LIGAND; P185ERBB2 AB The limited replicative life span of diploid human cells in vitro (cellular senescence) serves as a cellular model of aging. We examined the proliferative response of 2BS cells of different population doubling levels to epidermal growth factor (EGF). DNA synthesis was measured by thymidine incorporation. As the cells aged, there was a significant decrease both in the baseline level of DNA synthesis and in the stimulation of DNA synthesis by EGF addition. The effective concentration of EGF and the latent period prior to DNA synthesis did not change. EGF receptor mRNA expression also remained unchanged as the cells aged, in the absence or presence of EGF, suggesting that the defect in old cells lies downstream in the EGF signaling pathway. As the cells reached 100% of their life span, however, there was a 70% decrease in EGF receptor mRNA. Expression of the EGF receptor homologue HER-2 was also examined. The HER-2 mRNA level was significantly reduced in old cells. Moreover, HER-2 expression was stimulated by EGF addition in young cells but not in old cells. The results suggest that cell aging is associated with a progressive loss in the ability of cells to respond to growth factors. C1 BEIJING MED UNIV,DEPT BIOCHEM,BEIJING 100083,PEOPLES R CHINA. DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. NR 30 TC 44 Z9 55 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0047-6374 J9 MECH AGEING DEV JI Mech. Ageing. Dev. PD JAN PY 1994 VL 73 IS 1 BP 57 EP 67 DI 10.1016/0047-6374(94)90038-8 PG 11 WC Cell Biology; Geriatrics & Gerontology SC Cell Biology; Geriatrics & Gerontology GA NA021 UT WOS:A1994NA02100007 PM 8028398 ER PT J AU LEE, RS AUCHINCLOSS, H AF LEE, RS AUCHINCLOSS, H TI MECHANISMS OF TOLERANCE TO ALLOGRAFTS SO MECHANISMS OF IMMUNE REGULATION SE CHEMICAL IMMUNOLOGY LA English DT Review ID T-CELL RECEPTOR; CLASS-II MHC; MAJOR HISTOCOMPATIBILITY COMPLEX; TOTAL LYMPHOID IRRADIATION; MARROW GRAFT-REJECTION; VS-HOST DISEASE; NATURAL SUPPRESSOR CELLS; REACTIVE LYMPHOCYTES-B; ALLOGENEIC BONE-MARROW; PANCREATIC BETA-CELLS C1 MASSACHUSETTS GEN HOSP,DEPT SURG,TRANSPLANTAT UNIT,BOSTON,MA 02114. RP LEE, RS (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02114, USA. NR 199 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 1015-0145 J9 CHEM IMMUNOL JI Chem.Immunol. PY 1994 VL 58 BP 236 EP 258 PG 23 WC Allergy; Immunology SC Allergy; Immunology GA BA04B UT WOS:A1994BA04B00009 PM 8011154 ER PT J AU GRABBE, S GRANSTEIN, RD AF GRABBE, S GRANSTEIN, RD TI MECHANISMS OF ULTRAVIOLET-RADIATION CARCINOGENESIS SO MECHANISMS OF IMMUNE REGULATION SE CHEMICAL IMMUNOLOGY LA English DT Review ID ANTIGEN-PRESENTING CELLS; NECROSIS-FACTOR-ALPHA; TUMOR-BEARING MICE; EPIDERMAL LANGERHANS CELLS; UV-IRRADIATED MICE; SUPPRESSOR T-CELLS; CIS-UROCANIC ACID; CONTACT HYPERSENSITIVITY RESPONSES; PROSTAGLANDIN-DEPENDENT MECHANISM; KERATINOCYTE-DERIVED IL-10 C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA. RP GRABBE, S (reprint author), UNIV MUNSTER,DEPT DERMATOL,VON ESMARCH STR 56,D-48149 MUNSTER,GERMANY. FU NIAMS NIH HHS [AR40667] NR 163 TC 21 Z9 21 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 1015-0145 J9 CHEM IMMUNOL JI Chem.Immunol. PY 1994 VL 58 BP 291 EP 313 PG 23 WC Allergy; Immunology SC Allergy; Immunology GA BA04B UT WOS:A1994BA04B00011 PM 8011156 ER PT S AU SEED, B KOLANUS, W ROMEO, C XAVIER, R AF SEED, B KOLANUS, W ROMEO, C XAVIER, R BE Gupta, S Paul, WE DeFranco, A Perlmutter, R TI NONRECEPTOR TYROSINE KINASES IN AGGREGATION-MEDIATED CELL ACTIVATION SO MECHANISMS OF LYMPHOCYTE ACTIVATION AND IMMUNE REGULATION V: MOLECULAR BASIS OF SIGNAL TRANSDUCTION SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Mechanisms of Lymphocyte Activation and Immune Regulation CY FEB 04-06, 1994 CL NEWPORT BEACH, CA RP SEED, B (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44897-1 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1994 VL 365 BP 111 EP 119 PG 9 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA BB86U UT WOS:A1994BB86U00012 PM 7887297 ER PT J AU RUSSO, CL MCINTYRE, J GOORIN, AM LINK, MP GEBHARDT, MC FRIEND, SH AF RUSSO, CL MCINTYRE, J GOORIN, AM LINK, MP GEBHARDT, MC FRIEND, SH TI SECONDARY BREAST-CANCER IN PATIENTS PRESENTING WITH OSTEOSARCOMA - POSSIBLE INVOLVEMENT OF GERMLINE P53 MUTATIONS SO MEDICAL AND PEDIATRIC ONCOLOGY LA English DT Article DE SECOND MALIGNANCY; THERAPEUTIC CHEST IRRADIATION; TUMOR SUPPRESSOR GENE ID 2ND MALIGNANT NEOPLASMS; OSTEO-SARCOMA; CHILDHOOD-CANCER; PRIMARY TUMORS; CHILDREN; RISK; LEUKEMIA; IDENTIFICATION; SURVIVORS; THERAPY AB Second malignancies following treatment for osteosarcoma are unusual. Breast cancer occurring in patients with osteosarcoma has been reported following therapeutic chest irradiation. We now report three cases of breast cancer occurring in young women who were successfully treated for osteosarcoma. These women had not received therapeutic chest irradiation and in two of the three women there was no family history of breast cancer. Peripheral blood was available for study from one case. Of import, this case demonstrated a germline mutation in exon 7 of the tumor suppressor gene, p53. The mutation was detected by constant denaturing gradient gel electrophoresis and confirmed by DNA sequencing. In this particular patient, inactivation of the p53 gene may be involved in the development of both the first and second malignancy. (C) 1994 Wiley-Liss, Inc. C1 STANFORD UNIV,DEPT PEDIAT,STANFORD,CA 94305. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV MOLEC GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 28 TC 17 Z9 17 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 0098-1532 J9 MED PEDIATR ONCOL JI Med. Pediatr. Oncol. PY 1994 VL 23 IS 4 BP 354 EP 358 DI 10.1002/mpo.2950230407 PG 5 WC Oncology; Pediatrics SC Oncology; Pediatrics GA PD284 UT WOS:A1994PD28400006 PM 8058007 ER PT B AU LANE, L AYLIFFE, W FOSTER, CS AF LANE, L AYLIFFE, W FOSTER, CS BE Selser, RE TI MANAGEMENT STRATEGIES IN PERIPHERAL ULCERATIVE KERATITIS AND NECROTIZING SCLERITIS SO MEDICAL CORNEA: CORNEAL AND REFRACTIVE SURGERY LA English DT Proceedings Paper CT 42nd Annual Symposium on Medical Cornea - Corneal and Refractive Surgery CY FEB 26-28, 1993 CL NEW ORLEANS, LA SP NEW ORLEANS ACAD OPHTHALMOL C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,IMMUNOL SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KUGLER PUBLICATIONS BV PI AMSTELVEEN PA PO BOX 516, 1180 AM AMSTELVEEN, NETHERLANDS BN 90-6299-106-8 PY 1994 BP 39 EP 47 PG 9 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA BA56D UT WOS:A1994BA56D00005 ER PT B AU AYLIFFE, W FOSTER, CS AF AYLIFFE, W FOSTER, CS BE Selser, RE TI HIGH-RISK KERATOPLASTY SO MEDICAL CORNEA: CORNEAL AND REFRACTIVE SURGERY LA English DT Proceedings Paper CT 42nd Annual Symposium on Medical Cornea - Corneal and Refractive Surgery CY FEB 26-28, 1993 CL NEW ORLEANS, LA SP NEW ORLEANS ACAD OPHTHALMOL C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KUGLER PUBLICATIONS BV PI AMSTELVEEN PA PO BOX 516, 1180 AM AMSTELVEEN, NETHERLANDS BN 90-6299-106-8 PY 1994 BP 57 EP 69 PG 13 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA BA56D UT WOS:A1994BA56D00007 ER PT B AU FOSTER, CS LINDSTROM, R LEMP, M BUZARD, K AF FOSTER, CS LINDSTROM, R LEMP, M BUZARD, K BE Selser, RE TI THE CHRONIC RED EYE SO MEDICAL CORNEA: CORNEAL AND REFRACTIVE SURGERY LA English DT Proceedings Paper CT 42nd Annual Symposium on Medical Cornea - Corneal and Refractive Surgery CY FEB 26-28, 1993 CL NEW ORLEANS, LA SP NEW ORLEANS ACAD OPHTHALMOL C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,IMMUNOL SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KUGLER PUBLICATIONS BV PI AMSTELVEEN PA PO BOX 516, 1180 AM AMSTELVEEN, NETHERLANDS BN 90-6299-106-8 PY 1994 BP 143 EP 151 PG 9 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA BA56D UT WOS:A1994BA56D00014 ER PT J AU NIEMIERKO, A GOITEIN, M AF NIEMIERKO, A GOITEIN, M TI DOSE-VOLUME DISTRIBUTIONS - A NEW APPROACH TO DOSE-VOLUME HISTOGRAMS IN 3-DIMENSIONAL TREATMENT PLANNING SO MEDICAL PHYSICS LA English DT Article DE DOSE-VOLUME HISTOGRAM; DOSE-VOLUME DISTRIBUTION; HISTOGRAM; SAMPLING; RADIOTHERAPY PLANNING ID COMPLICATION PROBABILITY; RADIATION-THERAPY AB A new approach to calculating and displaying dose-volume relationships in 3D radiation therapy is presented. We have developed a concept of a dose-volume distribution (DVD) and its corresponding differential dose-volume distribution (DDVD), based on organization of the data in the volume rather than in the dose domain. The new concepts make full use of the information that can be obtained from the dose calculation points and the sampling pattern and are designed to overcome shortcomings of the classical concepts of dose-volume histograms (DVH) and differential dose-volume histograms (DDVH). The new concepts can be applied to any number of dose calculation points, but they are especially advantageous when a small number of points is used. DVDs are particularly well suited to pseudo- and quasirandom sampling of dose distributions. We have developed an error analysis for DVDs and DDVDs in the case of pseudorandom sampling. We also describe an adaptive technique for minimizing the amount of data needed for purposes of display. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP NIEMIERKO, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,DIV RADIAT BIOPHYS,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 21239, CA 50628] NR 15 TC 23 Z9 24 U1 0 U2 0 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0094-2405 J9 MED PHYS JI Med. Phys. PD JAN PY 1994 VL 21 IS 1 BP 3 EP 11 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MU896 UT WOS:A1994MU89600001 PM 8164585 ER PT J AU CASTILLO, L AJAMI, A BRANCH, S CHAPMAN, TE YU, YM BURKE, JF YOUNG, VR AF CASTILLO, L AJAMI, A BRANCH, S CHAPMAN, TE YU, YM BURKE, JF YOUNG, VR TI PLASMA ARGININE KINETICS IN ADULT MAN - RESPONSE TO AN ARGININE-FREE DIET SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID AMINO-ACIDS; NITROGEN-METABOLISM; GAS-CHROMATOGRAPHY; PROTEIN-DEGRADATION; UBIQUITIN PATHWAY; WHOLE-BODY; HUMANS; UREA; CITRULLINE; GLUTAMINE C1 MIT,HUMAN NUTR LAB,CAMBRIDGE,MA 02149. MIT,CLIN RES CTR,CAMBRIDGE,MA 02139. SHRINERS BURNS INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. TRACER TECHNOL,SOMERVILLE,MA. FU NIGMS NIH HHS [GM02700]; PHS HHS [R88, 15856] NR 75 TC 65 Z9 65 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD JAN PY 1994 VL 43 IS 1 BP 114 EP 122 DI 10.1016/0026-0495(94)90166-X PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MY189 UT WOS:A1994MY18900018 PM 8289668 ER PT J AU TOMERA, JF KUKULKA, SP LILFORD, K MARTYN, JAJ AF TOMERA, JF KUKULKA, SP LILFORD, K MARTYN, JAJ TI ESCHERICHIA-COLI ENDOTOXIN AFFINITY AT THE NICOTINIC(2) RECEPTOR - RECEPTOR THEORY REVISITED, ILUMINA NOSTROS OCCULAE SO METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY LA English DT Article DE DISSOCIATION CONSTANT; ENDOTOXIN; MOUSE; NICOTINIC RECEPTOR; SKELETAL MUSCLE ID CLINICAL-PHARMACOLOGY; GASTROCNEMIUS-MUSCLE; SENSITIVITY; DESENSITIZATION; ACETYLCHOLINE; PROTEIN; BINDING; CELLS AB This paper examines the interaction of endotoxin at the nicotinic(2) receptor (ACh-R(post)) with the adenylate cyclase signal transduction system in skeletal muscle. It reports the drug-receptor (DR) dissociation constant(K, 0.05020 +/-.0015 mg/kg) for E. coli endotoxin. It expands on a previous report (ii which presented the relevance of skeletal muscle cAMP as a metabolic indicator and second messenger influenced by endotoxicosis. The use of a murine endotoxic model allowed for the measuring of K for the antagonist DR affinity measures which relied on the constrained-slope Schild plot measured it. This report assessed dose-response relations of the the competitive antagonist dTC (ANI and their modification (AN') by advancing endotoxicosis. The presence of endotoxin al a fixed final concentration (i.e., 7.75 mg/kg) within the body at the end of a two week period caused a rightward shift in the dTC dose-response curve. Endotoxin desensitized cAMP and caused the dTC curve to be shifted rightward. This report differs from typical pharmacological applications where standard agonist curves are obtainable in the presence of an antagonist. This in vivo model did not allow for the measurement of agonist ACh concentration. Therefore, the use of a pair of compounds (i.e., antagonistic dTC and agonistic endotoxin) and their effects (i. e., suppression of active tension and cAMP desensitization, respectively) allowed us to quantitate K. In summary, this report supports the hypothesis linking the nicotinic(2) receptor to the adenylate cyclase signal transduction system and illustrates that endotoxicosis perturbed both. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIOL,BOSTON,MA. RP TOMERA, JF (reprint author), SHRINERS BURNS INST,CLIN PHARMACOL LAB,ANESTHESIA SERV,1 KENDALL SQ,BLDG 1400W,CAMBRIDGE,MA 02142, USA. FU PHS HHS [31569] NR 37 TC 2 Z9 2 U1 0 U2 0 PU J R PROUS SA PI BARCELONA PA APARTADO DE CORREOS 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 0379-0355 J9 METHOD FIND EXP CLIN JI Methods Find. Exp. Clin. Pharmacol. PY 1994 VL 16 IS 3 BP 191 EP 201 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NH834 UT WOS:A1994NH83400005 PM 8046953 ER PT J AU TOMERA, JF LILFORD, K AF TOMERA, JF LILFORD, K TI MULTIPLE STEPWISE REGRESSION-ANALYSIS OF PHYSIOLOGICAL TENSION AND SECONDARY MESSENGERS IN CHRONIC BURN TRAUMA SO METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY LA English DT Article DE ADENOSINE 3', 5' CYCLIC MONOPHOSPHATE; BURN TRAUMA; CALCIUM; DATA MATRIX; GASTROCNEMIUS; INOSITOL TRIPHOSPHATE; MULTIVARIATE; PHYSIOLOGICAL TENSION; POLYINOSITOLS; STEPWISE REGRESSION ANALYSIS AB In this report, we have used a multiple stepwise regression analysis to determine the best derived multivariate equation between a dependent and multiple independent parameters. All parameters were derived from harvested gastrocnemius muscle subjected to chronic burn trauma. Correlations between seven different parameters were tested. Physiologic tension, calcium, adenosine 3':5' cyclic monophosphate (cAMP), inositol 1,4, 5-triphosphate (IP3) and its catabolites comprised one large data matrix. From it, the various parameters were substituted as the dependent variable. The remaining parameters all comprised a multiple independent group. From such a format, the stepwise regression was run. The simultaneous co-governing of independent parameters over one dependent parameter provides a means of mathematically proving multiple correlations. Such findings provide a new perspective in interpreting chemical signalling. C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS RES CTR,ANESTHESIA SERV,CLIN PHARMACOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 16 TC 5 Z9 5 U1 0 U2 1 PU J R PROUS SA PI BARCELONA PA APARTADO DE CORREOS 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 0379-0355 J9 METHOD FIND EXP CLIN JI Methods Find. Exp. Clin. Pharmacol. PY 1994 VL 16 IS 4 BP 235 EP 246 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NL237 UT WOS:A1994NL23700001 PM 8051982 ER PT J AU LEECH, CA HOLT, GG AF LEECH, CA HOLT, GG TI APPLICATION OF PATCH-CLAMP METHODS TO THE STUDY OF CALCIUM CURRENTS AND CALCIUM CHANNELS SO METHODS IN CELL BIOLOGY, VOL 40 SE METHODS IN CELL BIOLOGY LA English DT Review ID PANCREATIC-BETA-CELLS; DEPENDENT CA2+ CHANNELS; ISLET B-CELLS; ION CHANNELS; SKELETAL-MUSCLE; INSULIN-SECRETION; FUNCTIONAL EXPRESSION; DIHYDROPYRIDINE RECEPTOR; CHROMAFFIN CELLS; MEMBRANE PATCHES RP LEECH, CA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [R01 DK045817] NR 68 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-679X J9 METHOD CELL BIOL PY 1994 VL 40 BP 135 EP 151 PG 17 GA BB09C UT WOS:A1994BB09C00006 PM 8201974 ER PT J AU LEU, AJ YANAR, A JOST, J HOFFMANN, U FRANZECK, UK BOLLINGER, A AF LEU, AJ YANAR, A JOST, J HOFFMANN, U FRANZECK, UK BOLLINGER, A TI MICROVASCULAR DYNAMICS IN NORMAL SKIN VERSUS SKIN OVERLYING KAPOSIS-SARCOMA SO MICROVASCULAR RESEARCH LA English DT Note ID CUTANEOUS BLOOD-FLOW; LIGHT C1 UNIV HOSP ZURICH,DEPT INTERNAL MED,DIV ANGIOL,CH-8091 ZURICH,SWITZERLAND. UNIV HOSP ZURICH,DEPT INTERNAL MED,DIV INFECTIOL,CH-8091 ZURICH,SWITZERLAND. RP LEU, AJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 9 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 0026-2862 J9 MICROVASC RES JI Microvasc. Res. PD JAN PY 1994 VL 47 IS 1 BP 140 EP 144 DI 10.1006/mvre.1994.1009 PG 5 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MW538 UT WOS:A1994MW53800009 PM 8022311 ER EF