FN Thomson Reuters Web of Science™ VR 1.0 PT J AU SPARR, LF RUUD, DH HICKAM, DH COONEY, TG AF SPARR, LF RUUD, DH HICKAM, DH COONEY, TG TI THE EFFECT OF HOUSE OFFICER ROTATION ON INPATIENT SATISFACTION AND WARD ATMOSPHERE - PRELIMINARY FINDINGS SO MILITARY MEDICINE LA English DT Article AB Continual rotation of house officers builds discontinuity into the physician-patient relationship in teaching hospitals. This has led to speculation about the problem of residents and interns leaving their patients in the midst of hospital treatment. This article uses prospective data to assess the effect of house officer turnover on levels of patient satisfaction with hospital care and on patient perception of the hospital environment. Two inpatient cohorts defined by whether or not they had undergone a house officer change were matched by age and diagnostic category. Although survey instruments were significantly correlated, there was no significant difference between the two inpatient cohorts overall or on any of the survey subscales. The survey showed good satisfaction with the hospital, doctors, and nurses in both test groups. The authors draw a preliminary conclusion that patient satisfaction with medical care and with the hospital atmosphere remains constant, independent of termination of the doctor-patient relationship. Results from other reports linking patient satisfaction with continuity of care have been mixed, In discussing the limitations of their study, the authors point out that their findings are based on single-site data. RP SPARR, LF (reprint author), PORTLAND VA MED CTR,OUTPATIENT PSYCHIAT SECT,PORTLAND,OR 97201, USA. NR 0 TC 3 Z9 3 U1 1 U2 1 PU ASSN MILITARY SURG US PI BETHESDA PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0026-4075 J9 MIL MED JI Milit. Med. PD JAN PY 1994 VL 159 IS 1 BP 47 EP 53 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA MZ440 UT WOS:A1994MZ44000017 PM 8164867 ER PT S AU SATTIN, A PEKARY, AE LLOYD, RL AF SATTIN, A PEKARY, AE LLOYD, RL BE Strand, FL Beckwith, B Chronwall, B Sandman, CA TI TRH GENE-PRODUCTS ARE IMPLICATED IN THE ANTIDEPRESSANT MECHANISMS OF SEIZURES SO MODELS OF NEUROPEPTIDE ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 15th Annual Winter Neuropeptide Conference: Models of Neuropeptide Action CY FEB 05-08, 1994 CL BRECKENRIDGE, CO SP Int Neuropeptide Soc ID THYROTROPIN-RELEASING-HORMONE; RAT LIMBIC FOREBRAIN; ELECTROCONVULSIVE-THERAPY; BRAIN; EXPRESSION; DEPRESSION; RECEPTORS; THRESHOLD; EFFICACY; REGIONS C1 VET ADM MED CTR,RES SERV,SEPULVEDA,CA 91343. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,ENDOCRINOL RES LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. RP SATTIN, A (reprint author), VET ADM MED CTR,PSYCHIAT SERV,ANTIDEPRESSANT NEUROPHARMACOL RES LAB,116A-11,16111 PLUMMER ST,SEPULVEDA,CA 91343, USA. NR 36 TC 28 Z9 28 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-912-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 739 BP 135 EP 153 DI 10.1111/j.1749-6632.1994.tb19815.x PG 19 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD10Q UT WOS:A1994BD10Q00012 PM 7832467 ER PT S AU PEKARY, AE LLOYD, RL SATTIN, A AF PEKARY, AE LLOYD, RL SATTIN, A BE Strand, FL Beckwith, B Chronwall, B Sandman, CA TI PREDOMINANCE OF PGLU-HIS-PRO-GLY AMONG ALL TRH PRECURSOR PEPTIDES IN RAT LIMBIC FOREBRAIN AFTER ELECTROCONVULSIVE SEIZURES SO MODELS OF NEUROPEPTIDE ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 15th Annual Winter Neuropeptide Conference: Models of Neuropeptide Action CY FEB 05-08, 1994 CL BRECKENRIDGE, CO SP Int Neuropeptide Soc ID PITUITARY; BIOSYNTHESIS; INCREASES; BRAIN C1 UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. VET ADM MED CTR,PSYCHIAT & RES SERV,ANTIDEPRESSANT NEUROPHARMACOL RES LAB,SEPULVEDA,CA 91343. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP PEKARY, AE (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINOL RES LAB,RES SERV,BLDG 114,RM 200,LOS ANGELES,CA 90073, USA. NR 8 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 0-89766-912-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 739 BP 330 EP 333 DI 10.1111/j.1749-6632.1994.tb19838.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD10Q UT WOS:A1994BD10Q00034 PM 7832488 ER PT J AU RUBIN, D HUDNALL, SD AISENBERG, A JACOBSON, JO HARRIS, NL AF RUBIN, D HUDNALL, SD AISENBERG, A JACOBSON, JO HARRIS, NL TI RICHTERS TRANSFORMATION OF CHRONIC LYMPHOCYTIC-LEUKEMIA WITH HODGKINS-LIKE CELLS IS ASSOCIATED WITH EPSTEIN-BARR-VIRUS INFECTION SO MODERN PATHOLOGY LA English DT Article ID REED-STERNBERG CELLS; IMMUNOGLOBULIN GENE REARRANGEMENTS; CLONAL ORIGIN; MALIGNANT-LYMPHOMA; DISEASE; EXPRESSION; PROLIFERATIONS; DISORDERS; FEATURES; ANTIBODY AB The appearance of a high-grade lymphoma in the setting of B-cell chronic lymphocytic leukemia (CLL) is termed Richter's syndrome. Usually the high-grade component is a monomorphous, large cell lymphoma, but occasionally the high-grade component takes the form of Hodgkin's disease or a Hodgkin's-like lymphoma. Although Richter's syndrome is thought to represent clonal evolution of the underlying B-cell neoplasm in most cases, such a progression is difficult to explain when the high-grade component is Hodgkin's disease. We report two cases of Richter's syndrome in which the large cells had a morphology consistent with Reed-Sternberg cells and were found in a background of CLL. The large cells in both cases expressed the CD15 and CD30 antigens in a pattern characteristic of Reed-Sternberg cells, and the large cells in one case also expressed monotypic cytoplasmic immunoglobulin of the same type as that expressed by the underlying CLL. In both cases, Southern blot analysis of DNA from lymph nodes that contained both CLL and the Hodgkin's-like component showed single immunoglobulin gene rearrangements. Using the polymerase chain reaction, we found Epstein-Barr virus DNA in lymph nodes from both cases, and in peripheral blood lymphoid cells from one case 4 yr before the onset of Richter's syndrome. Immunoperoxidase staining showed expression of EBV latent membrane protein only in the Reed-Sternberg-like cells. By in situ hybridization, EBV RNA was found only in the Reed-Sternberg-like cells, whereas in CLL tissues obtained before the onset of Richter's syndrome, scattered EBV-positive CLL cells were identified. Our results provide further support for the clonal association between CLL and a Hodgkin's-like large cell transformation, and strengthen the link between EBV infection and this form of Richter's syndrome. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. NR 44 TC 57 Z9 58 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD JAN PY 1994 VL 7 IS 1 BP 91 EP 98 PG 8 WC Pathology SC Pathology GA NF426 UT WOS:A1994NF42600019 PM 8159658 ER PT J AU BAUMANN, H SYMES, AJ COMEAU, MR MORELLA, KK WANG, YP FRIEND, D ZIEGLER, SF FINK, JS GEARING, DP AF BAUMANN, H SYMES, AJ COMEAU, MR MORELLA, KK WANG, YP FRIEND, D ZIEGLER, SF FINK, JS GEARING, DP TI MULTIPLE REGIONS WITHIN THE CYTOPLASMIC DOMAINS OF THE LEUKEMIA INHIBITORY FACTOR-RECEPTOR AND GP130 COOPERATE IN SIGNAL-TRANSDUCTION IN HEPATIC AND NEURONAL CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; RAT ALPHA-1-ACID GLYCOPROTEIN; CILIARY NEUROTROPHIC FACTOR; PLASMA-PROTEIN GENES; ACUTE PHASE RESPONSE; EXPRESSION; INTERLEUKIN-1; CYTOKINES; SUPERFAMILY; MEDIATORS AB The receptor for leukemia inhibitory factor (LIFR), in combination with the signal-transducing subunit for interleukin-6-type cytokine receptors, gp130, and LIF, activates transcription of acute-phase plasma protein genes in human and rat hepatoma cells and the vasoactive intestinal peptide gene in a human neuroblastoma cell line. To identify the regions within the cytoplasmic domain of LIFR that initiate signal transduction independently of gp130, we constructed a chimeric receptor by linking the extracellular domain of the granulocyte colony-stimulating factor receptor (G-CSFR) to the transmembrane and cytoplasmic domain of human LIFR. The function of the chimeric receptor protein in transcriptional activation was assessed by G-CSF-mediated stimulation of cotransfected cytokine-responsive reporter gene constructs in hepatoma and neuroblastoma cells. By using the full-length cytoplasmic domain and mutants with progressive carboxy-terminal deletions, internal deletions, or point mutations, we identified the first 150 amino acid residues of LIFR as the minimal region necessary for signaling. The signaling reaction appears to involve a cooperativity between the first 70-amino-acid region containing the two sequence motifs conserved among hematopoietin receptors (box 1 and box 2) and a critical sequence between residues 141 and 150 (box 3). Analogous analyses of the cytoplasmic domains of G-CSFR and gp130 indicated similar arrangements of functional domains in these receptor subunits and the requirement of a box 3-related motif for signaling. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. IMMUNEX CORP,SEATTLE,WA 98101. RP BAUMANN, H (reprint author), ROSWELL PK CANC INST,DEPT MOLEC & CELLULAR BIOL,BUFFALO,NY 14263, USA. RI Symes, Aviva/S-7471-2016 OI Symes, Aviva/0000-0003-2557-9939 FU NCI NIH HHS [NCI CA26122] NR 50 TC 106 Z9 109 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JAN PY 1994 VL 14 IS 1 BP 138 EP 146 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MM981 UT WOS:A1994MM98100015 PM 8264582 ER PT B AU TEDDER, TF AF TEDDER, TF BE Navarro, J TI REGULATION OF L-SELECTIN FUNCTION - A LEUKOCYTE RECEPTOR FOR ENDOTHELIUM SO MOLECULAR BASIS OF INFLAMMATION SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT International Symposium on Molecular Basis of Inflammation CY APR 21-23, 1993 CL HEIDELBERG, GERMANY SP ARES SERONO SYMPOSIA RP TEDDER, TF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-09-0 J9 CHALL MOD MED PY 1994 VL 3 BP 185 EP 200 PG 16 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA BA22U UT WOS:A1994BA22U00019 ER PT S AU DEMARTINO, J CARROLL, M MATHEYPREVOT, B DANDREA, AD AF DEMARTINO, J CARROLL, M MATHEYPREVOT, B DANDREA, AD BE Rich, IN Lappin, TRJ TI ERYTHROPOIETIN RECEPTOR CONTAINS BOTH GROWTH-PROMOTING ACTIVITY AND DIFFERENTIATION-PROMOTING ACTIVITY SO MOLECULAR, CELLULAR, AND DEVELOPMENTAL BIOLOGY OF ERYTHROPOIETIN AND ERYTHROPOIESIS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Workshop on Molecular, Cellular, and Developmental Biology of Erythropoietin and Erythropoiesis CY APR 26-30, 1993 CL IRSEE, GERMANY SP NEW YORK ACAD SCI ID COLONY-STIMULATING FACTOR; VIRUS GP55 GLYCOPROTEIN; IL-2 RECEPTOR; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; CYTOPLASMIC REGION; BETA-CHAIN; HEMATOPOIETIC-CELLS; LIGAND-BINDING; GENE INDUCTION C1 DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. FU NIDDK NIH HHS [R0I-DK43889-01A1] NR 37 TC 4 Z9 4 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 0-89766-837-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 718 BP 213 EP 222 PG 10 WC Biochemistry & Molecular Biology; Developmental Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Developmental Biology; Science & Technology - Other Topics GA BA22P UT WOS:A1994BA22P00022 PM 8185230 ER PT J AU CHU, HM TAN, Y KOBIERSKI, LA BALSAM, LB COMB, MJ AF CHU, HM TAN, Y KOBIERSKI, LA BALSAM, LB COMB, MJ TI ACTIVATING TRANSCRIPTION FACTOR-III STIMULATES 3',5'-CYCLIC ADENOSINE MONOPHOSPHATE-DEPENDENT GENE-EXPRESSION SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID GLUTATHIONE-S-TRANSFERASE; C-JUN; CYCLIC-AMP; PROTEIN-KINASE; MOUSE FIBROBLASTS; ESCHERICHIA-COLI; FOS PROTEINS; PHOSPHORYLATION; PROENKEPHALIN; PURIFICATION AB Activating transcription factor-3 (ATF-3) is one member of a large family of leucine zipper transcription factors which bind to promoters responsive to cAMP and phorbol ester at the related cAMP (CRE) and phorbol ester response elements. We report here that ATF-3 is coexpressed with the neuropeptide precursor proenkephalin in human neuroblastoma SK-N-MC cells. Cotransfection experiments indicate that activation of proenkephalin gene expression by ATF-3 is dependent upon both the catalytic subunit of the cAMP-dependent protein kinase and the CRE-2 element. The CRE-2 element is essential for second messenger-inducible expression and is known to bind AP-1-like transcription factors. ATF-3 expressed in;bacteria or from rabbit reticulocyte lysates binds to the proenkephalin CRE-2 element as a homodimer and as a heterodimer with Jun-D, another activator of proenkephalin transcription. ATF-3 stimulates binding of Jun-D to the proenkephalin CRE-2 element and acts synergistically with Jun-D to induce proenkephalin gene expression. Sequential immunoprecipations of ATF-3 from SK-N-MC cells expressing proenkephalin indicate that ATF-3 is complexed with Jun-D in vivo and that both proteins are highly phosphorylated. Together, our results;suggest that ATF-3 may play an important role in the regulation of gene expression by cAMP-dependent intracellular signaling pathways. C1 MASSACHUSETTS GEN HOSP, MOLEC NEUROBIOL LAB, CHARLESTON, MA 02129 USA. HARVARD MED SCH, PROGRAM NEUROSCI, BOSTON, MA 02114 USA. HARVARD UNIV, DEPT BIOL, CAMBRIDGE, MA 02138 USA. FU NIDA NIH HHS [DA-0151, DA-05706]; NIMH NIH HHS [F31-MH10073] NR 35 TC 54 Z9 55 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD JAN PY 1994 VL 8 IS 1 BP 59 EP 68 DI 10.1210/me.8.1.59 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MT064 UT WOS:A1994MT06400007 PM 8152431 ER PT J AU BORSOOK, D FALKOWSKI, O BURSTEIN, R STRASSMAN, A KONRADI, C DAUBER, A COMB, M HYMAN, SE AF BORSOOK, D FALKOWSKI, O BURSTEIN, R STRASSMAN, A KONRADI, C DAUBER, A COMB, M HYMAN, SE TI STRESS-INDUCED REGULATION OF A HUMAN PROENKEPHALIN-BETA-GALACTOSIDASE FUSION GENE IN THE HYPOTHALAMUS OF TRANSGENIC MICE SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN RELEASING-FACTOR; MESSENGER-RNA; SUPRAOPTIC NUCLEI; NERVOUS-SYSTEM; SPINAL-CORD; RAT; HYBRIDIZATION; LOCALIZATION; WITHDRAWAL; EXPRESSION AB Transgenic mice expressing an Escherichia coli beta-galactosidase reporter gene under the control of 3 kilobases of human proenkephalin gene 5'-flanking sequence and 1.2 kilobases of 3'-flanking sequence exhibited an anatomically correct pattern of basal and stress-regulated transgene expression within the hypothalamus. Acute osmotic stress and hypovolemia induced transgene expression in neurons within both the paraventricular and supraoptic nuclei. Chronic osmotic stress resulted in dramatic induction of transgene expression in both nuclei. These results demonstrate that the information required for correct hypothalamic expression and stress regulation of the proenkephalin gene is contained within our fusion construct. C1 MASSACHUSETTS GEN HOSP, MOLEC & DEV NEUROSCI LAB, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, HARVARD MED SCH, DEPT ANESTHESIA, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, HARVARD MED SCH, DEPT NEUROL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, HARVARD MED SCH, DEPT PSYCHIAT, BOSTON, MA USA. FU NIDA NIH HHS [DA-05706]; NIMH NIH HHS [MH-00892, MH-44160] NR 21 TC 25 Z9 25 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD JAN PY 1994 VL 8 IS 1 BP 116 EP 125 DI 10.1210/me.8.1.116 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MT064 UT WOS:A1994MT06400013 PM 8152426 ER PT J AU KOLODNER, R HALL, SD LUISIDELUCA, C AF KOLODNER, R HALL, SD LUISIDELUCA, C TI HOMOLOGOUS PAIRING PROTEINS ENCODED BY THE ESCHERICHIA-COLI RECE AND RECT GENES SO MOLECULAR MICROBIOLOGY LA English DT Review ID RECOMBINATION-DEFICIENT MUTANTS; BACTERIAL PLASMID DNA; BACTERIOPHAGE-LAMBDA; STRAND EXCHANGE; BETA-PROTEIN; EXONUCLEASE-VIII; SACCHAROMYCES-CEREVISIAE; PHAGE-LAMBDA; INTRAMOLECULAR RECOMBINATION; CONJUGATIONAL RECOMBINATION AB Early genetic analysis of alternate recombination pathways in Escherichia coli identified the RecE recombination pathway and the required exonuclease VIII encoded by the recE gene. Observations that not all recombination events promoted by the RecE pathway require recA suggest the existence of an additional homologous pairing protein besides RecA in E. coli. Genetic and biochemical analysis of the recE gene region indicates there are two partially overlapping genes, recE and recT, encoding at least two proteins: exoVIII and the RecT protein. Biochemical analysis has shown that the RecT protein, in combination with exoVIII, promotes homologous pairing and strand exchange in reactions containing linear duplex DNA and homologous, circular, single-stranded DNA as substrates. This reaction occurs in the absence of any high-energy cofactor. These two proteins, RecT and exoVIII, appear to be members of a second class of homologous pairing proteins that are required in genetic recombination and differ from the class of homologous pairing proteins that includes RecA. Members of this second class of proteins appear to include both bacteriophage-encoded proteins and proteins from eukaryotes and their viruses. C1 HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. UNIV PITTSBURGH, SCH MED, DEPT MOLEC GENET & BIOCHEM, PITTSBURGH, PA 15261 USA. RP KOLODNER, R (reprint author), DANA FARBER CANC INST, DIV CELLULAR & MOLEC BIOL, 44 BINNEY ST, BOSTON, MA 02115 USA. FU NIGMS NIH HHS [GM26017] NR 76 TC 64 Z9 66 U1 0 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0950-382X EI 1365-2958 J9 MOL MICROBIOL JI Mol. Microbiol. PD JAN PY 1994 VL 11 IS 1 BP 23 EP 30 DI 10.1111/j.1365-2958.1994.tb00286.x PG 8 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA MQ206 UT WOS:A1994MQ20600005 PM 8145642 ER PT B AU TAUBMAN, MA EASTCOTT, JW SHIMAUCHI, H TAKEICHI, O SMITH, DJ AF TAUBMAN, MA EASTCOTT, JW SHIMAUCHI, H TAKEICHI, O SMITH, DJ BE Genco, R Hamada, S Lehner, T McGhee, J Mergenhagen, S TI MODULATORY ROLE OF T-LYMPHOCYTES IN PERIODONTAL INFLAMMATION SO MOLECULAR PATHOGENESIS OF PERIODONTAL DISEASE LA English DT Proceedings Paper CT Symposium on Molecular Pathogenesis of Periodontal Disease CY JUN, 1993 CL BUFFALO, NY SP SUNSTAR INC, J O BUTLER CO, SUNY BUFFALO, SCH DENT MED C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 0 TC 32 Z9 32 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVE NW, WASHINGTON, DC 20005-4171 BN 1-55581-075-6 PY 1994 BP 147 EP 157 PG 11 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology; Pathology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology; Pathology GA BB59P UT WOS:A1994BB59P00013 ER PT B AU STASHENKO, P NGUYEN, L LI, YP AF STASHENKO, P NGUYEN, L LI, YP BE Genco, R Hamada, S Lehner, T McGhee, J Mergenhagen, S TI MECHANISMS OF REGULATION OF BONE-FORMATION BY PROINFLAMMATORY CYTOKINES SO MOLECULAR PATHOGENESIS OF PERIODONTAL DISEASE LA English DT Proceedings Paper CT Symposium on Molecular Pathogenesis of Periodontal Disease CY JUN, 1993 CL BUFFALO, NY SP SUNSTAR INC, J O BUTLER CO, SUNY BUFFALO, SCH DENT MED C1 FORSYTH DENT CTR,DEPT CYTOKINE BIOL,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVE NW, WASHINGTON, DC 20005-4171 BN 1-55581-075-6 PY 1994 BP 171 EP 181 PG 11 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology; Pathology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology; Pathology GA BB59P UT WOS:A1994BB59P00015 ER PT J AU WU, G TONNER, PH MILLER, KW AF WU, G TONNER, PH MILLER, KW TI ETHANOL STABILIZES THE OPEN-CHANNEL STATE OF THE TORPEDO NICOTINIC ACETYLCHOLINE-RECEPTOR SO MOLECULAR PHARMACOLOGY LA English DT Article ID FROG NEUROMUSCULAR-JUNCTION; ION CHANNELS; SELF-INHIBITION; ENDPLATE; ACTIVATION; AGONIST; ALCOHOLS; CURRENTS; BLOCK AB Ethanol is known to cause a leftward shift of the acetylcholine concentration-response curve for channel opening of the nicotinic acetylcholine receptor (nAcChoR). However, it remains uncertain whether the mechanism underlying ethanol's effect is an increase in the binding affinity of the agonist to the receptor or an increase in the open/closed equilibrium for those receptors occupied by agonist. In the present study, this question was resolved by measuring the efflux of Rb-86(+) over 9 msec from Torpedo vesicles after rapid mixing with the partial agonist suberyldicholine with or without ethanol as appropriate. Suberyldicholine's concentration-response curve is bell-shaped. Two actions underlie this bell-shaped curve, namely activation at low concentration (apparent dissociation constant for activation, K-a = 38 mu M) and self-inhibition at higher concentration (apparent dissociation constant for inhibition, K-b = 9 mM), but the overlap of these two actions only reduces the maximum observable flux by 20%. Increasing ethanol concentration from 0 to 0.9 M causes: a linear increase in the maximum response of the nAcChoR to suberyldicholine from 5 to 80% of the maximum induced by acetylcholine, a moderate increase in K-a, and no change in K-b. Analysis of our results using the sequential two-site binding model revealed that the main action of ethanol on nAcChoR was to increase the fraction of occupied receptors that open. The equilibrium constant describing this effect changed by 8-fold at anesthetic concentrations. Ethanol also decreased the affinity of suberyldicholine for its self-inhibition site by a comparable amount, suggesting that its main action is to stabilize the open state. In addition, ethanol caused a small increase in suberyldicholine's affinity for the agonist site. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIAAA NIH HHS [AA-07040] NR 27 TC 62 Z9 63 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JAN PY 1994 VL 45 IS 1 BP 102 EP 108 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MT928 UT WOS:A1994MT92800013 PM 8302268 ER PT J AU BORODIC, GE FERRANTE, R PEARCE, LB SMITH, K AF BORODIC, GE FERRANTE, R PEARCE, LB SMITH, K TI HISTOLOGIC ASSESSMENT OF DOSE-RELATED DIFFUSION AND MUSCLE-FIBER RESPONSE AFTER THERAPEUTIC BOTULINUM-A TOXIN INJECTIONS SO MOVEMENT DISORDERS LA English DT Article DE BOTULINUM TOXIN; BLEPHAROSPASM; SPASMODIC TORTICOLLIS; SPASMODIC DYSPHONIA; DYSTONIA MEIGE SYNDROME; HEMIFACIAL SPASM; MUSCLE FIBER ID SPASMODIC TORTICOLLIS; CHOLINESTERASE; BLEPHAROSPASM; INNERVATION AB Fiber diameter variability, acetylcholinesterase staining properties, and average fiber diameter were determined 5 weeks after varying doses of botulinum A toxin were administered into albino rabbit longissimus dorsi muscle. The average fiber diameter within the muscle appeared to be a function of the dose of botulinum toxin injected. Fiber diameter variability correlated with the dose of botulinum toxin administered. Both fiber diameter variability and acetylcholinesterase spread characteristics showed a distinct diffusion gradient over a defined field within a muscle. At lower doses (1 IU), collapse of the diffusion gradient occurred over a 15-30-mm segment of muscle. At higher doses (5-10 IU), diffusion of botulinum A toxin effect occurred throughout the entire muscle with no apparent end point. This study demonstrated that botulinum A toxin produces a gradient of denervation in a given muscle and that both the magnitude of denervation and the extent of the gradient are dose dependent. Furthermore, both muscle fiber diameter variability and acetylcholinesterase staining were useful as measures of chemodenervation. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. BOSTON UNIV,SCH MED,DEPT PHARMACOL,BOSTON,MA 02118. BEDFORD VET ADM MED CTR,BEDFORD,MA. BOSTON UNIV,DEPT NEUROL,BOSTON,MA 02215. BOSTON UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02118. BOSTON UNIV,DEPT PATHOL,BOSTON,MA 02215. NR 14 TC 155 Z9 160 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PD JAN PY 1994 VL 9 IS 1 BP 31 EP 39 DI 10.1002/mds.870090106 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA MP924 UT WOS:A1994MP92400005 PM 8139603 ER PT B AU ANDERSON, KC ANDERSEN, J SOIFFER, R FREEDMAN, AS RABINOWE, SN ROBERTSON, MJ SPECTOR, N FREEMAN, A MAUCH, P NADLER, LM RITZ, J AF ANDERSON, KC ANDERSEN, J SOIFFER, R FREEDMAN, AS RABINOWE, SN ROBERTSON, MJ SPECTOR, N FREEMAN, A MAUCH, P NADLER, LM RITZ, J BE Dammacco, F Barlogie, B TI MONOCLONAL-ANTIBODY PURGED BONE-MARROW TRANSPLANTATION THERAPY FOR MULTIPLE-MYELOMA SO MULTIPLE MYELOMA AND RELATED DISORDERS SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT International Symposium on Recent Advances on Monoclonal Grammapathies and Related Malignancies CY JUN 03-05, 1993 CL EVIAN LES BAINS, FRANCE SP ARES SERONO SYMPOSIA RP ANDERSON, KC (reprint author), DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, 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 88-85974-15-5 J9 CHALL MOD MED PY 1994 VL 4 BP 217 EP 232 PG 16 WC Oncology; Hematology; Immunology; Pathology SC Oncology; Hematology; Immunology; Pathology GA BA22V UT WOS:A1994BA22V00019 ER PT J AU CHURCH, DM STOTLER, CJ RUTTER, JL MURRELL, JR TROFATTER, JA BUCKLER, AJ AF CHURCH, DM STOTLER, CJ RUTTER, JL MURRELL, JR TROFATTER, JA BUCKLER, AJ TI ISOLATION OF GENES FROM COMPLEX SOURCES OF MAMMALIAN GENOMIC DNA USING EXON AMPLIFICATION SO NATURE GENETICS LA English DT Article ID SOMATIC-CELL HYBRIDS; SYNDROME TYPE-VII; MESSENGER-RNA; TRANSCRIBED SEQUENCES; EXPRESSION; CDNAS; MUTATION; CLONING; REGION; LOCUS AB Modifications to exon amplification have been instituted that increase its speed, efficiency and reliability. Exons were isolated from target human or mouse genomic DNA sources ranging from 30 kilobases (kb) to 3 megabases (Mb) in complexity. The efficiency was dependent upon the amount of input DNA, and ranged from isolation of an exon for every 20 kb to an exon for every 80 kb of target genomic DNA. In these studies, several novel genes and a smaller number of genes isolated previously that reside on human chromosome 9 have been identified. These results indicate that exon amplification is presently adaptable to large scale isolation of exons from complex sources of genomic DNA. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. OI Rutter, Joni/0000-0002-6502-2361 NR 52 TC 262 Z9 263 U1 0 U2 5 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD JAN PY 1994 VL 6 IS 1 BP 98 EP 105 DI 10.1038/ng0194-98 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA MQ177 UT WOS:A1994MQ17700021 PM 8136842 ER PT J AU URENA, P SEGRE, GV DRUEKE, TB AF URENA, P SEGRE, GV DRUEKE, TB TI PARATHYROID-HORMONE RECEPTOR SO NEPHROLOGY DIALYSIS TRANSPLANTATION LA English DT Editorial Material ID EXPRESSION CLONING; PEPTIDE RECEPTOR; MESSENGER-RNA; CELLS; CALCIUM; RESPONSES; PROTEIN; ACIDS; CAMP; BONE C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. RP URENA, P (reprint author), HOP NECKER ENFANTS MALAD,INSERM,U90,161 RUE SEVRES,F-75730 PARIS 15,FRANCE. NR 28 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 0931-0509 J9 NEPHROL DIAL TRANSPL JI Nephrol. Dial. Transplant. PY 1994 VL 9 IS 6 BP 593 EP 595 PG 3 WC Transplantation; Urology & Nephrology SC Transplantation; Urology & Nephrology GA NU883 UT WOS:A1994NU88300001 PM 7970082 ER PT J AU ARGILES, A MOURAD, G KERR, PG GARCIA, M COLLINS, B DEMAILLE, JG AF ARGILES, A MOURAD, G KERR, PG GARCIA, M COLLINS, B DEMAILLE, JG TI CELLS SURROUNDING HEMODIALYSIS-ASSOCIATED AMYLOID DEPOSITS ARE MAINLY MACROPHAGES SO NEPHROLOGY DIALYSIS TRANSPLANTATION LA English DT Article DE AMYLOID DEPOSITS; HEMODIALYSIS; MACROPHAGES; DIALYSIS RELATED AMYLOIDOSIS ID HEMODIALYSIS-ASSOCIATED AMYLOIDOSIS; BETA-2-MICROGLOBULIN; PROTEINS; FIBRILS; CULTURE; FORM AB Dialysis-related amyloidosis is a type of amyloidosis which has beta2-microglobulin as the major protein constituent and occurs predominantly in haemodialysis patients. Its prevalence is very high with increasing time on dialysis treatment and its pathogenesis, is not completely understood. While remarkable progress has been made in the identification of the components of the deposits, there are no reports characterizing the cells surrounding the amyloid fibrils. To characterize the cellular composition of the amyloid material, specimens from seven patients treated by maintenance haemodialysis were studied with immuno-peroxidase labelling using monoclonal antibodies to leukocytes (CD3, CD14, CD68, CD4, CD8, CD45). The results were very reproducible for the seven deposits assessed: Of the 182 +/- 26 leukocytes/0.2 mm2 of amyloid tissue expressing the 71.5-CD45 marker (common leukocyte), 91+/- 6% were CD68 (KP1) positive (monocyte macrophage). No CD3-positive cells (T-cell marker) were found in six of the seven patients, with only 1.6% in the remaining one. The present study shows that although amyloidosis has classically been considered as an acellular pathology, clearly there are cells surrounding amyloid fibrils. Strikingly, these cells are almost exclusively macrophages; there are no lymphocytes or granulocytes. The putative role of macrophages in the pathogenesis of beta2-microglobulin amyloidosis remains to be established. However, the identification and quantitation of the cells surrounding the amyloid deposits may be important for subsequent studies to elucidate amyloid pathogenesis and particularly protein-cell interactions. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MONASH MED CTR,DEPT NEPHROL,CLAYTON,VIC,AUSTRALIA. UNIV HOSP MONTPELLIER,DEPT NEPHROL,MONTPELLIER,FRANCE. RP ARGILES, A (reprint author), UNIV MONTPELLIER 1,FAC MED,CNRS,CRBM,UPR 9008,BP 5051,F-34033 MONTPELLIER,FRANCE. NR 30 TC 49 Z9 49 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0931-0509 J9 NEPHROL DIAL TRANSPL JI Nephrol. Dial. Transplant. PY 1994 VL 9 IS 6 BP 662 EP 667 PG 6 WC Transplantation; Urology & Nephrology SC Transplantation; Urology & Nephrology GA NU883 UT WOS:A1994NU88300013 PM 7970093 ER PT S AU HOLMES, LB AF HOLMES, LB BE Bock, G Marsh, J TI SPINA-BIFIDA - ANTICONVULSANTS AND OTHER MATERNAL INFLUENCES SO NEURAL TUBE EFFECTS SE CIBA FOUNDATION SYMPOSIA LA English DT Article; Proceedings Paper CT Symposium on Neural Tube Defects CY MAY 18-20, 1993 CL CIBA FOUNDATION, LONDON, ENGLAND SP CIBA SYMP HO CIBA FOUNDATION ID NEURAL-TUBE DEFECTS; DIABETIC MOTHERS; INFANTS; MALFORMATIONS; PREGNANCY; VALPROATE; FERTILITY; EXPOSURE; DRUGS; RISK AB At least two maternal conditions have been shown to be associated with an increased risk for the occurrence of anencephaly, spina bifida and encephalocele: insulin-dependent diabetes mellitus in the mother and maternal epilepsy for which anticonvulsant treatment is being used. Of 147 infants born at the Brigham and Women's Hospital with anencephaly, spina bifida and encephalocele among 123 489 live-born, still-born and elective terminations surveyed, 7.5% were infants of insulin-dependent diabetics and 0.7% had been exposed to anticonvulsants in utero. In addition to these proven causal associations neural tube defects have been postulated by some, but not all, studies as being more common among infants exposed to hyperthermia in utero and to drugs used to induce ovulation. RP HOLMES, LB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,EMBRYOL TERATOL UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. NR 25 TC 15 Z9 15 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, WEST SUSSEX, ENGLAND PO19 1UD SN 0300-5208 BN 0-471-94172-7 J9 CIBA F SYMP PY 1994 VL 181 BP 232 EP 238 PG 7 WC Developmental Biology; Medicine, General & Internal; Neurosciences SC Developmental Biology; General & Internal Medicine; Neurosciences & Neurology GA BZ87B UT WOS:A1994BZ87B00014 PM 8005027 ER PT S AU OAKLEY, GP NAU, H HALL, JG STANLEY, F OPITZ, JM HOLMES, LB SHURTLEFF, DB MILLS, JL LINDHOUT, D AF OAKLEY, GP NAU, H HALL, JG STANLEY, F OPITZ, JM HOLMES, LB SHURTLEFF, DB MILLS, JL LINDHOUT, D BE Bock, G Marsh, J TI ENVIRONMENTAL-FACTORS AFFECTING NEURAL-TUBE DEFECTS - GENERAL DISCUSSION SO NEURAL TUBE EFFECTS SE CIBA FOUNDATION SYMPOSIA LA English DT Discussion CT Symposium on Neural Tube Defects CY MAY 18-20, 1993 CL CIBA FOUNDATION, LONDON, ENGLAND SP CIBA SYMP HO CIBA FOUNDATION ID MOUSE; PREVENTION C1 FREE UNIV BERLIN,KLINIKUM RUDOLF VIRCHOW,INST TOXIKOL & EMBRYOPHARMAKOL,W-1000 BERLIN,GERMANY. UNIV BRITISH COLUMBIA,BRITISH COLUMBIA CHILDRENS HOSP,DEPT PEDIAT,VANCOUVER V6H 3V4,BC,CANADA. UNIV WESTERN AUSTRALIA,DEPT PAEDIAT,PERTH,WA 6001,AUSTRALIA. WESTERN AUSTRALIA RES INST CHILD HLTH,PERTH,WA 6001,AUSTRALIA. SHODAIR CHILDRENS HOSP,DEPT MED GENET,HELENA,MT 59604. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,EMBRYOL TERATOL UNIT,BOSTON,MA 02114. NICHHD,EPIDEMIOL BRANCH,PREVENT RES PROGRAM,BETHESDA,MD 20892. ERASMUS UNIV ROTTERDAM,ACAD HOSP ROTTERDAM DIJKZIGT,MGC,INST CLIN GENET,3000 DR ROTTERDAM,NETHERLANDS. UNIV WASHINGTON,DEPT PEDIAT,DIV CONGENITAL DEFECTS,BIRTH DEFECTS CLIN,SEATTLE,WA 98195. RP OAKLEY, GP (reprint author), CTR DIS CONTROL,NATL CTR ENVIRONM HLTH,DIV BIRTH DEFECTS & DEV DISABIL,BLDG 101,F34,ATLANTA,GA 30341, USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, WEST SUSSEX, ENGLAND PO19 1UD SN 0300-5208 BN 0-471-94172-7 J9 CIBA F SYMP PY 1994 VL 181 BP 245 EP 252 PG 8 WC Developmental Biology; Medicine, General & Internal; Neurosciences SC Developmental Biology; General & Internal Medicine; Neurosciences & Neurology GA BZ87B UT WOS:A1994BZ87B00015 ER PT J AU BEAL, MF AF BEAL, MF TI ENERGY, OXIDATIVE DAMAGE, AND ALZHEIMERS-DISEASE - CLUES TO THE UNDERLYING PUZZLE SO NEUROBIOLOGY OF AGING LA English DT Article; Proceedings Paper CT Fisher Symposium on Future Directions in Alzheimers Disease CY MAY 24-26, 1994 CL WASHINGTON, DC SP NIA, ZACHARY & ELIZABETH M FISHER MED FDN ID AMYOTROPHIC-LATERAL-SCLEROSIS; AGE-ASSOCIATED ACCUMULATION; MITOCHONDRIAL-DNA MUTATION; CYTOCHROME-OXIDASE; DEGENERATIVE DISEASES; HUMAN BRAIN; SUPEROXIDE-DISMUTASE; SKELETAL-MUSCLE; HUMAN HEARTS; GENE C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP BEAL, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,NEUROL SERV,WARREN 408,BOSTON,MA 02114, USA. FU NIA NIH HHS [P50AG05134, P01AG11337] NR 68 TC 8 Z9 8 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 2 BP S171 EP S174 PG 4 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA PW288 UT WOS:A1994PW28800044 PM 7700446 ER PT J AU BUSH, AI PETTINGELL, WH PARADIS, MD TANZI, RE AF BUSH, AI PETTINGELL, WH PARADIS, MD TANZI, RE TI THE ROLE OF ZINC IN A-BETA AMYLOIDOSIS SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GENET & AGING LAB,BOSTON,MA 02129. RI Bush, Ashley/A-1186-2007 OI Bush, Ashley/0000-0001-8259-9069 NR 1 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S50 EP S50 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900207 ER PT J AU CUPPLES, LA FARRER, LA FOLEY, EJ SOUZA, E LOCKE, P AUERBACH, SA GROWDON, JH HAINES, JL AF CUPPLES, LA FARRER, LA FOLEY, EJ SOUZA, E LOCKE, P AUERBACH, SA GROWDON, JH HAINES, JL TI GENETIC EPIDEMIOLOGIC STUDIES OF APOE AND ALZHEIMER-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,DEPT EPIDEMIOL,BOSTON,MA 02215. BOSTON UNIV,SCH MED,DEPT BIOSTAT,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S132 EP S132 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900546 ER PT J AU FARBER, SA SCHULZ, JG GROWDON, JH WURTMAN, RJ NITSCH, RM AF FARBER, SA SCHULZ, JG GROWDON, JH WURTMAN, RJ NITSCH, RM TI REGULATED APP(S) RELEASE FROM RAT-BRAIN SLICES SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. CHARITE HOSP,DEPT NEUROL,D-10098 BERLIN,GERMANY. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RI Schulz, Joachim/H-2430-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S63 EP S63 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900260 ER PT J AU FARRER, LA CUPPLES, LA VANDUIJN, CM CONNORLACKE, L KIELY, DK GROWDON, JH AF FARRER, LA CUPPLES, LA VANDUIJN, CM CONNORLACKE, L KIELY, DK GROWDON, JH TI RATE OF PROGRESSION OF ALZHEIMER-DISEASE IS ASSOCIATED WITH GENETIC RISK SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT EPIDEMIOL BIOSTAT,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. ERASMUS UNIV ROTTERDAM,DEPT EPIDEMIOL,ROTTERDAM,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S28 EP S28 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900119 ER PT J AU GEARING, M SCHNEIDER, JA ROBBINS, RS REBECK, GW HYMAN, BT MIRRA, SS AF GEARING, M SCHNEIDER, JA ROBBINS, RS REBECK, GW HYMAN, BT MIRRA, SS TI APOLIPOPROTEIN-E AND REGIONAL VARIATION IN DIFFUSE PLAQUES IN ALZHEIMERS-DISEASE (AD) WITH AND WITHOUT PARKINSONS-DISEASE (PD) CHANGES - AN IMMUNOHISTOCHEMICAL AND MOLECULAR STUDY SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 VET ADM MED CTR,DEPT PATHOL & LAB MED,ATLANTA,GA 30033. EMORY UNIV,ATLANTA,GA 30033. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S118 EP S119 PG 2 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900490 ER PT J AU GROWDON, JH AF GROWDON, JH TI ADVANCES IN THE DIAGNOSIS OF AD SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S5 EP S5 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900022 ER PT J AU HAINES, JL LOCKE, PA TANZI, RE GUSELLA, JF PERICAKVANCE, MA CONNEALLY, PN AF HAINES, JL LOCKE, PA TANZI, RE GUSELLA, JF PERICAKVANCE, MA CONNEALLY, PN TI FAMILY STUDIES OF APOE IN EARLY AND LATE-ONSET ALZHEIMER DISEASES SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S131 EP S131 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900543 ER PT J AU HARR, SD MENDEZ, AJ UINT, L REBECK, GW HYMAN, BT AF HARR, SD MENDEZ, AJ UINT, L REBECK, GW HYMAN, BT TI EXCHANGEABLE APOLIPOPROTEINS EXPRESSION IN THE BRAIN AND THE NEUROPATHOLOGY OF AD SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S117 EP S118 PG 2 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900486 ER PT J AU HYMAN, BT AF HYMAN, BT TI STUDYING THE ALZHEIMERS-DISEASE BRAIN - INSIGHTS, PUZZLES, AND OPPORTUNITIES SO NEUROBIOLOGY OF AGING LA English DT Article; Proceedings Paper CT Fisher Symposium on Future Directions in Alzheimers Disease CY MAY 24-26, 1994 CL WASHINGTON, DC SP NIA, ZACHARY & ELIZABETH M FISHER MED FDN ID BETA-PROTEIN PRECURSOR; RECEPTOR-RELATED PROTEIN; APOLIPOPROTEIN-E; SENILE PLAQUES; HIPPOCAMPAL-FORMATION; MULTIFUNCTIONAL RECEPTOR; NEUROFIBRILLARY TANGLES; PATHOLOGICAL-CHANGES; PERFORANT PATHWAY; PYRAMIDAL NEURONS RP HYMAN, BT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,32 FRUIT ST,BOSTON,MA 02114, USA. FU NIA NIH HHS [AG08487, P50AG05134, P01AG11337] NR 59 TC 1 Z9 2 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 2 BP S79 EP S83 PG 5 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA PW288 UT WOS:A1994PW28800023 PM 7700469 ER PT J AU HYMAN, BT WEST, HL HARR, SD GOMEZISLA, T MUI, S AF HYMAN, BT WEST, HL HARR, SD GOMEZISLA, T MUI, S TI QUANTITATIVE NEUROPATHOLOGY IN ALZHEIMER-DISEASE - NEURONAL LOSS IN HIGH-ORDER ASSOCIATION CORTEX PARALLELS DEMENTIA SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S141 EP S141 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900583 ER PT J AU KOVACS, DM WASCO, W TANZI, RE AF KOVACS, DM WASCO, W TANZI, RE TI A CDEI-LIKE E-BOX IN THE APP PROMOTER PROVIDES A POSSIBLE ROLE FOR APLP2 IN TRANSCRIPTIONAL REGULATION SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GENET & AGING LAB,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S86 EP S86 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900356 ER PT J AU MILBURY, PE BEAL, MF MATSON, WR AF MILBURY, PE BEAL, MF MATSON, WR TI THE POTENTIAL OF DEGENERATIVE DISORDER DIAGNOSIS BASED ON BIOCHEMICAL PATTERN OR PROFILE ANALYSIS SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 ESA INC,BEDFORD,MA 01730. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S95 EP S95 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900392 ER PT J AU NITSCH, RM SLACK, BE FARBER, SA BORGHESANI, PR DENG, M WURTMAN, RJ GROWDON, JH AF NITSCH, RM SLACK, BE FARBER, SA BORGHESANI, PR DENG, M WURTMAN, RJ GROWDON, JH TI REGULATION OF APP PROCESSING BY CELL-SURFACE RECEPTORS SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S75 EP S76 PG 2 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900312 ER PT J AU PERLS, TT REBECK, GW WEST, HL SODHI, P LIPSITZ, LA HYMAN, BT AF PERLS, TT REBECK, GW WEST, HL SODHI, P LIPSITZ, LA HYMAN, BT TI APOLIPOPROTEIN EPSILON-4 ALLOTYPE PREVALENCE IS LOW IN BOTH NORMAL AND ALZHEIMERS-DISEASE OLDEST-OLD SUBJECTS - THE EFFECT OF SELECTIVE SURVIVAL SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEACONESS HOSP,HEBREW REHABIL CTR AGED,DEPT NEUROL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DIV AGING,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S73 EP S73 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900303 ER PT J AU REBECK, GW HARR, SD STRICKLAND, DK HYMAN, BT AF REBECK, GW HARR, SD STRICKLAND, DK HYMAN, BT TI APOLIPOPROTEIN-E END ITS RECEPTOR LRP IN AD AND CONTROL BRAIN SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. AMER RED CROSS,BIOCHEM LAB,ROCKVILLE,MD 20855. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S117 EP S117 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900485 ER PT J AU SIMONIAN, NA HYMAN, BT AF SIMONIAN, NA HYMAN, BT TI FUNCTIONAL ALTERATIONS IN ALZHEIMERS-DISEASE - SELECTIVE LOSS OF MITOCHONDRIAL ENCODED CYTOCHROME-OXIDASE MESSENGER-RNA IN THE HIPPOCAMPAL-FORMATION SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S125 EP S125 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900518 ER PT J AU SMALL, GW COLLINS, MT MAZZIOTTA, JC BAXTER, LR PHELPS, ME MANDELKERN, MA KAPLAN, A ADAMSON, CF CHANG, L GUZE, BH CORDER, EH SAUNDERS, AM CONNEALLY, PM HAINES, JL PERICAKVANCE, MA ROSES, AD AF SMALL, GW COLLINS, MT MAZZIOTTA, JC BAXTER, LR PHELPS, ME MANDELKERN, MA KAPLAN, A ADAMSON, CF CHANG, L GUZE, BH CORDER, EH SAUNDERS, AM CONNEALLY, PM HAINES, JL PERICAKVANCE, MA ROSES, AD TI APOLIPOPROTEIN-E TYPE-4 ALLELE LOWERS CEREBRAL PARIETAL METABOLISM IN RELATIVES AT RISK FOR FAMILIAL ALZHEIMER-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHARMACOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. INDIANA UNIV,MED CTR,DEPT MED & MOLEC GENET,INDIANAPOLIS,IN 46202. MASSACHUSETTS GEN HOSP E,MOLEC NEUROGEN UNIT,BOSTON,MA 02129. DUKE UNIV,MED CTR,ALZHEIMER DIS RES CTR,DURHAM,NC 27710. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S155 EP S155 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900638 ER PT J AU TANZI, RE BUSH, AI WASCO, W AF TANZI, RE BUSH, AI WASCO, W TI GENETIC-STUDIES OF ALZHEIMERS-DISEASE - LESSONS LEARNED AND FUTURE IMPERATIVES SO NEUROBIOLOGY OF AGING LA English DT Article; Proceedings Paper CT Fisher Symposium on Future Directions in Alzheimers Disease CY MAY 24-26, 1994 CL WASHINGTON, DC SP NIA, ZACHARY & ELIZABETH M FISHER MED FDN ID AMYLOID PRECURSOR PROTEIN; CEREBRAL-HEMORRHAGE; MESSENGER-RNA; MUTATION; LOCUS; LINKAGE; CDNA; CHROMOSOME-14; PEPTIDES; BRAIN RP TANZI, RE (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,CTR NEUROSCI, DEPT NEUROL, GENET & AGING LAB, BOSTON, MA 02129 USA. RI Bush, Ashley/A-1186-2007 OI Bush, Ashley/0000-0001-8259-9069 NR 28 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 2 BP S145 EP S148 PG 4 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA PW288 UT WOS:A1994PW28800039 PM 7700440 ER PT J AU TANZI, RE ROMANO, DM CROWLEY, AC PARADIS, MD GASTON, SM BUCKLER, A WASCO, W AF TANZI, RE ROMANO, DM CROWLEY, AC PARADIS, MD GASTON, SM BUCKLER, A WASCO, W TI CANDIDATE GENES FOR THE MAJOR EARLY-ONSET FAD LOCUS ON CHROMOSOME-14 - ASCERTAINMENT AND ANALYSIS SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GENET & AGING LAB,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S155 EP S156 PG 2 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900641 ER PT J AU WASCO, W KOVACS, DM CROWLEY, A PARADIS, M FELSENSTEIN, KM TANZI, RE AF WASCO, W KOVACS, DM CROWLEY, A PARADIS, M FELSENSTEIN, KM TANZI, RE TI MOLECULAR CHARACTERIZATION OF THE MEMBERS OF THE APP LIKE GENE FAMILY SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GENET & AGING LAB,BOSTON,MA. BRISTOL MYERS SQUIBB CO,WALLINGFORD,CT 06492. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S159 EP S160 PG 2 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900657 ER PT J AU WEST, HL REBECK, GW GROWDON, JH HYMAN, BT AF WEST, HL REBECK, GW GROWDON, JH HYMAN, BT TI APOLIPOPROTEIN E4 AFFECTS NEUROPATHOLOGY BUT NOT CLINICAL PROGRESSION IN ALZHEIMERS-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 1 BP S28 EP S29 PG 2 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA NV609 UT WOS:A1994NV60900120 ER PT J AU YOUNG, AB AF YOUNG, AB TI FUTURE-DIRECTIONS FOR RESEARCH ON ALZHEIMERS-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Article; Proceedings Paper CT Fisher Symposium on Future Directions in Alzheimers Disease CY MAY 24-26, 1994 CL WASHINGTON, DC SP NIA, ZACHARY & ELIZABETH M FISHER MED FDN RP YOUNG, AB (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,SERV NEUROL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PY 1994 VL 15 SU 2 BP S73 EP S73 PG 1 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA PW288 UT WOS:A1994PW28800021 PM 7700467 ER PT S AU LIPTON, SA SINGEL, DJ STAMLER, JS AF LIPTON, SA SINGEL, DJ STAMLER, JS BE Chiueh, CC Gilbert, DL Colton, CA TI NEUROPROTECTIVE AND NEURODESTRUCTIVE EFFECTS OF NITRIC-OXIDE AND REDOX CONGENERS SO NEUROBIOLOGY OF NO- AND -OH SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 1993 Symposium on the Neurobiology of NO- and -OH CY NOV 07, 1993 CL NIH, BETHESDA, MD SP NIH, NIMH, NINDS, NIA, NHLBI, NCI HO NIH C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,DEPT CHEM,CAMBRIDGE,MA 02138. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV RESP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BROCKTON W ROXBURY VET ADM MED CTR,CARDIOL SECT,BOSTON,MA 02115. NR 9 TC 44 Z9 46 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-873-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 738 BP 382 EP 387 PG 6 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD10R UT WOS:A1994BD10R00044 PM 7832446 ER PT B AU BEAL, MF AF BEAL, MF BE Jolles, G Stutzmann, JM TI Huntington's disease SO NEURODEGENERATIVE DISEASES LA English DT Proceedings Paper CT 8th International Round Table of the Rhone-Poulenc-Rorer-Foundation - Neurodegenerative Diseases CY 1993 CL ANNECY, FRANCE SP RHONE POULENC RORER FDN, INST SCI VIVANT RP HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL ROAD, LONDON, ENGLAND NW1 7DX BN 0-12-388185-4 PY 1994 BP 169 EP 181 PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA BC44Y UT WOS:A1994BC44Y00009 ER PT J AU WALTER, KA NEWMAN, NJ LESSELL, S AF WALTER, KA NEWMAN, NJ LESSELL, S TI OCULOMOTOR PALSY FROM MINOR HEAD TRAUMA - INITIAL SIGN OF INTRACRANIAL ANEURYSM SO NEUROLOGY LA English DT Note ID CEREBRAL ANEURYSMS AB Minor head trauma precipitated oculomotor nerve palsies in two patients who subsequently were discovered to have ipsilateral posterior communicating artery aneurysms. A history of minor trauma should not dissuade investigation for underlying causes of oculomotor nerve palsy, including intracranial aneurysm. C1 EMORY UNIV,SCH MED,DEPT OPHTHALMOL,ATLANTA,GA 30322. EMORY UNIV,SCH MED,DEPT NEUROL,ATLANTA,GA 30322. EMORY UNIV,SCH MED,DEPT NEUROSURG,ATLANTA,GA. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA. NR 10 TC 28 Z9 29 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1994 VL 44 IS 1 BP 148 EP 150 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA MR371 UT WOS:A1994MR37100030 PM 8290050 ER PT J AU DASHEIFF, RM AF DASHEIFF, RM TI THE FIRST AMERICAN EPILEPTOLOGISTS - SPRATLING,WILLIAM,P.,MD, AND PARK,ROSWELL, MD SO NEUROLOGY LA English DT Editorial Material C1 UNIV PITTSBURGH,SCH MED,DEPT NEUROL,PITTSBURGH,PA 15261. US DEPT VET AFFAIRS,NEUROL SERV,PITTSBURGH,PA. RP DASHEIFF, RM (reprint author), UNIV PITTSBURGH,CTR EPILEPSY,3515 5TH AVE,ROOM 625,PITTSBURGH,PA 15213, USA. NR 9 TC 3 Z9 3 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1994 VL 44 IS 1 BP 171 EP 174 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA MR371 UT WOS:A1994MR37100039 PM 8290059 ER PT J AU GRIFFITH, JM ADLER, LE FREEDMAN, R AF GRIFFITH, JM ADLER, LE FREEDMAN, R TI FINE MOTOR-PERFORMANCE IN SCHIZOPHRENIA SO NEUROPSYCHOBIOLOGY LA English DT Article DE SMOOTH PURSUIT EYE MOVEMENT; SCHIZOPHRENIA; NEUROMOTOR PERFORMANCE ID EYE-TRACKING DYSFUNCTIONS; PSYCHOTIC-PATIENTS; ABNORMALITIES AB Peripheral and central aspects of motor dysfunction were assessed in 12 schizophrenic and 12 normal subjects, using a test of control of finger movement based on the widely used smooth pursuit eye movement task. This was performed in order to investigate the basis of neuromotor dysfunction in schizophrenia. In this task, subjects used finger movement to track a visual target. Simultaneously, an electromyogram of the extensor digitorum communis, the primary muscle utilized in the task, was recorded. Smooth pursuit eye movements were also assessed. Accuracy of finger-based and smooth-pursuit eye movement tracking was analyzed by fast Fourier transform and expressed as a log signal-to-noise ratio. The electromyograms were analyzed by motor unit potential discrimination and by interspike interval histography. Schizophrenics demonstrated significantly poorer finger tracking than did controls, with a mean score of 2.01 +/- 0.63 (SD) versus 2.81 +/- 0.42 (t = 3.52, d.f. = 21, p < 0.005). However, there was no evidence for motor-unit dysfunction. Schizophrenics also performed more poorly on smooth-pursuit eye movement, with a mean score of 2.06 +/- 0.62 versus 3.33 +/- 1.21 (t = 3.21, d.f. = 22, p < 0.005). Severity of extrapyramidal symptoms was correlated with poorer performance on the finger tracking task, but not smooth-pursuit eye movement. These findings support the hypothesis that schizophrenics' tracking abnormalities are due to central nervous system deficits rather than peripheral pathology. C1 UNIV COLORADO,HLTH SCI CTR,DEPT PSYCHIAT,DENVER,CO 80262. DENVER VA MED CTR,DEPT PSYCHIAT,DENVER,CO. NR 15 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0302-282X J9 NEUROPSYCHOBIOLOGY JI Neuropsychobiology PY 1994 VL 29 IS 4 BP 179 EP 184 DI 10.1159/000119084 PG 6 WC Neurosciences; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA NP336 UT WOS:A1994NP33600005 PM 8047244 ER PT B AU GREEN, MF NUECHTERLEIN, KH AF GREEN, MF NUECHTERLEIN, KH BE David, AS Cutting, JC TI MECHANISMS OF BACKWARD-MASKING IN SCHIZOPHRENIA SO NEUROPSYCHOLOGY OF SCHIZOPHRENIA SE BRAIN DAMAGE, BEHAVIOUR AND COGNITION : DEVELOPMENTS IN CLINICAL NEUROPSYCHOLOGY LA English DT Proceedings Paper CT International Symposium on Neuropsychology of Schizophrenia CY OCT 10-11, 1991 CL INST PSYCHIAT LONDON, LONDON, ENGLAND SP INST PSYCHIAT LONDON, WELLCOME TRUST, LUNDBECK PHARM, SANDOZ HO INST PSYCHIAT LONDON C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RI David, Anthony/C-1315-2011 OI David, Anthony/0000-0003-0967-774X NR 0 TC 2 Z9 2 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC PUBL PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430 BN 0-86377-303-6 J9 BRAIN DAM B PY 1994 BP 79 EP 95 PG 17 WC Psychology, Clinical; Neurosciences; Psychiatry; Psychology SC Psychology; Neurosciences & Neurology; Psychiatry GA BA10R UT WOS:A1994BA10R00005 ER PT J AU SIMONIAN, NA REBECK, GW HYMAN, BT AF SIMONIAN, NA REBECK, GW HYMAN, BT TI FUNCTIONAL INTEGRITY OF NEURAL SYSTEMS RELATED TO MEMORY IN ALZHEIMERS-DISEASE SO NEUROSCIENCE: FROM THE MOLECULAR TO THE COGNITIVE SE PROGRESS IN BRAIN RESEARCH LA English DT Review ID PERFORANT PATHWAY ZONE; NITRIC-OXIDE SYNTHASE; CYTOCHROME-OXIDASE; NEUROFIBRILLARY TANGLES; HIPPOCAMPAL-FORMATION; ENERGY-METABOLISM; SENILE PLAQUES; VISUAL-CORTEX; PATTERN; NEURONS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP SIMONIAN, NA (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. FU NIA NIH HHS [AG08487] NR 41 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 J9 PROG BRAIN RES PY 1994 VL 100 BP 245 EP 254 PG 10 WC Neurosciences SC Neurosciences & Neurology GA BB62A UT WOS:A1994BB62A00030 PM 7938525 ER PT J AU UHLER, TA FRIM, DM PAKZABAN, P ISACSON, O SIESJO, BK YOUNG, W AF UHLER, TA FRIM, DM PAKZABAN, P ISACSON, O SIESJO, BK YOUNG, W TI THE EFFECTS OF MEGADOSE METHYLPREDNISOLONE AND U-78517F ON TOXICITY MEDIATED BY GLUTAMATE RECEPTORS IN THE RAT NEOSTRIATUM SO NEUROSURGERY LA English DT Article DE EXCITOTOXICITY; LAZAROIDS; METHYLPREDNISOLONE; NEUROPROTECTION; RAT; STRIATUM ID SPINAL-CORD INJURY; HIGH-DOSE METHYLPREDNISOLONE; NERVE GROWTH-FACTOR; HIPPOCAMPAL-NEURONS; LIPID-PEROXIDATION; BRAIN INJURY; DISEASES; ACID; NEUROTOXICITY; METABOLISM AB MECHANISMS OF NEURONAL death after acute insults are unknown but may involve energy depletion and resultant glutamate toxicity. One potential pathway leading to cell death is the formation of oxygen free radicals in an energy-depleted state. Megadoses of glucocorticoids as well as the lazaroid compounds (e.g., 21-aminosteroids and 2-methylaminochromans) have been shown to be potent antioxidants, capable of mitigating the effects of oxygen radicals on lipid membranes in vitro. The authors investigated the protective antioxidant effects of megadose methylprednisolone (MPSS) and the lazaroid 2-methylaminochroman (U-78517F) on the size of striatal lesions caused by quinolinic acid, an N-methyl-D-aspartate (NMDA) receptor agonist that mimics certain aspects of the secondary injury surrounding the pan-necrosis central to stroke or cerebral contusion. Treatment with MPSS (60 mg/kg/day) before quinolinate infusion and continuing through the first postoperative day caused a significant (P < 0.01) 56% increase in the size of striatal lesions. In contrast, treatment with MPSS given 2 to 6 hours after creation of the lesion did not affect lesion size. Animals treated with U-78517F also failed to exhibit any neuroprotective effects. The detrimental effect of pretreatment with megadose MPSS is likely the result of deleterious energy-depleting glucocorticoid effects that outweigh any positive antioxidant effects. We conclude that megadose MPSS, although found to be beneficial in the treatment of spinal cord injury, may not be beneficial in the treatment of intracranial insults involving glutamate toxicity. C1 MCLEAN HOSP, NEUROREGENERAT LAB, MRC 119, 115 MILL ST, BELMONT, MA 02178 USA. HARVARD UNIV, SCH MED, PROGRAM NEUROSCI, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, NEUROSURG SERV, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROL SERV, BOSTON, MA 02114 USA. FU NINDS NIH HHS [5 T32 NS07340-03, NS 29178, NS 30064] NR 43 TC 23 Z9 25 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD JAN PY 1994 VL 34 IS 1 BP 122 EP 128 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA MN504 UT WOS:A1994MN50400018 PM 7907169 ER PT J AU FISCHMAN, AJ SOLOMON, HF BABICH, JW ABRAMS, MJ CALLAHAN, RJ STRAUSS, HW RUBIN, RH AF FISCHMAN, AJ SOLOMON, HF BABICH, JW ABRAMS, MJ CALLAHAN, RJ STRAUSS, HW RUBIN, RH TI IMAGING OF FOCAL SITES OF INFLAMMATION IN RHESUS-MONKEYS WITH TC-99M-LABELED HUMAN POLYCLONAL IGG SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article ID IMMUNOGLOBULIN; INFECTION; QUANTITATION; LOCALIZATION AB The biological behavior of human polyclonal immunoglobulin G (IgG) radiolabeled with Tc-99m via a nicotinyl hydrazine derivative, was evaluated in Rhesus monkeys. Tc-99m-IgG and In-111-MACROSCINT(R) DTPA-IgG were co-administered to Rhesus monkeys with focal sites of sterile inflammation and scintillation camera images were acquired at 6 and 19 h after injection. The biodistribution of the two antibody preparations were similar, however, small differences were detected: Tc-99m-IgG > In-111-IgG in spleen and lung; Tc-99m-IgG < In-111-IgG in bone and skeletal muscle. A linear correlation of the tissue-to-blood ratios of Tc-99m- and In-111-labeled IgG was observed at both times (r(2) > 0.98). The slopes of the regression lines were not significantly different from unity: 6 h-0.982 +/- 0.018; 19 h 1.0334 +/- 0.0226. Also, at both 6 and 19 h after injection, the target-to-background ratios (T/B) for the sites of inflammation were remarkably similar for In-111 and Tc-99m. These studies establish that human polyclonal IgG labeled with Tc-99m via a nicotinyl hydrazine modified intermediate is equivalent to In-111-MACROSCINT(R) DTPA-IgG for imaging focal sites of inflammation in monkeys. C1 MASSACHUSETTS GEN HOSP,MED SERV,CLIN INVEST UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. RW JOHNSON PHARMACEUT RES INST,SPRING HOUSE,PA. JOHNSON MATTHEY PHARMACEUT RES,W CHESTER,PA. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 15 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 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD JAN PY 1994 VL 21 IS 1 BP 111 EP 116 DI 10.1016/0969-8051(94)90137-6 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MU096 UT WOS:A1994MU09600016 PM 9234272 ER PT J AU JONES, GS ELMALEH, DR STRAUSS, HW FISCHMAN, AJ AF JONES, GS ELMALEH, DR STRAUSS, HW FISCHMAN, AJ TI SYNTHESIS AND BIODISTRIBUTION OF A NEW (99M)TECHNETIUM FATTY-ACID SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article ID IMAGING AGENTS AB The synthesis and biodistribution is described for a new Tc-99m-labeled fatty acid. The requisite diaminodithiol (N2S2) ligand, 9,10-bis[N-(2'-methyl-2'-mercapto)propyl] aminooctadecanoic acid, was prepared in nine steps from ethyl oleate and characterized by fast atom bombardment mass spectrometry and elemental analysis of its nickell(II) complex. The radiolabeling procedure provided a liposoluble Tc-99m-labeled complex (Tc-99m-11) which was administered intravenously to rats concomitantly with 15-(p-[I-125]-iodophenyl) pentadecanoic acid (IPPA). The myocardial profile of Tc-99m-11 was inferior to that of IPPA. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,PHYS RES LAB,RESH 517,BOSTON,MA 02114. NR 17 TC 21 Z9 22 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD JAN PY 1994 VL 21 IS 1 BP 117 EP 123 DI 10.1016/0969-8051(94)90138-4 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MU096 UT WOS:A1994MU09600017 PM 9234273 ER PT J AU BROWN, EN SCHMID, CH AF BROWN, EN SCHMID, CH TI APPLICATION OF THE KALMAN FILTER TO COMPUTATIONAL PROBLEMS IN STATISTICS SO NUMERICAL COMPUTER METHODS, PT B SE METHODS IN ENZYMOLOGY LA English DT Review ID MAXIMUM-LIKELIHOOD; EXPERT-SYSTEMS; TIME-SERIES; REGRESSION; ALGORITHM C1 TUFTS UNIV,NEW ENGLAND MED CTR,BIOSTAT RES CTR,DIV CLIN CARE RES,BOSTON,MA 02111. RP BROWN, EN (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,STAT RES LAB,BOSTON,MA 02114, USA. OI Schmid, Christopher/0000-0002-0855-5313 NR 25 TC 4 Z9 4 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 240 BP 171 EP 181 PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BB62P UT WOS:A1994BB62P00009 PM 7823830 ER PT B AU ZIELSTORFF, RD BARNETT, GO FITZMAURICE, JB OLIVER, DE FORDCARLETON, P THOMPSON, BT ESTEY, G ECCLES, R MARTIN, M AF ZIELSTORFF, RD BARNETT, GO FITZMAURICE, JB OLIVER, DE FORDCARLETON, P THOMPSON, BT ESTEY, G ECCLES, R MARTIN, M BE Grobe, SJ PluyterWenting, ESP TI A DECISION SUPPORT SYSTEM FOR TROUBLESHOOTING PULMONARY ARTERY CATHETER WAVEFORMS SO NURSING INFORMATICS: AN INTERNATIONAL OVERVIEW FOR NURSING IN A TECHNOLOGICAL ERA LA English DT Proceedings Paper CT 5th IMIA International Conference on Nursing Use of Computers and Information Science CY JUN 17-22, 1994 CL SAN ANTONIO, TX SP INT MED INFORMAT ASSOC C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 1 U2 1 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-81851-0 PY 1994 BP 362 EP 366 PG 5 WC Computer Science, Information Systems; Information Science & Library Science; Nursing SC Computer Science; Information Science & Library Science; Nursing GA BC30F UT WOS:A1994BC30F00075 ER PT J AU ABATE, M AF ABATE, M TI THE WOMAN SCIENTIST - MEETING THE CHALLENGES FOR A SUCCESSFUL CAREER - YENTSCH,CM, SINDERMANN,CJ SO NURSING RESEARCH LA English DT Book Review RP ABATE, M (reprint author), MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,GRAD PROGRAM NURSING,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER J NURSING CO PI NEW YORK PA 555 W 57TH ST, NEW YORK, NY 10019-2961 SN 0029-6562 J9 NURS RES JI Nurs. Res. PD JAN-FEB PY 1994 VL 43 IS 1 BP 37 EP 37 PG 1 WC Nursing SC Nursing GA PB300 UT WOS:A1994PB30000007 ER PT J AU CARLESSO, N GRIFFIN, JD DRUKER, BJ AF CARLESSO, N GRIFFIN, JD DRUKER, BJ TI USE OF A TEMPERATURE-SENSITIVE MUTANT TO DEFINE THE BIOLOGICAL EFFECTS OF THE P210(BCR-ABL) TYROSINE KINASE ON PROLIFERATION OF A FACTOR-DEPENDENT MURINE MYELOID CELL-LINE SO ONCOGENE LA English DT Article ID CHRONIC MYELOGENOUS LEUKEMIA; COLONY-STIMULATING FACTOR; MIDDLE-T-ANTIGEN; V-ABL ONCOGENE; BCR-ABL; INTERLEUKIN-3 DEPENDENCE; PHILADELPHIA-CHROMOSOME; INVITRO TRANSFORMATION; HEMATOPOIETIC-CELLS; PROTEIN-KINASE AB The Philadelphia chromosome, detected in virtually all cases of chronic myelogenous leukemia, is formed by a reciprocal translocation between chromosomes 9 and 22 that fuses BCR encoded sequences upstream of exon 2 of c-ABL. This oncogene produces a fusion protein, p210(BCR-ABL), in which the ABL tyrosine kinase activity is elevated. This elevated kinase activity is essential for transformation, but the mechanisms involved are unknown. To investigate p210(BCR-ABL) function we constructed a model system in which the tyrosine kinase activity of p210(BCR-ABL) was inducible. Two amino acid substitutions, Arg to His at amino acid 457 and Tyr to His at amino acid 469 of c-abl, modeled on mutations known to render v-src temperature-sensitive for tyrosine kinase activity, were introduced into p210(BCR-ABL). This mutant was characterized in an IL-3 growth factor dependent murine myeloid cell line, 32Dc13. Cell lines expressing the temperature-sensitive mutant remained factor dependent at the non-permissive temperature, but at the permissive temperature displayed a marked reduction in cell death in the absence of growth factor and an exaggerated proliferative response to low levels of IL-3. Both the kinase activity of the mutant and the levels of tyrosine phosphorylated proteins are increased in the temperature-sensitive mutant at the permissive temperature. Further, tyrosine phosphorylation of potential substrates of the p210(BCR-ABL) tyrosine kinase, p120 rasGAP and its associated proteins of p190 and p62, only occurs at the permissive temperature in cells expressing the temperature-sensitive mutant. C1 DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV TURIN,DEPT EXPTL MED & ONCOL,HEMATOL SECT,TURIN,ITALY. DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. FU NCI NIH HHS [CA36167, CA01422] NR 49 TC 84 Z9 85 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN PY 1994 VL 9 IS 1 BP 149 EP 156 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA MW247 UT WOS:A1994MW24700018 PM 8302574 ER PT J AU SCHMIDTERFURTH, U BAUMAN, W GRAGOUDAS, E FLOTTE, TJ MICHAUD, NA BIRNGRUBER, R HASAN, T AF SCHMIDTERFURTH, U BAUMAN, W GRAGOUDAS, E FLOTTE, TJ MICHAUD, NA BIRNGRUBER, R HASAN, T TI PHOTODYNAMIC THERAPY OF EXPERIMENTAL CHOROIDAL MELANOMA USING LIPOPROTEIN-DELIVERED BENZOPORPHYRIN SO OPHTHALMOLOGY LA English DT Article ID HEMATOPORPHYRIN PHOTORADIATION THERAPY; MALIGNANT-MELANOMA; INTRAOCULAR TUMORS; CELLS; PHOTOIMMUNOTHERAPY; OXYGEN; CANCER; INVIVO; AGENT AB Background: Benzoporphyrin derivative monoacid (BPD) is a new photosensitizer currently undergoing clinical trial for cutaneous malignancies. Compared with the clinically most frequently used sensitizer, Photofrin, BPD may offer higher tumor phototoxicity, better tissue penetration, and absence of significant skin sensitization. Low-density lipoprotein (LDL) carriers heighten efficiency and selectivity of BPD because neovascular and tumor cells express an increased number of LBL receptors. Hence, in addition to the vaso-occlusive effects similar to most other photosensitizers, LDL-BPD also has been shown to cause direct tumor cell damage. Methods: Benzoporphyrin derivative monoacid was complexed with human LDL and used in photodynamic treatment of choroidal melanomas experimentally induced in eight albino rabbits. Five rabbits served as controls. Three hours after intravenous injection of 2 mg/kg body weight of LDL-BPD, eight tumors were irradiated at 692 nm and 100 J/cm(2) via an argon-pumped dye laser coupled into a slit lamp. Results: Angiography and histologic findings showed immediate photothrombosis after disintegration of endothelial membranes. After complete necrosis of tumor cells within 24 hours, a small fibrotic scar slowly developed. No tumor regrowth was noted up to 6 weeks when animals were killed. Conclusion: These data suggest that photodynamic treatment with LDL-BPD may be a promising modality for multiple clinical applications, including tumors and neovascularizations II. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,RETINA SERV,BOSTON,MA 02115. RI Birngruber, Reginald/Q-2342-2016 NR 32 TC 83 Z9 90 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD JAN PY 1994 VL 101 IS 1 BP 89 EP 99 PG 11 WC Ophthalmology SC Ophthalmology GA MV308 UT WOS:A1994MV30800018 PM 8302569 ER PT J AU NETLAND, PA SUGRUE, SP ALBERT, DM SHORE, JW AF NETLAND, PA SUGRUE, SP ALBERT, DM SHORE, JW TI HISTOPATHOLOGIC FEATURES OF THE FLOPPY EYELID SYNDROME - INVOLVEMENT OF TARSAL ELASTIN SO OPHTHALMOLOGY LA English DT Article ID MANAGEMENT; PINGUECULA AB Purpose: Patients with the floppy eyelid syndrome have chronic papillary conjunctivitis with easily everted upper eyelids and a soft, pliant upper tarsus. The purpose of this study is to describe the clinical features and the histopathologic correlate in a group of patients with floppy eyelid syndrome. Methods: The authors examined eight patients with floppy eyelid syndrome, four of whom underwent surgical management with horizontal eyelid shortening. Eyelid tissue from these patients was examined using light microscopy, electron microscopy, and immunohistochemistry and compared with controls with unrelated eyelid or orbital disorders. Results: Clinical findings included obesity or eye rubbing, lash ptosis, and, less commonly, blepharoptosis. Two patients had documented sleep apnea with abnormal sleep electroencephalogram. Light microscopy of the surgical specimens showed chronic conjunctival inflammation, papillary conjunctivitis, and meibomian gland abnormalities, including granuloma formation. Verhoeff's modified elastin stain demonstrated a marked decrease in the amount of elastin fibers in tarsus from patients with floppy eyelid syndrome compared with controls. Immunohistochemical staining for elastin also showed a marked decrease of tarsal elastin in floppy eyelid patients compared with controls. In contrast, immunohistochemical stains showed that the distribution of collagen types I and III was similar between patients with floppy eyelid syndrome and controls. Electron microscopy demonstrated that tarsal collagen was comparable in patients and controls, and that there was a reduced amount of tarsal elastin in floppy eyelid syndrome compared with controls. Conclusions: These findings demonstrate that tarsal elastin is decreased in the floppy eyelid syndrome, which may contribute to the laxity of the tarsus in this disorder. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. UNIV WISCONSIN,SCH MED,DEPT OPHTHALMOL,MADISON,WI 53706. NR 21 TC 59 Z9 63 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD JAN PY 1994 VL 101 IS 1 BP 174 EP 181 PG 8 WC Ophthalmology SC Ophthalmology GA MV308 UT WOS:A1994MV30800031 PM 8302552 ER PT B AU CARIANI, P AF CARIANI, P BE Pribram, K TI AS IF TIME REALLY MATTERED - TEMPORAL STRATEGIES FOR NEURAL CODING OF SENSORY INFORMATION SO ORIGINS: BRAIN AND SELF ORGANIZATION LA English DT Proceedings Paper CT 2nd Appalachian Conference on Neurodynamics - Origins, Brain and Self Organization CY OCT 03-06, 1993 CL RADFORD UNIV, RADFORD, VA HO RADFORD UNIV RP CARIANI, P (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB AUDITORY PHYSIOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC PUBL PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430 BN 0-8058-1786-7 PY 1994 BP 208 EP 252 PG 45 WC Psychology, Experimental SC Psychology GA BB47H UT WOS:A1994BB47H00009 ER PT S AU MARTIN, KA HALL, J ADAMS, J CROWLEY, WF AF MARTIN, KA HALL, J ADAMS, J CROWLEY, WF BE Filicori, M Flamigni, C TI PULSATILE GNRH IN HYPOGONADOTROPIC HYPOGONADISM SO OVULATION INDUCTION: BASIC SCIENCE AND CLINICAL ADVANCES SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT Symposium on Ovulation Induction: Basic Science and Clinical Advances CY JAN 20-22, 1994 CL PALM BEACH, FL C1 MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINE UNIT,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 0-444-81696-8 J9 INT CONGR SER PY 1994 VL 1046 BP 255 EP 266 PG 12 WC Endocrinology & Metabolism; Obstetrics & Gynecology; Reproductive Biology SC Endocrinology & Metabolism; Obstetrics & Gynecology; Reproductive Biology GA BB16D UT WOS:A1994BB16D00029 ER PT J AU KRON, J SILKA, MJ OHM, OJ BARDY, G BENDITT, D CHILSON, D GILLIS, AM MITCHELL, LB GULAMHUSEIN, S KUCK, K SIEBELS, J BREITHARDT, G BLOCK, M TOUBOUL, P PRADEL, L BRACHMANN, J RUSKIN, J HAFFAJEE, C AF KRON, J SILKA, MJ OHM, OJ BARDY, G BENDITT, D CHILSON, D GILLIS, AM MITCHELL, LB GULAMHUSEIN, S KUCK, K SIEBELS, J BREITHARDT, G BLOCK, M TOUBOUL, P PRADEL, L BRACHMANN, J RUSKIN, J HAFFAJEE, C TI PRELIMINARY EXPERIENCE WITH NONTHORACOTOMY IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS IN YOUNG-PATIENTS SO PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY LA English DT Article DE SUDDEN DEATH; IMPLANTABLE CARDIOVERTER DEFIBRILLATOR; PEDIATRIC CARDIOLOGY ID MALIGNANT VENTRICULAR ARRHYTHMIAS; SYSTEM AB Implantable cardioverter defibrillators represent an important treatment option for patients with life-threatening tachyarrhythmias. However, the requirement for surgical access to the thorax contributes to significant procedural morbidity with ICD implantation. This study was performed to assess an initial experience with a nonthoracotomy approach to ICD lead implantation in young patients. An international survey identified 17 patients, ranging in age from 12-20 years (mean = 16.7 +/- 2.4) and weighing from 33-89 kg (mean = 60.6 +/- 13.3), who had undergone placement of the Medtronic Transvene(R) defibrillator lead system. Implant indications were aborted sudden cardiac death in 15 patients and recurrent ventricular tachycardia or familial sudden death in 2 patients. At a median follow-up of 7.9 months, 9 of 17 patients had received at least one ICD therapy. There have been no deaths, Complications included patch or generator erosion (3 patients), lead dislodgement (1 patient), and ICD system infection requiring explanation (1 patient]. The initial experience with nonthoracotomy ICDs in young patients appears promising. This approach may be particularly advantageous for patients who have undergone prior thoracotomy. Prospective clinical trials will be required to establish the applicability of these lead systems to select patient populations. C1 OREGON HLTH SCI UNIV,DEPT PEDIAT,PORTLAND,OR 97201. UNIV BERGEN,SCH MED,BERGEN,NORWAY. UNIV WASHINGTON,SEATTLE,WA. UNIV MINNESOTA,MINNEAPOLIS,MN. MEDTRONIC INC,MINNEAPOLIS,MN. SACRED HEART HOSP,SPOKANE,WA. UNIV CALGARY,CALGARY,AB,CANADA. UNIV ALBERTA,EDMONTON,AB,CANADA. UNIV HAMBURG,HAMBURG,GERMANY. UNIV MUNSTER,MUNSTER,GERMANY. HOSP CARDIOVASC L PRADEL,LYON,FRANCE. UNIV HEIDELBERG,MED KLIN,W-6900 HEIDELBERG,GERMANY. MASSACHUSETTS GEN HOSP,BOSTON,MA. ST ELIZABETHS HOSP BOSTON,BOSTON,MA. RP KRON, J (reprint author), OREGON HLTH SCI UNIV,DEPT MED,DIV CARDIOL,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. NR 9 TC 26 Z9 26 U1 0 U2 1 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 0147-8389 J9 PACE JI PACE-Pacing Clin. Electrophysiol. PD JAN PY 1994 VL 17 IS 1 BP 26 EP 30 DI 10.1111/j.1540-8159.1994.tb01347.x PG 5 WC Cardiac & Cardiovascular Systems; Engineering, Biomedical SC Cardiovascular System & Cardiology; Engineering GA MU094 UT WOS:A1994MU09400006 PM 8139991 ER PT S AU LOPESVIRELLA, MF AF LOPESVIRELLA, MF BE Sakamoto, N Alberti, KGM Hotta, N TI INTERRELATED METABOLISM IMBALANCES LINKED TO HYPERGLYCEMIA-INDUCED VASCULAR DYSFUNCTION SO PATHOGENESIS AND TREATMENT OF NIDDM AND ITS RELATED PROBLEMS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 4th International Symposium on Treatment of Diabetes Mellitus: Pathogenesis and Treatment of NIDDM and Its Related Problems CY OCT 26-27, 1993 CL NAGOYA, JAPAN SP NAGOYA UNIV, JAPAN DIABETES SOC, FDN ADV INT SCI, AICHI PREFECTURE, NAGOYA CITY C1 MED UNIV S CAROLINA,RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29425. 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 0-444-81712-3 J9 INT CONGR SER PY 1994 VL 1057 BP 29 EP 36 PG 8 WC Endocrinology & Metabolism; Pathology SC Endocrinology & Metabolism; Pathology GA BB08V UT WOS:A1994BB08V00005 ER PT S AU ARAKI, E KAHN, CR SHICHIRI, M AF ARAKI, E KAHN, CR SHICHIRI, M BE Sakamoto, N Alberti, KGM Hotta, N TI STRUCTURE AND REGULATION OF THE INSULIN-RECEPTOR SUBSTRATE-1 (IRS-1) SO PATHOGENESIS AND TREATMENT OF NIDDM AND ITS RELATED PROBLEMS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 4th International Symposium on Treatment of Diabetes Mellitus: Pathogenesis and Treatment of NIDDM and Its Related Problems CY OCT 26-27, 1993 CL NAGOYA, JAPAN SP NAGOYA UNIV, JAPAN DIABETES SOC, FDN ADV INT SCI, AICHI PREFECTURE, NAGOYA CITY C1 BRIGHAM & WOMENS HOSP,DEPT MED,CTR JOSLIN DIABET,DIV RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 2 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81712-3 J9 INT CONGR SER PY 1994 VL 1057 BP 243 EP 249 PG 7 WC Endocrinology & Metabolism; Pathology SC Endocrinology & Metabolism; Pathology GA BB08V UT WOS:A1994BB08V00038 ER PT J AU KOERNER, FC OCONNELL, JX AF KOERNER, FC OCONNELL, JX TI FIBROADENOMA - MORPHOLOGICAL OBSERVATIONS AND A THEORY OF PATHOGENESIS SO PATHOLOGY ANNUAL 1994, VOL 29, PT 1 SE PATHOLOGY ANNUAL LA English DT Review ID HUMAN-BREAST; GROWTH-FACTOR; MAMMARY-TUMORS; LOCALIZATION; LESIONS RP KOERNER, FC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT LAB,DEPT PATHOL,BOSTON,MA 02114, USA. NR 31 TC 12 Z9 12 U1 1 U2 1 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0079-0184 J9 PATHOL ANNU PY 1994 VL 29 BP 1 EP 19 PN 1 PG 19 WC Pathology SC Pathology GA BB35F UT WOS:A1994BB35F00001 PM 8127621 ER PT J AU SHADY, JA BLACK, PM KUPSKY, WJ TARBELL, NJ SCOTT, RM LEONG, T HOLMES, G AF SHADY, JA BLACK, PM KUPSKY, WJ TARBELL, NJ SCOTT, RM LEONG, T HOLMES, G TI SEIZURES IN CHILDREN WITH SUPRATENTORIAL ASTROGLIAL NEOPLASMS SO PEDIATRIC NEUROSURGERY LA English DT Article DE ASTROCYTOMAS; GANGLIOGLIOMAS; GLIOBLASTOMAS; NEOPLASMS, PEDIATRIC; SEIZURES; CEREBRAL NEOPLASMS ID CHILDHOOD BRAIN-TUMORS; COMPUTED-TOMOGRAPHY; EPILEPSY; ASTROCYTOMAS; PROGNOSIS; GLIOMA AB We reviewed the records of 98 consecutive patients, 18 years of age or younger, with pathologically confirmed supratentorial astroglial neoplasms at the Children's Hospital, Boston, to evaluate the importance of seizures in their presentation and natural history. Tumors were diagnosed using the WHO criteria as pilocytic astrocytomas, astrocytomas, anaplastic astrocytomas, glioblastomas, giant cell glioblastomas, oligoastrocytomas and gangliogliomas. Our results were as follows. (1) Fifty percent of children had seizures as part of their presentation and 30% had seizures as their only presenting phenomenon. (2) The seizures varied in nature, but complex (55%) or simple (28%) partial seizures were by far the most common types, occurring in 77% of cases. (3) Preoperative electroencephalography (EEG) accurately lateralized to the tumor side in 88% of the cases and localized to the correct lobe in 56%. (4) Tumors involving cerebral cortex significantly correlated with seizures at presentation as compared to noncortical locations; 59% of patients with cortical tumors presented with seizures, and only 15% of patients with noncortical tumors experienced seizures. Lesions in the temporal and frontal lobes had the highest incidence of seizures. (5) Patients with gangliogliomas and oligoastrocytomas had the highest incidence of seizures, 88 and 86%, respectively, whereas patients with anaplastic astrocytoma had the lowest incidence, 21%. (6) Histopathologic calcification was associated with seizures at presentation approaching significance (p = 0.06). (7) Seizures at presentation were significantly associated with good prognosis (p = 0.02). C1 CHILDRENS HOSP,DEPT NEUROSURG,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,MED CTR,SCH MED,DEPT NEUROPATHOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,CTR MED,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,MED CTR,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 37 TC 18 Z9 18 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1016-2291 J9 PEDIATR NEUROSURG JI Pediatr. Neurosurg. PY 1994 VL 21 IS 1 BP 23 EP 30 DI 10.1159/000120810 PG 8 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA NX906 UT WOS:A1994NX90600005 PM 7947306 ER PT J AU CHAPMAN, PH COSMAN, ER ZERVAS, NT AF CHAPMAN, PH COSMAN, ER ZERVAS, NT TI EXPERIENCE WITH TELEMETRIC PRESSURE MEASUREMENTS IN SHUNT SYSTEMS SO PEDIATRIC NEUROSURGERY LA English DT Article ID FLOW RP CHAPMAN, PH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV NEUROSURG,BOSTON,MA 02114, USA. NR 16 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1016-2291 J9 PEDIATR NEUROSURG JI Pediatr. Neurosurg. PY 1994 VL 21 IS 3 BP 179 EP 183 DI 10.1159/000120831 PG 5 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA PM386 UT WOS:A1994PM38600005 PM 7803307 ER PT J AU RIORDAN, LL KELLY, DH SHANNON, DC AF RIORDAN, LL KELLY, DH SHANNON, DC TI SLOW WEIGHT-GAIN IS ASSOCIATED WITH INCREASED PERIODIC BREATHING IN HEALTHY INFANTS SO PEDIATRIC PULMONOLOGY LA English DT Article DE PERCENT PERIODIC BREATHING; 2 WEEKS VS 2 MOS TESTING ID DEATH SYNDROME VICTIMS; FULL-TERM INFANTS; PRETERM INFANTS; HEART-RATE; PATTERNS; APNEA; SLEEP AB To investigate the hypothesis that weight gain can influence periodic breathing in healthy infants, we prospectively studied, by nocturnal pneumogram technique, respiration and heart rate in 99 full-term infants during the first month of life. Eighty-eight infants had a repeat study at about 2 months of age. Pneumograms were analyzed visually for percent periodic breathing (%PB), and by computer for mean respiratory rate and mean heart rate. We found a median %PB of 0.9 initially and of 0.3 at about 2 months of age. The 95th percentile was 13.5 at 2 weeks and 7.3 at 2 months, higher than previously reported. Between the two ages tested, %PB was inversely correlated with weight gain (P < 0.001, < 0.03, respectively). Infants with greater weight gain had a greater fall in %PB (P < 0.03). We conclude that in the first 2 months of life, slow weight gain is associated with increased periodic breathing. (C) 1994 Wiley-Liss, Inc. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHILDRENS SERV,PEDIAT PULM UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL 07354] NR 35 TC 1 Z9 1 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 8755-6863 J9 PEDIATR PULM JI Pediatr. Pulmonol. PD JAN PY 1994 VL 17 IS 1 BP 22 EP 25 DI 10.1002/ppul.1950170105 PG 4 WC Pediatrics; Respiratory System SC Pediatrics; Respiratory System GA MP341 UT WOS:A1994MP34100004 PM 8108172 ER PT J AU OLSTAD, OK MORRISON, NE JEMTLAND, R JUPPNER, H SEGRE, GV GAUTVIK, KM AF OLSTAD, OK MORRISON, NE JEMTLAND, R JUPPNER, H SEGRE, GV GAUTVIK, KM TI DIFFERENCES IN BINDING AFFINITIES OF HUMAN PTH(1-84) DO NOT ALTER BIOLOGICAL POTENCY - A COMPARISON BETWEEN CHEMICALLY SYNTHESIZED HORMONE, NATURAL AND MUTANT FORMS SO PEPTIDES LA English DT Article DE RECOMBINANT PARATHYROID HORMONES; RECOMBINANT PTH/PTHRP RECEPTOR; CAMP RESPONSE; RATS ID HUMAN PARATHYROID-HORMONE; SACCHAROMYCES-CEREVISIAE; ALPHA-FACTOR; RECEPTOR; PEPTIDE; CELLS; SECRETION; MEMBRANE; REGION; IDENTIFICATION AB The purpose of this study was to evaluate receptor binding affinities and biological properties in vitro and in vivo of various recombinant hPTH(1-84) forms representing the natural hormone and a mutagenized hPTH form, [Gln(26)]hPTH(1-84)(QPTH), after expression in E. coli and Saccharomyces cerevisiae. In LLC-PK1 cells stably transformed with the rat PTH/PTHrP receptor, chemically synthesized hPTH(1-84) and QPTH showed a reduced binding affinity (apparent K-d is and 23 nM, respectively) than the recombinant, hPTH(1-84) (apparent K-d 9.5 nM). All recombinant hPTH forms showed a similar potency to stimulate cellular cAMP production (EC(50) 1.5 nM) and significantly better than chemically synthesized hPTH (EC(50) 5.7 nM). All hormone forms showed an about equipotent activity in causing elevation in serum calcium, increased excretion of urine phosphate, and cAMP. Thus, the natural recombinant PTH forms showed higher binding affinities and adenylate cyclase activation potencies in LLC-PK1 cells, but the reduced receptor binding affinity exerted by QPTH did not transcend differences in cAMP generation and in vivo biological activities. C1 ZYMOGENET,SEATTLE,WA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA. RP OLSTAD, OK (reprint author), UNIV OSLO,INST MED BIOCHEM,POB 1112,N-0317 OSLO,NORWAY. NR 29 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 0196-9781 J9 PEPTIDES JI Peptides PY 1994 VL 15 IS 7 BP 1261 EP 1265 DI 10.1016/0196-9781(94)90151-1 PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA PM187 UT WOS:A1994PM18700015 PM 7854979 ER PT B AU MOSKOWITZ, MA CUTRER, FM AF MOSKOWITZ, MA CUTRER, FM BE Fields, HL Liebeskind, JC TI POSSIBLE IMPORTANCE OF NEUROGENIC INFLAMMATION WITHIN THE MENINGES TO MIGRAINE HEADACHES SO PHARMACOLOGICAL APPROACHES TO THE TREATMENT OF CHRONIC PAIN: NEW CONCEPTS & CRITICAL ISSUES SE PROGRESS IN PAIN RESEARCH AND MANAGEMENT LA English DT Proceedings Paper CT 4th Annual Bristol-Myers Squibb Symposium on Pain Research - Pharmacological Approaches to the Treatment of Chronic Pain: New Concepts and Critical Issues CY JUN 13-15, 1993 CL MONTEREY, CA SP BRISTOL MYERS SQUIBB CO, UNIV CALIF SCH MED SAN FRANCISCO, DEPT NEUROL, UNIV CALIF LOS ANGELES, DEPT PSYCHOL C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. NR 0 TC 15 Z9 15 U1 0 U2 1 PU INT ASSOC STUDY PAIN (IASP) PRESS PI SEATTLE PA 909 NE 43RD ST, SUITE 304, SEATTLE, WA 98105 BN 0-931092-04-3 J9 PROG PAIN RES MANAG PY 1994 VL 1 BP 43 EP 49 PG 7 WC Pharmacology & Pharmacy; Rehabilitation SC Pharmacology & Pharmacy; Rehabilitation GA BB55R UT WOS:A1994BB55R00004 ER PT B AU YOSHIDA, T DALKARA, T IRIKURA, K MOSKOWITZ, MA AF YOSHIDA, T DALKARA, T IRIKURA, K MOSKOWITZ, MA BE Krieglstein, J OberpichlerSchwenk, H TI Inhibition of neuronal nitric oxide production by 7-nitro-indazole decreases infarct size in focal cerebral ischemia SO PHARMACOLOGY OF CEREBRAL ISCHEMIA 1994 LA English DT Proceedings Paper CT 5th Symposium on Pharmacology of Cerebral Ischemia CY JUL, 1994 CL MARBURG, GERMANY SP Deut Forschungsgemeinsch, Bonn, Hess Minist Wissensch & Kunst, Wiesbaden, Philipps Univ, Marburg C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROSURG,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU WISSENSCHAFTLICHE verlagsgesellschaft mbh PI STUTTGART PA POSTFACH 40, BIRKENWALDSTRASSE 44, 70191 STUTTGART, GERMANY BN 3-88763-029-7 PY 1994 BP 329 EP 334 PG 6 WC Biochemistry & Molecular Biology; Clinical Neurology; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BD29C UT WOS:A1994BD29C00032 ER PT J AU HOLMBERG, EB PERKELL, JS HILLMAN, RE GRESS, C AF HOLMBERG, EB PERKELL, JS HILLMAN, RE GRESS, C TI INDIVIDUAL VARIATION IN MEASURES OF VOICE SO PHONETICA LA English DT Article ID GLOTTAL AIR-FLOW; FEMALE; WAVEFORM; PRESSURE; SPEECH AB Measures of inferred subglottal air pressure, glottal airflow waveform characteristics, sound pressure level (SPL) and the acoustic spectral slope were studied for individual speakers with normal voices. Combinations of different levels of subglottal air pressure and varying glottal configurations could result in the same SPL. Relatively high air pressure levels were associated with a steep spectral slope, reflecting a more sinusoidal glottal waveform and a relatively abducted membranous glottis, which would result in damping of F-1. Data suggested that the interarytenoid glottal opening could vary without systematically affecting SPL or voice quality. The results indicate that the principles of production-related economy of effort and physiological, acoustic and perceptual constraints may apply to voice production. C1 MASSACHUSETTS EYE & EAR INFIRM,VOICE & SPEECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. RP HOLMBERG, EB (reprint author), MIT,ELECTR RES LAB,BLDG 36,ROOM 521,50 VASSAR ST,CAMBRIDGE,MA 02139, USA. FU NIDCD NIH HHS [DC 00266] NR 29 TC 14 Z9 14 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0031-8388 J9 PHONETICA JI Phonetica PY 1994 VL 51 IS 1-3 BP 30 EP 37 PG 8 WC Acoustics; Audiology & Speech-Language Pathology; Linguistics; Language & Linguistics SC Acoustics; Audiology & Speech-Language Pathology; Linguistics GA NU539 UT WOS:A1994NU53900004 PM 8052674 ER PT B AU HOHMANN, EL MILLER, SI AF HOHMANN, EL MILLER, SI BE TorrianiGorini, A Yagil, E Silver, S TI THE SALMONELLA PHOR VIRULENCE REGULON SO PHOSPHATE IN MICROORGANISMS: CELLULAR AND MOLECULAR BIOLOGY LA English DT Proceedings Paper CT International Symposium on Cellular and Molecular Biology of Phosphate and Phosphorylated Compounds in Microorganisms CY SEP 12-17, 1993 CL WOODS HOLE, MA SP FDN MICROBIOL, INT UNION BIOCHEM & MOLEC BIOL, AUSTRALIA, US DOE C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. NR 0 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVE NW, WASHINGTON, DC 20005-4171 BN 1-55581-080-2 PY 1994 BP 120 EP 125 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Microbiology SC Biochemistry & Molecular Biology; Cell Biology; Microbiology GA BB56S UT WOS:A1994BB56S00021 ER PT B AU VENEGAS, JG TREPPO, S MIJAILOVICH, SM AF VENEGAS, JG TREPPO, S MIJAILOVICH, SM BE Hoffman, EA Acharya, RS TI CONTRIBUTIONS STATISTICAL NOISE TO SPATIAL HETEROGENEITY OF PET IMAGES OF PULMONARY-FUNCTION SO PHYSIOLOGY AND FUNCTION FROM MULTIDIMENSIONAL IMAGES: MEDICAL IMAGING 1994 SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Physiology and Function from Multidimensional Images CY FEB 13-14, 1994 CL NEWPORT BEACH, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS, AMER ASSOC PHYSICISTS MED, BIOMED OPT SOC, US FDA, CTR DEVICES & RADIOL HLTH, NATL ELEC MANUFACTURERS ASSOC, DIAGNOST IMAGING & THERAPY SYS DIV, SOC IMAGING SCI & TECHNOL, RADIOL INFORMAT SYST CONSORTIUM, RADIOL SOC N AMER, SOC COMP APPLICAT RADIOL C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 0 TC 5 Z9 5 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1463-8 J9 P SOC PHOTO-OPT INS PY 1994 VL 2168 BP 361 EP 368 DI 10.1117/12.174410 PG 8 WC Cardiac & Cardiovascular Systems; Engineering, Biomedical; Optics SC Cardiovascular System & Cardiology; Engineering; Optics GA BA56T UT WOS:A1994BA56T00033 ER PT J AU WANG, J ZHANG, H GOODMAN, HM AF WANG, J ZHANG, H GOODMAN, HM TI AN ARABIDOPSIS CAB GENE HOMOLOGOUS TO CAB-8 OF TOMATO SO PLANT PHYSIOLOGY LA English DT Note ID THALIANA; FAMILY C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 4 TC 6 Z9 8 U1 0 U2 0 PU AMER SOC PLANT PHYSIOLOGISTS PI ROCKVILLE PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 SN 0032-0889 J9 PLANT PHYSIOL JI Plant Physiol. PD JAN PY 1994 VL 104 IS 1 BP 297 EP 297 DI 10.1104/pp.104.1.297 PG 1 WC Plant Sciences SC Plant Sciences GA MR629 UT WOS:A1994MR62900040 PM 8115553 ER PT J AU YAREMCHUK, MJ FIALA, TGS BARKER, F RAGLAND, R AF YAREMCHUK, MJ FIALA, TGS BARKER, F RAGLAND, R TI THE EFFECTS OF RIGID FIXATION ON CRANIOFACIAL GROWTH OF RHESUS-MONKEYS SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID CRANIAL GROWTH; CRANIOSYNOSTOSIS; RABBITS; BRAIN AB A male infant rhesus monkey model was used to examine the growth effect on the craniofacial skeleton caused by osteotomy and three types of fixation: interfragmentary wiring, microplate and screw fixation, and ''extensive'' microplate and screw fixation. The animals (n=12) were allowed to mature until cranial growth was at least 95 percent complete. Direct craniometric measurements were obtained and analyzed for differences in the three treated groups. A group of unoperated male animal skulls also was analyzed as controls (n=5). A subtle visible and measurable restriction of growth in the operated area occurred in all treatment groups. Significant differences (p<0.05) were found in only 4 of the 39 craniometric chords measured. Interfragmentary wiring showed fewer growth-restrictive effects than standard use of microfixation plates. Extensive use of rigid fixation devices caused the greatest degree of growth disturbance. Osteotomy and fixation in the infant rhesus monkey affect craniofacial growth, with the degree of growth restriction increasing with the amount of fixation hardware. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV PLAST SURG,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT SURG,DIV NEUROSURG,BOSTON,MA. UNIV MASSACHUSETTS,MED CTR,DEPT RADIOL,WORCESTER,MA 01655. NR 24 TC 41 Z9 42 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JAN PY 1994 VL 93 IS 1 BP 1 EP 10 PG 10 WC Surgery SC Surgery GA MP565 UT WOS:A1994MP56500001 PM 8278464 ER PT S AU VACANTI, CA VACANTI, JP LANGER, R AF VACANTI, CA VACANTI, JP LANGER, R BE Shalaby, SW Ikada, Y Langer, R Williams, J TI TISSUE ENGINEERING USING SYNTHETIC BIODEGRADABLE POLYMERS SO POLYMERS OF BIOLOGICAL AND BIOMEDICAL SIGNIFICANCE SE ACS SYMPOSIUM SERIES LA English DT Article; Proceedings Paper CT Symposium on Polymers of Biological and Biomedical Significance, at the 204th National Meeting of the American Chemical Society CY AUG 24-28, 1992 CL WASHINGTON, DC SP AMER CHEM SOC, DIV POLYM CHEM INC ID TRANSPLANTATION; HEPATOCYTES; CELLS; GUNN; RATS; INVITRO; GROWTH; MODEL AB A new approach to create new animal tissues utilizing biodegradable polymer is presented. The use of this approach to create cartilage, liver and other tissues are reviewed. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP,DEPT SURG,BOSTON,MA 02115. MIT,DEPT CHEM ENGN,BOSTON,MA 02139. RP VACANTI, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG & ANESTHESIOL,BOSTON,MA 02115, USA. NR 36 TC 9 Z9 9 U1 2 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0097-6156 BN 0-8412-2732-2 J9 ACS SYM SER PY 1994 VL 540 BP 16 EP 34 PG 19 WC Chemistry, Multidisciplinary; Medicine, Research & Experimental; Polymer Science SC Chemistry; Research & Experimental Medicine; Polymer Science GA BZ58M UT WOS:A1994BZ58M00003 ER PT J AU ABRAMS, DB BOUTWELL, WB GRIZZLE, J HEIMENDINGER, J SORENSEN, G VARNES, J AF ABRAMS, DB BOUTWELL, WB GRIZZLE, J HEIMENDINGER, J SORENSEN, G VARNES, J TI CANCER CONTROL AT THE WORKPLACE - THE WORKING WELL TRIAL SO PREVENTIVE MEDICINE LA English DT Article ID SMOKING CESSATION; HEALTH PROMOTION; COMMUNITY INTERVENTION; PROGRAMS; MODELS; RISK AB Background. Few research studies have been conducted on cancer prevention and control at the workplace. This article presents an overview of the largest worksite cancer control trial in the United States-The Working Well Trial-conducted in 114 worksites by four study centers, a coordinating center, and the National Cancer Institute. The trial's organizational structure, research design, dependent measures, and theoretical model for intervention are described. Special features of the trial include using the worksite as the unit of randomization, intervention, and evaluation and a theory-driven conceptual model of intervention that places emphasis on individual and organizational targets for change, uses the transtheoretical stage of change model to guide a sustained 2-year multiple risk factor intervention, and makes use of volunteer resources within the worksite to reduce cost, increase participation, and improve tailoring to individual needs. The trial will have a potential impact on over 25,000 workers. Conclusion. The issues raised in this overview have implications for the evaluation and dissemination of cancer prevention and control programs to defined populations. (C) 1994 Academic Press, Inc. C1 FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. UNIV TEXAS,M D ANDERSON CANC CTR,HOUSTON,TX 77025. NCI,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV FLORIDA,GAINESVILLE,FL 32611. RP ABRAMS, DB (reprint author), BROWN UNIV,MIRIAM HOSP,PROVIDENCE,RI 02912, USA. FU NCI NIH HHS [U01 CA51686, U01 CA51671, U01 CA51687] NR 54 TC 88 Z9 88 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 0091-7435 J9 PREV MED JI Prev. Med. PD JAN PY 1994 VL 23 IS 1 BP 15 EP 27 DI 10.1006/pmed.1994.1003 PG 13 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA ND355 UT WOS:A1994ND35500003 PM 8016028 ER PT B 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 BE Gebhart, GF Hammond, DL Jensen, TS TI GENE DELIVERY TO MOUSE SENSORY NEURONS USING HERPES VIRUS VECTORS SO PROCEEDINGS OF THE 7TH WORLD CONGRESS ON PAIN: PROGRESS IN PAIN RESEARCH AND MANAGEMENT SE PROGRESS IN PAIN RESEARCH AND MANAGEMENT LA English DT Proceedings Paper CT 7th World Congress on Pain CY 1993 CL PARIS, FRANCE SP INT ASSOC STUDY PAIN C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT ASSOC STUDY PAIN (IASP) PRESS PI SEATTLE PA 909 NE 43RD ST, SUITE 304, SEATTLE, WA 98105 BN 0-931092-07-8 J9 PROG PAIN RES MANAG PY 1994 VL 2 BP 385 EP 394 PG 10 WC Anesthesiology; Clinical Neurology SC Anesthesiology; Neurosciences & Neurology GA BC03R UT WOS:A1994BC03R00027 ER PT B AU EISENBERG, E BERKEY, C CARR, DB CHALMERS, TC MOSTELLER, F AF EISENBERG, E BERKEY, C CARR, DB CHALMERS, TC MOSTELLER, F BE Gebhart, GF Hammond, DL Jensen, TS TI NSAIDS FOR CANCER PAIN - META-ANALYSIS OF EFFICACY SO PROCEEDINGS OF THE 7TH WORLD CONGRESS ON PAIN: PROGRESS IN PAIN RESEARCH AND MANAGEMENT SE PROGRESS IN PAIN RESEARCH AND MANAGEMENT LA English DT Proceedings Paper CT 7th World Congress on Pain CY 1993 CL PARIS, FRANCE SP INT ASSOC STUDY PAIN C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU INT ASSOC STUDY PAIN (IASP) PRESS PI SEATTLE PA 909 NE 43RD ST, SUITE 304, SEATTLE, WA 98105 BN 0-931092-07-8 J9 PROG PAIN RES MANAG PY 1994 VL 2 BP 697 EP 707 PG 11 WC Anesthesiology; Clinical Neurology SC Anesthesiology; Neurosciences & Neurology GA BC03R UT WOS:A1994BC03R00046 ER PT B AU MOSKOWITZ, MA AF MOSKOWITZ, MA BE Gebhart, GF Hammond, DL Jensen, TS TI DRUG MECHANISMS IN ACUTE MIGRAINE SO PROCEEDINGS OF THE 7TH WORLD CONGRESS ON PAIN: PROGRESS IN PAIN RESEARCH AND MANAGEMENT SE PROGRESS IN PAIN RESEARCH AND MANAGEMENT LA English DT Proceedings Paper CT 7th World Congress on Pain CY 1993 CL PARIS, FRANCE SP INT ASSOC STUDY PAIN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,NEUROL SERV,STROKE RES LAB,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU INT ASSOC STUDY PAIN (IASP) PRESS PI SEATTLE PA 909 NE 43RD ST, SUITE 304, SEATTLE, WA 98105 BN 0-931092-07-8 J9 PROG PAIN RES MANAG PY 1994 VL 2 BP 755 EP 764 PG 10 WC Anesthesiology; Clinical Neurology SC Anesthesiology; Neurosciences & Neurology GA BC03R UT WOS:A1994BC03R00050 ER PT J AU TYAN, ML AF TYAN, ML TI FETAL WEIGHT AT TERM INFLUENCED BY H-2-ASSOCIATED LOCI SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; GROWTH; PHENOTYPE; STRAINS; RAT AB Pregnant mice which in theory differ only in the region of the major histocompatibility complex (MHC) on chromosome 17 (C57BL/10, the inbred partner [host strain], and B10.D2, B10.BR, B10.A, B10.A[2R], B10.A[5R], B10.A[15R] and B10.A[18R]) were sacrificed on the 11th and 18th days of gestation, and the fetuses were sexed and weighed. Fetuses from reciprocal crosses between B10.A and B10.BR, B10.D2 and C57BL/10 were weighed and sexed on the 18th day of gestation. It was found that (i) fetal weights were not significantly different among the strains examined on day 11 (B10.BR, B10.A[15R] and B10.A[18R]), (ii) B10.BR fetuses of both sexes weighed significantly less than fetuses from the other strains on day 18, (iii) B10.D2 18-day-old male but not female fetuses were heavier than the males from the other strains (this difference was not present when corrections for litter size were made), (iv) the fetuses from the B10.A x B10.BR cross were the smallest, those from the B10.D2 x B10.A cross the largest, and those from the B10.A x C57BL/10 crosses intermediate, and (v) maternal effects were noted in the B10.A x B10.BR and B10.A x B10.D2 but not the B10.A x C57BL/10 crosses. The results suggest that there are two or more MHC associated loci that influence growth rate in late gestation. Among the candidate genes are Ped and Igfr II. RP TYAN, ML (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073, USA. NR 17 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD JAN PY 1994 VL 205 IS 1 BP 85 EP 88 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF384 UT WOS:A1994NF38400013 PM 8115355 ER PT J AU LESLIE, CA DUBEY, DP AF LESLIE, CA DUBEY, DP TI INCREASED PGE(2) FROM HUMAN MONOCYTES ISOLATED IN THE LUTEAL-PHASE OF THE MENSTRUAL-CYCLE - IMPLICATIONS FOR IMMUNITY SO PROSTAGLANDINS LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; SYNTHASE CYCLOOXYGENASE; MONOCLONAL-ANTIBODIES; GONADAL-STEROIDS; CANDIDA-ALBICANS; MESSENGER-RNA; CELL-ACTIVITY; PROSTAGLANDINS; PROGESTERONE; MACROPHAGES AB The reproductive hormones are implicated in the well documented sexual dimorphism in cellular and immune responses. Prostaglandins (PGs) are mediators of the immune response with their concentration and relative amounts being pivotal to their impact. In resident peritoneal macrophages isolated from mice we had previously noted that the cells from females synthesized significantly more PG than males. In these experiments we investigated whether PG metabolism in the human monocyte was influenced by gender and by stage of the menstrual cycle. Monocytes isolated from the female and activated in vitro with LPS produced on average significantly more PG into the medium than the males. Among females, significantly more PG was found in the medium from cells isolated during the luteal phase of the cycle than during the early follicular phase. It was also in this luteal phase in which the female differed substantially from males. We suggest that the in vivo hormonal changes associated with the menstrual cycle modulate monocyte synthesis of PG and other immune modulators such as IL-1. This could be a key to understanding differences in vulnerability between males and females as well as within phases of the cycle, to immune and inflammatory insult. C1 BOSTON UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02118. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP LESLIE, CA (reprint author), VET ADM MED CTR,ENRM,BEDFORD,MA 01730, USA. FU NIAID NIH HHS [AI 26817] NR 47 TC 30 Z9 30 U1 0 U2 2 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0090-6980 J9 PROSTAGLANDINS JI Prostaglandins PD JAN PY 1994 VL 47 IS 1 BP 41 EP 54 DI 10.1016/0090-6980(94)90073-6 PG 14 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MR647 UT WOS:A1994MR64700005 PM 8140261 ER PT J AU SHIPLEY, WU AF SHIPLEY, WU TI PHASE-III TRIAL OF ANDROGEN SUPPRESSION BEFORE AND DURING RADIATION-THERAPY FOR LOCALLY ADVANCED PROSTATIC-CANCER - ABSTRACT REPORT OF RTOG-8610 SO PROSTATE LA English DT Article; Proceedings Paper CT Satellite Symposium on Clinical Developments in Prostate Cancer, at the 2nd International Congress of the Dutch-Urological-Association CY NOV, 1993 CL AMSTERDAM, NETHERLANDS SP DUTCH UROL ASSOC DE ANDROGEN ABLATION; FLUTAMIDE; ZOLADEX(R); MAXIMAL ANDROGEN BLOCKADE; PELVIC IRRADIATION; STAGE T3 PROSTATE CANCER ID IRRADIATION; CARCINOMA; RTOG-77-06 C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SHIPLEY, WU (reprint author), HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 9 TC 1 Z9 1 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 0270-4137 J9 PROSTATE JI Prostate PY 1994 SU 5 BP 2 EP 3 PG 2 WC Endocrinology & Metabolism; Urology & Nephrology SC Endocrinology & Metabolism; Urology & Nephrology GA NM063 UT WOS:A1994NM06300002 ER PT J AU IVERSEN SHIPLEY, WU NEWLING, DWW KURTH VOGES, GE SCHULMAN, CC DENIS, L AF IVERSEN SHIPLEY, WU NEWLING, DWW KURTH VOGES, GE SCHULMAN, CC DENIS, L TI CLINICAL DEVELOPMENTS IN PROSTATE-CANCER - PANEL DISCUSSION-I SO PROSTATE LA English DT Discussion C1 HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ACAD ZIEKENHUIS,DEPT UROL,AMSTERDAM,NETHERLANDS. MAINZ MED SCH,DEPT UROL,D-55131 MAINZ,GERMANY. ERASME UNIV HOSP,UNIV CLIN BRUSSELS,DEPT UROL,B-1070 BRUSSELS,BELGIUM. ACAD ZIEKENHUIS MIDDELHEIM,DEPT UROL,B-2020 ANTWERP,BELGIUM. 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 0270-4137 J9 PROSTATE JI Prostate PY 1994 SU 5 BP 15 EP 16 PG 2 WC Endocrinology & Metabolism; Urology & Nephrology SC Endocrinology & Metabolism; Urology & Nephrology GA NM063 UT WOS:A1994NM06300005 ER PT J AU LENDERKING, WR WORTH, JL BECKETT, A AF LENDERKING, WR WORTH, JL BECKETT, A TI QUALITY-OF-LIFE ASSESSMENT IN HIV-INFECTED PSYCHIATRIC OUTPATIENTS - PERCEIVED HEALTH, FUNCTIONAL STATUS, SYMPTOMS, AND PREFERENCES FOR CARDIOPULMONARY-RESUSCITATION SO PSYCHOLOGY & HEALTH LA English DT Article; Proceedings Paper CT Amsterdam Conference of the Symposium on Quality of Life and HIV Infection: The Biopsychosocial Dimension CY JUL 16-17, 1992 CL UNIV AMSTERDAM, AMSTERDAM, NETHERLANDS SP UNIV AMSTERDAM, FAC PSYCHOL, UNIV LEIDEN, DEPT CLIN & HLTH PSYCHOL, JOHNS HOPKINS UNIV, SCH HYGIENE & PUBLIC HLTH, WHO, AMSTERDAM COLLABORAT CTR QUAL LIFE HO UNIV AMSTERDAM DE HIV AIDS; QUALITY OF LIFE; DEPRESSION; PREFERENCES FOR RESUSCITATION; SUICIDE ID IMMUNODEFICIENCY-VIRUS-INFECTION; HOMOSEXUAL MEN; STATUS QUESTIONNAIRE; DEPRESSIVE SYMPTOMS; MEDICAL OUTCOMES; VALIDITY; AIDS; RELIABILITY; ZIDOVUDINE; VALIDATION AB The current study had two purposes: (1) to describe the reliability and validity of a measure of quality of life (QOL) in HIV-infected psychiatric outpatients, and (2) to predict cardiopulmonary resuscitation (CPR) preferences from disease stage, depression, and other QOL factors. We studied 63 patients, who were seen in one year at an HIV/AIDS psychiatry clinic. The results provide evidence for the validity of our instrument as a measure of health status in an HIV-infected psychiatric population. Overall symptoms were the strongest associates of functional limitations, disability, and perceived health, but depression was also significantly associated with all measures of QOL. Twenty-two patients (35.5%) would not have wanted to be revived if their heart stopped beating the day of the study. Disease stage and poor mental health were independent predictors of this preference, but severity of depression, social support, fatigue, perceived health, functional limitations, and life satisfaction were not. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT PSYCHIAT,BOSTON,MA 02215. RP LENDERKING, WR (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTATIST,BOSTON,MA 02115, USA. NR 27 TC 5 Z9 5 U1 2 U2 2 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0887-0446 J9 PSYCHOL HEALTH JI Psychol. Health PY 1994 VL 9 IS 1-2 BP 51 EP 64 DI 10.1080/08870449408407459 PG 14 WC Public, Environmental & Occupational Health; Psychology, Multidisciplinary SC Public, Environmental & Occupational Health; Psychology GA NB876 UT WOS:A1994NB87600004 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI THE PSYCHIATRIC MENTAL STATUS EXAMINATION - TRZEPACZ,PT, BAKER,RW SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GREENBERG, DB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JAN-FEB PY 1994 VL 35 IS 1 BP 94 EP 95 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MN516 UT WOS:A1994MN51600014 ER PT J AU RABINOWITZ, T AF RABINOWITZ, T TI PSYCHOPHARMACOLOGY OF PANIC - MONTGOMERY,SA SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RABINOWITZ, T (reprint author), MASSACHUSETTS GEN HOSP,AVERY D WEISMAN PSYCHIAT CONSULTAT SERV,BOSTON,MA, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JAN-FEB PY 1994 VL 35 IS 1 BP 95 EP 96 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MN516 UT WOS:A1994MN51600015 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI DEMENTIA - A CLINICAL APPROACH - CUMMINGS,JL, BENSON,DF SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GREENBERG, DB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JAN-FEB PY 1994 VL 35 IS 1 BP 97 EP 97 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MN516 UT WOS:A1994MN51600016 ER PT J AU FAVA, M BOUFFIDES, E PAVA, JA MCCARTHY, MK STEINGARD, RJ ROSENBAUM, JF AF FAVA, M BOUFFIDES, E PAVA, JA MCCARTHY, MK STEINGARD, RJ ROSENBAUM, JF TI PERSONALITY-DISORDER COMORBIDITY WITH MAJOR DEPRESSION AND RESPONSE TO FLUOXETINE TREATMENT SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Article DE MAJOR DEPRESSION; PERSONALITY DISORDER; FLUOXETINE; ANTIDEPRESSANT DRUGS ID STATE; PHARMACOTHERAPY; PLACEBO AB The relationship between depression and comorbid personality disorders is still poorly understood. The aims of this study were to examine differences in depression severity between depressed outpatients with and without comorbid personality disorders, to determine the effect of a fixed dose of fluoxetine on personality disorders, and to assess the predictive value of personality disorder diagnoses at baseline with regard to response to fluoxetine. Eighty-three outpatients with major depressive disorder (MDD) were assessed with a self-rating scale, the Personality Diagnostic Questionnaire-Revised (PDQ-R), before and after 8 weeks of treatment with fluoxetine 20 mg/day. The presence of a cluster B diagnosis before treatment predicted positive outcome as measured by the change in score on the modified 17-item Hamilton Rating Scale for Depression (HAM-D-17*). Following treatment, we found significant reductions in the frequency of most individual personality disorder diagnoses and total PDQ-R score. While patients no longer meeting criteria for cluster B personality disorders after treatment had similar reductions in depressive symptoms compared to those maintaining the diagnoses, subjects no longer meeting criteria for cluster A and cluster C diagnoses after treatment exhibited significantly greater decreases in depression severity than those who maintained the diagnoses. Overall, these results suggest that fluoxetine may be beneficial in the treatment of certain personality disorder traits in patients with MDD. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP FAVA, M (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WACC 815,PARKMAN ST,BOSTON,MA 02114, USA. NR 23 TC 70 Z9 70 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1994 VL 62 IS 3-4 BP 160 EP 167 PG 8 WC Psychiatry; Psychology SC Psychiatry; Psychology GA PP416 UT WOS:A1994PP41600003 PM 7846259 ER PT J AU AHLES, TA SILBERFARB, PM RUNDLE, AC HOLLAND, JC KORNBLITH, AB CANELLOS, GP GREEN, MR PERRY, MC AF AHLES, TA SILBERFARB, PM RUNDLE, AC HOLLAND, JC KORNBLITH, AB CANELLOS, GP GREEN, MR PERRY, MC TI QUALITY-OF-LIFE IN PATIENTS WITH LIMITED SMALL-CELL CARCINOMA OF THE LUNG RECEIVING CHEMOTHERAPY WITH OR WITHOUT RADIATION-THERAPY, FOR CANCER AND LEUKEMIA GROUP-B SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Article DE QUALITY OF LIFE; CARCINOMA OF THE LUNG; RADIOTHERAPY; CHEMOTHERAPY; SURVIVAL ID ACUTE LYMPHOCYTIC-LEUKEMIA; CRANIAL IRRADIATION; OF-LIFE; SURVIVORS AB Quality of life was assessed in 57 patients with limited small-cell carcinoma of the lung utilizing psychological scales that measured mood, functional status, and cognitive impairment. These patients received chemotherapy with or without radiotherapy to the primary tumor. All patients received prophylactic cranial radiation. Patients who received the combination of chemotherapy and radiotherapy to both the primary tumor and CNS had an increase in overall survival. However, because of the increased toxicity experienced by these patients, a decrease in quality of life was documented by measures of psychological distress when compared to patients receiving chemotherapy alone. The findings support the importance of utilizing quality of life measures in addition to measures of physical toxicity so that patients can make an informed choice regarding treatment options. C1 NORRIS COTTON CANC CTR,LEBANON,NH. GENENTECH INC,S SAN FRANCISCO,CA 94080. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. DANA FARBER CANC INST,BOSTON,MA. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. UNIV MISSOURI,ELLIS FISCHEL CANC CTR,COLUMBIA,MO. RP AHLES, TA (reprint author), DARTMOUTH HITCHCOCK MED CTR,CTR PSYCHOONCOL RES,1 MED CTR DR,LEBANON,NH 03756, USA. NR 19 TC 14 Z9 14 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1994 VL 62 IS 3-4 BP 193 EP 199 PG 7 WC Psychiatry; Psychology SC Psychiatry; Psychology GA PP416 UT WOS:A1994PP41600007 PM 7846263 ER PT J AU COPELAND, PM AF COPELAND, PM TI RENAL-FAILURE ASSOCIATED WITH LAXATIVE ABUSE SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Article DE LAXATIVES; BULIMIA NERVOSA; HYPOKALEMIA; RHABDOMYOLYSIS; ACUTE RENAL FAILURE ID ANOREXIA-NERVOSA; BULIMIA; RHABDOMYOLYSIS AB Eating disorder patients often abuse laxatives in an attempt to purge excess food. Laxative abuse can cause hypokalemia and volume depletion. Hypokalemia, in turn, can lead to rhabdomyolysis. Laxative-induced hypokalemia and volume depletion have been previously reported to cause renal insufficiency, but not severe enough to require hemodialysis. A 27-year-old woman with a long history of laxative abuse presented with severe renal failure associated with hypokalemia and volume depletion. She required acute hemodialysis for worsening acidosis (pH 7.05) despite assisted ventilation. A prior episode of hypokalemic rhabdomyolysis at age 23 had resulted in only mild renal insufficiency. Her later episode of severe renal failure was linked to profound volume depletion (blood urea nitrogen 135 mg/dl). This patient calls attention to a potentially life-threatening complication of laxative abuse and indicates that volume depletion can exacerbate laxative-associated renal failure. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP COPELAND, PM (reprint author), SALEM HOSP,EATING DISORDERS PROGRAM,SALEM,MA 01970, USA. NR 11 TC 15 Z9 16 U1 0 U2 7 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1994 VL 62 IS 3-4 BP 200 EP 202 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA PP416 UT WOS:A1994PP41600008 PM 7531354 ER PT J AU BALL, SG OTTO, MW AF BALL, SG OTTO, MW TI COGNITIVE-BEHAVIORAL TREATMENT OF CHOKING PHOBIA - 3 CASE-STUDIES SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Note DE CHOKING PHOBIA; COGNITIVE-BEHAVIORAL TREATMENT AB The present study describes 3 case examples of patients with choking phobia who were given a brief, cognitive-behavioral treatment that combined the interventions of psychoeducation, cognitive restructuring interoceptive and in vivo exposure. This program was designed to address fears of anxiety and choking sensations as well as fears of swallowing. The patients were treated for 11-13 sessions. All 3 patients responded to the program as measured by their progression on their food hierarchy and by weight gain. Issues in the treatment of these patients are discussed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CAMBRIDGE,MA. RP BALL, SG (reprint author), INDIANA UNIV,SCH MED,CLIN BLDG 291,541 CLIN DR,INDIANAPOLIS,IN 46202, USA. NR 6 TC 9 Z9 10 U1 0 U2 7 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1994 VL 62 IS 3-4 BP 207 EP 211 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA PP416 UT WOS:A1994PP41600010 PM 7846265 ER PT J AU PAVA, JA FAVA, M LEVENSON, JA AF PAVA, JA FAVA, M LEVENSON, JA TI INTEGRATING COGNITIVE THERAPY AND PHARMACOTHERAPY IN THE TREATMENT AND PROPHYLAXIS OF DEPRESSION - A NOVEL-APPROACH SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Note DE DEPRESSION; COGNITIVE THERAPY; DRUG THERAPY; NOVEL APPROACH ID COMPARATIVE EFFICACY; MAJOR DEPRESSION; COMBINATION; RELAPSE AB Psychiatric clinicians frequently prescribe biologic treatments such as antidepressant medication in combination with psychologic treatments such as psychotherapy. In the present article we propose a model integrating antidepressant treatment with Beck's cognitive therapy, a form of psychotherapy with established efficacy in the acute treatment of depression. We argue for adding cognitive therapy following successful pharmacological treatment, i.e., for spending cognitive therapy resources in the continuation phase of treatment, where they are most likely to make a unique and separate contribution to patient well-being, particularly in the areas of relapse prevention and treating residual symptoms. We encourage researchers to compare this treatment strategy to other approaches in terms of its ability to (1) prevent relapses and recurrences of depressive episodes, and (2) to impact positively on the overall quality of life in recovered depressed patients. RP PAVA, JA (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,DEPRESS RES PROGRAM,WACC 815,PARKMAN ST,BOSTON,MA 02114, USA. NR 29 TC 28 Z9 29 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1994 VL 61 IS 3-4 BP 211 EP 219 PG 9 WC Psychiatry; Psychology SC Psychiatry; Psychology GA NL593 UT WOS:A1994NL59300013 PM 8066160 ER PT J AU BRINK, JA KAMMER, B MUELLER, PR BALFE, DM PRIEN, EL FERRUCCI, JT AF BRINK, JA KAMMER, B MUELLER, PR BALFE, DM PRIEN, EL FERRUCCI, JT TI PREDICTION OF GALLSTONE COMPOSITION - SYNTHESIS OF CT AND RADIOGRAPHIC FEATURES IN-VITRO SO RADIOLOGY LA English DT Article DE CHOLESTEROL; COMPUTED TOMOGRAPHY (CT), TISSUE CHARACTERIZATION; GALLBLADDER, CALCULI; GALLBLADDER, CT; GALLBLADDER, RADIOGRAPHY ID CHOLESTEROL; INVITRO; INVIVO AB PURPOSE: To test a morphoradiographic algorithm designed to predict the composition of gallstones with use of computed tomography (CT) to define calcification patterns. MATERIALS AND METHODS: Two reviewers retrospectively evaluated the radiographic features of 120 separate in vitro specimens (59 radiopaque and 61 radiolucent), then classified the stones into several categories of composition with the algorithm. RESULTS: The most useful features for prediction of cholesterol composition were, in order of decreasing importance, stone shape, absence of dense calcification on plain radiographs, overall CT attenuation not higher than that of water, presence of a second generation of smaller stones, and a peripheral cover of calcification detected on CT scans of aging cholesterol stones. The greatest error occurred in distinction between stones with mixed composition (50%-79% cholesterol) and older stones with higher cholesterol content (80%-95% cholesterol). CONCLUSION: The range of qualitative CT appearances advances the possibility of predicting gallstone composition and potential outcome of nonsurgical treatment. C1 MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT MED SERV,BOSTON,MA. WASHINGTON UNIV,SCH MED,MALLINCKRODT INST RADIOL,ST LOUIS,MO. RP BRINK, JA (reprint author), MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT RADIOL,BOSTON,MA, USA. NR 18 TC 15 Z9 15 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JAN PY 1994 VL 190 IS 1 BP 69 EP 75 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MW253 UT WOS:A1994MW25300016 PM 8259431 ER PT J AU KOPANS, DB AF KOPANS, DB TI MAMMOGRAPHIC FOLLOW-UP TO DETECT BREAST-CANCER RECURRENCE AFTER CONSERVATIVE TREATMENT SO RADIOLOGY LA English DT Letter RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 1 TC 2 Z9 2 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JAN PY 1994 VL 190 IS 1 BP 286 EP 286 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MW253 UT WOS:A1994MW25300056 PM 8259422 ER PT S AU BEAL, MF AF BEAL, MF BE Racagni, G Brunello, N Langer, SZ TI MOLECULAR MECHANISMS OF EXCITOTOXICITY SO RECENT ADVANCES IN THE TREATMENT OF NEURODEGENERATIVE DISORDERS AND COGNITIVE DYSFUNCTION SE INTERNATIONAL ACADEMY FOR BIOMEDICAL AND DRUG RESEARCH LA English DT Proceedings Paper CT Collegium-Internationale-Neuro-Psychopharmacologicum Presidents Workshop on Recent Advances in the Treatment of Neurodegenerative Disorders and Cognitive Dysfunction CY MAY 01-03, 1993 CL CAPRI, ITALY SP COLLEGIUM INT NEURO PSYCHOPHARM RP BEAL, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,WARREN 408,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 1019-2029 BN 3-8055-5838-4 J9 INT ACAD B JI Int.Acad.Biomed.Drug Res. PY 1994 VL 7 BP 102 EP 111 PG 10 WC Neurosciences; Pathology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pathology; Pharmacology & Pharmacy GA BA44A UT WOS:A1994BA44A00015 ER PT S AU CALDERWOOD, SB AF CALDERWOOD, SB BE Karmali, MA Goglio, AG TI SECTION-II OVERVIEW - TOXIN STRUCTURE-FUNCTION, RECEPTORS, CELL BIOLOGY SO RECENT ADVANCES IN VEROCYTOTOXIN-PRODUCING ESCHERICHIA COLI INFECTIONS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 2nd International Symposium and Workshop on Verocytotoxin (Shiga-like toxin)-producing Escherichia Coli infections CY JUN 27-30, 1994 CL BERGAMO, ITALY SP ASSOC MICROBIOL CLIN ITALIANI, HOSPIT SICK CHILDREN, RES INST, TORONTO, CANADA, OSPEDALI RIUNITI, BERGAMO, ITALY, IST RIC FARMACOL MARIO NEGRI, BERGAMO, ITALY, IST SUPER SANITA, ROMA, ITALY, LOIS JOY GALLER FDN HEMOLYT UREM SYNDROME INC, NY C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. NR 0 TC 4 Z9 4 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 0-444-81840-5 J9 INT CONGR SER PY 1994 VL 1072 BP 119 EP 122 PG 4 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA BC58C UT WOS:A1994BC58C00028 ER PT S AU RUSKIN, JN AF RUSKIN, JN BE Hayakawa, H Kanno, M Mandel, WJ TI THE UNITED-STATES PERSPECTIVE ON DRUG TREATMENT FOR LETHAL ARRHYTHMIAS SO RECENT DEVELOPMENTS IN THE MANAGEMENT OF ARRHYTHMIAS SE ROYAL SOCIETY OF MEDICINE INTERNATIONAL CONGRESS AND SYMPOSIUM SERIES LA English DT Proceedings Paper CT Symposium on Recent Developments in the Management of Arrhythmias CY NOV 11-12, 1993 CL ATLANTA, GA SP WARNER LAMBERT KK, JAPAN C1 MASSACHUSETTS GEN HOSP,CARDIAC ARRHYTHMIA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ROYAL SOC MEDICINE PRESS LTD PI LONDON PA 1 WIMPOLE STREET, LONDON, ENGLAND W1M 8AE SN 0142-2367 BN 1-85315-216-1 J9 ROY SOC MED INT CONG PY 1994 IS 207 BP 79 EP 85 PG 7 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA BC21N UT WOS:A1994BC21N00011 ER PT S AU BONNERWEIR, S AF BONNERWEIR, S BE Bardin, CW TI REGULATION OF PANCREATIC BETA-CELL MASS IN-VIVO SO RECENT PROGRESS IN HORMONE RESEARCH, VOL 49 SE RECENT PROGRESS IN HORMONE RESEARCH LA English DT Article; Proceedings Paper CT 1992 Laurentian Hormone Conference CY NOV 14-18, 1992 CL PR SP MERCK SHARP & DOHME, POPULAT COUNCIL ID GROWTH FACTOR-I; MESSENGER RIBONUCLEIC-ACID; REGENERATING RAT PANCREAS; INVIVO GLUCOSE INFUSIONS; INSULIN-SECRETION; B-CELL; DIABETIC RATS; MORPHOMETRIC QUANTITATION; PLACENTAL-LACTOGEN; GENE-EXPRESSION RP BONNERWEIR, S (reprint author), HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,ELLIOT P JOSLIN RES LAB,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK-35449, DK-36836, DK-44523] NR 76 TC 111 Z9 114 U1 0 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0079-9963 BN 0-12-571149-2 J9 RECENT PROG HORM RES PY 1994 VL 49 BP 91 EP 104 PG 14 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BB16S UT WOS:A1994BB16S00004 PM 8146438 ER PT J AU KOLAKOWSKI, LF AF KOLAKOWSKI, LF TI GCRDB - A G-PROTEIN-COUPLED RECEPTOR DATABASE SO RECEPTORS & CHANNELS LA English DT Review DE SEQUENCE DATABASE; RECEPTOR FAMILIES; PROTEIN ANALYSIS ID SEQUENCES; RHODOPSIN; PATTERNS; CLONING; PEPTIDE; DISEASE; GENE AB G-protein-coupled receptors (GCRs) are a very large protein family and are critical components in many different autocrine, paracrine and endocrine signaling systems in animals. Current estimates are that humans have several thousand GCRs encoded by only slightly fewer genes. I have developed GCRDb, a database of sequences and other data relevant to the study of the biology of the receptors. The database implementation, data collection, and query system are described. An integral component of the design of GCRDb is the classification of GCRs in families. The current composition of GCRDb is presented in a table showing the number of entries in each family and group as derived from accepted mutation parsimony analyses. RP KOLAKOWSKI, LF (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL UNIT,BOSTON,MA 02129, USA. NR 23 TC 312 Z9 313 U1 4 U2 22 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1060-6823 J9 RECEPTOR CHANNEL JI Recept. Channels PY 1994 VL 2 IS 1 BP 1 EP 7 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NT283 UT WOS:A1994NT28300001 PM 8081729 ER PT J AU YOUNG, LHY GRAGOUDAS, ES AF YOUNG, LHY GRAGOUDAS, ES TI MACULAR UVEAL MELANOMA TREATED WITH PROTON-BEAM IRRADIATION - 10-YEAR FOLLOW-UP OBSERVATION WITH HISTOPATHOLOGIC CORRELATION SO RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES LA English DT Article DE MACULAR UVEAL MELANOMA; PROTON BEAM IRRADIATION AB Background: Although patients with choroidal melanoma within 3 mm of both the optic nerve and fovea are at higher risk for visual loss after proton beam irradiation, half of the patients in this study with visual acuity better than 20/200 before treatment maintained this level of vision for at least 2 years. Findings at a 10-year follow-up examination of a patient with macular uveal melanoma treated with proton beam irradiation are presented. Methods: A 65-year-old woman with macular uveal melanoma in one eye and optic atrophy in the fellow eye was treated with proton beam irradiation and evaluated for 10 years. The clinical course and histopathologic findings are presented. Results: The patient had optic atrophy in the fellow eye with visual acuity of 20/200, but maintained reading vision with the irradiated eye until she died of cardiac arrest, Histopathologic examination of the tumor-bearing eye showed a pigmented choroidal mass involving the macula. The mass consisted of plump spindle-shaped cells with small nuclei and indistinct nucleoli and a large number of pigment-laden macrophages. Conclusion: It is demonstrated that long-term useful vision can be preserved in patients afflicted with macular uveal melanoma after proton beam irradiation. RP YOUNG, LHY (reprint author), MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0275-004X J9 RETINA-J RET VIT DIS JI Retin.-J. Retin. Vitr. Dis. PY 1994 VL 14 IS 1 BP 43 EP 46 PG 4 WC Ophthalmology SC Ophthalmology GA NE115 UT WOS:A1994NE11500010 PM 8016461 ER PT J AU HU, LK HUH, K GRAGOUDAS, ES YOUNG, LHY AF HU, LK HUH, K GRAGOUDAS, ES YOUNG, LHY TI ESTABLISHMENT OF PIGMENTED CHOROIDAL MELANOMAS IN A RABBIT MODEL SO RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES LA English DT Article DE PIGMENTED CHOROIDAL MELANOMA; ANIMAL MODEL AB Purpose: To establish an animal model of pigmented choroidal melanoma. Methods: Four melanoma cell lines originally isolated from melanotic tumors (B16F10, RPMI 1846, OCM 1, and IIB) were used to establish choroidal melanomas in 105 rabbits; 88 animals were immunosuppressed with cyclosporine. Tumor cells were implanted transclerally and examined with indirect ophthalmoscopy, ultrasound, and photography. Results: Characteristic growth patterns were noted for each cell line. Animal cell lines typically produced choroidal tumors 3 to 4 mm in height within 2 weeks; human cell lines took an additional 7 to 10 days to achieve tumors of similar height. Tumors of heaviest pigmentation were generated consistently with the B16F10 cells, and with the other three cell lines only mild pigmentation was observed. Tumor shape varied depending on the source of implantation: diffuse, flat tumors were observed when cell suspensions were implanted, and nodular tumors were obtained with tumor fragments. Histopathologically, lesions were highly cellular, with rich vascularity and large numbers of mitotic figures. Conclusion: As the majority of human uveal melanomas are pigmented, the added feature of pigmentation associated with this model makes it more suitable for evaluating the role of newly developed phototherapies in the management of uveal melanoma. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,243 CHARLES ST,BOSTON,MA 02114. FU NCRR NIH HHS [SOJRR0548528] NR 0 TC 30 Z9 34 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0275-004X J9 RETINA-J RET VIT DIS JI Retin.-J. Retin. Vitr. Dis. PY 1994 VL 14 IS 3 BP 264 EP 269 DI 10.1097/00006982-199414030-00014 PG 6 WC Ophthalmology SC Ophthalmology GA PC419 UT WOS:A1994PC41900012 PM 7973123 ER PT B AU PARRISH, JA AF PARRISH, JA BE Grundfest, WS TI LASER TECHNOLOGY IN THE COST OF HEALTH CARE SO ROLE OF TECHNOLOGY IN THE COST OF HEALTH CARE: HEALTH CARE TECHNOLOGY POLICY I SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Health Care Technology Policy I - The Role of Technology in the Cost of Health Care CY APR 27-29, 1994 CL ARLINGTON, VA SP IEEE, USA ACTIV BOARD, WHITAKER FDN, MEDALLIONS CHARITABLE FUND, SOC PHOTO OPT INSTRUMENTAT ENGINEERS, HAMAMATSU CORP C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,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 0-8194-1631-2 J9 P SOC PHOTO-OPT INS PY 1994 VL 2307 BP 132 EP 133 DI 10.1117/12.195441 PG 2 WC Health Policy & Services SC Health Care Sciences & Services GA BC03K UT WOS:A1994BC03K00015 ER PT J AU SAZON, DA SHARMA, O SANTIAGO, S WILLIAMS, AJ AF SAZON, DA SHARMA, O SANTIAGO, S WILLIAMS, AJ TI FLUORODEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY IN PULMONARY SARCOIDOSIS SO SARCOIDOSIS LA English DT Article ID LAVAGE RP SAZON, DA (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VET ADM MED CTR, SCH MED, DIV PULM & CRIT CARE, LOS ANGELES, CA USA. NR 5 TC 4 Z9 4 U1 0 U2 0 PU PCA-PUBLISHING COMMUNICATION ADVERTISING PI MILAN PA VIA CLERICI 12, 20032 MILAN, ITALY SN 0393-1447 J9 SARCOIDOSIS JI Sarcoidosis PD JAN PY 1994 VL 11 SU 1 BP 363 EP 367 PG 5 WC Respiratory System SC Respiratory System GA NJ447 UT WOS:A1994NJ44700076 ER PT J AU CLOUD, ML OFFEN, W AF CLOUD, ML OFFEN, W TI CONTINUOUS INFUSIONS OF NIZATIDINE ARE SAFE AND EFFECTIVE IN THE TREATMENT OF INTENSIVE-CARE UNIT PATIENTS AT RISK FOR STRESS GASTRITIS SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY LA English DT Article; Proceedings Paper CT Round-Table Meeting on Nizatidine - A Clinical Up-Date, Including a Quality of Life Perspective CY OCT, 1993 CL LONDON, ENGLAND DE ANTACID; CONTINUOUS INFUSIONS; GASTRIC ASPIRATE PH; NIZATIDINE; PLACEBO; STRESS GASTRITIS; UPPER GASTROINTESTINAL BLEEDING ID CRITICALLY ILL PATIENT; ULCER PROPHYLAXIS; DUODENAL-ULCER; DOUBLE-BLIND; CIMETIDINE; RANITIDINE; DISEASE; TRIAL; PH; MULTICENTER AB This multicentre, randomized, parallel, double-blind study compared the safety and efficacy of nizatidine 20 and 10 mg/h with placebo. The objective was to maintain gastric pH > 4 in seriously ill patients at risk for stress gastritis. Gastric aspirate was obtained at 2-h intervals through a nasogastric tube after beginning study drug, and tested for pH and the presence of blood. Antacid doses (15 ml per dose) were individually adjusted and administered whenever the gastric pH was < 4. Significant gastrointestinal bleeding was assessed clinically by Hemmocult(R) results, presence of frank bleeding from the GI tract, number of transfusions and vital signs. One hundred and twenty-six patients, 43 nizatidine 20 mg/h, 43 nizatidine 10 mg/h and 40 placebo were admitted to the study. For the treatment period, patients treated with either dose of nizatidine required significantly less antacid than placebo treated patients to maintain gastric acid pH greater than or equal to 4 (median total: 45 ml versus 180 ml, p < 0.001). Adverse clinical and laboratory events were similar or less frequent in the nizatidine groups compared with placebo. Nosocomial pneumonia occurred with very low frequency in all treatment groups. C1 UNIV CALIF SAN DIEGO,MED CTR,SAN DIEGO,CA 92103. ST PAUL RAMSEY MED CTR,ST PAUL,MN 55101. RUTGERS STATE UNIV,COOPER HOSP,MED CTR,CAMDEN,NJ. BLAKE MEM HOSP,HCALW,BRADENTON,FL. UNIV SO ALABAMA,MOBILE,AL 36688. UNIV MARYLAND,CTR TRAUMA,BALTIMORE,MD. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HENRY FORD HOSP,DETROIT,MI 48202. UNIV TEXAS,CTR HLTH & SCI,HOUSTON,TX. RP CLOUD, ML (reprint author), ELI LILLY & CO,LILLY CORP CTR,LILLY RES LABS,DROP 2146,INDIANAPOLIS,IN 46285, USA. NR 24 TC 1 Z9 1 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5521 J9 SCAND J GASTROENTERO JI Scand. J. Gastroenterol. PY 1994 VL 29 SU 206 BP 29 EP 34 DI 10.3109/00365529409091418 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA PX124 UT WOS:A1994PX12400007 ER PT J AU KANE, JM MARDER, SR AF KANE, JM MARDER, SR TI CLOZAPINE - BENEFITS AND RISKS - REPLY SO SCHIZOPHRENIA BULLETIN LA English DT Letter C1 ALBERT EINSTEIN COLL MED,GLEN OAKS,NY 11004. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90073. RP KANE, JM (reprint author), LONG ISL JEWISH MED CTR,HILLSIDE HOSP,DEPT PSYCHIAT,GLEN OAKS,NY 11004, USA. NR 2 TC 3 Z9 3 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1994 VL 20 IS 1 BP 23 EP 24 PG 2 WC Psychiatry SC Psychiatry GA MY468 UT WOS:A1994MY46800004 ER PT J AU GREEN, MF SATZ, P CHRISTENSON, C AF GREEN, MF SATZ, P CHRISTENSON, C TI MINOR PHYSICAL ANOMALIES IN SCHIZOPHRENIA-PATIENTS, BIPOLAR PATIENTS, AND THEIR SIBLINGS SO SCHIZOPHRENIA BULLETIN LA English DT Article ID ADULT SCHIZOPHRENIA; PRENATAL EXPOSURE; INFLUENZA; CLASSIFICATION; DISORDERS; CHILDREN; ETIOLOGY; EPIDEMIC AB Minor physical anomalies (MPAs) are believed to reflect abnormalities in fetal neurodevelopment. Several studies have shown that schizophrenia patients have more MPAs than normal controls, but little is known about the meaning of this increased rate of MPAs. The current study first attempted to determine whether the increased MPAs are associated with schizophrenia in particular or with psychosis in general. Second, the study tested whether the patients' siblings also show an increased rate of MPAs by assessing MPAs in schizophrenia patients, bipolar manic patients, the siblings from each group of patients, and normal controls. The schizophrenia patients had significantly more MPAs than normal controls and bipolar patients. The rate of MPAs in bipolar patients did not differ from normal controls. This pattern suggests that MPAs have some degree of specificity to schizophrenia. Both sibling groups had fewer MPAs than the patients, and this difference was significant for the comparison between schizophrenia patients and their siblings. When viewed within a vulnerability-stress model, the results are consistent with the theory that MPAs may reflect early, largely extra-genetic, stressful events. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. FU NIMH NIH HHS [MH-43292] NR 30 TC 116 Z9 117 U1 2 U2 2 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1994 VL 20 IS 3 BP 433 EP 440 PG 8 WC Psychiatry SC Psychiatry GA PB173 UT WOS:A1994PB17300004 PM 7973464 ER PT J AU DAVIDSON, M HAROUTUNIAN, V GABRIEL, SM POWCHIK, P HARVEY, PD MOHS, RC DAVIS, KL AF DAVIDSON, M HAROUTUNIAN, V GABRIEL, SM POWCHIK, P HARVEY, PD MOHS, RC DAVIS, KL TI COGNITIVE IMPAIRMENT IN ELDERLY SCHIZOPHRENIC-PATIENTS SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT 116A,BRONX,NY 10468. NR 0 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1994 VL 11 IS 2 BP 162 EP 163 PG 2 WC Psychiatry SC Psychiatry GA MT535 UT WOS:A1994MT53500203 ER PT J AU SALLES, G SHIPP, MA COIFFIER, B AF SALLES, G SHIPP, MA COIFFIER, B TI CHEMOTHERAPY OF NON-HODGKINS AGGRESSIVE LYMPHOMAS SO SEMINARS IN HEMATOLOGY LA English DT Review ID LARGE-CELL LYMPHOMA; BONE-MARROW TRANSPLANTATION; DIFFUSE HISTIOCYTIC LYMPHOMA; SOUTHWEST-ONCOLOGY-GROUP; HIGH-DOSE THERAPY; COLONY-STIMULATING FACTOR; TERM FOLLOW-UP; NERVOUS-SYSTEM COMPLICATIONS; BRIEF-DURATION CHEMOTHERAPY; POPULATION-BASED REGISTRY C1 UNIV CLAUDE BERNARD,HOSP CIVILS LYON,SERV HEMATOL,PARIS,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. NR 207 TC 39 Z9 39 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD JAN PY 1994 VL 31 IS 1 BP 46 EP 69 PG 24 WC Hematology SC Hematology GA MR066 UT WOS:A1994MR06600005 PM 8122135 ER PT J AU GROSSBARD, ML NADLER, LM AF GROSSBARD, ML NADLER, LM TI IMMUNOTOXIN THERAPY OF LYMPHOID NEOPLASMS SO SEMINARS IN HEMATOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; B-CELL LYMPHOMA; PHASE-I TRIAL; CHRONIC LYMPHOCYTIC-LEUKEMIA; RICIN-A-CHAIN; MONOCLONAL-ANTIBODY; LYMPHOBLASTIC-LEUKEMIA; IMMUNOCONJUGATE; INTERLEUKIN-2; SEROTHERAPY C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. FU NCI NIH HHS [CA34183, 1K12CA01730] NR 46 TC 17 Z9 17 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD JAN PY 1994 VL 31 IS 1 BP 88 EP 97 PG 10 WC Hematology SC Hematology GA MR066 UT WOS:A1994MR06600007 PM 8122137 ER PT J AU GLASS, WF TROYER, DA KREISBERG, JI AF GLASS, WF TROYER, DA KREISBERG, JI TI REGULATION OF MESANGIAL CELL-FUNCTION BY THROMBIN SO SEMINARS IN THROMBOSIS AND HEMOSTASIS LA English DT Article ID EXTRACELLULAR-MATRIX; CYCLIC-AMP; TYROSINE PHOSPHORYLATION; PROTEIN-KINASE; SHAPE CHANGE; RECEPTOR; ADHESION; CAMP; TRANSFORMATION; FIBROBLASTS C1 UNIV TEXAS, HLTH SCI CTR, DEPT PATHOL, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP GLASS, WF (reprint author), UNIV VIRGINIA, HLTH SCI CTR, DEPT PATHOL, BOX 214, CHARLOTTESVILLE, VA 22908 USA. FU NIDDK NIH HHS [DK29787, DK46735, DK34234] NR 39 TC 1 Z9 1 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0094-6176 J9 SEMIN THROMB HEMOST JI Semin. Thromb. Hemost. PY 1994 VL 20 IS 4 BP 333 EP 338 DI 10.1055/s-2007-1001923 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA PW767 UT WOS:A1994PW76700006 PM 7899864 ER PT B AU TALAL, N AF TALAL, N BE Homma, M Sugai, S Tojo, T Miyasaka, N Akizuki, M TI SUMMARY - IV INTERNATIONAL-SYMPOSIUM ON SJOGRENS-SYNDROME SO SJOGREN'S SYNDROME: STATE OF THE ART LA English DT Proceedings Paper CT 4th International Symposium on Sjogrens Syndrome CY AUG 11-13, 1993 CL TOKYO, JAPAN C1 AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. 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 90-6299-107-6 PY 1994 BP 93 EP 98 PG 6 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BB01Y UT WOS:A1994BB01Y00018 ER PT J AU BARRACK, RL TANZER, M KATTAPURAM, SV HARRIS, WH AF BARRACK, RL TANZER, M KATTAPURAM, SV HARRIS, WH TI THE VALUE OF CONTRAST ARTHROGRAPHY IN ASSESSING LOOSENING OF SYMPTOMATIC UNCEMENTED TOTAL HIP COMPONENTS SO SKELETAL RADIOLOGY LA English DT Article DE ARTHROGRAPHY; UNCEMENTED LOOSENING; TOTAL HIP REPLACEMENT ID ARTHROPLASTY; REPLACEMENT; PAIN AB Twenty-five patients with symptomatic uncemented total hip components were studied with contrast arthrography prior to surgical exploration. All but one had uncemented femoral stems and 16 had an uncemented acetabular component. As judged by the findings at surgery, on the femoral side the sensitivity, specificity, and accuracy of arthrography were 57%, 60%, and 58% respectively. There was a relatively high incidence of both false positives (17%) and false negatives (25%). On the acetabular side sensitivity, specificity, and accuracy were 29%, 89%, and 62.5%. False negatives were common (31%), while there was only one false positive. The results in this small series show that arthrography has distinct limitations in identifying the fixation status of uncemented total hip components. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. NR 22 TC 15 Z9 15 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2348 J9 SKELETAL RADIOL JI Skeletal Radiol. PD JAN PY 1994 VL 23 IS 1 BP 37 EP 41 PG 5 WC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging SC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging GA MU587 UT WOS:A1994MU58700006 PM 8160035 ER PT J AU STOECKLE, JD AF STOECKLE, JD TI THE LAST TENEMENT, CONFRONTING COMMUNITY AND URBAN-RENEWAL ON BOSTON WEST END - FISHER,SM, HUGHES,C SO SOCIAL SCIENCE & MEDICINE LA English DT Book Review RP STOECKLE, JD (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0277-9536 J9 SOC SCI MED JI Soc. Sci. Med. PD JAN PY 1994 VL 38 IS 1 BP 198 EP 199 PG 2 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA MK270 UT WOS:A1994MK27000025 ER PT B AU ARYSTARKHOVA, E SWEADNER, KJ AF ARYSTARKHOVA, E SWEADNER, KJ BE Bamberg, E Schoner, W TI DIFFERENTIAL EXPRESSION OF NA+/K+-ATPASE ISOFORMS IN CULTURED RODENT CARDIAC AND SKELETAL-MUSCLE CELLS SO SODIUM PUMP: STRUCTURE MECHANISM, HORMONAL CONTROL AND ITS ROLE IN DISEASE LA English DT Proceedings Paper CT 7th International Conference on The Sodium Pump, organized as the 105th Conference of the Gesellschaft-fur-Biologische-Chemie CY SEP 05-11, 1993 CL TODTMOOS, GERMANY SP GESELL BIOL CHEM C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU DR DIETRICH STEINKOPFF VERLAG PI BERLIN 33 PA C/O SPRINGER VERLAG, HEIDELBERGER PLATZ 3, 1000 BERLIN 33, GERMANY BN 3-7985-0961-1 PY 1994 BP 230 EP 233 PG 4 WC Cell Biology SC Cell Biology GA BB12E UT WOS:A1994BB12E00040 ER PT B AU HAUPERT, GT AF HAUPERT, GT BE Bamberg, E Schoner, W TI STRUCTURE AND BIOLOGICAL-ACTIVITY OF THE NA+/K+-ATPASE INHIBITOR ISOLATED FROM BOVINE HYPOTHALAMUS - DIFFERENCE FROM OUABAIN SO SODIUM PUMP: STRUCTURE MECHANISM, HORMONAL CONTROL AND ITS ROLE IN DISEASE LA English DT Proceedings Paper CT 7th International Conference on The Sodium Pump, organized as the 105th Conference of the Gesellschaft-fur-Biologische-Chemie CY SEP 05-11, 1993 CL TODTMOOS, GERMANY SP GESELL BIOL CHEM C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL UNIT,BOSTON,MA 02129. NR 0 TC 6 Z9 6 U1 0 U2 0 PU DR DIETRICH STEINKOPFF VERLAG PI BERLIN 33 PA C/O SPRINGER VERLAG, HEIDELBERGER PLATZ 3, 1000 BERLIN 33, GERMANY BN 3-7985-0961-1 PY 1994 BP 732 EP 742 PG 11 WC Cell Biology SC Cell Biology GA BB12E UT WOS:A1994BB12E00133 ER PT J AU AMBROSE, CM DUYAO, MP BARNES, G BATES, GP LIN, CS SRINIDHI, J BAXENDALE, S HUMMERICH, H LEHRACH, H ALTHERR, M WASMUTH, J BUCKLER, A CHURCH, D HOUSMAN, D BERKS, M MICKLEM, G DURBIN, R DODGE, A READ, A GUSELLA, J MACDONALD, ME AF AMBROSE, CM DUYAO, MP BARNES, G BATES, GP LIN, CS SRINIDHI, J BAXENDALE, S HUMMERICH, H LEHRACH, H ALTHERR, M WASMUTH, J BUCKLER, A CHURCH, D HOUSMAN, D BERKS, M MICKLEM, G DURBIN, R DODGE, A READ, A GUSELLA, J MACDONALD, ME TI STRUCTURE AND EXPRESSION OF THE HUNTINGTONS-DISEASE GENE - EVIDENCE AGAINST SIMPLE INACTIVATION DUE TO AN EXPANDED CAG REPEAT SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID TRINUCLEOTIDE REPEAT; CANDIDATE REGION; DNA MARKERS; LENGTH; LOCUS AB Huntington's disease, a neurodegenerative disorder characterized by loss of stratal neurons, is caused by an expanded, unstable trinucleotide repeat in a novel 4p16.3 gene. To lay the foundation for exploring the pathogenic mechanism in HD, we have determined the structure of the disease gene and examined its expression. The HD locus spans 180 kb and consists of 67 exons ranging in size from 48 bp to 341 bp with an average of 138 bp. Scanning of the HD transcript failed to reveal any additional sequence alterations characteristic of HD chromosomes. A codon loss polymorphism in linkage disequilibrium with the disorder revealed that both normal and HD alleles are represented in the mRNA population in HD heterozygotes, indicating that the defect does not eliminate transcription. The gene is ubiquitously expressed as two alternatively polyadenylated forms displaying different relative abundance in various fetal and adult tissues, suggesting the operation of interacting factors in determining specificity of cell loss. The HD gene was disrupted in a female carrying a balanced translocation with a breakpoint between exons 40 and 41. The absence of any abnormal phenotype in this individual argues against simple inactivation of the gene as the mechanism by which the expanded trinucleotide repeat causes HD. Taken together; these observations suggest that the dominant HD mutation either confers a new property on the mRNA or, more likely, alters an interaction at the protein level. C1 IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. SANGER CTR,CAMBRIDGE CB10 1RQ,CAMBS,ENGLAND. ST MARYS HOSP,DEPT MED GENET,MANCHESTER M13 0JH,LANCS,ENGLAND. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. RP AMBROSE, CM (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114, USA. RI Bates, Gillian/E-1146-2012 OI Bates, Gillian/0000-0002-4041-6305 FU NINDS NIH HHS [NS16367]; Wellcome Trust NR 23 TC 174 Z9 178 U1 1 U2 16 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD JAN PY 1994 VL 20 IS 1 BP 27 EP 38 DI 10.1007/BF02257483 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA NM895 UT WOS:A1994NM89500003 PM 8197474 ER PT J AU LIPSITZ, SR ZHAO, LP AF LIPSITZ, SR ZHAO, LP TI ESTIMATION IN CONTINGENCY-TABLES WITH GIVEN MARGINALS SO STATISTICIAN LA English DT Article DE CONTINGENCY TABLE; ITERATIVE PROPORTIONAL FITTING; LINEAR MODEL; MARGINAL CONSTRAINTS ID CATEGORICAL-DATA AB Pelz and Good showed how several methods of estimating cell probabilities in contingency tables with known marginal probabilities can be expressed in terms of optimizing additive objective functions (such as the log-likelihood or minimum chi2). They used constrained optimization with Lagrange multipliers to obtain the estimates from the objective function. In this paper, we show that, by linearly transforming the parameter space of the cell probabilities, the estimates from any of the objective functions can be obtained without the need for constrained optimization. Then, commonly used statistical packages can be used to estimate the cell probabilities without the need for constrained optimization. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. UNIV HAWAII,HONOLULU,HI 96822. NR 10 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0039-0526 J9 STATISTICIAN JI Statistician PY 1994 VL 43 IS 2 BP 223 EP 230 DI 10.2307/2348339 PG 8 WC Statistics & Probability SC Mathematics GA NN465 UT WOS:A1994NN46500001 ER PT J AU MCLAREN, CE LEGLER, JM BRITTENHAM, GM AF MCLAREN, CE LEGLER, JM BRITTENHAM, GM TI THE GENERALIZED CHI(2) GOODNESS-OF-FIT TEST SO STATISTICIAN LA English DT Article DE ANEMIA; PEARSON CHI(2)-TEST; POWER DIVERGENCE STATISTIC; RED BLOOD CELL VOLUME DISTRIBUTIONS ID EXPECTATION-MAXIMIZATION ALGORITHM; IRON-DEFICIENCY ANEMIA; VOLUME DISTRIBUTIONS; GROUPED DATA; RED AB Because the power of the chi2 goodness-of-fit test depends on sample size, small and unimportant departures from a specified theoretical distribution may be detected with large samples. To adjust for data with extremely large sample sizes, a generalization of the chi2-test was developed that tests for the equality of an observed and fitted distribution to within a specified amount. Procedures for estimating the true amount of lack of fit between two distributions and for a calculation of the power of the generalized chi2-test under specified alternatives were devised. These techniques were applied to the analysis of red blood cell volume distributions in healthy individuals and patients with anaemia. To be consistent with the physiology of red blood cell production, the explicit models examined were a single log-normal distribution and a mixture of two log-normal distributions. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. MOORHEAD STATE UNIV,DEPT MATH,MOORHEAD,MN 56560. NR 26 TC 7 Z9 7 U1 1 U2 2 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0039-0526 J9 STATISTICIAN JI Statistician PY 1994 VL 43 IS 2 BP 247 EP 258 DI 10.2307/2348342 PG 12 WC Statistics & Probability SC Mathematics GA NN465 UT WOS:A1994NN46500004 ER PT J AU NATHAN, DG AF NATHAN, DG TI STUDIES OF HYBRID HEMATOPOIETIC GROWTH-FACTOR RECEPTORS SO STEM CELLS LA English DT Article DE GROWTH FACTOR RECEPTOR; ERYTHROPOIETIN; GM-CSF; SIGNALING PROLIFERATION ID COLONY-STIMULATING FACTOR; EXPRESSION CLONING; GM-CSF; ERYTHROPOIETIN RECEPTOR; SIGNAL-TRANSDUCTION; BETA-SUBUNIT; ALPHA-CHAIN; DOMAINS AB To gain further insight into the mechanisms by which both granulocyte-macrophage-colony stimulating factor (GM-CSF) and erythropoietin receptors function, we have utilized a GM-CSP erythropoietin hybrid receptor with GM-CSF as the external domain and erythropoietin as the intracellular domain. Results show that the beta common GM-CSF receptor both enhances the affinity binding of GM-CSF to the receptor and plays an important role in signaling through the receptor. A truncated form of the beta common receptor actually acts as a dominant negative regulatory factor. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP NATHAN, DG (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01CA45559]; NHLBI NIH HHS [P01HL32262] NR 15 TC 1 Z9 1 U1 0 U2 0 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 1066-5099 J9 STEM CELLS JI Stem Cells PY 1994 VL 12 SU 1 BP 27 EP 35 PG 9 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA PY200 UT WOS:A1994PY20000006 PM 7696966 ER PT J AU DRANOFF, G MULLIGAN, RC AF DRANOFF, G MULLIGAN, RC TI ACTIVITIES OF GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR REVEALED BY GENE-TRANSFER AND GENE KNOCKOUT STUDIES SO STEM CELLS LA English DT Article DE GM-CSF; GENE THERAPY; TUMOR VACCINE; KNOCKOUT; SURFACTANT; RETROVIRUS ID TUMOR-NECROSIS-FACTOR; PULMONARY ALVEOLAR PROTEINOSIS; LASTING ANTITUMOR IMMUNITY; MURINE GM-CSF; LANGERHANS CELLS; DENDRITIC CELLS; FACTOR-ALPHA; REDUCED TUMORIGENICITY; EXPRESSION; SURFACTANT AB We used retroviral mediated gene transfer and gene knockout technologies to explore the in vivo functions of murine granulocyte-macrophage colony-stimulating factor (GM-CSF) [1, 2]. In tumor vaccination experiments, GM-CSP was the most potent molecule of a large number of cytokines, adhesion molecules and other immunomodulators for the induction of specific and long-lasting anti-tumor immunity. Vaccination required activities of both CD4 and CDS positive lymphocytes, and likely involved the augmentation by GM-CSF of host professional antigen-presenting cell function. Mice engineered by homologous recombination techniques in embryonic stem cells to lack GM-CSF demonstrated no significant perturbations in steady-state hematopoiesis. All mutant animals, however, developed the accumulation of surfactant proteins and lipids in the alveolar space, the defining feature of the idiopathic human disorder pulmonary alveolar proteinosis. Surfactant lipid and protein content were increased in the absence of alterations in surfactant protein mRNA, supporting the concept that surfactant clearance or catabolism was perturbed. Extensive lymphoid hyperplasia associated with lung airways and blood vessels was also found, yet no infectious agents could be isolated. These results demonstrate that GM-CSF is not an essential growth factor for basal hematopoiesis and reveal an unexpected, critical role for GM-CSF in pulmonary homeostasis. It is tempting to speculate that the ability of GM-CSF to modulate the uptake and processing of particulate material underlies the mechanisms of immunostimulation and surfactant accumulation. C1 HARVARD UNIV,SCH MED,BOSTON,MA. MIT,DEPT BIOL,CAMBRIDGE,MA. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. RP DRANOFF, G (reprint author), DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 65 TC 40 Z9 41 U1 1 U2 1 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 1066-5099 J9 STEM CELLS JI Stem Cells PY 1994 VL 12 SU 1 BP 173 EP 184 PG 12 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA PY200 UT WOS:A1994PY20000018 PM 7696961 ER PT J AU METCALF, D WILLIAMS, DA BEGLEY, G WARNER SHERIDAN HAWLEY, RG KRIEGER DRANOFF, G STANLEY, ER BONAFE TESTA GIANELLABORRADORI, A RAK REVOLTELLA MURPHY, MJ MARMONT AF METCALF, D WILLIAMS, DA BEGLEY, G WARNER SHERIDAN HAWLEY, RG KRIEGER DRANOFF, G STANLEY, ER BONAFE TESTA GIANELLABORRADORI, A RAK REVOLTELLA MURPHY, MJ MARMONT TI PROCEEDINGS OF THE METCALF FORUM - DISCUSSION SO STEM CELLS LA English DT Discussion C1 JAMES WHITCOMB RILEY HOSP CHILDREN,INDIANAPOLIS,IN 46202. SUNNYBROOK HLTH SCI CTR,TORONTO,ON M4N 3M5,CANADA. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT DEV & MOLEC BIOL,BRONX,NY 10461. SANDOZ PHARMA LTD,CLIN RES & DEV,CH-4002 BASEL,SWITZERLAND. HIPPLE CANC RES CTR,DAYTON,OH 45439. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP METCALF, D (reprint author), ROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,HUMAN LEUKEMIA LAB,PO ROYAL MELBOURNE HOSP,MELBOURNE,VIC 3050,AUSTRALIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 1066-5099 J9 STEM CELLS JI Stem Cells PY 1994 VL 12 SU 1 BP 277 EP 287 PG 11 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA PY200 UT WOS:A1994PY20000026 ER PT J AU ACKERMAN, RH CANDIA, MR AF ACKERMAN, RH CANDIA, MR TI IDENTIFYING CLINICALLY RELEVANT CAROTID DISEASE SO STROKE LA English DT Editorial Material DE CAROTID ARTERY DISEASES; CAROTID ENDARTERECTOMY; CLINICAL TRIALS; DIAGNOSTIC IMAGING C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ACKERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,NEUROVASC LAB,GRAY 2,BOSTON,MA 02114, USA. NR 17 TC 37 Z9 37 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1994 VL 25 IS 1 BP 1 EP 3 PG 3 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA MP106 UT WOS:A1994MP10600001 PM 8266354 ER PT J AU SAKAS, DE CROWELL, RM KIM, K KOROSUE, K ZERVAS, NT AF SAKAS, DE CROWELL, RM KIM, K KOROSUE, K ZERVAS, NT TI THE PERFLUOROCARBON FLUOROMETHYLOADAMANTANE OFFERS CEREBRAL PROTECTION IN A MODEL OF ISOVOLEMIC HEMODILUTION IN RABBITS SO STROKE LA English DT Article DE CEREBRAL INFARCTION; CEREBRAL ISCHEMIA; HEMODILUTION; PERFLUOROCARBONS ID BLOOD-FLOW; FLUOSOL-DA; FLUOROCARBON EMULSION; OXYGEN AVAILABILITY; ARTIFICIAL BLOOD; ISCHEMIA; SIZE; OCCLUSION; INFARCTION; REDUCTION AB Background and Purpose Perfluorocarbons (PFCs) are considered promising cerebral protection agents because they could combine the beneficial effects of decreased blood viscosity with enhanced oxygen-carrying capacity and oxygen tissue delivery, but trials of PFCs as hemodilutants have been very limited. We evaluated fluoromethyloadamantane (FMA), a new perfluorocarbon compound, as an isovolemic hemodilutant and compared it with low-molecular-weight dextran 40 (D40) and a control group. Methods Through a transorbital craniectomy, the internal carotid, anterior, and middle cerebral arteries were coagulated to create a cerebral infarction in anesthetized, mechanically ventilated rabbits. No other experimental procedure was performed in control animals. In the two other groups, hemodilution was commenced 30 minutes after the arterial occlusion with either D40 or FMA. Hemodynamic parameters and brain and systemic temperature were monitored throughout the experiments. All animals were killed 6 hours after the arterial occlusion. Results Hemodynamic and metabolic parameters and blood oxygen content were not affected by the infusion of either FMA or D40. Brain and systemic temperature remained constant. The ratio of infarct volume to the hemispheric volume was 19.6+/-3.7% in the FMA group (n=17), 19.9+/-4.6% in the D40 group (n=16), and 40.3+/-5.7% in the control group (n=17). The difference in infarct volume of both FMA and D40 animals compared with controls was statistically significant (P<.01) when tested with Student's t test. There was no significant difference between FMA and D40 groups. Conclusions These results suggest that FMA has cerebral protective properties and should be purified, optimized, and further tested experimentally to develop a stable, efficient, and safe oxygen carrier, potentially suitable for clinical trials. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT SURG,NEUROSURG SERV,BOSTON,MA 02114. BEAUMONT HOSP,NATL CTR NEUROSURG,DUBLIN 9,IRELAND. NR 33 TC 15 Z9 15 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1994 VL 25 IS 1 BP 197 EP 201 PG 5 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA MP106 UT WOS:A1994MP10600169 PM 7505493 ER PT J AU DALKARA, T MORIKAWA, E PANAHIAN, N MOSKOWITZ, MA AF DALKARA, T MORIKAWA, E PANAHIAN, N MOSKOWITZ, MA TI BLOOD-FLOW DEPENDENT FUNCTIONAL RECOVERY IN A RAT MODEL OF FOCAL CEREBRAL-ISCHEMIA SO STROKE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1994 VL 25 IS 1 BP 255 EP 255 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA MP106 UT WOS:A1994MP10600077 ER PT J AU IRIKURA, K MAYNARD, KI LEE, WS MOSKOWITZ, MA AF IRIKURA, K MAYNARD, KI LEE, WS MOSKOWITZ, MA TI NITRIC-OXIDE SYNTHASE (NOS) INHIBITION CORRELATES WITH THE REDUCED RCBF RESPONSE TO HYPERCAPNIA SO STROKE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1994 VL 25 IS 1 BP 263 EP 263 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA MP106 UT WOS:A1994MP10600122 ER PT J AU MAYNARD, KI OGILVY, CS AF MAYNARD, KI OGILVY, CS TI ARTERIOVENOUS-MALFORMATIONS DO NOT POSSESS PEPTIDERGIC PERIVASCULAR NERVES SO STROKE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1994 VL 25 IS 1 BP 268 EP 268 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA MP106 UT WOS:A1994MP10600184 ER PT J AU LO, EH MATSUMOTO, K PIERCE, AR GARRIDO, L LUTTINGER, D AF LO, EH MATSUMOTO, K PIERCE, AR GARRIDO, L LUTTINGER, D TI MONITORING STROKE THERAPY IN REAL-TIME WITH DIFFUSION-WEIGHTED MRI SO STROKE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1994 VL 25 IS 1 BP 270 EP 270 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA MP106 UT WOS:A1994MP10600195 ER PT B AU CAVINESS, VS TAKAHASHI, T NOWAKOWSKI, RS TSAI, LH AF CAVINESS, VS TAKAHASHI, T NOWAKOWSKI, RS TSAI, LH BE Albowitz, B Albus, K Kuhnt, U Nothdurft, HC Wahle, P TI REGULATED AND NONREGULATED PARAMETERS OF NEOCORTICAL CYTOGENESIS SO STRUCTURAL AND FUNCTIONAL ORGANIZATION OF THE NEOCORTEX: PROCEEDINGS OF A SYMPOSIUM IN THE MEMORY OF OTTO D. CREUTZFELDT SE EXPERIMENTAL BRAIN RESEARCH SERIES LA English DT Proceedings Paper CT Symposium on Structural and Functional Organization of the Neocortex, in the Memory of Otto D Creutzfeldt CY MAY, 1993 CL MAX PLANCK INST BIOPHYS CHEM, GOTTINGEN, GERMANY HO MAX PLANCK INST BIOPHYS CHEM RP CAVINESS, VS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,25 FRUIT ST,BOSTON,MA 02114, USA. RI Nowakowski, Richard/C-3217-2016 NR 0 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN 33 PA HEIDELBERGER PLATZ 3, W-1000 BERLIN 33, GERMANY BN 3-540-57205-8 J9 EXP BR RES PY 1994 VL 24 BP 8 EP 22 PG 15 WC Anatomy & Morphology; Developmental Biology; Neurosciences SC Anatomy & Morphology; Developmental Biology; Neurosciences & Neurology GA BB91W UT WOS:A1994BB91W00002 ER PT B AU GREEN, R SZOSTAK, JW AF GREEN, R SZOSTAK, JW BE Sarma, RH Sarma, MH TI TEMPLATE-DIRECTED OLIGONUCLEOTIDE-ASSEMBLY REACTIONS CATALYZED BY A MINIMALLY STRUCTURED RIBOZYME DERIVED FROM A GROUP-I INTRON SO STRUCTURAL BIOLOGY: THE STATE OF THE ART, VOL 1 LA English DT Proceedings Paper CT 8th Conversation in the Discipline Biomolecular Stereodynamics CY JUN 22-26, 1993 CL SUNY ALBANY, ALBANY, NY SP SUNY ALBANY, DEPT CHEM, SUNY ALBANY, INST BIOMOLEC STEREODYNAM HO SUNY ALBANY C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ADENINE PRESS PI SCHENECTADY PA 2066 CENTRAL AVE, SCHENECTADY, NY 12304 BN 0-940030-43-8 PY 1994 BP 277 EP 283 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA69K UT WOS:A1994BA69K00021 ER PT J AU RUBIN, D WARSHAW, AL SOUTHERN, JF PINS, M COMPTON, CC LEWANDROWSKI, KB AF RUBIN, D WARSHAW, AL SOUTHERN, JF PINS, M COMPTON, CC LEWANDROWSKI, KB TI EXPRESSION OF CA-15.3 PROTEIN IN THE CYST CONTENTS DISTINGUISHES BENIGN FROM MALIGNANT PANCREATIC MUCINOUS CYSTIC NEOPLASMS SO SURGERY LA English DT Article ID CARCINOEMBRYONIC ANTIGEN; CYSTADENOCARCINOMA; CYSTADENOMA; DIAGNOSIS; LESIONS; TUMORS; FLUID AB Background. Inflammatory pseudocysts, serous cystadenomas, and mucinous cystic tumors comprise most cystic lesions of the pancreas. The mucinous tumors include mucinous cystic neoplasms, which are benign on histologic examination but have the potential for malignant transformation, and mucinous cystadenocarcinomas. Accurate preoperative classification of pancreatic cysts with clinical and radiologic criteria is often impossible, and as a result many cystic tumors are inappropriately treated as pseudocysts. Analysis of percutaneous needle-aspirated cyst fluid for tumor markers, enzymes, viscosity, and cytologic study has been proposed as a useful modality to distinguish mucinous from nonmucinous cystic lesions. However, no reliable cyst fluid parameter distinguishes benign from malignant mucinous tumors. Methods. The concentration of the tumor marker CA 15-3 was measured by immunoassay in cyst fluid from six pseudocysts, five serous cystadenomas, three mucinous cystic neoplasms, and six mucinous cystadenocarcinomas. Results. The concentration of CA 15-3 in the cyst fluid of mucinous cystadenocarcinomas was higher (mean, 178 units/ml; range, 40 to 392) than that of mucinous cystic neoplasms (mean, 4.7 units/ml; range 0 to 14), serous cystadenomas (mean, 9.2 units/ml; range, 0 to 32), and pseudocysts (mean, 15.3 units/ml; range, 0 to 66). An upper cutoff value of 30 units/ml distinguished mucinous cystic neoplasms from mucinous cystadenocarcinomas with 100% sensitivity and 100% specificity (p = 0.01). Conclusions. Production of CA 15-3 appears to coincide with malignant transformation in pancreatic mucinous cystic neoplasms. We conclude that measurement of CA 15-3 levels in the cyst fluid is useful in the differentiation of benign from malignant pancreatic mucinous cysts. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 14 TC 47 Z9 50 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD JAN PY 1994 VL 115 IS 1 BP 52 EP 55 PG 4 WC Surgery SC Surgery GA MR827 UT WOS:A1994MR82700009 PM 8284761 ER PT J AU FISHER, CM OJEMANN, RG AF FISHER, CM OJEMANN, RG TI BILATERAL DECOMPRESSIVE CRANIECTOMY FOR WORSENING COMA IN ACUTE SUBARACHNOID HEMORRHAGE - OBSERVATIONS IN SUPPORT OF THE PROCEDURE SO SURGICAL NEUROLOGY LA English DT Article DE CEREBRAL ANEURYSM; SUBARACHNOID HEMORRHAGE; CRANIECTOMY AB Bilateral craniectomy in a woman comatose and decerebrate after a subarachnoid hemorrhage, resulted in normal mentation in 3 days. The dramatic recovery is unmatched in our experience. The rationale rested on clinicopathologic studies showing that in such cases brain swelling was the cause of death, the brain being otherwise intact. Emergency surgery to relieve the tamponade seemed reasonable. The question is whether the procedure has a role in those patients who fail to respond to current therapeutic measures. The arguments in favor, presented herein, are illustrated by three pathologic studies selected from our longtime experience. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. RP FISHER, CM (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 22 TC 57 Z9 57 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0090-3019 J9 SURG NEUROL JI Surg. Neurol. PD JAN PY 1994 VL 41 IS 1 BP 65 EP 74 DI 10.1016/0090-3019(94)90210-0 PG 10 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA NL662 UT WOS:A1994NL66200013 PM 8310390 ER PT J AU COLLEN, D LU, HR STASSEN, JM VREYS, I YASUDA, T BUNTING, S GOLD, HK AF COLLEN, D LU, HR STASSEN, JM VREYS, I YASUDA, T BUNTING, S GOLD, HK TI ANTITHROMBOTIC EFFECTS AND BLEEDING-TIME PROLONGATION WITH SYNTHETIC PLATELET GPIIB/IIIA INHIBITORS IN ANIMAL-MODELS OF PLATELET-MEDIATED THROMBOSIS SO THROMBOSIS AND HAEMOSTASIS LA English DT Article ID ARG-GLY-ASP; GLYCOPROTEIN-IIB/IIIA RECEPTOR; ACUTE MYOCARDIAL-INFARCTION; PLASMINOGEN-ACTIVATOR; ARTERIAL THROMBOSIS; MONOCLONAL-ANTIBODY; CANINE PREPARATION; UNSTABLE ANGINA; FACTOR BINDING; FEMORAL VEIN AB Cyclic Arg-Gly-Asp (RGD) containing synthetic peptides such as L-cysteine, N-(mercaptoacetyl)-D-tyrosyl-L-arginylglycyl-Lalphaaspartylcyclic (1-5)-sulfide, 5-oxide (G4120) and acetyl-L-cysteinyl-L-asparaginyl-L-prolyl-L-arginyl-glycyl-L-alpha-aspartyl-[0-methyttyrosyl]-L-arginyl-L-cysteinamide, cyclic 1-9-sulfide (TP9201) bind with high affinity to the platelet GPIIb/IIIa receptor. The relationship between antithrombotic effect, ex vivo platelet aggregation and bleeding time prolongation with both agents was studied in hamsters with a standardized femoral vein endothelial cell injury predisposing to platelet-rich mural thrombosis, and in dogs with a carotid arterial eversion graft inserted in the femoral artery. Intravenous administration of G4120 in hamsters inhibited in vivo thrombus formation with a 50% inhibitory bolus dose (ID50) of approximately 20 mug/kg, ex vivo ADP-induced platelet aggregation with ID50 of 10 mug/kg, and bolus injection of 1 mg/kg prolonged the bleeding time from 38 +/- 9 to 1,100 +/- 330 s. Administration of TP9201 in hamsters inhibited in vivo thrombus formation with ID50 of 30 mug/kg, ex vivo platelet aggregation with an ID50 of 50 mug/kg and bolus injection of 1 mg/kg did not prolong the template bleeding time. In the dog eversion graft model, infusion of 100 mug/kg of G4120 over 60 min did not fully inhibit platelet-mediated thrombotic occlusion but was associated with inhibition of ADP-induced ex vivo platelet aggregation and with prolongation of the template bleeding time from 1.3 +/- 0.4 to 12 +/- 2 min. Infusion of 300 mug/kg Of TP9201 over 60 min completely prevented thrombotic occlusion, inhibited ex vivo platelet aggregation, but was not associated with prolongation of the template bleeding time. TP9201, unlike G4120, inhibits in vivo platelet-mediated thrombus formation without associated prolongation of the template bleeding time. C1 CATHOLIC UNIV LEUVEN,CTR THROMBOSIS & VASC RES,B-3000 LOUVAIN,BELGIUM. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. GENENTECH INC,DEPT CARDIOVASC PHARMACOL,S SAN FRANCISCO,CA 94080. NR 46 TC 62 Z9 62 U1 0 U2 1 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JAN PY 1994 VL 71 IS 1 BP 95 EP 102 PG 8 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA MQ902 UT WOS:A1994MQ90200016 PM 8165652 ER PT J AU YUNIS, JJ KINEKE, E YUNIS, EJ AF YUNIS, JJ KINEKE, E YUNIS, EJ TI CHARACTERIZATION OF A NEW DRB1 ALLELE, DRB1-ASTERISK-1309, BY PCR-SSOP AND SEQUENCING SO TISSUE ANTIGENS LA English DT Note DE DRB1; PCR; ALLELE; SSO; MHC-HLA ID OLIGONUCLEOTIDE PROBES; CHAIN-REACTION; CLASS-II; DNA; POLYMERASE; AMPLIFICATION C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA. AMER RED CROSS BLOOD SERV,NE REG,DEDHAM,MA. RP YUNIS, JJ (reprint author), DANA FARBER CANC INST,HISTOCOMPATIBIL LAB,DIV IMMUNOGENET,D271,44 BINNEY ST,BOSTON,MA 02115, USA. NR 22 TC 6 Z9 7 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD JAN PY 1994 VL 43 IS 1 BP 54 EP 57 DI 10.1111/j.1399-0039.1994.tb02298.x PG 4 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA MU528 UT WOS:A1994MU52800010 PM 8023320 ER PT J AU LATINNE, D VITIELLO, DM SACHS, DH SYKES, M AF LATINNE, D VITIELLO, DM SACHS, DH SYKES, M TI TOLERANCE TO DISCORDANT XENOGRAFTS .1. SHARING OF HUMAN NATURAL ANTIBODY DETERMINANTS ON MINIATURE SWINE BONE-MARROW CELLS AND ENDOTHELIAL-CELLS SO TRANSPLANTATION LA English DT Article ID TRANSPLANTATION; SPECIFICITY; PRIMATES; SURVIVAL; REGIMEN; MODEL; RAT AB Xenotransplantation could potentially overcome the organ shortage that currently limits the field of transplantation. Because of their breeding characteristics as well as their size and physiologic similarities to humans, we have chosen miniature swine as possible xenograft donors, and are currently attempting to develop a means of using mixed xenogeneic chimerism as an approach to tolerance induction in swine-to-primate species combinations. One major barrier to organ grafting from pig to man is the presence in human serum of preformed natural antibodies (NAb) reacting with antigens expressed on porcine endothelial cells and causing hyperacute rejection. Previous experiments performed in our laboratory have shown that both humoral and cellular tolerance can be induced in a concordant xenogeneic species combination (rat --> mouse) using donor bone marrow infusion following conditioning with a nonmyeloablative regimen. Induction of chimerism in these animals was associated with a marked reduction in the level of IgM natural antibodies that recognize rat bone marrow cells. A similar approach could also lead to humoral and cellular tolerance induction in the swine --> human species combination, permitting transplantation of vascularized organs from the swine donor. To determine the potential of bone marrow transplantation to induce a state of ''natural antibody tolerance,'' it was essential to determine whether or not all human NAb target antigens expressed on swine EC are also expressed on cells derived from swine bone marrow. We have addressed this question by evaluating the ability of various swine bone marrow-derived cells to absorb human IgM and IgG NAb that bind to swine EC. Our results demonstrate that swine bone marrow cells and their progeny can absorb almost all IgM NAb that bind to swine EC, as detected by flow cytometric and ELISA assays. Specificity of absorption was demonstrated, as total serum IgM levels declined only minimally after absorption on swine BMC and to an extent comparable to that observed following absorption with human cells, which did not deplete swine EC-binding NAb. Human IgG binding to swine EC was also completely absorbed by swine BMC. These results suggest that a state of ''NAb tolerance'' could be induced by successful swine marrow engraftment in man. Furthermore, swine PBL, platelets, and EC were able to absorb most IgM NAb that bound to swine BMC, suggesting that absorption using antigen from any of these tissues might facilitate marrow engraftment, and hence tolerance induction, in this species combination. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,BOSTON,MA 02129. NR 36 TC 16 Z9 16 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD JAN PY 1994 VL 57 IS 2 BP 238 EP 245 DI 10.1097/00007890-199401001-00015 PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA MU939 UT WOS:A1994MU93900015 PM 8310515 ER PT B AU FERRANTE, RJ KOWALL, NW RICHARDSON, EP AF FERRANTE, RJ KOWALL, NW RICHARDSON, EP BE Fuxe, K Agnati, LF Bjelke, B Ottoson, D TI NEURONAL PLASTICITY - A POTENTIAL ROLE IN SPINY STRIATAL NEURON DEGENERATION IN HUNTINGTONS DISEASE SO TROPHIC REGULATION OF THE BASAL GANGLIA: FOCUS ON DOPAMINE NEURONS SE WENNER-GREN INTERNATIONAL SERIES LA English DT Proceedings Paper CT 1992 Wenner-Gren-Center Symposium on Trophic Regulation of the Basal Ganglia - Focus on Dopamine Neurons CY 1992 CL STOCKHOLM, SWEDEN SP Wenner Gren Ctr C1 MASSACHUSETTS GEN HOSP,CS KUBIK NEUROPATHOL LAB,BOSTON,MA 02114. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON PRESS LTD PI OXFORD PA THE BOULEVARD LANGFORD LANE KIDLINGTON, OXFORD, ENGLAND OX5 1GB BN 0-08-042276-4 J9 WENN GR INT PY 1994 VL 62 BP 465 EP 477 PG 13 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA BD25V UT WOS:A1994BD25V00030 ER PT S AU SEARLES, JS ALTERMAN, AI AF SEARLES, JS ALTERMAN, AI BE Babor, TF Hesselbrock, V Meyer, RE Shoemaker, W TI ENVIRONMENTAL DIFFERENCES IN YOUNG MEN WITH AND WITHOUT A FAMILY HISTORY OF ALCOHOLISM SO TYPES OF ALCOHOLICS: EVIDENCE FROM CLINICAL, EXPERIMENTAL, AND GENETIC RESEARCH SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Genetic Susceptibility, Biological Markers of Vulnerability and Alcoholic Subtypes CY OCT 22-23, 1992 CL FARMINGTON, CT SP NIAAA ID CROSS-FOSTERING ANALYSIS; ANTISOCIAL PERSONALITY; INHERITANCE; ABUSE C1 UNIV VERMONT,COLCHESTER,VT. UNIV PENN,VET AFFAIRS MED CTR,ADDICT RES CTR,PHILADELPHIA,PA 19104. RP SEARLES, JS (reprint author), VERMONT ALCOHOL RES CTR,2000 MT VIEW DR,COLCHESTER,VT, USA. NR 27 TC 8 Z9 8 U1 2 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-799-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 708 BP 147 EP 156 DI 10.1111/j.1749-6632.1994.tb24707.x PG 10 WC Substance Abuse; Genetics & Heredity; Multidisciplinary Sciences; Psychiatry SC Substance Abuse; Genetics & Heredity; Science & Technology - Other Topics; Psychiatry GA BA04C UT WOS:A1994BA04C00015 PM 8154675 ER PT B AU DRETLER, SP ROSEN, DI AF DRETLER, SP ROSEN, DI BE Ryall, R Bais, R Marshall, VR Rofe, AM Smith, LH Walker, VR TI THE ELECTROMECHANICAL IMPACTOR (EMI) - A DEVICE FOR INTRACORPOREAL LITHOTRIPSY SO UROLITHIASIS 2 LA English DT Proceedings Paper CT 7th International Symposium on Urolithiasis CY AUG 24-27, 1992 CL CAIRNS, AUSTRALIA C1 MASSACHUSETTS GEN HOSP,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 BN 0-306-44727-4 PY 1994 BP 551 EP 551 PG 1 WC Endocrinology & Metabolism; Urology & Nephrology SC Endocrinology & Metabolism; Urology & Nephrology GA BB17Y UT WOS:A1994BB17Y00222 ER PT B AU DEMAY, MB KRONENBERG, HM HEYMONT, JL BOGADO, CE MACKEY, SL AF DEMAY, MB KRONENBERG, HM HEYMONT, JL BOGADO, CE MACKEY, SL BE Norman, AW Bouillon, R Thomasset, M TI 1,25(OH)(2)D-3 response elements: Is there an order? SO VITAMIN D: PLURIPOTENT STEROID HORMONE: STRUCTURAL STUDIES, MOLECULAR ENDOCRINOLOGY AND CLINICAL APPLICATIONS LA English DT Proceedings Paper CT 9th Workshop on Vitamin D CY MAY 28-JUN 02, 1994 CL ORLANDO, FL SP Chugai Pharm Co Ltd, Japan, Hoffmann La Roche Ltd, Switzerland, Hoffmann La Roche Inc, US, Inst Sci Roussel, France, Lab Leo SA, France, Leo Pharm Prod Ltd A S, Denmark, Novo Nordisk A S, Denmark, Procter & Gamble Pharm, US, Solvay Duphar BV, Netherlands, Sumitomo Pharm Co Ltd, Japan, Teijin Ltd, Japan, Westwood Squibb Pharm Res Inst, US C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WALTER DE GRUYTER PI BERLIN 30 PA GENTHINER STRASSE 13, W-1000 BERLIN 30, GERMANY BN 3-11-014157-4 PY 1994 BP 259 EP 263 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD64B UT WOS:A1994BD64B00087 ER PT B AU COBURN, JW AF COBURN, JW BE Norman, AW Bouillon, R Thomasset, M TI Use of calcitriol in treating the secondary hyperparathyroidism of uremia: What are the differences between oral and intravenous therapy? SO VITAMIN D: PLURIPOTENT STEROID HORMONE: STRUCTURAL STUDIES, MOLECULAR ENDOCRINOLOGY AND CLINICAL APPLICATIONS LA English DT Proceedings Paper CT 9th Workshop on Vitamin D CY MAY 28-JUN 02, 1994 CL ORLANDO, FL SP Chugai Pharm Co Ltd, Japan, Hoffmann La Roche Ltd, Switzerland, Hoffmann La Roche Inc, US, Inst Sci Roussel, France, Lab Leo SA, France, Leo Pharm Prod Ltd A S, Denmark, Novo Nordisk A S, Denmark, Procter & Gamble Pharm, US, Solvay Duphar BV, Netherlands, Sumitomo Pharm Co Ltd, Japan, Teijin Ltd, Japan, Westwood Squibb Pharm Res Inst, US C1 UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WALTER DE GRUYTER PI BERLIN 30 PA GENTHINER STRASSE 13, W-1000 BERLIN 30, GERMANY BN 3-11-014157-4 PY 1994 BP 649 EP 657 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD64B UT WOS:A1994BD64B00208 ER PT J AU GORLIN, JB KELLY, L AF GORLIN, JB KELLY, L TI ALLOIMMUNIZATION VIA PREVIOUS TRANSFUSION PLACES FEMALE KP(B)-NEGATIVE RECIPIENTS AT RISK FOR HAVING CHILDREN WITH CLINICALLY SIGNIFICANT HEMOLYTIC-DISEASE OF THE NEWBORN SO VOX SANGUINIS LA English DT Article ID MANAGEMENT; SEVERITY; CLONING; PATIENT AB We report a case of clinically significant hemolytic disease of the newborn due to Kp(b) alloimmunisation requiring obstetric intervention. This case and a review of the literature are in contrast to reviews of hemolytic disease of the newborn that either ascribe no significance to the Kp(b) antigen or suggest that it causes only rare or mild disease. Analysis of our Kp(b)-negative donor pool suggests that prior transfusion greatly increases the chance of alloimmunisation. The role of frozen rare donor registry cells as a public resource is emphasised. C1 PUGET SOUND BLOOD CTR SEATTLE,WASHINGTON,DC. CHILDRENS HOSP,DIV HEMATOL,BOSTON,MA. DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA. NR 15 TC 7 Z9 8 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0042-9007 J9 VOX SANG JI Vox Sang. PY 1994 VL 66 IS 1 BP 46 EP 48 PG 3 WC Hematology SC Hematology GA MR731 UT WOS:A1994MR73100008 PM 8146981 ER PT J AU CHURCHILL, WH CHAPMAN, RH RUTHERFORD, CJ POSS, R WALLACE, EL SURGENOR, DM AF CHURCHILL, WH CHAPMAN, RH RUTHERFORD, CJ POSS, R WALLACE, EL SURGENOR, DM TI BLOOD PRODUCT UTILIZATION IN HIP AND KNEE ARTHROPLASTY - EFFECT OF GENDER AND AUTOLOGOUS BLOOD ON TRANSFUSION PRACTICE SO VOX SANGUINIS LA English DT Article ID RED-CELL TRANSFUSIONS; REPLACEMENT SURGERY; INFECTION AB Analysis of total blood product support for a 1-year cohort of patients undergoing hip or knee total joint arthroplasty showed significant differences in transfusion therapy between patients who predeposited autologous blood and those who did not. In primary joint arthroplasty, 51% of nonpredepositing patients undergoing hip replacement and 28% of nonpredepositing patients undergoing knee replacement required red cell transfusions. In revision procedures, 58-61% were transfused. Predepositors requiring only autologous blood received less blood per patient than nonpredepositors; however, 73-87% of primary and 86-88% of revision arthroplasty patients were transfused. Predepositors receiving supplemental allogeneic blood used a volume of red cells comparable to nonpredepositing patients, which was significantly greater than the red cell requirement of predepositors using only autologous blood. Moreover, regardless of predeposit status, the extent of red cell replacement differed between men and women. Male patients presented with significantly higher hematocrits and were less likely to be transfused than females undergoing the same procedure. However, once the transfusion-decision was made, the average amount of red cells given for each procedure did not show gender-related variation. Despite differences in admission and lowest observed hematocrits, all patients were discharged with hematocrits in the same range, suggesting that men were replaced with relatively less blood than women. These differences in transfusion practice relating to gender and predeposit status could not be associated with identifiable changes in clinical outcome which might provide rationale for the observed differences in practice. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT ORTHOPED,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT CLIN LABS,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT ORTHOPED,BOSTON,MA. CTR BLOOD RES,BOSTON,MA 02115. RP CHURCHILL, WH (reprint author), BRIGHAM & WOMENS HOSP,DEPT CLIN LABS,BLOOD BANK,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-33774] NR 11 TC 28 Z9 28 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0042-9007 J9 VOX SANG JI Vox Sang. PY 1994 VL 66 IS 3 BP 182 EP 187 PG 6 WC Hematology SC Hematology GA NF014 UT WOS:A1994NF01400006 PM 8036787 ER PT J AU HUANG, PL DAWSON, TM BREDT, DS SNYDER, SH FISHMAN, MC AF HUANG, PL DAWSON, TM BREDT, DS SNYDER, SH FISHMAN, MC TI TARGETED DISRUPTION OF THE NEURONAL NITRIC-OXIDE SYNTHASE GENE SO CELL LA English DT Article ID LONG-TERM POTENTIATION; HYPERTROPHIC PYLORIC-STENOSIS; RAT ANOCOCCYGEUS MUSCLE; MONOMETHYL-L-ARGININE; NADPH-DIAPHORASE; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; HUNTINGTONS-DISEASE; ADP-RIBOSYLATION; STRIATAL NEURONS; PENILE ERECTION AB By homologous recombination, we have generated mice that lack the neuronal nitric oxide synthase (NOS) gene. Neuronal NOS expression and NADPH-diaphorase (NDP) staining are absent in the mutant mice. Very low level residual catalytic activity suggests that other enzymes in the brain may generate nitric oxide. The neurons normally expressing NOS appear intact, and the mutant NOS mice are viable, fertile, and without evident histopathological abnormalities in the central nervous system. The most evident effect of disrupting the neuronal NOS gene is the development of grossly enlarged stomachs, with hypertrophy of the pyloric sphincter and the circular muscle layer. This phenotype resembles the human disorder infantile pyloric stenosis, in which gastric outlet obstruction is associated with the lack of NDP neurons in the pylorus. C1 JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROSCI, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT PHARMACOL & MOLEC SCI, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT PSYCHIAT & BEHAV SCI, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROL, BALTIMORE, MD 21205 USA. RP HUANG, PL (reprint author), MASSACHUSETTS GEN HOSP, CARDIOVASC RES CTR, BOSTON, MA 02129 USA. FU NHLBI NIH HHS [HL-02792-02]; NIMH NIH HHS [MH-18501]; NINDS NIH HHS [CIDA NS-01578] NR 71 TC 1043 Z9 1059 U1 1 U2 9 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0092-8674 J9 CELL JI Cell PD DEC 31 PY 1993 VL 75 IS 7 BP 1273 EP 1286 DI 10.1016/0092-8674(93)90615-W PG 14 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MP869 UT WOS:A1993MP86900007 PM 7505721 ER PT J AU LEEHUANG, S LIN, JJ KUNG, HF HUANG, PL LEE, L HUANG, PL AF LEEHUANG, S LIN, JJ KUNG, HF HUANG, PL LEE, L HUANG, PL TI THE 3' FLANKING REGION OF THE HUMAN ERYTHROPOIETIN-ENCODING GENE CONTAINS NITROGEN-REGULATORY OXYGEN-SENSING CONSENSUS SEQUENCES AND TISSUE-SPECIFIC TRANSCRIPTIONAL REGULATORY ELEMENTS SO GENE LA English DT Article DE DNA SEQUENCE; ENHANCER ELEMENTS; GROWTH HORMONE; ERYTHROPOIESIS ID ACUTE-PHASE GENES; NUCLEAR FACTORS; LIVER; EXPRESSION; PROMOTER; PROTEIN; HYPOXIA; BINDING; ENHANCER; ALPHA-1-ANTITRYPSIN AB We have reported the identification of a classical canonical CAAT box, TATA boxes and other transcriptional regulatory elements in the 5' flanking region of the human erythropoietin (hEp)-encoding gene (Lee-Huang et al., Gene 128 (1993) 227-236]. These elements were not found in the hEp genomic clones reported by others. Our genomic clone extends in both directions beyond any reported clones, by 3.9 kb on the 5' side and by 1.8 kb on the 3' side. Many important regulatory elements are found in these extended flanking regions. We report here the genomic structure of the extended 3' flanking region of hEp. This region contains the following regulatory elements: nitrogen-regulatory/oxygen-sensing consensus sequences, 5'TTTTGCA and 5'-CCCTGCA; tissue-specific regulatory elements, including binding sites for A-activator, 5'-GTGGTGCAA; for;DBP, 5'-TGATTTTGT; for HNF, 5'-T(A/G)TTTGT; and fbr C/EBP, 5'-T(T/G) (T/G)TGCAAT; a lymphokine-responsive element, 5'-GTGAAACCCC (Rev), as well as binding sites for AP and Spl. In addition, the nucleotide (nt) sequence in this region is rich in inverted repeats (palindromes) that allow the formation of hairpin loops. A total of 14 potential stem loops with a maximum loop size of 20 nt are found. The identification of these regulatory elements in hEp should provide further insight into the tissue-specific and inducible expression of hEp. Such knowledge should be useful in the clinical modulation of erythropoiesis under physiologic and pathologic conditions. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAMME,FREDERICK,MD 21701. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP LEEHUANG, S (reprint author), NYU,SCH MED,DEPT BIOCHEM,NEW YORK,NY 10016, USA. FU NHLBI NIH HHS [HL30862, HL21683] NR 43 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD DEC 31 PY 1993 VL 137 IS 2 BP 203 EP 210 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA MW218 UT WOS:A1993MW21800007 PM 8299948 ER PT J AU ZUSMAN, RM AF ZUSMAN, RM TI ANGIOTENSIN-CONVERTING ENZYME-INHIBITORS - MORE DIFFERENT THAN ALIKE - FOCUS ON CARDIAC-PERFORMANCE SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article; Proceedings Paper CT ACE Portfolio Speakers Conference CY APR 29-MAY 02, 1993 CL SAN ANTONIO, TX SP BRISTOL MYERS SQUIBB CO ID LEFT-VENTRICULAR HYPERTROPHY; CONGESTIVE HEART-FAILURE; ANTIHYPERTENSIVE THERAPY; SYSTOLIC FUNCTION; LIPID-METABOLISM; BLOOD-PRESSURE; ACE INHIBITORS; HYPERTENSION; CAPTOPRIL; GLUCOSE AB Development of an increased systemic vascular resistance and the concomitant Increase in blood pressure are associated with significant changes in left ventricular structure and function. The plasma and tissue renin-angiotensin systems play an important, but variable, role in the regulation of blood pressure and systemic vascular resistance in normotensive and hypertensive patients. Non-angiotensin-mediated effects of angiotensin-converting enzyme (ACE) inhibitors and/or differential tissue specificities may result in a variable hemodynamic response to individual therapies. Using first-pass radionuclide cineangiography, the hemodynamic effects of captopril, lisinopril, and fosinopril were compared. Fosinopril induced a greater reduction in systemic vascular resistance than did equipotent hypotensive doses of captopril or lisinopril and was associated with an increase in cardiac output, left ventricular peak ejection rate, and left ventricular peak filling rate. Along with previously accumulated data, these results suggest that structural differences among ACE inhibitors may result in unique physiologic effects. Fosinopril appears to have a cardiotropic effect that causes Improved left ventricular diastolic performance; this effect is unique among currently available ACE inhibitors. The clinical significance of the unique profiles of Individual ACE inhibitors awaits assessment via comparative clinical investigations. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ZUSMAN, RM (reprint author), MASSACHUSETTS GEN HOSP,DIV HYPERTENS & VASC MED,CARDIAC UNIT,15 PARKMAN ST,WACC-482,BOSTON,MA 02114, USA. NR 56 TC 18 Z9 18 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD DEC 30 PY 1993 VL 72 IS 20 BP H25 EP H36 DI 10.1016/0002-9149(93)91052-J PG 12 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MP706 UT WOS:A1993MP70600006 PM 8285179 ER PT J AU WINAWER, SJ ZAUBER, AG HO, MN OBRIEN, MJ GOTTLIEB, LS STERNBERG, SS WAYE, JD SCHAPIRO, M BOND, JH PANISH, JF ACKROYD, F SHIKE, M KURTZ, RC HORNSBYLEWIS, L GERDES, H STEWART, ET AF WINAWER, SJ ZAUBER, AG HO, MN OBRIEN, MJ GOTTLIEB, LS STERNBERG, SS WAYE, JD SCHAPIRO, M BOND, JH PANISH, JF ACKROYD, F SHIKE, M KURTZ, RC HORNSBYLEWIS, L GERDES, H STEWART, ET TI PREVENTION OF COLORECTAL-CANCER BY COLONOSCOPIC POLYPECTOMY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID SCREENING SIGMOIDOSCOPY; SUBSEQUENT CARCINOMA; NATURAL-HISTORY; POLYPS; RISK; MORTALITY; INDIVIDUALS; POPULATION; ADENOMAS; RECTUM AB Background. The current practice of removing adenomatous polyps of the colon and rectum is based on the belief that this will prevent colorectal cancer. To address the hypothesis that colonoscopic polypectomy reduces the incidence of colorectal cancer, we analyzed the results of the National Polyp Study with reference to other published results. Methods. The study cohort consisted of 1418 patients who had a complete colonoscopy during which one or more adenomas of the colon or rectum were removed. The patients subsequently underwent periodic colonoscopy during an average follow-up of 5.9 years, and the incidence of colorectal cancer was ascertained. The incidence rate of colorectal cancer was compared with that in three reference groups, including two cohorts in which colonic polyps were not removed and one general-population registry, after adjustment for sex, age, and polyp size. Results. Ninety-seven percent of the patients were followed clinically for a total of 8401 person-years, and 80 percent returned for one or more of their scheduled colonoscopies. Five asymptomatic early-stage colorectal cancers (malignant polyps) were detected by colonoscopy (three at three years, one at six years, and one at seven years). No symptomatic cancers were detected. The numbers of colorectal cancers expected on the basis of the rates in the three reference groups were 48.3, 43.4, and 20.7, for reductions in the incidence of colorectal cancer of 90, 88, and 76 percent, respectively (P<0.001). Conclusions. Colonoscopic polypectomy resulted in a lower-than-expected incidence of colorectal cancer. These results support the view that colorectal adenomas progress to adenocarcinomas, as well as the current practice of searching for and removing adenomatous polyps to prevent colorectal cancer. C1 BOSTON CITY HOSP,MALLORY INST PATHOL,BOSTON,MA 02118. MT SINAI MED CTR,NEW YORK,NY 10029. VALLEY PRESBYTERIAN HOSP,VAN NUYS,CA. VET AFFAIRS MED CTR,MINNEAPOLIS,MN. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MILWAUKEE CTY MED CTR,MILWAUKEE,WI. RP WINAWER, SJ (reprint author), MEM SLOAN KETTERING CANC CTR,GASTROENTEROL & NUTR SERV,NATL POLYP STUDY HEADQUARTERS,NEW YORK,NY 10021, USA. FU NCI NIH HHS [CA 26852] NR 24 TC 2581 Z9 2650 U1 5 U2 64 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 DEC 30 PY 1993 VL 329 IS 27 BP 1977 EP 1981 DI 10.1056/NEJM199312303292701 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MN573 UT WOS:A1993MN57300001 PM 8247072 ER PT J AU WONG, TY MIHM, MC AF WONG, TY MIHM, MC TI MYCOSIS-FUNGOIDES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note RP WONG, TY (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 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 DEC 30 PY 1993 VL 329 IS 27 BP 2001 EP 2001 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MN573 UT WOS:A1993MN57300005 PM 8247076 ER PT J AU GIVER, L BARTEL, DP ZAPP, ML GREEN, MR ELLINGTON, AD AF GIVER, L BARTEL, DP ZAPP, ML GREEN, MR ELLINGTON, AD TI SELECTION AND DESIGN OF HIGH-AFFINITY RNA LIGANDS FOR HIV-1 REV SO GENE LA English DT Article DE APTAMER; SELEX; REV-RESPONSIVE ELEMENT; AIDS; NUCLEIC ACID PHARMACEUTICAL ID VIRUS TYPE-1 REV; RESPONSIVE ELEMENT RNA; TARGET SEQUENCE; MUTATIONAL ANALYSIS; TRANS-ACTIVATOR; MESSENGER-RNA; PROTEIN; BINDING; REPLICATION; EXPRESSION AB We have used in vitro selection to isolate minimal, high-affinity RNA ligands for the Rev protein of HIV-1. Sequence analysis reveals that the tightest binding aptamers exhibit some similarity to a Rev-binding element (RBE) localized within the Rev-responsive element (RRE), but also contain novel sequence and structural motifs. A short helical stem and bulged nucleotides (nt) CUC...UYGAG that have no counterpart in the wild-type (wt) element contribute to high-affinity binding. We have designed and synthesized a short (37 nt) RNA molecule that incorporates this motif; this RNA ligand has from three- to fivefold tighter binding than the full-length wt element, and up to 16-fold tighter than minimal wt RBEs. A guanosine:guanosine pairing that is postulated to occur in the wt element has been altered to other base pairings in the context of our optimized minimal element. RNAs that contain non-Watson-Crick base pairings, that can be modeled as isosteric to the wt G:G pair, bind Rev up to 160-fold tighter than elements that contain canonical Watson-Crick pairings or non-isosteric mismatches. These results support the hypothesis that Rev recognizes structural features associated with a non-Watson-Crick base pair. C1 INDIANA UNIV,DEPT CHEM,BLOOMINGTON,IN 47405. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02118. UNIV MASSACHUSETTS,MED CTR,PROGRAM MOLEC MED,WORCESTER,MA 01605. NR 31 TC 41 Z9 42 U1 3 U2 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD DEC 27 PY 1993 VL 137 IS 1 BP 19 EP 24 DI 10.1016/0378-1119(93)90246-Y PG 6 WC Genetics & Heredity SC Genetics & Heredity GA MW217 UT WOS:A1993MW21700004 PM 7506689 ER PT J AU VANDENHEUVEL, S HARLOW, E AF VANDENHEUVEL, S HARLOW, E TI DISTINCT ROLES FOR CYCLIN-DEPENDENT KINASES IN CELL-CYCLE CONTROL SO SCIENCE LA English DT Article ID PROTEIN-KINASE; SACCHAROMYCES-CEREVISIAE; CATALYTIC SUBUNIT; CDC28 MUTATION; ACTIVATION; MITOSIS; FAMILY; YEAST; PHASE; GENE AB The key cell-cycle regulator Cdc2 belongs to a family of cyclin-dependent kinases in higher eukaryotes. Dominant-negative mutations were used to address the requirement for kinases of this family in progression through the human cell cycle. A dominant-negative Cdc2 mutant arrested cells at the G2 to M phase transition, whereas mutants of the cyclin-dependent kinases Cdk2 and Cdk3 caused a G1 block. The mutant phenotypes were specifically rescued by the corresponding wild-type kinases. These data reveal that Cdk3, in addition to Cdc2 and Cdk2, executes a distinct and essential function in the mammalian cell cycle. RP VANDENHEUVEL, S (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129, USA. RI van den Heuvel, Sander/B-8892-2011 NR 45 TC 896 Z9 900 U1 2 U2 23 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD DEC 24 PY 1993 VL 262 IS 5142 BP 2050 EP 2054 DI 10.1126/science.8266103 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MN108 UT WOS:A1993MN10800043 PM 8266103 ER PT J AU HABER, DA PARK, S MAHESWARAN, S ENGLERT, C RE, GG HAZENMARTIN, DJ SENS, DA GARVIN, AJ AF HABER, DA PARK, S MAHESWARAN, S ENGLERT, C RE, GG HAZENMARTIN, DJ SENS, DA GARVIN, AJ TI WT1-MEDIATED GROWTH SUPPRESSION OF WILMS-TUMOR CELLS EXPRESSING A WT1 SPLICING VARIANT SO SCIENCE LA English DT Article ID GENOMIC STRUCTURE; GENE WT1; RB GENE; FORM; TUMORIGENICITY; TRANSFORMATION; CHROMOSOME-11; PROTEIN; BINDING; FOSB AB A human Wilms tumor cell line (RM1) was developed to test the tumor suppressor activity of WT1, a zinc finger transcription factor that is expressed in the developing human kidney and is mutationally inactivated in a subset of Wilms tumors. Transfection of each of four wild-type WT1 isoforms suppressed the growth of RM1 cells. The endogenous WT1 transcript in these cells was devoid of exon 2 sequences, a splicing alteration that was also detected in varying amounts in all Wilms tumors tested but not in normal kidney. Production of this abnormal transcript, which encodes a functionally altered protein, may represent a distinct mechanism for inactivating WT1 in Wilms tumors. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. RP HABER, DA (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC GENET LAB,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA58596, CA37887] NR 30 TC 169 Z9 170 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD DEC 24 PY 1993 VL 262 IS 5142 BP 2057 EP 2059 DI 10.1126/science.8266105 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MN108 UT WOS:A1993MN10800045 PM 8266105 ER PT J AU OSSWALD, S TROUTON, TG MCGOVERN, BA AF OSSWALD, S TROUTON, TG MCGOVERN, BA TI NEUROCARDIOGENIC SYNCOPE - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP OSSWALD, S (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 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 DEC 23 PY 1993 VL 329 IS 26 BP 1967 EP 1967 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MM885 UT WOS:A1993MM88500021 ER PT J AU DINARELLO, CA WEBB, AC ROSENWASSER, LJ RICH, A WOLFF, SM AURON, PE AF DINARELLO, CA WEBB, AC ROSENWASSER, LJ RICH, A WOLFF, SM AURON, PE TI MOLECULAR-CLONING OF HUMAN INTERLEUKIN-1B - A CITATION-CLASSIC COMMENTARY ON NUCLEOTIDE-SEQUENCE OF HUMAN MONOCYTE INTERLEUKIN-1 PRECURSOR CDNA BY AURON,P.E., WEBB,A.C., ROSENWASSER,L.J., MUCCI,S.F., RICH,A., WOLFF,S.M., AND DINARELLO,C.A. SO CURRENT CONTENTS/LIFE SCIENCES LA English DT Article C1 WELLESLEY COLL,DEPT BIOL,WELLESLEY,MA 02181. UNIV COLORADO,NATL JEWISH HOSP,SCH MED,DENVER,CO 80207. MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP DINARELLO, CA (reprint author), TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,BOSTON,MA 02111, USA. NR 3 TC 0 Z9 0 U1 0 U2 8 PU INST SCI INFORM INC PI PHILADELPHIA PA 3501 MARKET ST, PHILADELPHIA, PA 19104 SN 0011-3409 J9 CC/LIFE SCI PD DEC 20 PY 1993 IS 51-52 BP 8 EP 8 PG 1 WC Multidisciplinary Sciences; Social Sciences, Interdisciplinary SC Science & Technology - Other Topics; Social Sciences - Other Topics GA MJ841 UT WOS:A1993MJ84100001 ER PT J AU GOLDHIRSCH, A GELBER, RD CASTIGLIONE, M SENN, HJ AF GOLDHIRSCH, A GELBER, RD CASTIGLIONE, M SENN, HJ TI DOXORUBICIN ADJUVANT COMBINATIONS FOR BREAST-CANCER - REPLY SO LANCET LA English DT Letter ID CHEMOTHERAPY; CYCLOPHOSPHAMIDE; METHOTREXATE; FLUOROURACIL; TAMOXIFEN; TUMORS C1 IBCSG,FDN COUNCIL,T GALLEN,SWITZERLAND. IBCSG,BERN,SWITZERLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GOLDHIRSCH, A (reprint author), OSPED CIVICO,DEPT ONCOL,IBCSG,CH-6900 LUGANO,SWITZERLAND. NR 8 TC 0 Z9 0 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD DEC 18 PY 1993 VL 342 IS 8886-7 BP 1551 EP 1551 DI 10.1016/S0140-6736(05)80117-5 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MM402 UT WOS:A1993MM40200036 ER PT J AU POLLACK, AE HARRISON, MB WOOTEN, GF FINK, JS AF POLLACK, AE HARRISON, MB WOOTEN, GF FINK, JS TI DIFFERENTIAL LOCALIZATION OF A2A ADENOSINE RECEPTOR MESSENGER-RNA WITH D1 AND D2 DOPAMINE-RECEPTOR MESSENGER-RNA IN STRIATAL OUTPUT PATHWAYS FOLLOWING A SELECTIVE LESION OF STRIATONIGRAL NEURONS SO BRAIN RESEARCH LA English DT Note DE IN SITU HYBRIDIZATION; VOLKENSIN; BASAL GANGLIA; STRIATUM; A2 ADENOSINE RECEPTOR ID TERM RESERPINIZED MICE; GENE-EXPRESSION; STRIATOPALLIDAL NEURONS; MESSENGER-RNA; RAT STRIATUM; VOLKENSIN; CLONING; BINDING AB We have used the suicide transport agent volkensin to produce selective lesions of striatonigral neurons. By in situ hybridization histochemistry unilateral volkensin injections in the substantia nigra decreased the number of D1 receptor mRNA-expressing neurons in the ipsilateral striatum but did not change the number of D2 receptor and A2a adenosine receptor mRNA-expressing neurons. These findings confirm that striatonigral neurons express D1 receptors and suggest that D2-A2a receptor expressing neurons are predominantly localized to other neuronal populations within the striatum. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02114. UNIV VIRGINIA,DEPT NEUROL,CHARLOTTESVILLE,VA 22908. FU NIDA NIH HHS [DA07496]; NINDS NIH HHS [NS01454, NS30024] NR 24 TC 60 Z9 60 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD DEC 17 PY 1993 VL 631 IS 1 BP 161 EP 166 DI 10.1016/0006-8993(93)91204-6 PG 6 WC Neurosciences SC Neurosciences & Neurology GA MK991 UT WOS:A1993MK99100026 PM 8298989 ER PT J AU CHESEBRO, JH BADIMON, JJ ORTIZ, AF MEYER, BJ FUSTER, V AF CHESEBRO, JH BADIMON, JJ ORTIZ, AF MEYER, BJ FUSTER, V TI CONJUNCTIVE ANTITHROMBOTIC THERAPY FOR THROMBOLYSIS IN MYOCARDIAL-INFARCTION SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Unresolved Issues in Thrombolysis CY MAY 05-06, 1993 CL COMO, ITALY ID UNSTABLE ANGINA-PECTORIS; PLASMINOGEN-ACTIVATOR; PLATELET-AGGREGATION; RECOMBINANT HIRUDIN; ARTERIAL THROMBOSIS; HEPARIN; INHIBITION; DEPOSITION; DISEASE; ASPIRIN AB Disruption of an atherosclerotic plaque in coronary arteries with a minor stenosis Is the usual stimulus for acute coronary thrombosis and myocardial infarction. In this article the pathogenesis of arterial thrombosis and contributions of local arterial wall substrates, the theology of blood flow, systemic factors, and the critical role of thrombin in the formation of thrombus are discussed. More potent antithrombotic therapy may accelerate exogenous thrombolysis, allows endogenous thrombolysis, and should reduce recurrent infarction and ischemia and death, as well as need for coronary revascularization. Maximal antithrombotic therapy for acute myocardial infarction includes an Intravenous bolus of heparin at 100 U/kg followed by an intravenous infusion-at 1,200 U/hr for patients weighing 60-80 kg, 1,300 U/hr for those weighing >80 kg, and 1,000 U/hr for those weighing <60 kg (or 1;1 U/kg/hr)-to maintain the activated partial thromboplastin time at 2-3 times control (60-90 sec) for at least 5-7 days. To convert intravenous to subcutaneous administration, use 14,000-17,000 U every 12 hours and Initially overlap the intravenous infusion by 2 hours. The loading dose of aspirin on admission to the hospital is 160 mg followed by 80 mg/day. High risk patients should be considered for conversion of heparin to warfarin therapy for at least 3 months at an international normalized ratio of 2.5-4.0 for the prevention of recurrent ischemia, reinfarction, death, thromboembolism, reactivation of thrombosis, and reduced necessity for revascularization. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CHESEBRO, JH (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,JACKSON 1402,32 FRUIT ST,BOSTON,MA 02114, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 52 TC 4 Z9 4 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD DEC 16 PY 1993 VL 72 IS 19 BP G66 EP G74 DI 10.1016/0002-9149(93)90110-X PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MP705 UT WOS:A1993MP70500011 PM 8279364 ER PT J AU BURTON, MD WAIN, JC AF BURTON, MD WAIN, JC TI CLUBBING AND HYPERTROPHIC OSTEOARTHROPATHY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note RP BURTON, MD (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 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 DEC 16 PY 1993 VL 329 IS 25 BP 1861 EP 1861 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA ML588 UT WOS:A1993ML58800007 PM 8247039 ER PT J AU COCKRILL, BA MCLOUD, TC KAZEMI, H WAIN, JC MARK, EJ AF COCKRILL, BA MCLOUD, TC KAZEMI, H WAIN, JC MARK, EJ TI A 46-YEAR-OLD MAN WITH POSTOBSTRUCTIVE PNEUMONIA AND A PULMONARY MASS - BRONCHIECTASIS, LEFT LOWER LOBE, SACCULAR AND ANEURYSMAL, WITH COLLAPSE AND CHRONIC ORGANIZING PNEUMONIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID CYSTIC ADENOMATOID MALFORMATION; PLASMA-CELL GRANULOMA; INFLAMMATORY PSEUDOTUMORS; PLEURAL MESOTHELIOMA; SURGICAL-TREATMENT; FIBROUS TUMORS; LUNG; SEQUESTRATION; BRONCHOPULMONARY; HISTIOCYTOMA C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP COCKRILL, BA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 47 TC 1 Z9 1 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 DEC 16 PY 1993 VL 329 IS 25 BP 1873 EP 1880 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA ML588 UT WOS:A1993ML58800009 ER PT J AU BLACKER, D LAVORI, PW FARAONE, SV TSUANG, MT AF BLACKER, D LAVORI, PW FARAONE, SV TSUANG, MT TI UNIPOLAR RELATIVES IN BIPOLAR PEDIGREES - A SEARCH FOR INDICATORS OF UNDERLYING BIPOLARITY SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE MANIC-DEPRESSIVE ILLNESS; DEPRESSION; LINKAGE ANALYSIS; CASENESS INDEX ID MANIC-DEPRESSIVE ILLNESS; AFFECTIVE-DISORDERS; GENETIC-LINKAGE; COLLABORATIVE PROGRAM; PSYCHIATRIC-DISORDERS; DIAGNOSTIC CRITERIA; COMPLEX DISEASES; RELIABILITY; FAMILY; SCHIZOPHRENIA AB In an effort to identify features indicative of underlying bipolarity within the unipolar relatives of bipolar probands, we compared unipolar relatives of bipolars with unipolar relatives of unipolars. Using data from the Collaborative Study of the Psychobiology of Depression, we compared a number of demographic and clinical features individually, and then developed a logistic regression model for the differences found. Unipolar relatives of bipolars were somewhat more likely to be male and to have subthreshold bipolar features, and less likely to have panic symptoms. In addition, they had a small but significant decrease in the number of depressive symptoms and a large decrease in all treatment indicators. A multiple logistic regression model for these differences was highly significant, but had limited ability to discriminate between the two groups. These differences are not large enough to effectively discriminate between the groups for the purposes of classification. These particular results may result from a number of factors, most likely the choice of comparison group. Nonetheless, the work demonstrates a potential method for the construction of caseness indices for use in genetic studies of bipolar and other psychiatric disorders. (C) 1993 Wiley-Liss, Inc. C1 HARVARD UNIV, SCH PUBL HLTH, PROGRAM PSYCHIAT EPIDEMIOL, BOSTON, MA 02115 USA. BROWN UNIV, DEPT PSYCHIAT & HUMAN BEHAV, PROVIDENCE, RI 02912 USA. VET ADM MED CTR, BROCKTON, MA USA. RP BLACKER, D (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT PSYCHIAT, CNY-9, BOSTON, MA 02114 USA. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [5T32-MH17119-08, 3-U01-MH25478-18, U01-MH46318] NR 51 TC 19 Z9 19 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 EI 1096-8628 J9 AM J MED GENET JI Am. J. Med. Genet. PD DEC 15 PY 1993 VL 48 IS 4 BP 192 EP 199 DI 10.1002/ajmg.1320480405 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA ML602 UT WOS:A1993ML60200004 PM 8135302 ER PT J AU SALLES, G ZAIN, M JIANG, WM BOUSSIOTIS, VA SHIPP, MA AF SALLES, G ZAIN, M JIANG, WM BOUSSIOTIS, VA SHIPP, MA TI ALTERNATIVELY SPLICED CD44 TRANSCRIPTS IN DIFFUSE LARGE-CELL LYMPHOMAS - CHARACTERIZATION AND COMPARISON WITH NORMAL ACTIVATED B-CELLS AND EPITHELIAL MALIGNANCIES SO BLOOD LA English DT Note ID LYMPHOCYTE HOMING RECEPTOR; NON-HODGKINS-LYMPHOMA; MONOCLONAL-ANTIBODIES; ADHESION MOLECULES; TUMOR-GROWTH; ANTIGEN; EXPRESSION; PROTEIN; HYALURONATE; EXONS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 46 TC 78 Z9 80 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 DEC 15 PY 1993 VL 82 IS 12 BP 3539 EP 3547 PG 9 WC Hematology SC Hematology GA MM263 UT WOS:A1993MM26300004 PM 7505117 ER PT J AU UCHIYAMA, H BARUT, BA MOHRBACHER, AF CHAUHAN, D ANDERSON, KC AF UCHIYAMA, H BARUT, BA MOHRBACHER, AF CHAUHAN, D ANDERSON, KC TI ADHESION OF HUMAN MYELOMA-DERIVED CELL-LINES TO BONE-MARROW STROMAL CELLS STIMULATES INTERLEUKIN-6 SECRETION SO BLOOD LA English DT Article ID HUMAN MULTIPLE-MYELOMA; PLASMA-CELLS; PERIPHERAL-BLOOD; B-CELLS; GROWTH; EXPRESSION; DIFFERENTIATION; PROLIFERATION; MOLECULES; RECEPTORS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA50947] NR 44 TC 328 Z9 335 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 DEC 15 PY 1993 VL 82 IS 12 BP 3712 EP 3720 PG 9 WC Hematology SC Hematology GA MM263 UT WOS:A1993MM26300027 PM 8260708 ER PT J AU MELDER, RJ BROWNELL, AL SHOUP, TM BROWNELL, GL JAIN, RK AF MELDER, RJ BROWNELL, AL SHOUP, TM BROWNELL, GL JAIN, RK TI IMAGING OF ACTIVATED NATURAL-KILLER-CELLS IN MICE BY POSITRON EMISSION TOMOGRAPHY - PREFERENTIAL UPTAKE IN TUMORS SO CANCER RESEARCH LA English DT Note ID INFILTRATING LYMPHOCYTES; LOCALIZATION; MELANOMA; INVIVO AB Optimal delivery of immunologically active cells to target tissue(s) is important for improving adoptive immunotherapy of neoplastic diseases. By using positron emission tomography, we have measured the systemic distribution and tumor localization of locally injected, activated natural killer (NK) cells or nonactivated lymphocytes in the FSaII fibrosarcoma grown s.c. in the tail of C3H mice. Murine NK cells were isolated and expanded in the presence of interleukin 2 and collected at 5 to 7 days after culture. These cells were then washed and labeled with [C-11]methyl iodide, a positron-emitting isotope. Ten million activated or nonactivated cells were injected into the lateral tail vein distal to the tumor over a period of 2 min, and the accumulation of counts in the tumor was monitored during the injection and at 30-60 min postinjection. There was no significant difference in the rate of accumulation of activated NK cells (685 +/- 264 (SE); n = 5) versus nonactivated splenic lymphocytes (595 +/- 105; n = 5) during the injection period. Whole body scans of the mice done at 30 min to 1 h postinjection showed that the number of activated cells retained within the tumor ranged from 4 to 30% (15.3 +/- 4.9%; n = 5) of the injected dose. Activated NK cells which were not retained by the tumor accumulated in the lungs, liver, and spleen. In contrast, from 3 to 4% (3.4 +/- 0.2%; n = 5) of nonactivated lymphocytes remained within the tumor by 1 h. Nonactivated cells were distributed more homogeneously throughout the systemic circulation than the activated cells, although these cells also demonstrated increased retention in the lungs, liver, and spleen. The present study demonstrates that positron emission tomography may be used to quantify the number of effector cells which accumulate within tumors and to determine their biodistribution. The retention of labeled cells within the tumor may also be used as a means of imaging the tumor. Finally, the preferential accumulation of effector cells in the tumor vasculature following local injection has useful implications for adoptive immunotherapy. C1 HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP MELDER, RJ (reprint author), HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115, USA. NR 20 TC 49 Z9 49 U1 0 U2 5 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 15 PY 1993 VL 53 IS 24 BP 5867 EP 5871 PG 5 WC Oncology SC Oncology GA ML589 UT WOS:A1993ML58900008 PM 8261395 ER PT J AU FRISOLI, JK TUDOR, EG FLOTTE, TJ HASAN, T DEUTSCH, TF SCHOMACKER, KT AF FRISOLI, JK TUDOR, EG FLOTTE, TJ HASAN, T DEUTSCH, TF SCHOMACKER, KT TI PHARMACOKINETICS OF A FLUORESCENT DRUG USING LASER-INDUCED FLUORESCENCE SO CANCER RESEARCH LA English DT Article ID PHOTODYNAMIC THERAPY; SULFONATED PHTHALOCYANINE; CEREBRAL GLIOMA; ALUMINUM PHTHALOCYANINE; TISSUE DISTRIBUTION; MICE BEARING; PHOTOFRIN-II; TUMORS; HEMATOPORPHYRIN; CANCER AB Laser-induced fluorescence has been used to measure tissue levels of chloroaluminum sulfonated phthalocyanine in vivo in an implanted hamster cheek pouch carcinoma tumor model. The drug was excited at 610 nm via a pulsed nitrogen laser-pumped dye laser, and fluorescence intensity was monitored at 684 nm for up to 30 days after drug administration. Data were acquired noninvasively with high temporal and spatial resolution using the laser-induced fluorescence apparatus and were analyzed with a multicompartment pharmacokinetic model. In addition, our published data on a C6-BAG glioma rat brain tumor model were analyzed to illustrate the effect of different tumor models on the rates. The rates extracted from the pharmacokinetic model elucidate the mechanisms of drug uptake and retention in the cheek pouch and brain tumor models. The laser-induced fluorescence approach should lead to better drug dosimetry for photochemotherapy and allow quick characterization of the pharmacokinetics of new photosensitizers in tissue. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTODED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. FU NCI NIH HHS [R01 CA156177]; NHLBI NIH HHS [HL46384] NR 37 TC 36 Z9 38 U1 1 U2 5 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 15 PY 1993 VL 53 IS 24 BP 5954 EP 5961 PG 8 WC Oncology SC Oncology GA ML589 UT WOS:A1993ML58900023 PM 8261409 ER PT J AU GALLUSSER, A KIRCHHAUSEN, T AF GALLUSSER, A KIRCHHAUSEN, T TI THE BETA-1-SUBUNIT AND BETA-2-SUBUNIT OF THE AP COMPLEXES ARE THE CLATHRIN COAT ASSEMBLY COMPONENTS SO EMBO JOURNAL LA English DT Article DE AP-CLATHRIN INTERACTION; CLATHRIN-ASSOCIATED PROTEINS; ENDOCYTOSIS; MEMBRANE TRAFFIC; RECOMBINANT AP SUBUNITS ID PLASMA-MEMBRANE; PROTEIN COMPLEX; BOVINE BRAIN; VESICLES; BINDING; IDENTIFICATION; PURIFICATION; POLYPEPTIDES; RECEPTOR; DOMAINS AB The beta1 and beta2 subunits are the closely-related large chains of the trans-Golgi network AP-1 and the plasma membrane AP-2 clathrin-associated protein complexes, respectively. Recombinant beta1 and beta2 subunits have been generated in Escherichia coli. It was found that, in the absence of alt the other AP subunits, beta1 and beta2 interact with clathrin and drive the efficient assembly of clathrin coats. In addition, beta2 subunits and AP complexes compete for the same clathrin binding site. The appearance of the clathrin/beta coats is the same as the barrel-shaped structures formed with native AP complexes. It is proposed that the principal function of the beta subunits is to initiate coat formation, while the remaining subunits of the AP complexes have other roles in coated pit and coated vesicle function. C1 HARVARD UNIV,SCH MED,DEPT CELL BIOL,200 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. NR 39 TC 122 Z9 123 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD DEC 15 PY 1993 VL 12 IS 13 BP 5237 EP 5244 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MM120 UT WOS:A1993MM12000036 PM 8262066 ER PT J AU PIGNATA, C PRASAD, KVS ROBERTSON, MJ LEVINE, H RUDD, CE RITZ, J AF PIGNATA, C PRASAD, KVS ROBERTSON, MJ LEVINE, H RUDD, CE RITZ, J TI FC-GAMMA-RIIIA-MEDIATED SIGNALING INVOLVES SRC-FAMILY LCK IN HUMAN NATURAL-KILLER-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TYROSINE-PROTEIN-KINASE; GROWTH-FACTOR RECEPTOR; LYMPHOCYTES-T; CD3 COMPLEX; IGG FC; PHOSPHORYLATION; EXPRESSION; TRANSDUCTION; CD16; ACTIVATION AB The cell surface receptor for IgG Fc domain (FcgammaRIIIA, CD16) is present as a multimeric complex on human NK cells and is essential for antibody-dependent cellular cytotoxicity. Although CD16 engagement induces tyrosine phosphorylation of several substrates, the intracytoplasmic domains of the CD16 molecule lack intrinsic protein tyrosine kinase consensus sequences. We report here that, in human NK cells, engagement of the CD16 receptor induces tyrosine phosphorylation of p56lck tyrosine kinase. CD16 triggering through anti-receptor antibody enhances in vitro kinase activity of phosphotyrosyl proteins and autophosphorylation activity of anti-/ck immunoprecipitates. Similar results were obtained after stimulation with IL-1 2. In vivo labeling experiments showed that CD16 cross-linking primarily induces in vivo phosphorylation of p56lck at the tyr-394 autophosphorylation site. Using in vitro kinase assay of CD16 immunoprecipitates from lysates of human NK cells, we demonstrated that a phosphorylated protein of 62 to 65 kDa was co-precipitated with CD16. Reprecipitation experiments also suggested that a small amount of p56lck may interact with this complex. These results indicate that CD16 triggering involves p56lck and that this kinase is therefore involved in the signaling pathways regulating NK cell cytolytic functions. However, additional kinases not yet identified are also likely to play a role in the early signaling events through CD16. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV TUMOR IMMUNOL,BOSTON,MA 02115. 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 34 TC 55 Z9 55 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 DEC 15 PY 1993 VL 151 IS 12 BP 6794 EP 6800 PG 7 WC Immunology SC Immunology GA MM036 UT WOS:A1993MM03600019 PM 8258691 ER PT J AU DANG, H OGAWA, N TAKEI, M LAZARIDIS, K TALAL, N AF DANG, H OGAWA, N TAKEI, M LAZARIDIS, K TALAL, N TI INDUCTION OF LUPUS-ASSOCIATED AUTOANTIBODIES BY IMMUNIZATION WITH NATIVE AND RECOMBINANT IG POLYPEPTIDES EXPRESSING A CROSS-REACTIVE IDIOTYPE 4B4 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTI-SM AUTOANTIBODY; INTERSPECIES IDIOTYPE; DNA IDIOTYPE; NAIVE MICE; CELL LINES; ERYTHEMATOSUS; ANTIBODIES; ACTIVATION; DISEASE; GENE AB A human mAb designated 4B4 with anti-Sm activity was derived from a patient with systemic lupus erythematosus. This antibody expressed a lupus-associated cross-reactive Id, partially related to the monoclonal murine anti-Sm (Y2) from MRL/lpr mice. Studies were performed to investigate the ability of 4B4 to induce lupus in nonautoimmune-prone mice. BALB/c mice immunized with 4B4 produced antibodies to dsDNA, ssDNA, Sm ribonucleoprotein, and mouse Fc fragment. There was no antibody activity against SSA/Ro, SSB/La, and hen egg lysozyme. Ag inhibition studies show that the autoantibodies were not polyreactive. Mice were also immunized with r4B4 polypeptides representing the H/L heterodimer, H chain and L chain. Autoantibodies were induced in mice immunized against the H/L and H polypeptides. No autoantibodies were induced in mice immunized with recombinant L chain. Furthermore, from 20 to 68% of antibody activity to Sm or dsDNA could be inhibited with anti-Id antiserum (either anti-4B4 or Y2). The autoantibody was initially IgM and then underwent an isotype switch to IgG. These results show that lupus-associated autoantibodies can be induced by immunization with 4B4 and that the 4B4 V(H) region is important in this induction process. The finding of murine IgG autoantibody expressing a cross-reactive Id similar to the immunizing 4B4 suggests a role for anti-idiotypic Th cells in this autoimmune response. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP DANG, H (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [DE 09311] NR 33 TC 46 Z9 46 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 DEC 15 PY 1993 VL 151 IS 12 BP 7260 EP 7267 PG 8 WC Immunology SC Immunology GA MM036 UT WOS:A1993MM03600066 PM 8258723 ER PT J AU SANDLER, DP SHORE, DL ANDERSON, JR DAVEY, FR ARTHUR, D MAYER, RJ SILVER, RT WEISS, RB MOORE, JO SCHIFFER, CA WURSTERHILL, DH MCINTYRE, OR BLOOMFIELD, CD AF SANDLER, DP SHORE, DL ANDERSON, JR DAVEY, FR ARTHUR, D MAYER, RJ SILVER, RT WEISS, RB MOORE, JO SCHIFFER, CA WURSTERHILL, DH MCINTYRE, OR BLOOMFIELD, CD TI CIGARETTE-SMOKING AND RISK OF ACUTE-LEUKEMIA - ASSOCIATIONS WITH MORPHOLOGY AND CYTOGENETIC ABNORMALITIES IN BONE-MARROW SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; ACUTE MYELOID-LEUKEMIA; UNITED-STATES VETERANS; ADULT LEUKEMIA; EXPOSURES; OCCUPATION; KARYOTYPE; BENZENE; CRISIS AB Background: Cigarette smoking may be a risk factor for leukemia. No detailed biological mechanism has been proposed, but a causal link is made plausible by evidence of systemic effects of cigarette smoke and the presence in cigarette smoke of chemicals that have been associated with leukemia risk. Purpose: Our purpose was to investigate the leukemia risk associated with cigarette smoking in a multicenter case-control study of acute leukemias in adults. Methods: Adults aged 18-79 with newly diagnosed leukemia were contacted to participate in this epidemiologic study when they entered a clinical trial to be treated under protocols sponsored by Cancer and Leukemia Group B. Smoking histories for 610 patients with acute leukemia and 618 population control subjects were obtained by telephone interviews. We examined bone marrow samples and classified patients by morphology of leukocyte precursor cells according to the French-American-British (FAB) classification system and, for 378 patients, by the presence or absence of specific clonal chromosome abnormalities. We calculated odds ratios (ORs) for risk of leukemia associated with smoking cigarettes. ORs were adjusted for age, race, and sex. Results: Smoking was associated with only a modest increase in risk for leukemia overall (adjusted OR = 1.13; 95% confidence interval [CI] = 0.89-1.44). However, among participants aged 60 and older, smoking was associated with a twofold increase in risk for acute myeloid leukemia (AML) (OR = 1.96; 95% CI = 1.17-3.28) and a threefold increase in risk for acute lymphocytic leukemia (ALL) (OR = 3.40; 95% CI 0.97-11.9). Among older persons, risks increased with amount and duration of smoking. Smoking was associated with increased risk for AML classified as FAB type M2 at all ages, with ORs of 1.70 (95% CI = 1.00-2.90) for those younger than 60 and 3,50 (95% CI = 1.53-8.03) for those aged 60 and older. Smoking was also associated with ALL type L2 at all ages, with ORs of 1.72 (95% CI = 0.90-3.27) for those younger than 60 and 5.34 (95% CI = 1.03-27.6) for those who were older. Smoking was more common among patients with specific chromosome abnormalities in AML [-7 or 7q-, -Y, +13] and in ALL [t(9;22)(q34;q11)]. Conclusions: Cigarette smoking is associated with increased risk for leukemia and may lead to leukemias of specific morphologic and chromosomal types. The association varies with age. Implication: Examining discrete subtypes of disease may permit more accurate assessment of risk. As standardized morphologic classification and cytogenetic and molecular evaluation of leukemia patients becomes more common, epidemiologic studies that take advantage of these advances will begin to contribute to the identification of additional risk factors and mechanisms in acute leukemia. C1 WESTAT CORP,DURHAM,NC. NEBRASKA MED CTR,DEPT PREVENT & SOCIETAL MED,OMAHA,NE. SUNY HLTH SCI CTR,DEPT PATHOL,SYRACUSE,NY. UNIV MINNESOTA,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CORNELL UNIV,MED CTR,NEW YORK HOSP,CLIN ONCOL SECT,NEW YORK,NY 10021. WALTER REED ARMY MED CTR,MED ONCOL SECT,WASHINGTON,DC 20307. DUKE UNIV,MED CTR,DEPT HEMATOL ONCOL,DURHAM,NC 27710. UNIV MARYLAND,CTR CANC,CATONSVILLE,MD 21228. UNIV MARYLAND,MED CTR,CATONSVILLE,MD 21228. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,CANC & LEUKEMIA GRP B,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PATHOL,HANOVER,NH 03756. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT MED,BUFFALO,NY 14263. RP SANDLER, DP (reprint author), NIEHS,EPIDEMIOL BRANCH,ENVIRONM & MOLEC EPIDEMIOL SECT,MAIL DROP A3-05,POB 12233,RES TRIANGLE PK,NC 27709, USA. OI Sandler, Dale/0000-0002-6776-0018 FU NCI NIH HHS [CA31946, CA33601, CA37027] NR 55 TC 74 Z9 75 U1 1 U2 3 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD DEC 15 PY 1993 VL 85 IS 24 BP 1994 EP 2003 DI 10.1093/jnci/85.24.1994 PG 10 WC Oncology SC Oncology GA ML155 UT WOS:A1993ML15500010 PM 8246285 ER PT J AU ANDREWS, NC KOTKOW, KJ NEY, PA ERDJUMENTBROMAGE, H TEMPST, P ORKIN, SH AF ANDREWS, NC KOTKOW, KJ NEY, PA ERDJUMENTBROMAGE, H TEMPST, P ORKIN, SH TI THE UBIQUITOUS SUBUNIT OF ERYTHROID TRANSCRIPTION FACTOR NF-E2 IS A SMALL BASIC-LEUCINE ZIPPER PROTEIN RELATED TO THE V-MAF ONCOGENE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GLOBIN GENE EXPRESSION; LOCUS CONTROL REGION; AP-1 MOTIF ID DOMINANT CONTROL REGION; LOCUS-CONTROL REGION; PORPHOBILINOGEN DEAMINASE GENE; DNA-BINDING PROTEIN; BETA-GLOBIN GENE; REGULATORY ELEMENT; MAMMALIAN-CELLS; JUN-B; C-JUN; INVIVO AB Erythroid transcription factor NF-E2 is a tissue-restricted heterodimeric protein which recognizes an extended AP-1 motif [(T/C)TGCTGA(C/G)TCA(T/C)] found in the upstream locus control regions of the alpha- and beta-globin gene clusters. A cDNA clone encoding a cell-type-specific subunit of NF-E2, designated p45 NF-E2, has previously been characterized and shown to encode a basic-leucine zipper DNA-binding protein. Here we describe protein purification and cloning of cDNA that encodes the second basic-leucine zipper subunit of the native NF-E2 heterodimer. This polypeptide, designated p18, is widely expressed. It displays extensive homology to the v-maf oncogene product and a human retinal-specific protein, NRL. Unusual features in the basic region shared by v-Maf, NRL, and p18 place them in a distinct subfamily of AP-1-like proteins. C1 HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. HOWARD HUGHES MED INST, BOSTON, MA 02115 USA. ST JUDE CHILDRENS RES HOSP, DEPT BIOCHEM, MEMPHIS, TN 38101 USA. MEM SLOAN KETTERING CANC CTR, MOLEC BIOL PROGRAM, NEW YORK, NY 10021 USA. RP ANDREWS, NC (reprint author), HARVARD UNIV, CHILDRENS HOSP, SCH MED, DANA FARBER CANC INST, DIV HEMATOL ONCOL, BOSTON, MA 02115 USA. OI Andrews, Nancy/0000-0003-0243-4462 NR 42 TC 233 Z9 235 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 15 PY 1993 VL 90 IS 24 BP 11488 EP 11492 DI 10.1073/pnas.90.24.11488 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MM515 UT WOS:A1993MM51500012 PM 8265578 ER PT J AU ARULANANDAM, ARN WITHKA, JM WYSS, DF WAGNER, G KISTER, A PALLAI, P RECNY, MA REINHERZ, EL AF ARULANANDAM, ARN WITHKA, JM WYSS, DF WAGNER, G KISTER, A PALLAI, P RECNY, MA REINHERZ, EL TI THE CD58 (LFA-3) BINDING-SITE IS A LOCALIZED AND HIGHLY-CHARGED SURFACE-AREA ON THE AGFCC'C'' FACE OF THE HUMAN CD2 ADHESION DOMAIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CELL ADHESION; T-CELL RECEPTOR; NMR; SITE-DIRECTED MUTAGENESIS ID FUNCTION-ASSOCIATED ANTIGEN-3; CELL ERYTHROCYTE RECEPTOR; LYMPHOCYTE-T; 3-DIMENSIONAL STRUCTURE; MOLECULAR-CLONING; PROTEIN; RECOGNITION; ACTIVATION; COMPLEX; SHEEP AB Using site-directed mutagenesis in conjunction with NMR structural data on the adhesion domain of human CD2, we have defined the binding region for CD58. Previous structural studies of rat and human CD2 indicate that this adhesion domain is immunoglobulin-like. Here we report that the CD58 binding site is a well-circumscribed, charged surface area covering almost-equal-to 770 angstrom2 on the AGFCC'C'' face of the CD2 beta barrel. This site contains beta-strand residues in the carboxyl-terminal half of the F strand (including Lys-82 and Tyr-86), the top of the C strand (Asp-32 and Lys-34), and the C' strand (Gln-46), which are all solvent exposed. In addition, several exposed residues on the FG loop (Gly-90, Lys-91, Asn-92, and Val-93), the CC' loop (Lys-41 and Lys-43), and the C'C'' loop (Arg-48 and Lys-51) form this site. In contrast, neither residues on the more peripheral G and C'' strands of the same CD2 surface nor residues on B, E, and D strands of the opposite face are involved in CD58 binding. This CD58 binding site is predicted to lie most distal to the T-lymphocyte surface membrane, with ready access to CD58 on the surface of the opposing antigen-presenting cell. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP ARULANANDAM, ARN (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115, USA. NR 39 TC 77 Z9 78 U1 3 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 15 PY 1993 VL 90 IS 24 BP 11613 EP 11617 DI 10.1073/pnas.90.24.11613 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MM515 UT WOS:A1993MM51500037 PM 7505442 ER PT J AU LEE, CH LI, W NISHIMURA, R ZHOU, M BATZER, AG MYERS, MG WHITE, MF SCHLESSINGER, J SKOLNIK, EY AF LEE, CH LI, W NISHIMURA, R ZHOU, M BATZER, AG MYERS, MG WHITE, MF SCHLESSINGER, J SKOLNIK, EY TI NCK-ASSOCIATES WITH THE SH2 DOMAIN-DOCKING PROTEIN IRS-1 IN INSULIN-STIMULATED CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID RECEPTOR TYROSINE KINASES; PHOSPHATIDYLINOSITOL 3'-KINASE; SIGNAL TRANSDUCTION; GROWTH-FACTOR; PHOSPHORYLATION; BINDING; TARGET; REGION; GAP; P85 AB Nck, an oncogenic protein composed of one SH2 and three SH3 domains, is a common target for various cell surface receptors. Nck is thought to function as an adaptor protein to couple cell surface receptors to downstream effector molecules that regulate cellular responses induced by receptor activation. In this report, we show that Nck forms a stable complex in vivo with IRS-1 in insulin-stimulated cells. The interaction between IRS-1 and Nck is mediated by the binding of the SH2 domain of Nck to tyrosine-phosphorylated IRS-1. Although Nck associates with IRS-1, Nck phosphorylation is not affected by insulin stimulation. Furthermore, in vitro and in vivo studies show that the SH2 domains of Nck, GRB2, and p85 bind distinct phosphotyrosine residues in IRS-1. After insulin stimulation all three signaling molecules can be found complexed to a single IRS-1 molecule. These findings provide further evidence that, in response to insulin stimulation, IRS-1 acts as an SH2 docking protein that coordinates the regulation of various different signaling pathways activated by the insulin receptor. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,BOSTON,MA 02115. RP LEE, CH (reprint author), NYU MED CTR,DEPT PHARMACOL,NEW YORK,NY 10016, USA. RI Lee, Chi-Hon/G-9190-2012 FU NIDDK NIH HHS [DK438080] NR 38 TC 195 Z9 198 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 DEC 15 PY 1993 VL 90 IS 24 BP 11713 EP 11717 DI 10.1073/pnas.90.24.11713 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MM515 UT WOS:A1993MM51500057 PM 8265614 ER PT J AU BROOKS, EG BALK, SP AUPEIX, K COLONNA, M STROMINGER, JL GROHSPIES, V AF BROOKS, EG BALK, SP AUPEIX, K COLONNA, M STROMINGER, JL GROHSPIES, V TI HUMAN T-CELL RECEPTOR (TCR) ALPHA/BETA+ CD4-CD8- T-CELLS EXPRESS OLIGOCLONAL TCRS, SHARE JUNCTIONAL MOTIFS ACROSS TCR V(BETA)-GENE FAMILIES, AND PHENOTYPICALLY RESEMBLE MEMORY T-CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DOUBLE-NEGATIVE CD4-CD8; MAJOR HISTOCOMPATIBILITY COMPLEX; ALPHA-BETA; LYMPHOCYTES-T; GENE FAMILIES; COMBINED IMMUNODEFICIENCY; FUNCTIONAL-PROPERTIES; POPULATION; THYMOCYTES; ANTIGEN AB Most human T cells express the TCR alpha/beta and either CD4 or CD8 molecules (single positive, SP); however, small numbers lack CD4 and CD8. In inbred mice, alpha/beta CD4-CD8- (double negative, DN) T cells preferentially express certain beta variable region (V(beta)) families and may arise via unique developmental pathways. Increased percentages of alpha/beta DN T cells have been identified in some human and murine autoimmune and immunodeficiency diseases. However, their contribution to disease pathology or normal immunity is unknown. To study the cell surface phenotype and TCR diversity of human alpha/beta DN T cells, these cells were isolated from the peripheral blood of healthy adults. The proportion of alpha/beta DN T cells expressing molecules associated with activation (HLA-DR), previous exposure to antigen (CD45RO), and cytotoxic function (CD56, CD57, and CD11b) was increased relative to SP T cells. The TCR V(beta) repertoire of alpha/beta DN T cells was different from that of alpha/beta SP T cells, although most major gene families were present. For example, higher proportions of V(beta)11, a minor gene family in peripheral blood leukocytes, were found in most alpha/beta DN T-cell samples. In contrast to mice, no dominant V(beta) family was used consistently in different human individuals. Within an individual alpha/beta DN T cells possessed an oligoclonal TCRbeta repertoire with conservation of several distinct junctional amino acid motifs with one joined to three different V(beta) genes in two individuals, suggesting that these cells have undergone a selection process driven by a limited set of ligands. The possibility that they may represent, at least in part, originally SP T cells anergized by down-modulation of CD4 or CD8 must also be entertained. Overall, this study demonstrates that human peripheral blood alpha/beta DN T cells possess unique phenotypic and TCRbeta repertoire characteristics when compared with the major alpha/beta SP T cell populations and thus may serve specialized immunologic functions and/or have an unusual origin. C1 BETH ISRAEL HOSP,DIV HEMATOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. FU NCI NIH HHS [CA-47554]; NIAID NIH HHS [K08 AI01064] NR 50 TC 33 Z9 34 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 15 PY 1993 VL 90 IS 24 BP 11787 EP 11791 DI 10.1073/pnas.90.24.11787 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MM515 UT WOS:A1993MM51500072 PM 7505446 ER PT J AU COLLINS, TL BURAKOFF, SJ AF COLLINS, TL BURAKOFF, SJ TI TYROSINE KINASE-ACTIVITY OF CD4-ASSOCIATED P56(LCK) MAY NOT BE REQUIRED FOR CD4-DEPENDENT T-CELL ACTIVATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE T-CELL SIGNALING ID PROTEIN-KINASE; SIGNAL TRANSDUCTION; CROSS-LINKING; ANTIGEN RECEPTOR; CD4 RECEPTOR; PHYSICAL ASSOCIATION; LYMPHOCYTES-T; PHOSPHORYLATION; P56LCK; RESPONSIVENESS AB The lymphoid-specific tyrosine kinase p56lck (Lck) is critical for the development and activation of T lymphocytes, and Lck kinase activity has been implicated in both T-cell antigen receptor/CD3- and CD4-mediated signaling. CD4-dependent T-cell activation has been demonstrated to be dependent upon the association of CD4 with Lck. To examine the role of the kinase activity of Lck in CD4-dependent T-cell activation, we have generated several kinase-deficient mutants of Lck. When transfected into CD4+ murine T-cell hybridoma cells, these mutants cause almost-equal-to 90% diminution in CD4-associated Lck kinase activity. Specifically, upon CD4 crosslinking there is decreased Lck autophosphorylation and decreased phosphorylation of an exogenous substrate. When CD4 is crosslinked to the T-cell antigen receptor-CD3 complex, decreased phosphorylation of associated substrates is also observed. In spite of this striking inhibition of Lck kinase function, cells expressing the kinase-deficient mutants demonstrate normal or enhanced CD4-dependent antigen responsiveness. These data demonstrate that the level of Lck kinase activity does not correlate with its CD4-associated function and suggest that the kinase activity of Lck may not be required for CD4-mediated signaling. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP COLLINS, TL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI17258] NR 35 TC 31 Z9 31 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 15 PY 1993 VL 90 IS 24 BP 11885 EP 11889 DI 10.1073/pnas.90.24.11885 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MM515 UT WOS:A1993MM51500092 PM 7505449 ER PT J AU KING, CY WEISS, MA AF KING, CY WEISS, MA TI THE SRY HIGH-MOBILITY-GROUP BOX RECOGNIZES DNA BY PARTIAL INTERCALATION IN THE MINOR-GROOVE - A TOPOLOGICAL MECHANISM OF SEQUENCE SPECIFICITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE TESTIS-DETERMINING FACTOR; TRANSCRIPTION FACTORS; DNA-BINDING PROTEINS; 2-DIMENSIONAL-NMR SPECTROSCOPY ID NUCLEAR-MAGNETIC-RESONANCE; BINDING PROPERTIES; CRYSTAL-STRUCTURE; DETERMINING GENE; TATA-BOX; PROTEIN; TRANSCRIPTION; COMPLEX; HMG; HELIX AB SRY, a putative transcription factor encoded by the sex-determining region of the human Y chromosome, regulates a genetic switch in male development. Impairment of this switch leads to intersex abnormalities of the newborn and is observed in association with mutations in the SRY DNA-binding domain [the high-mobility-group (HMG) box]. Here we show that the SRY HMG box exhibits a novel mechanism of DNA recognition: partial intercalation of a nonpolar side chain in the DNA minor groove. Base stacking (but not base pairing) is interrupted at the site of insertion. Sequence specificity reflects topological requirements of partial intercalation rather than direct readout of base-specific functional groups. Our results predict that the SRY HMG box inserts an alpha-helix into a widened minor groove at the center of a sharp DNA bend. A similar mechanism may underlie binding of SRY and homologous HMG proteins to four-way junctions (Holliday intermediates) and other noncanonical DNA structures. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NICHD NIH HHS [HD26465] NR 37 TC 115 Z9 116 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 15 PY 1993 VL 90 IS 24 BP 11990 EP 11994 DI 10.1073/pnas.90.24.11990 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MM515 UT WOS:A1993MM51500114 PM 8265659 ER PT J AU ROSENZWEIG, AC FREDERICK, CA LIPPARD, SJ NORDLUND, P AF ROSENZWEIG, AC FREDERICK, CA LIPPARD, SJ NORDLUND, P TI CRYSTAL-STRUCTURE OF A BACTERIAL NONHEME IRON HYDROXYLASE THAT CATALYZES THE BIOLOGICAL OXIDATION OF METHANE SO NATURE LA English DT Article ID METHYLOCOCCUS-CAPSULATUS-BATH; METHYLOSINUS-TRICHOSPORIUM OB3B; ACTIVE-SITE; RIBONUCLEOTIDE REDUCTASE; MONO-OXYGENASE; GENE-CLUSTER; COMPONENT-C; PROTEIN-A; OIL-SPILL; MONOOXYGENASE AB The 2.2 angstrom crystal structure of the 251K alpha2beta2gamma2 dimeric hydroxylase protein of methane mono-oxygenase from Methylococcus capsulatus (Bath) reveals the geometry of the catalytic di-iron core. The two iron atoms are bridged by exogenous hydroxide and acetate ligands and further coordinated by four glutamate residues, two histidine residues and a water molecule. The dinuclear iron centre lies in a hydrophobic active-site cavity for binding methane. An extended canyon runs between alphabeta pairs, which have many long alpha-helices, for possible docking of the reductase and coupling proteins required for catalysis. C1 MIT,DEPT CHEM,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV STOCKHOLM,DEPT MOLEC BIOL,S-10691 STOCKHOLM,SWEDEN. RI reddy, indra/C-5363-2011 NR 57 TC 725 Z9 741 U1 27 U2 305 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD DEC 9 PY 1993 VL 366 IS 6455 BP 537 EP 543 DI 10.1038/366537a0 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ML218 UT WOS:A1993ML21800061 PM 8255292 ER PT J AU BRENNICK, J DUNCAN, L AF BRENNICK, J DUNCAN, L TI IMAGES IN CLINICAL MEDICINE - VULVAR HERPES-SIMPLEX INFECTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note RP BRENNICK, J (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 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 DEC 9 PY 1993 VL 329 IS 24 BP 1783 EP 1783 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MK096 UT WOS:A1993MK09600006 PM 8232487 ER PT J AU BLUMENTHAL, D MEYER, GS AF BLUMENTHAL, D MEYER, GS TI THE FUTURE OF THE ACADEMIC-MEDICAL-CENTER UNDER HEALTH-CARE REFORM SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material C1 UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. RP BLUMENTHAL, D (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 11 TC 67 Z9 67 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 DEC 9 PY 1993 VL 329 IS 24 BP 1812 EP 1814 DI 10.1056/NEJM199312093292413 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA MK096 UT WOS:A1993MK09600013 PM 8232494 ER PT J AU ANDERSEN, JW SMALLEY, RV AF ANDERSEN, JW SMALLEY, RV TI INTERFERON-ALFA COMBINED WITH CYTOTOXIC CHEMOTHERAPY FOR PATIENTS WITH NON-HODGKINS-LYMPHOMA (VOL 327, PG 1336, 1992) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Correction, Addition C1 SYNERTRON INC,MADISON,WI 53705. RP ANDERSEN, JW (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 1 TC 33 Z9 33 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 DEC 9 PY 1993 VL 329 IS 24 BP 1821 EP 1822 DI 10.1056/NEJM199312093292419 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MK096 UT WOS:A1993MK09600033 PM 8232506 ER PT J AU ANDERSON, JW SMALLEY, RV AF ANDERSON, JW SMALLEY, RV TI INTERFERON-ALFA PLUS CHEMOTHERAPY FOR NON-HODGKINS-LYMPHOMA - 5-YEAR FOLLOW-UP SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 SYNERTRON INC,MADISON,WI 53705. RP ANDERSON, JW (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 1 TC 33 Z9 33 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 DEC 9 PY 1993 VL 329 IS 24 BP 1821 EP 1822 DI 10.1056/NEJM199312093292419 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MK096 UT WOS:A1993MK09600032 PM 8232506 ER PT J AU DREYER, EB AF DREYER, EB TI INHALED STEROID USE AND GLAUCOMA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP DREYER, EB (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. NR 3 TC 36 Z9 36 U1 0 U2 2 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 DEC 9 PY 1993 VL 329 IS 24 BP 1822 EP 1822 DI 10.1056/NEJM199312093292420 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MK096 UT WOS:A1993MK09600034 PM 8232507 ER PT J AU HENDRICKSON, BA ZHANG, W CRAIG, RJ JIN, YJ BIERER, BE BURAKOFF, S DILELLA, AG AF HENDRICKSON, BA ZHANG, W CRAIG, RJ JIN, YJ BIERER, BE BURAKOFF, S DILELLA, AG TI STRUCTURAL ORGANIZATION OF THE GENES ENCODING HUMAN AND MURINE FK506-BINDING PROTEIN (FKBP)13 AND COMPARISON TO FKBP1 SO GENE LA English DT Note DE IMMUNOSUPPRESSANT; IMMUNOPHILIN; GENOMIC LIBRARY; RECOMBINANT DNA; RAPAMYCIN ID RAPAMYCIN-BINDING-PROTEIN; MOLECULAR-CLONING; SACCHAROMYCES-CEREVISIAE; CYCLOSPORINE-A; LYMPHOCYTES-T; FK506; IMMUNOPHILIN; SEQUENCES; CALCINEURIN; NUCLEOTIDE AB FK506-binding protein (FKBP)12 and FKBP13 are members of a family of proteins which bind the immunosuppressant drugs, FK506 and rapamycin. FKBP12 and FKBP13 are encoded by distinct genes, designated FKBP1 and FKBP2, respectively. The structure of human FKBP1 was previously characterized. We now report the genomic structure of the human and murine FKBP2 genes. Comparison of FKBP1 and FKBP2 reveals significant homology and correlation of intron positions in the C-terminal region, suggesting that these genes may have evolved from a common ancestral gene. C1 CHILDRENS HOSP,DIV INFECT DIS,BOSTON,MA 02115. SMITHKLINE BEECHAM PHARMACEUT CO,DEPT MOLEC GENET,KING OF PRUSSIA,PA 19406. DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT MED,BOSTON,MA 02115. RP HENDRICKSON, BA (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,200 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 27 TC 14 Z9 15 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD DEC 8 PY 1993 VL 134 IS 2 BP 271 EP 275 DI 10.1016/0378-1119(93)90106-D PG 5 WC Genetics & Heredity SC Genetics & Heredity GA MM727 UT WOS:A1993MM72700019 PM 7505249 ER PT J AU WENG, SA SPIRO, RG AF WENG, SA SPIRO, RG TI DEMONSTRATION THAT A KIFUNENSINE-RESISTANT ALPHA-MANNOSIDASE WITH A UNIQUE PROCESSING ACTION ON N-LINKED OLIGOSACCHARIDES OCCURS IN RAT-LIVER ENDOPLASMIC-RETICULUM AND VARIOUS CULTURED-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRIMMING MAN9-MANNOSIDASE; GLYCOPROTEIN-BIOSYNTHESIS; PURIFICATION; PROTEIN; RECEPTOR; COMPLEX; ENZYME; SLICES AB A novel alpha-mannosidase has been identified in rat liver endoplasmic reticulum (ER) which at neutral pH processes the Man9GlcNAc oligosaccharide of glycoproteins by specifically cleaving the terminal mannose residue of the alpha1,6-linked chain to yield Man8GlcNAc, isomer C. This enzyme accounted for about half of the total ER a-mannosidase activity and was fully active at the concentration (0.25 muM) of kifunensine (KIF) completely inhibitory to the action of the ER enzyme which by removing the terminal sugar of the middle chain converts Man9GlcNAc to Man8GlcNAc isomer B; both ER enzymes, however, were inhibited in a similar manner by 1-deoxymannojirimycin (IC50 = 0.2 mM) and their action could not be distinguished with this agent. The KIF-resistant mannosidase which functioned optimally in the presence of 0.1-0.5% Triton X-100 did not show the high susceptibility to EDTA demonstrated by the KIF-sensitive enzyme and unlike the latter had the capacity to hydrolyze p-nitrophenyl-alpha-D-mannoside (K(m) = 0.45 mM); it had no specific cation requirements, but its activity was greatly reduced in the presence of Zn2+. In isolated ER membranes as well as in intact carbonyl cyanide m-chlorophenylhydrazone-treated cells, the processing pattern was substantially different in the presence of KIF than in its absence; while in the latter instance Man9GlcNAc was readily converted to Man63GlcNAc, the KIF-resistant enzyme was limited in its capacity to go beyond Man8GlcNAc. The KIF-resistant alpha-mannosidase was found in substantial amounts in all cell lines examined (HL-60, BW5147.3, MOLT-4, K-562, HepG2, Chinese hamster ovary, F-9, Madin-Darby canine kidney, FRTL-5). The finding that mannose removal from N-linked oligosaccharides can be initiated in two distinctive manners substantially broadens our concept of the processing events which can occur before a glycoprotein reaches the Golgi complex or to which ER resident molecules can be exposed. C1 JOSLIN DIABET CTR,ELLIOTT P JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 17477] NR 33 TC 89 Z9 90 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD DEC 5 PY 1993 VL 268 IS 34 BP 25656 EP 25663 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MK100 UT WOS:A1993MK10000056 PM 8245001 ER PT J AU WIGHTMAN, B HA, I RUVKUN, G AF WIGHTMAN, B HA, I RUVKUN, G TI POSTTRANSCRIPTIONAL REGULATION OF THE HETEROCHRONIC GENE LIN-14 BY LIN-4 MEDIATES TEMPORAL PATTERN-FORMATION IN C-ELEGANS SO CELL LA English DT Article ID DOUBLE-STRANDED-RNA; CAENORHABDITIS-ELEGANS; MESSENGER-RNA; COVALENT MODIFICATION; DEVELOPMENTAL SWITCH; ELEMENTS; EXPRESSION; SEQUENCES; PROTEIN; REGION AB During C. elegans development, the temporal pattern of many cell lineages is specified by graded activity of the heterochronic gene Lin-14. Here we demonstrate that a temporal gradient in Lin-14 protein is generated posttranscriptionally by multiple elements in the lin-14 3'UTR that are regulated by the heterochronic gene Lin-4. The lin-14 3'UTR is both necessary and sufficient to confer lin-4-mediated posttranscriptional temporal regulation. The function of the lin-14 3'UTR is conserved between C. elegans and C. briggsae. Among the conserved sequences are seven elements that are each complementary to the lin-4 RNAs. A reporter gene bearing three of these elements shows partial temporal gradient activity. These data suggest a molecular mechanism for Lin-14p temporal gradient formation: the lin-4 RNAs base pair to sites in the lin-14 3'UTR to form multiple RNA duplexes that down-regulate lin-14 translation. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. FU NIGMS NIH HHS [GM44619] NR 27 TC 1995 Z9 2152 U1 14 U2 118 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD DEC 3 PY 1993 VL 75 IS 5 BP 855 EP 862 DI 10.1016/0092-8674(93)90530-4 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MK966 UT WOS:A1993MK96600006 PM 8252622 ER PT J AU SADOSHIMA, J XU, YH SLAYTER, HS IZUMO, S AF SADOSHIMA, J XU, YH SLAYTER, HS IZUMO, S TI AUTOCRINE RELEASE OF ANGIOTENSIN-II MEDIATES STRETCH-INDUCED HYPERTROPHY OF CARDIAC MYOCYTES IN-VITRO SO CELL LA English DT Article ID GENE-EXPRESSION; CONVERTING ENZYME; PRESSURE-OVERLOAD; GROWTH; RENIN; RAT; SYSTEM; CELLS; IMMUNOREACTIVITY; REGRESSION AB Hypertrophy is a fundamental adaptive process employed by postmitotic cardiac and skeletal muscle in response to mechanical load. How muscle cells convert mechanical stimuli into growth signals has been a long-standing question. Using an in vitro model of load (stretch)-induced cardiac hypertrophy, we demonstrate that mechanical stretch causes release of angiotensin II (Ang II) from cardiac myocytes and that Ang II acts as an initial mediator of the stretch-induced hypertrophic response. The results not only provide direct evidence for the autocrine mechanism in load-induced growth of cardiac muscle cells, but also define the pathophysiological role of the local (cardiac) renin-angiotensin system. C1 BETH ISRAEL HOSP,DIV CARDIOVASC,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM CELL & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. RP SADOSHIMA, J (reprint author), BETH ISRAEL HOSP,DIV MOLEC MED,BOSTON,MA 02215, USA. NR 37 TC 1023 Z9 1042 U1 0 U2 11 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD DEC 3 PY 1993 VL 75 IS 5 BP 977 EP 984 DI 10.1016/0092-8674(93)90541-W PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MK966 UT WOS:A1993MK96600017 PM 8252633 ER PT J AU FISHEL, R LESCOE, MK RAO, MRS COPELAND, NG JENKINS, NA GARBER, J KANE, M KOLODNER, R AF FISHEL, R LESCOE, MK RAO, MRS COPELAND, NG JENKINS, NA GARBER, J KANE, M KOLODNER, R TI THE HUMAN MUTATOR GENE HOMOLOG MSH2 AND ITS ASSOCIATION WITH HEREDITARY NONPOLYPOSIS COLON-CANCER SO CELL LA English DT Article ID DNA MISMATCH CORRECTION; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE; HUMAN-CELLS; COLORECTAL-CANCER; NUCLEAR EXTRACTS; G.T MISPAIRS; REPAIR; CONVERSION; PROTEIN AB We have identified a human homolog of the bacterial MutS and S. cerevisiae MSH proteins, called hMSH2. Expression of hMSH2 in E. coli causes a dominant mutator phenotype, suggesting that hMSH2, like other divergent MutS homologs, interferes with the normal bacterial mismatch repair pathway. hMSH2 maps to human chromosome 2p22-21 near a locus implicated in hereditary nonpolyposis colon cancer (HNPCC). A T to C transition mutation has been detected in the -6 position of a splice acceptor site in sporadic colon tumors and in affected individuals of two small HNPCC kindreds. These data and reports indicating that S. cerevisiae msh2 mutations cause an instability of dinucleotide repeats like those associated with HNPCC suggest that hMSH2 is the HNPCC gene. C1 NCI, FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS, BASIC RES PROGRAM,MAMMALIAN GENET LAB, FREDERICK, MD 21702 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV CANC EPIDEMIOL & CONTROL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV CELLULAR & MOLEC BIOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. RP UNIV VERMONT, SCH MED, MARKEY CTR MOLEC GENET, DEPT MICROBIOL & MOLEC GENET, BURLINGTON, VT 05405 USA. FU NCI NIH HHS [CA56542]; NHGRI NIH HHS [HG00305]; NIGMS NIH HHS [GM50006] NR 70 TC 2266 Z9 2309 U1 8 U2 167 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0092-8674 EI 1097-4172 J9 CELL JI Cell PD DEC 3 PY 1993 VL 75 IS 5 BP 1027 EP 1038 DI 10.1016/0092-8674(93)90546-3 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MK966 UT WOS:A1993MK96600022 PM 8252616 ER PT J AU KREK, W LIVINGSTON, DM SHIRODKAR, S AF KREK, W LIVINGSTON, DM SHIRODKAR, S TI BINDING TO DNA AND THE RETINOBLASTOMA GENE-PRODUCT PROMOTED BY COMPLEX-FORMATION OF DIFFERENT E2F FAMILY MEMBERS SO SCIENCE LA English DT Article ID TRANSCRIPTION FACTOR E2F; CELL-CYCLE; SUSCEPTIBILITY GENE; PROTEIN; PHOSPHORYLATION; IDENTIFICATION; CLONING AB The E2F family of transcription factors functions in the control of the mammalian cell cycle. Here it is shown that two family members, E2F-1 and DP-1, form specific heterodimers in vivo, a process that enhances DNA binding, transactivation, and the binding of the retinoblastoma gene product. These results suggest that heterodimerization regulates E2F function and contributes to cell cycle control. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 27 TC 235 Z9 235 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD DEC 3 PY 1993 VL 262 IS 5139 BP 1557 EP 1560 DI 10.1126/science.8248803 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK329 UT WOS:A1993MK32900036 PM 8248803 ER PT J AU BONNI, A FRANK, DA SCHINDLER, C GREENBERG, ME AF BONNI, A FRANK, DA SCHINDLER, C GREENBERG, ME TI CHARACTERIZATION OF A PATHWAY FOR CILIARY NEUROTROPHIC FACTOR SIGNALING TO THE NUCLEUS SO SCIENCE LA English DT Article ID LEUKEMIA INHIBITORY FACTOR; PROTEIN-TYROSINE KINASES; C-FOS PROMOTER; TRANSCRIPTION FACTOR; CYTOPLASMIC ACTIVATION; BINDING PROTEIN; FACTOR PREVENTS; FACTOR RECEPTOR; MOTOR NEURONS; IFN-GAMMA AB Components of a signaling pathway that couples the ciliary neurotrophic factor (CNTF) receptor to induction of transcription were identified. CNTF stimulated the tyrosine phosphorylation of p91, a protein implicated in interferon signaling pathways, and of two proteins that are distinct but related to p91. Tyrosine-phosphorylated p91 translocated to the nucleus, where p91 and p91-related proteins bound to a DNA sequence found in promoters of genes responsive to CNTF. This DNA sequence, when inserted upstream of a reporter gene, conferred a transcriptional response to CNTF. A pathway that transduces interferon signals may therefore have a more general function in the propagation of responses to certain neurotrophic factors. C1 HARVARD UNIV, SCH MED, PROGRAM NEUROSCI, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MICROBIOL & MOLEC GENET, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. COLUMBIA UNIV, DEPT MED, NEW YORK, NY 10032 USA. FU NCI NIH HHS [R01 CA43855]; NHLBI NIH HHS [HL21006-17] NR 57 TC 174 Z9 175 U1 0 U2 3 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 EI 1095-9203 J9 SCIENCE JI Science PD DEC 3 PY 1993 VL 262 IS 5139 BP 1575 EP 1579 DI 10.1126/science.7504325 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK329 UT WOS:A1993MK32900042 PM 7504325 ER PT J AU LIPES, MA ROSENZWEIG, A TAN, KN TANIGAWA, G SEIDMAN, JG EISENBARTH, GS AF LIPES, MA ROSENZWEIG, A TAN, KN TANIGAWA, G SEIDMAN, JG EISENBARTH, GS TI T-CELL RECEPTOR SPECIFICITY AND DIABETES IN NONOBESE DIABETIC MICE - REPLY SO SCIENCE LA English DT Article ID DESTRUCTION; LYT-2+; L3T4+ C1 BRIGHAM & WOMENS HOSP,DIV VASC RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MEM SLOAN KETTERING CANC CTR,PROGRAM CELLULAR BIOCHEM & BIOPHYS,NEW YORK,NY 10021. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. BARBARA DAVIS CTR CHILDHOOD DIABET,DENVER,CO 80262. RP LIPES, MA (reprint author), JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215, USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD DEC 3 PY 1993 VL 262 IS 5139 BP 1584 EP 1584 DI 10.1126/science.262.5139.1584 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK329 UT WOS:A1993MK32900047 PM 17829386 ER PT J AU SUMNER, DR JASTY, M JACOBS, JJ URBAN, RM BRAGDON, CR HARRIS, WH GALANTE, JO AF SUMNER, DR JASTY, M JACOBS, JJ URBAN, RM BRAGDON, CR HARRIS, WH GALANTE, JO TI HISTOLOGY OF POROUS-COATED ACETABULAR COMPONENTS - 25 CEMENTLESS CUPS RETRIEVED AFTER ARTHROPLASTY SO ACTA ORTHOPAEDICA SCANDINAVICA LA English DT Article ID INGROWTH AB 25 hemispherical acetabular components retrieved from patients who had a total hip arthroplasty (THA) were studied histologically. All of the components had titanium fiber metal porous coatings and were implanted with adjuvant screw fixation, 18 in primary THA and 7 in revision THA. None of the cups had been removed because of infection or failure of fixation. The components had been in place an average of 30 (1-140) weeks. 18 cups had bone ingrowth into the porous coating. Up to one third of the available void space within the porous coating was occupied by bone, while the maximal proportion of the area of the bone-implant interface with bone ingrowth was over 80 percent. Bone ingrowth was more often observed at the dome and in the vicinity of sites of screw fixation than elsewhere. Peripherally, bone ingrowth was less consistent, and in isolated areas fibrocartilage and mineralized fibrocartilage were occasionally observed. The longer-term cases had more bone ingrowth than the shorter-term cases. Apparent metallic debris was observed within histiocytes adjacent to screw holes, and the amount of this material increased with duration of implantation. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SUMNER, DR (reprint author), RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT ORTHOPED,1653 W CONGRESS PKWY,CHICAGO,IL 60612, USA. NR 20 TC 57 Z9 59 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6470 J9 ACTA ORTHOP SCAND JI Acta Orthop. Scand. PD DEC PY 1993 VL 64 IS 6 BP 619 EP 626 DI 10.3109/17453679308994584 PG 8 WC Orthopedics SC Orthopedics GA MU335 UT WOS:A1993MU33500003 PM 8291405 ER PT J AU MORGAN, JR TOMPKINS, RG YARMUSH, ML AF MORGAN, JR TOMPKINS, RG YARMUSH, ML TI ADVANCES IN RECOMBINANT RETROVIRUSES FOR GENE DELIVERY SO ADVANCED DRUG DELIVERY REVIEWS LA English DT Review DE GENE THERAPY; RECOMBINANT RETROVIRUS; GENE TRANSFER ID HEMATOPOIETIC STEM-CELLS; HUMAN ADENOSINE-DEAMINASE; LONG-TERM EXPRESSION; BETA-GLOBIN GENE; MEDIATED TRANSFER; SKIN FIBROBLASTS; BONE-MARROW; MAMMALIAN-CELLS; ENDOTHELIAL-CELLS; STABLE EXPRESSION AB A naturally occurring murine retrovirus has been adapted to serve as a safe and effective vehicle for the transfer of genes to human cells. This process of gene transfer, known as ''retroviral-mediated gene transfer'', facilitates the efficient introduction and expression of stable gene copies in human diploid cells from a variety of tissues. Using this approach, numerous genes have been introduced into human cells and attention has been focused on the use of this technology to achieve therapeutic goals. Gene transfer technology has the potential for the correction of genetic diseases as well as the development of novel solutions to the problems involved with delivery of therapeutic proteins. C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,SURG SERV,BOSTON,MA 02114. RUTGERS UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. OI Morgan, Jeffrey/0000-0002-7546-3443 NR 106 TC 26 Z9 26 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-409X J9 ADV DRUG DELIVER REV JI Adv. Drug Deliv. Rev. PD DEC PY 1993 VL 12 IS 3 BP 143 EP 158 DI 10.1016/0169-409X(93)90056-A PG 16 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MP864 UT WOS:A1993MP86400003 ER PT J AU MORGAN, JR AF MORGAN, JR TI GENE THERAPEUTICS - PREFACE SO ADVANCED DRUG DELIVERY REVIEWS LA English DT Editorial Material RP MORGAN, JR (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,BOSTON,MA 02114, USA. OI Morgan, Jeffrey/0000-0002-7546-3443 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-409X J9 ADV DRUG DELIVER REV JI Adv. Drug Deliv. Rev. PD DEC PY 1993 VL 12 IS 3 BP R7 EP R8 DI 10.1016/0169-409X(93)90054-8 PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MP864 UT WOS:A1993MP86400001 ER PT J AU MOORE, JP YOSHIYAMA, H HO, DD ROBINSON, JE SODROSKI, J AF MOORE, JP YOSHIYAMA, H HO, DD ROBINSON, JE SODROSKI, J TI ANTIGENIC VARIATION IN GP120S FROM MOLECULAR CLONES OF HIV-1 LAI SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; NEUTRALIZING MONOCLONAL-ANTIBODY; HTLV-III; TYPE-1 GP120; ENVELOPE GLYCOPROTEIN; AIDS VIRUS; NUCLEOTIDE-SEQUENCE; ESCHERICHIA-COLI; GENE-PRODUCTS; SOLUBLE CD4 AB To address the relationship between primary sequence variation in HIV-1 gp120 and its antigenic structure in a simple system, we have measured the binding of human and murine monoclonal antibodies (MAbs) to gp120 from four molecular clones of HIV-1 LAI: HxB2, HxB3, Hx10, and NL4-3. Despite the close relationship between these clones, and their relatively conserved gp120 sequences, there is considerable variation in their antigenic structure, judged by MAb reactivities to the V2, V3, and C4 domains and to discontinuous epitopes. Because of our prior studies of the determinants of MAb binding to HxB2 gp120, we can make reasonable estimates of how sequence variation among the LAI clone gp120s affects their binding of some MAbs; for other MAbs our current knowledge of gp120 structure is too limited to allow such estimates. These results indicate that small variations in primary gp120 amino acid sequence can profoundly affect recognition of this glycoprotein by all five groups of defined anti-gp120 neutralizing antibodies. C1 NYU,SCH MED,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10018. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RI Yoshiyama, Hironori/D-7902-2012; OI Yoshiyama, Hironori/0000-0001-7588-278X FU NIAID NIH HHS [1 P30 AI27742-04, AI 24755, AI 25542-05A1] NR 67 TC 26 Z9 26 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD DEC PY 1993 VL 9 IS 12 BP 1185 EP 1193 DI 10.1089/aid.1993.9.1185 PG 9 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA MQ904 UT WOS:A1993MQ90400003 PM 7511394 ER PT J AU BECKER, HC HALE, RL BOGGAN, WO RANDALL, CL AF BECKER, HC HALE, RL BOGGAN, WO RANDALL, CL TI EFFECTS OF PRENATAL ETHANOL EXPOSURE ON LATER SENSITIVITY TO THE LOW-DOSE STIMULANT ACTIONS OF ETHANOL IN MOUSE OFFSPRING - POSSIBLE ROLE OF CATECHOLAMINES SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE PRENATAL ETHANOL; ETHANOL-STIMULATED ACTIVITY; BRAIN CATECHOLAMINES; FETAL ALCOHOL SYNDROME; ETHANOL SENSITIVITY ID ALCOHOL EXPOSURE; ADULT-RATS; LOCOMOTOR-ACTIVITY; BEHAVIOR; INUTERO; MICE; CONSUMPTION; AMPHETAMINE; BRAIN; METHYLPHENIDATE AB The purpose of this study was to examine whether prenatal ethanol (EtOH) exposure alters later sensitivity to the low-dose stimulant effects of EtOH. Because the locomotor stimulant effects of EtOH are thought to be mediated, at least in part, by activation of brain monoamine systems, and because prenatal EtOH exposure has been shown to alter brain monoamine activity, it was hypothesized that prenatal EtOH exposure may alter sensitivity to the stimulant actions of EtOH. To test this hypothesis, sensitivity to the locomotor stimulant effects of various challenge doses of EtOH was examined in male and female offspring from prenatal alcohol (A), pair-fed (PF), and lab chow (LC) groups at different ages. In addition, to address the hypothesis further, sensitivity to the catecholamine synthesis inhibitor alpha-methyl-p-tyrosine (AMPT) was examined in these offspring, as well. Results indicated that male offspring prenatally exposed to EtOH exhibited reduced baseline activity and a blunted stimulant response to all challenge doses of EtOH (0.75-1.5 g/kg) in comparison with control offspring at 30 days of age, but these effects appeared to ''normalize'' at 70 days of age. Female EtOH-exposed offspring also exhibited a reduced baseline level of activity relative to control offspring, as well as a blunted stimulant response to the lowest challenge dose of EtOH (0.75 g/kg) at 30 days of age, and these effects persisted into adulthood. The stimulant response to higher doses of EtOH did not significantly differ among prenatal treatment groups in young or adult female offspring. However, because baseline activity was significantly lower in female EtOH exposed offspring than control offspring, the stimulant response to these doses of EtOH (1.125 and 1.5 g/kg) was relatively greater than that for PF and LC offspring. Importantly, none of the differences in performance among the prenatal treatment groups could be attributed to an alteration in EtOH pharmacokinetics, because blood ROH levels measured immediately following the 10-min test session were similar for all prenatal treatment groups across all of the EtOH test doses. Further, a similar response profile as that observed following EtOH challenge at 70 days of age was obtained following phenobarbital challenge (10-40 mg/kg). Finally, whereas AMPT (50-400 mg/ kg) dose-dependently antagonized the stimulant effects of EtOH in all prenatal treatment groups, this effect of AMPT was significantly greater in mice prenatally exposed to RON in comparison with control offspring. Thus, sensitivity to the stimulant effects of EtOH was significantly altered in adult male mice when these animals were additionally challenged with a drug that further reduced central catecholamine activity. Taken together, these results provide support for the hypothesis that prenatal EtOH exposure alters later sensitivity to the low-dose stimulant properties of the drug, and that this effect may be the result of an alteration in brain monoamine activity in these offspring. C1 MED UNIV S CAROLINA,RALPH H JOHNSON VET ADM MED CTR,CHARLESTON,SC. MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC. FU NIAAA NIH HHS [AA07791] NR 48 TC 25 Z9 25 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD DEC PY 1993 VL 17 IS 6 BP 1325 EP 1336 DI 10.1111/j.1530-0277.1993.tb05249.x PG 12 WC Substance Abuse SC Substance Abuse GA MN395 UT WOS:A1993MN39500033 PM 8116850 ER PT J AU RIVERA, JM VANDERVOORT, PM DEPRADA, JAV MELE, D KARSON, TH MOREHEAD, A MORRIS, E WEYMAN, A THOMAS, JD AF RIVERA, JM VANDERVOORT, PM DEPRADA, JAV MELE, D KARSON, TH MOREHEAD, A MORRIS, E WEYMAN, A THOMAS, JD TI WHICH PHYSICAL FACTORS DETERMINE TRICUSPID REGURGITATION JET AREA IN THE CLINICAL SETTING SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID DIMENSIONAL DOPPLER ECHOCARDIOGRAPHY; PROXIMAL FLOW CONVERGENCE; SYSTEMIC BLOOD-FLOW; MITRAL REGURGITATION; VALVULAR REGURGITATION; QUANTIFICATION; VALVE; VALIDATION; PULMONARY; MOMENTUM AB The visual assessment of jet area has become the most common method used in daily clinical practice to evaluate valvular regurgitation. Despite the high prevalence of tricuspid regurgitation, however, few studies have systematically compared TR jet areas with a quantitative standard. To evaluate this, 40 patients in sinus rhythm with tricuspid regurgitation were analyzed: 16 with centrally directed free jets and 24 with impinging wall jets. The size of the maximal planimetered color jet area (cm2) was compared with parameters derived using the pulsed Doppler 2-dimensional echocardiographic method: regurgitant fraction and the flow convergence method (peak flow rate, effective regurgitant orifice area and momentum). Mean tricuspid regurgitant fraction averaged 33 +/- 15%, peak flow rate 76 +/- 54 cm3/s, effective regurgitant orifice area 27 +/- 21 mm2 and momentum 21,717 +/- 15,014 cm4/s2. An average of 4-chamber, and long- and short-axis areas in free jets correlated well with regurgitant fraction (r = 0.81, p < 0.001), better with peak flow rate (r = 0.94, p < 0.001), effective regurgitant orifice (r = 0.92, p < 0.001) and momentum (r = 0.94, p < 0.001). The correlation was worse, but still significant, in wall jets. For the same peak flow rate, wall jets were 75% of the size of a corresponding free jet. Jet area measurement is a good semiquantitative tool to measure tricuspid regurgitation in free jets, which correlates well with regurgitant fraction and better with new parameters available from analysis of the proximal acceleration field. In patients with eccentrically directed wall jets the correlation with planimetered jet area was worse, but still significant. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NONINVAS CARDIAC LAB,BOSTON,MA 02114. RP RIVERA, JM (reprint author), CLEVELAND CLIN FDN,DEPT CARDIOL,DESK F15,9500 EUCLID AVE,CLEVELAND,OH 44195, USA. RI rivera, miguel/D-5026-2014 NR 30 TC 30 Z9 30 U1 0 U2 2 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD DEC 1 PY 1993 VL 72 IS 17 BP 1305 EP 1309 DI 10.1016/0002-9149(93)90302-S PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MJ980 UT WOS:A1993MJ98000017 PM 8256709 ER PT J AU KANTOFF, PW BLOCK, C LETVAK, L GEORGE, M AF KANTOFF, PW BLOCK, C LETVAK, L GEORGE, M TI 14-DAY CONTINUOUS-INFUSION OF MITOXANTRONE IN HORMONE-REFRACTORY METASTATIC ADENOCARCINOMA OF THE PROSTATE SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE ADENOCARCINOMA; PROSTATE; CONTINUOUS INFUSION; MITOXANTRONE; METASTATIC; HORMONE-REFRACTORY; CHEMOTHERAPY ID CANCER AB A dose-finding investigation was conducted with mitoxantrone administered as 14-day continuous infusions to patients with hormone-refractory metastatic adenocarcinoma of the prostate. Fifteen men participated in four dosage groups: mitoxantrone 1.0, 1.25, 1.4, and 1.5 mg/m2/day: a treatment cycle was defined as a dose of mitoxantrone given over 2 weeks, followed by 2 weeks of monitoring prior to the next course. The patients received 1 to 10 courses, with the majority receiving 1 to 3. The maximum tolerated dose was 1.25 mg/m2/day for 14 days of continuous infusion. Two patients discontinued treatment because of gastrointestinal effects. Most adverse clinical experiences were mild or moderate in intensity. A decrease in prostate-specific antigen (PSA) response was seen after one course in 6 of 14 patients who had PSA measurements. Stable disease was achieved in 40% of the evaluable patients, and some quality of life parameters improved. Further clinical trials with mitoxantrone are indicated in patients with prostatic cancer, especially in those who have had less previous treatment. C1 AMER CYANAMID CO,LEDERLE LABS,PEARL RIVER,NY 10965. RP KANTOFF, PW (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 11 TC 20 Z9 20 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3732 J9 AM J CLIN ONCOL-CANC JI Am. J. Clin. Oncol.-Cancer Clin. Trials PD DEC PY 1993 VL 16 IS 6 BP 489 EP 491 DI 10.1097/00000421-199312000-00005 PG 3 WC Oncology SC Oncology GA MM257 UT WOS:A1993MM25700005 PM 8256762 ER PT J AU CENTENO, BA LOUIS, DN KUPSKY, WJ PREFFER, FI SOBEL, RA AF CENTENO, BA LOUIS, DN KUPSKY, WJ PREFFER, FI SOBEL, RA TI THE AGNOR TECHNIQUE, PCNA IMMUNOHISTOCHEMISTRY, AND DNA-PLOIDY IN THE EVALUATION OF CHOROID-PLEXUS BIOPSY SPECIMENS SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE AGNOR TECHNIQUE; CHOROID PLEXUS TUMORS; DNA PLOIDY; FLOW CYTOMETRY; NORMAL CHOROID PLEXUS; NUCLEOLAR ORGANIZER REGIONS; PCNA IMMUNOHISTOCHEMISTRY ID CELL NUCLEAR ANTIGEN; CENTRAL-NERVOUS-SYSTEM; FLOW-CYTOMETRIC DNA; PARAFFIN-EMBEDDED TISSUE; FALSE ANEUPLOID PEAKS; HUMAN-BRAIN-TUMORS; AUXILIARY PROTEIN; POLYMERASE-DELTA; NEOPLASMS; PROLIFERATION AB The histologic distinctions between normal choroid plexus and choroid plexus papilloma and between choroid plexus papilloma and choroid plexus carcinoma are sometimes difficult. The authors performed the silver nucleolar organizer region (AgNOR) technique, immunohistochemistry for proliferating cell nuclear antigen (PCNA), and DNA ploidy analysis by flow cytometry on 9 samples of normal choroid plexus, 8 papillomas, and 13 carcinomas to evaluate whether these techniques can aid in these differential diagnoses. Significant differences were found in the mean AgNOR count between normal choroid plexus (1.35 +/- 0.11) and choroid plexus papillomas (2.42 +/- 0.81) (P < 0.001), but not between choroid plexus papillomas and carcinomas. In the normal choroid plexus, AgNORs were smooth and round; in the papillomas and carcinomas, however, they varied in size and shape. Compound AgNORs were commonly present in the tumors but were essentially absent in controls. Antibody to PCNA did not stain normal choroid plexus cells (except for focal staining in one sample of normal choroid plexus adjacent to a carcinoma) but stained many papilloma and carcinoma cells. DNA ploidy analysis demonstrated aneuploidy in some papillomas and carcinomas but could not be used for the distinction of normal choroid plexus from papillomas. These results suggested that the AgNOR technique and PCNA immunohistochemistry could be used to distinguish normal choroid plexus from choroid plexus papilloma in small, diagnostically difficult biopsy specimens. C1 MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. CHILDRENS HOSP MED CTR, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. NR 38 TC 23 Z9 23 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9173 EI 1943-7722 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD DEC PY 1993 VL 100 IS 6 BP 690 EP 696 PG 7 WC Pathology SC Pathology GA ML604 UT WOS:A1993ML60400018 PM 7902669 ER PT J AU RABENECK, L RISSER, JMH MURRAY, NGB MCCABE, BK LACKE, CE LUCCO, LJ AF RABENECK, L RISSER, JMH MURRAY, NGB MCCABE, BK LACKE, CE LUCCO, LJ TI FAILURE OF PROVIDERS TO VACCINATE HIV-INFECTED MEN AGAINST HEPATITIS-B - A MISSED OPPORTUNITY SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID HOMOSEXUAL MEN; ANTIBODY; ANTIGEN AB Objective: To carry out an audit of hepatitis B immunization practices in an out patient HIV clinic. Methods: We reviewed the medical records of all new HIV-infected patients seen between October 1, 1990 and December 31, 1991. Results: The 125 patients were men with a mean age and CD4 count of 43 yr and 240 cells/mm3, respectively. Fourteen percent (14%) of men who showed a clear need for vaccine, having no HBV markers, were not vaccinated by the clinic staff. Further, 16% whose susceptibility to HBV infection was unclear, with anti-HBc as a sole HBV marker, were not evaluated with a booster dose of hepatitis B vaccine in an attempt to elicit an anamnestic response. Conclusions: In failing to vaccinate or evaluate the 30% of patients without HBsAg or anti-HBs, our providers are missing an important opportunity in preventive medicine. We urge others to examine their own hepatitis B screening and vaccination practices. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. VET ADM RES CTR AIDS & HIV INFECT,HOUSTON,TX. RP RABENECK, L (reprint author), VET ADM MED CTR 111D,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 18 TC 17 Z9 17 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD DEC PY 1993 VL 88 IS 12 BP 2015 EP 2018 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MK860 UT WOS:A1993MK86000006 PM 8249965 ER PT J AU KWIATKOWSKI, DJ DIB, C SLAUGENHAUPT, SA POVEY, S GUSELLA, JF HAINES, JL AF KWIATKOWSKI, DJ DIB, C SLAUGENHAUPT, SA POVEY, S GUSELLA, JF HAINES, JL TI AN INDEX MARKER MAP OF CHROMOSOME-9 PROVIDES STRONG EVIDENCE FOR POSITIVE INTERFERENCE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID DINUCLEOTIDE REPEAT POLYMORPHISM; GENETIC-LINKAGE MAP; HUMAN GENOME; LOCUS; IDENTIFICATION; PROGRAM; 9Q32-34 AB An index marker map of chromosome 9 has been constructed using the Centre d'Etude du Polymorphisme Humain reference pedigrees. The map comprises 26 markers, with a maximum intermarker interval of 13.1 cM and only two intervals >10 cM. Placement of all but one marker into the map was achieved with >10,000:1 odds. The sex-equal length is 151 cM, with male length of 121 cM and female length of 185 cM. The map extends to within 2%-3% of physical length at the telomeres, and its coverage therefore is expected to be within 20-30 cM of full map length. The markers are all of the GT/CA repeat type and have average heterozygosity .77, with a range of .60-.89. The map shows both marked contraction of genetic distance relative to physical distance in the pericentromeric region and expansion in the telomeric regions. Genotypic data were carefully examined for errors by using the crossover routine of the program DATAMAN. Five new mutations were observed among 17,316 meiotic events examined. There were two double-crossover events occurring within an interval of 0-10 cM, and another eight were observed within an interval of 10-20 cM. Many of these could be due to additional mutational events in which one parental allele converted to the other by either gene conversion or random strand slippage. When there was no correction for these possible mutational events, the number of crossovers displayed by the maternal and paternal chromosomes was significantly different (P<.001) from that predicted by the Poisson distribution, which would be expected in the absence of interference. In addition, the observed crossover distribution for paternally derived chromosomes was similar to that predicted from cytogenetic chiasma frequency observations. In all, the data strongly support the occurrence of strong positive interference on human chromosome 9 and suggest that flanking markers at an interval of less than or equal to 20 cM are generally sufficient for disease gene inheritance predictions in presymptomatic genetic counseling by Linkage analysis. C1 HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DIV EXPTL MED & HEMATOL ONCOL, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, NEUROGENET LAB, BOSTON, MA 02114 USA. GENETHON, EVRY, FRANCE. UCL, MRC, HUMAN BIOCHEM GENET UNIT, LONDON, ENGLAND. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00324, HG00169, HG00598] NR 27 TC 46 Z9 46 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD DEC PY 1993 VL 53 IS 6 BP 1279 EP 1288 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA MJ818 UT WOS:A1993MJ81800015 PM 8250044 ER PT J AU EMANUEL, EJ WEINBERG, DS GONIN, R HUMMEL, LR EMANUEL, LL AF EMANUEL, EJ WEINBERG, DS GONIN, R HUMMEL, LR EMANUEL, LL TI HOW WELL IS THE PATIENT SELF-DETERMINATION ACT WORKING - AN EARLY ASSESSMENT SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID ADVANCE DIRECTIVES; CARDIOPULMONARY RESUSCITATION; ELDERLY OUTPATIENTS; LIVING WILLS; CARE; ATTITUDES; PROXY AB OBJECTIVES: To assess the association between implementation of the Patient Self-Determination Act (PSDA) and (1) the use of formal, written advance directives, (2) the use of informal advance care arrangements, and (3) discussions between patients and their physicians and proxies on advance care planning and end-of-life treatment preferences. DESIGN: A time-sequence study in which patients discharged from acute care hospitals 1 month before the implementation of the PSDA and 5 months after implementation of the PSDA were interviewed. SETTING: Two medical school-affiliated, major teaching hospitals with more than 500 beds and 3 nonteaching community hospitals with fewer than 400 beds in eastern Massachusetts. PATIENTS: A total of 579 adult patients were interviewed: 258 patients discharged before the implementation of the PSDA (pre-PSDA) and 321 patients discharged 5 months after implementation of the PSDA (post-PSDA). MEASUREMENTS: Patients were asked about their formal, written or informal advance care planning arrangements, about the frequency of inquiries and information provided on advance care planning by the hospitals, and about their discussions of advance care planning and end-of-life treatment preferences with physicians and their proxies. RESULTS: In the pre-PSDA cohort, 60.9% of the patients had some kind of advance care planning, whereas in the post-PSDA cohort, 72.6% did (p = 0.01). However, there was not a significant increase in the proportion of patients who had advance care planning ''In a written document'' (19.8% of the pre-PSDA cohort compared with 25.5% of the post-PSDA cohort, p = 0.11). The increase in written advance care planning was concentrated in the community, nonteaching hospitals (10.7% pre-PSDA versus 23.7% post-PSDA). Overall, 41.4% of patients recalled inquiries or information about advance care planning during their hospitalization. Implementation of the PSDA was not associated with a significant change in the proportion of patients who discussed advance care planning or end-of-life issues with their physicians (13.6% pre-PSDA versus 17.1% post-PSDA, p = 0.25). However, there was an increase in the proportion of patients with poorer health who spoke with their physicians (15.4% pre-PSDA versus 24.8% post-PSDA). Implementation of the PSDA was associated with an increase in the proportion of patients who had general discussions with proxies about end-of-life issues (61.8% pre-PSDA versus 73.0% post-PSDA, p = 0.024). However, 33.6% of pre-PSDA and 33.2% of post-PSDA patients had detailed discussions with their proxy about specific interventions such as mechanical ventilation or artificial nutrition. Patients with formal proxies had detailed discussions significantly more frequently than other patients (50.0% versus 26.8%, p <0.0001). CONCLUSIONS: The PSDA was associated with significant effects on general advance care planning issues, increasing the proportion of patients who had (1) some kind of advance care arrangements and (2) general discussions of end-of-life issues with their proxies. However, the PSDA did not appear associated with significant increases (1) in the use of formal, written advance care documents, (2) in the frequency of discussions between patients and their physicians on advance care documents or end-of-life issues, or (3) in the frequency of discussions about specific treatment preferences between patients and their proxies. C1 BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV MED ETH,BOSTON,MA 02115. RP EMANUEL, EJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 27 TC 96 Z9 97 U1 2 U2 6 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD DEC PY 1993 VL 95 IS 6 BP 619 EP 628 DI 10.1016/0002-9343(93)90358-V PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA MN550 UT WOS:A1993MN55000010 PM 8259779 ER PT J AU BREUER, W SLOTKI, IN AUSIELLO, DA CABANTCHIK, IZ AF BREUER, W SLOTKI, IN AUSIELLO, DA CABANTCHIK, IZ TI INDUCTION OF MULTIDRUG-RESISTANCE DOWN-REGULATES THE EXPRESSION OF CFTR IN COLON EPITHELIAL-CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Note DE CYSTIC FIBROSIS; CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR; P-GLYCOPROTEIN; HT-29 CELLS ID TRANSMEMBRANE-CONDUCTANCE REGULATOR; CYSTIC-FIBROSIS GENE; CHLORIDE CHANNEL; P-GLYCOPROTEIN; SECRETORY EPITHELIUM; LOCALIZATION; TRANSPORT; PATTERNS; PROTEINS; UTERUS AB The epithelial cell line HT-29, which constitutively expresses the cystic fibrosis transmembrane conductance regulator (CFTR), was induced to become drug resistant by cultivation in the presence of colchicine. The gradual acquisition of drug resistance was associated with a corresponding increase in the expression of the multidrug resistance P-glycoprotein (P-gp) and a marked (>80%) decrease in the constitutive levels of CTFR protein, as determined by immunoblotting. The reduction in CFTR content occurred at the onset of acquisition of drug resistance when P-gp expression was still relatively low. Reversal of drug resistance by removal of colchicine from the culture medium led to a 70% decrease in P-gp levels and a concomitant 40% increase in CFTR. The levels of other membrane proteins such as Na+-K+-ATPase and alkaline phosphatase remained relatively constant (<26% variation). We propose that a selective downregulation of CFTR is elicited by acquisition of the multidrug resistance (MDR) phenotype and that induction of P-gp expression leads to a reversible repression of CFTR biosynthesis. These findings provide an experimental foundation for the complementary patterns of expression of the CFTR and MDR1 genes observed in vivo. C1 SHARE ZEDEK MED CTR,RENAL UNIT,IL-91035 JERUSALEM,ISRAEL. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL SECT,BOSTON,MA 02114. RP BREUER, W (reprint author), HEBREW UNIV JERUSALEM,INST LIFE SCI,DEPT BIOL CHEM,IL-91904 JERUSALEM,ISRAEL. NR 24 TC 49 Z9 49 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 DEC PY 1993 VL 265 IS 6 BP C1711 EP C1715 PN 1 PG 5 WC Physiology SC Physiology GA MQ656 UT WOS:A1993MQ65600031 ER PT J AU BONADONNA, RC DELPRATO, S BONORA, E GULLI, G SOLINI, A DEFRONZO, RA AF BONADONNA, RC DELPRATO, S BONORA, E GULLI, G SOLINI, A DEFRONZO, RA TI EFFECTS OF PHYSIOLOGICAL HYPERINSULINEMIA ON THE INTRACELLULAR METABOLIC PARTITION OF PLASMA-GLUCOSE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INSULIN; GLYCOLYSIS; SUBSTRATE COMPETITION ID MAGNETIC-RESONANCE SPECTROSCOPY; MUSCLE GLYCOGEN-SYNTHESIS; WHOLE-BODY; INDIRECT CALORIMETRY; SUBSTRATE OXIDATION; SKELETAL-MUSCLE; INSULIN; HUMANS; INVIVO; TURNOVER AB Methodology for assessing the glycolytic and oxidative fluxes from plasma glucose, by measuring (H2O)-H-3 and (CO2)-C-14 rates of production during [3-H-3]- and [U-C-14]glucose infusion, was tested in healthy subjects. In study 1, during staircase (H2O)-H-3 infusion in six subjects, calculated rates of (H2O)-H-3 appearance agreed closely with (H2O)-H-3 infusion rates. In study 2, when [2-H-3]glucose and (NaHCO3)-C-14 were infused in four subjects in the basal state and during a 4-h euglycemic insulin (approximately 70 muU/ml) clamp, accurate estimates of the rates of [2-H-3]glucose detritiation were obtained (94-97% of the expected values), and the recovery factor of (NaHCO3)-C-14 did not change during hyperinsulinemia. In study 3, 11 subjects underwent a 4-h euglycemic insulin (approximately 70 muU/ml) clamp with [3-H-3]- and [U-C-14]glucose infusion and measurement of gaseous exchanges by indirect calorimetry to estimate the rates of total glycolysis, glycogen synthesis, glucose oxidation, nonoxidative glycolysis, hepatic glucose production, glucose recycling, and glucose conversion to fat. Hyperinsulinemia stimulated glycogen synthesis above baseline more than glycolysis [increment of 4.78 +/- 0.37 vs. 2.0 +/- 0. 17 mg . min-1 . kg-1 of lean body mass (LBM), respectively, P < 0.011 and incompletely suppressed (approximately 87%) hepatic glucose production. The major component of nonoxidative glycolysis shifted from glucose recycling in the postabsorptive state (approximately 57% of nonoxidative glycolysis) to glucose conversion to fat during hyperinsulinemia (approximately 59% of nonoxidative glycolysis). Lipid oxidation during the insulin clamp was negatively correlated with both isotopic glucose oxidation (r = -0.822, P < 0.002) and glycolysis (r = -0.582, P < 0.07). In conclusion, in healthy subjects, glycogen synthesis plays a greater role than glycolysis and glucose oxidation in determining insulin-mediated glucose disposal. Part of insulin-mediated increase in glycolysis/oxidation might be secondary to the relief of the competition between fat and glucose for oxidation. C1 UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. RP BONADONNA, RC (reprint author), CNR,INST CLIN PHYSIOL,METAB UNIT,VIA SAVI 8,I-56100 PISA,ITALY. RI Del Prato, Stefano/K-3405-2016; Solini, Anna/K-4666-2016 OI Del Prato, Stefano/0000-0002-5388-0270; Solini, Anna/0000-0002-7855-8253 FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK-24092] NR 53 TC 24 Z9 24 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 DEC PY 1993 VL 265 IS 6 BP E943 EP E953 PN 1 PG 11 WC Physiology SC Physiology GA MQ656 UT WOS:A1993MQ65600052 PM 8279550 ER PT J AU BIEDERMAN, J FARAONE, SV SPENCER, T WILENS, T NORMAN, D LAPEY, KA MICK, E LEHMAN, BK DOYLE, A AF BIEDERMAN, J FARAONE, SV SPENCER, T WILENS, T NORMAN, D LAPEY, KA MICK, E LEHMAN, BK DOYLE, A TI PATTERNS OF PSYCHIATRIC COMORBIDITY, COGNITION, AND PSYCHOSOCIAL FUNCTIONING IN ADULTS WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID RISK-FACTORS; CHILDREN; SAMPLE AB Objective: Although attention deficit hyperactivity disorder is a common disorder of childhood, its status as a disorder in adults is not clear. The authors reasoned that if the adult diagnosis of the disorder is a valid clinical entity, it should be similar to the childhood disorder with regard to patterns of psychiatric and cognitive findings. Method: Eighty-four adults with a clinical diagnosis of childhood-onset attention deficit hyperactivity disorder confirmed by structured interview who were referred for treatment were studied. Findings were compared with those from a preexisting study group of referred children with attention deficit hyperactivity disorder, nonreferred adult relatives of those children who also bad attention deficit hyperactivity disorder, and adults without the disorder who were relatives of normal children. Subjects were evaluated with a comprehensive battery of psychiatric, cognitive, and psychosocial assessments. Results: The referred and nonreferred adults with attention deficit hyperactivity disorder were similar to one another but more disturbed and impaired than the comparison subjects without the disorder. The pattern of psychopathology, cognition, and functioning among the adults with attention deficit hyperactivity disorder approximated the findings for children with the disorder. Conclusions: These results show that referred and nonreferred adults with attention deficit hyperactivity disorder have a pattern of demographic, psychosocial, psychiatric, and cognitive features that mirrors well-documented findings among children with the disorder. These findings further support the validity of the diagnosis for adults. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT ACC 725,FRUIT ST,BOSTON,MA 02114, USA. OI Mick, Eric/0000-0001-8505-8145; Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [NIMH MH-41314] NR 25 TC 552 Z9 560 U1 5 U2 25 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 DEC PY 1993 VL 150 IS 12 BP 1792 EP 1798 PG 7 WC Psychiatry SC Psychiatry GA MK054 UT WOS:A1993MK05400005 PM 8238632 ER PT J AU GERVAIS, DA WHITMAN, GJ CHEW, FS AF GERVAIS, DA WHITMAN, GJ CHEW, FS TI PULMONARY EOSINOPHILIC GRANULOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note ID HISTIOCYTOSIS-X; ADULT; LUNG; CT C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 5 TC 4 Z9 4 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 DEC PY 1993 VL 161 IS 6 BP 1158 EP 1158 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MJ634 UT WOS:A1993MJ63400004 PM 8249718 ER PT J AU YOUNG, RH AF YOUNG, RH TI NEW AND UNUSUAL ASPECTS OF OVARIAN GERM-CELL TUMORS SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE OVARY; GERM CELL TUMORS; PATHOLOGY, ADVANCES, UNUSUAL FEATURES ID ENDODERMAL SINUS TUMOR; MALIGNANT STRUMA OVARII; YOLK-SAC TUMOR; SERTOLI-LEYDIG CELL; TRABECULAR CARCINOID-TUMOR; CLINICOPATHOLOGICAL ANALYSIS; DERMOID CYST; INTESTINAL DIFFERENTIATION; HEPATOID CARCINOMA; ALPHA-FETOPROTEIN AB Ovarian germ cell tumors are reviewed with emphasis on recent developments. In the primitive germ cell tumor group the recently recognized subtypes of yolk sac tumor, the hepatoid and glandular variants are described. Hepatoid tumors, which resemble hepatocellular carcinomas, are usually admixed with other patterns of yolk sac neoplasia but when the hepatoid component predominates, distinction from metastatic hepatocellular carcinoma may be difficult. Glandular yolk sac tumors include those with a cribriform pattern as well as tumors that may be confused with endometrioid carcinoma. Within the teratoma category, a recent paper exploring the occasional relation between immature teratomas and dermoid cysts is reviewed. Problems caused by some of the monodermal teratomas are also highlighted. Struma ovarii may be the source of many diagnostic problems. It may be cystic and microscopic examination may reveal inconspicuous numbers of clearly recognizable thyroid follicles, resulting in confusion with other cystic ovarian tumors. In noncystic strumas many patterns, such as solid or pseudotubular, may be seen and the presence of cells with abundant clear or eosinophilic cytoplasm may add to the diagnostic difficulty, particularly if other teratomatous elements are lacking. Immunohistochemical staining for thyroglobulin may be crucial in establishing the diagnosis of a struma in these situations. The problem of identifying reliable criteria for malignancy of struma ovarii is explored on the basis of recent information. The two most recently recognized subtypes of carcinoid tumor, strumal and mucinous, are reviewed as are primary neuroectodermal and sebaceous tumors of the ovary. Unusual clinical features of germ cell tumors are discussed under three main categories: endocrine syndromes, paraendocrine and paraneoplastic syndromes, and miscellaneous. Included in these categories are disorders such as sexual precocity in association with germ cell tumors containing syncytiotrophoblast cells, endocrine abnormalities associated with the recently described functioning ovarian tumors with peripheral steroid cell proliferation, hyperthyroidism with struma ovarii, the carcinoid syndrome, autoimmune hemolytic anemia associated with dermoid cysts, complications of dermoid cyst rupture, which may simulate disseminated carcinomatosis, and ascites and Meigs' syndrome associated with struma ovarii. RP YOUNG, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT PATHOL,HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 106 TC 45 Z9 48 U1 1 U2 5 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 DEC PY 1993 VL 17 IS 12 BP 1210 EP 1224 DI 10.1097/00000478-199312000-00002 PG 15 WC Pathology; Surgery SC Pathology; Surgery GA MJ161 UT WOS:A1993MJ16100002 PM 7694512 ER PT J AU FINE, HA MAYER, RJ AF FINE, HA MAYER, RJ TI PRIMARY CENTRAL-NERVOUS-SYSTEM LYMPHOMA SO ANNALS OF INTERNAL MEDICINE LA English DT Review ID IMMUNE-DEFICIENCY-SYNDROME; NON-HODGKINS-LYMPHOMA; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PRIMARY MALIGNANT-LYMPHOMA; EPSTEIN-BARR-VIRUS; PRIMARY CEREBRAL LYMPHOMA; PRIMARY BRAIN LYMPHOMA; PRIMARY CNS LYMPHOMA; RETICULUM-CELL SARCOMA; HIGH-DOSE METHOTREXATE AB Objective: To compare the pathogenesis, clinical presentation, therapy, and prognosis of primary central nervous system lymphoma in immunocompetent persons with these characteristics of the disease in patients with AIDS. Data Sources and Extraction: All English-language papers published between 1980 and 1992 dealing with either lymphoma and the central nervous system or AIDS were reviewed. Patient characteristics, clinical presentation, histologic findings, and treatment and survival data were extracted from each case report and review. Data Synthesis: Data were available on 792 patients (from 40 reported series) with non-AIDS-associated primary central nervous system lymphoma and 315 patients (from 32 series) with AIDS-associated primary central nervous system lymphoma. Patients with AIDS initially consulted a physician more often when they had global neurologic symptoms compared with patients without AIDS, with more than 50% of the lesions on computed tomographic (CT) scans in patients with AIDS being ring-enhancing and multifocal, a pattern rarely described in immunocompetent patients. The overall survival of the patients without AIDS was 18.9 months compared with 2.6 months for patients with AIDS, with substantial differences remaining even for subgroups of patients similarly treated with radiation and chemotherapy. Conclusion: Primary central nervous system lymphoma is probably a substantially different disease in persons with and without AIDS with regard to patient characteristics, clinical and radiographic presentation, and prognosis. Recent advances in the treatment of this disease in patients without AIDS have not largely affected patients with AIDS. Substantial improvements in survival in these patients await advances in controlling their human immunodeficiency virus-associated disease. C1 BRAIN TUMOR CTR,BOSTON,MA. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FINE, HA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 112 TC 296 Z9 310 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD DEC 1 PY 1993 VL 119 IS 11 BP 1093 EP 1104 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA MJ335 UT WOS:A1993MJ33500007 PM 8239229 ER PT J AU HAYES, DF AF HAYES, DF TI TUMOR-MARKERS FOR BREAST-CANCER SO ANNALS OF ONCOLOGY LA English DT Review DE TUMOR MARKERS; BREAST CANCER; PROGNOSIS; DIAGNOSIS ID EPITHELIAL MEMBRANE ANTIGEN; AXILLARY MICRO-METASTESES; DUCTAL CARCINOMA INSITU; HER-2 NEU ONCOGENE; TERM FOLLOW-UP; MONOCLONAL-ANTIBODIES; PROGNOSTIC-SIGNIFICANCE; ESTROGEN-RECEPTOR; FLOW-CYTOMETRY; BONE-MARROW RP HAYES, DF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BREAST EVALUAT,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [5 R03 CA 53336] NR 109 TC 39 Z9 40 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. PD DEC PY 1993 VL 4 IS 10 BP 807 EP 819 PG 13 WC Oncology SC Oncology GA MP520 UT WOS:A1993MP52000004 PM 8117599 ER PT J AU BROUMAND, SR LABS, JD NOVELLINE, RA MARKOWITZ, BL YAREMCHUK, MJ AF BROUMAND, SR LABS, JD NOVELLINE, RA MARKOWITZ, BL YAREMCHUK, MJ TI THE ROLE OF 3-DIMENSIONAL COMPUTED-TOMOGRAPHY IN THE EVALUATION OF ACUTE CRANIOFACIAL TRAUMA SO ANNALS OF PLASTIC SURGERY LA English DT Article ID DIMENSIONAL CT RECONSTRUCTION; FACIAL STRUTS; FRACTURES; SURGERY; REFORMATIONS AB Three-dimensional computed tomographic (3-D CT) reformations together with their corresponding conventional axial two-dimensional (2-D) CT images of 20 patients with facial fractures were compared with 2-D CT alone to define their usefulness in the determination of facial skeletal fracture patterns. Nine surgeons with three different levels of experience and training evaluated the presence and spatial arrangement of fractures in all 2-D CT and 3-D CT scans. Comparisons were made between their evaluations of 2-D CT alone and 2-D CT plus 3-D CT scans. Statistical analyses with Friedman's test were performed. The addition of 3-D CT did not alter the interpretation of 2-D CT in 75% of evaluations. The number and accuracy of the changes made with the aid of 3-D CT reflected the experience of the observers. Overall, there was no improvement in the accuracy of interpretations with the addition of 3-D CT. C1 MASSACHUSETTS GEN HOSP, DEPT SURG,DIV PLAST SURG,15 PARKMAN ST,SUITE 453, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, DIV PLAST SURG, BOSTON, MA 02114 USA. UNIV CALIF LOS ANGELES, MED CTR, DEPT SURG, DIV PLAST SURG, LOS ANGELES, CA USA. NR 25 TC 8 Z9 9 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0148-7043 J9 ANN PLAS SURG JI Ann. Plast. Surg. PD DEC PY 1993 VL 31 IS 6 BP 488 EP 494 DI 10.1097/00000637-199312000-00002 PG 7 WC Surgery SC Surgery GA ML232 UT WOS:A1993ML23200002 PM 8297077 ER PT J AU SOUBA, WW AF SOUBA, WW TI GLUTAMINE AND CANCER SO ANNALS OF SURGERY LA English DT Review ID TOTAL PARENTERAL-NUTRITION; TUMOR-BEARING MICE; AMINO-ACID; PROTEIN-SYNTHESIS; INTESTINAL-MUCOSA; RADIATION-INJURY; HOST TISSUES; METABOLISM; MUSCLE; RATS AB Objective: This overview on glutamine and cancer discusses the importance of glutamine for tumor growth, summarizes the alterations in interorgan glutamine metabolism that develop in the tumor-bearing host, and reviews the potential benefits of glutamine nutrition in the patient with cancer. Summary Background Data: Glutamine is the most abundant amino acid in the blood and tissues. It is essential for tumor growth and marked changes in organ glutamine metabolism are characteristic of the host with cancer. Because host glutamine depletion has adverse effects, it is important to study the regulation of glutamine metabolism in cancer and to evaluate the impact of glutamine nutrition in the tumor-bearing state. Methods: Data from a variety of investigations on glutamine metabolism and nutrition related to the host with cancer were compiled and summarized. Results: Numerous studies on glutamine metabolism in cancer indicate that many tumors are avid glutamine consumers in vivo and in vitro. As a consequence of progressive tumor growth, host glutamine depletion develops and becomes a hallmark. This glutamine depletion occurs in part because the tumor behaves as a ''glutamine trap'' but also because of cytokine-mediated alterations in glutamine metabolism in host tissues. Animal and human studies that have investigated the use of glutamine-supplemented nutrition in the host with cancer suggest that pharmacologic doses of dietary glutamine may be beneficial. Conclusions: Understanding the control of glutamine metabolism in the tumor-bearing host not only improves the knowledge of metabolic regulation in the patient with cancer but also will lead to improved nutritional support regimens targeted to benefit the host. RP SOUBA, WW (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,DIV SURG ONCOL,FRUIT ST,BOSTON,MA 02114, USA. NR 77 TC 188 Z9 198 U1 1 U2 9 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD DEC PY 1993 VL 218 IS 6 BP 715 EP 728 DI 10.1097/00000658-199312000-00004 PG 14 WC Surgery SC Surgery GA ML605 UT WOS:A1993ML60500004 PM 8257221 ER PT J AU MEYERS, BF MCCABE, CJ AF MEYERS, BF MCCABE, CJ TI TRAUMATIC DIAPHRAGMATIC-HERNIA OCCULT MARKER OF SERIOUS INJURY SO ANNALS OF SURGERY LA English DT Article ID RUPTURE; EXPERIENCE AB Recent experience with traumatic diaphragmatic hernias at the Massachusetts General Hospital was reviewed to identify pitfalls in the diagnosis and treatment of this injury. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA. NR 25 TC 120 Z9 128 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD DEC PY 1993 VL 218 IS 6 BP 783 EP 790 DI 10.1097/00000658-199312000-00013 PG 8 WC Surgery SC Surgery GA ML605 UT WOS:A1993ML60500013 PM 8257229 ER PT J AU SACHS, DH AF SACHS, DH TI TRANSPLANTATION TOLERANCE SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT 29TH Annual Meeting of the Society-of-Thoracic-Surgeons CY JAN 25-27, 1993 CL SAN ANTONIO, TX SP SOC THORAC SURGEONS ID BONE-MARROW CHIMERAS; RADIATION CHIMERAS; IMMUNOCOMPETENCE; XENOGRAFTS; IRRADIATION; SPECIFICITY; INDUCTION AB Two major factors currently limiting the field of transplantation are (1) treatment-related complications and (2) donor organ availability. This article reviews progress from our laboratory in research directed at solutions to both of these limitations. The induction of specific tolerance could eliminate many of the treatment-related complications currently attributable to nonspecific immunosuppressive drug therapy. The methodology being investigated involves use of mixed chimerism as an approach to transplantation tolerance. In this case, the presence of certain donor bone marrow-derived elements induces specific tolerance, whereas host-type antigen presenting cells confer normal immunocompetence. In addition, extension of this work toward tolerance across xenogeneic barriers could eliminate the limitation of organ donor availability. A nonmyeloablative preparative regimen capable of inducing mixed chimerism and tolerance has previously been described from our laboratory for both allogeneic murine systems and concordant xenogeneic rat --> mouse systems. Current studies attempting to extend this regimen to a discordant pig --> monkey xenograft model are reviewed. If successful, these studies could provide a virtually limitless source of xenogeneic donor organs. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SACHS, DH (reprint author), MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,SURG SERV,BOSTON,MA 02129, USA. FU NIAID NIH HHS [AI31046] NR 20 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD DEC PY 1993 VL 56 IS 6 BP 1221 EP 1227 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA MP525 UT WOS:A1993MP52500001 PM 8267417 ER PT J AU SOUSSY, CJ WOLFSON, JS NG, EY HOOPER, DC AF SOUSSY, CJ WOLFSON, JS NG, EY HOOPER, DC TI LIMITATIONS OF PLASMID COMPLEMENTATION TEST FOR DETERMINATION OF QUINOLONE RESISTANCE DUE TO CHANGES IN THE GYRASE A PROTEIN AND IDENTIFICATION OF CONDITIONAL QUINOLONE RESISTANCE LOCUS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID ESCHERICHIA-COLI; DNA GYRASE; GENE; CIPROFLOXACIN; MUTATIONS; MECHANISMS; MUTANTS; CLONING; SUBUNIT; STRAINS AB Plasmid pJSW101 derived from pUC19 and carrying the wild-type gyrA gene was found to be unstable in HM72, a quinolone-resistant (QR) clinical isolate of Escherichia coli, and resulted in no change in quinolone MICs. MICs determined in the presence of ampicillin to ensure plasmid presence, however, resulted in complementation. HM72 was proved to have a gyrA mutation based on the DNA sequence of a 418-bp fragment of gyrA. DNA sequencing identified a common mutation encoding Leu-83 as the cause of QR. To identify loci other than gyrA and nfxB contributing to QR in KF111b, zgh-3075::Tn10 (67 min) in CAG12152 was transduced into KF111b. Sixteen percent of the transductants had a fourfold decrease in norfloxacin MIC, indicating the presence of a locus, nfxD, which contributes to QR. Outcross of of nfxD from DH151 (gvrA nfxB nfxD zgh-3075::Tn10) resulted in 8% of the KF130 gyrA, 2% of the EN226-3 gyrA, and none of the KL16 (wild-type) transductants, with a four- to eightfold increase in norfloxacin MIC. In the presence of ampicillin, the resistance of a gyrA nfxD double mutant, DH161 nfxD gvrA (from EN226-3), was fully complemented by gvrA(+). Thus, gyrA(+) plasmid complementation tests for QR may be falsely negative with plasmid instability, a difficulty which may be circumvented by maintenance of plasmid selection. In addition, if nfxD-like mutations occur in gyrA clinical isolates, a positive test may overestimate the level of resistance attributable to gyrA alone. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,INFECT DIS UNIT,BOSTON,MA 02114. RP SOUSSY, CJ (reprint author), UNIV PARIS 12,HOP HENRI MONDOR,SERV BACTERIOL VIROL HYG,F-94010 CRETEIL,FRANCE. NR 27 TC 34 Z9 34 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 DEC PY 1993 VL 37 IS 12 BP 2588 EP 2592 PG 5 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA MK853 UT WOS:A1993MK85300013 PM 8109921 ER PT J AU RICE, LB MARSHALL, SH CARIAS, LL SUTTON, L JACOBY, GA AF RICE, LB MARSHALL, SH CARIAS, LL SUTTON, L JACOBY, GA TI SEQUENCES OF MGH-1, YOU-1, AND YOU-2 EXTENDED-SPECTRUM BETA-LACTAMASE GENES SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID ESCHERICHIA-COLI; CEFTAZIDIME RESISTANCE; BROAD-SPECTRUM; KLEBSIELLA-PNEUMONIAE; NUCLEOTIDE-SEQUENCES; ENTEROBACTERIACEAE; AZTREONAM; OUTBREAK AB Genes for MOB-I, YOU-1, and YOU-2 extended-spectrum beta-lactamases have been cloned and sequenced. The gene for MGH-1 has the sequence of bla(TEM-10), YOU-2 has that of bla(TEM-12), and YOU-1 has that of bla(TEM-26). All have evolved from bla(TEM-1b) but have the strong dual promoter sequence of bla(TEM-2). C1 DEPT VET AFFAIRS MED CTR,RES SERV,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,SCH MED,DEPT MED,CLEVELAND,OH 44106. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. FU NIAID NIH HHS [NIAID AI20415] NR 19 TC 30 Z9 30 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 DEC PY 1993 VL 37 IS 12 BP 2760 EP 2761 PG 2 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA MK853 UT WOS:A1993MK85300046 PM 8109951 ER PT J AU WEBER, GF WAXMAN, DJ AF WEBER, GF WAXMAN, DJ TI DENITROSATION OF THE ANTICANCER DRUG 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA CATALYZED BY MICROSOMAL GLUTATHIONE-S-TRANSFERASE AND CYTOCHROME-P450 MONOOXYGENASES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID RAT-LIVER MICROSOMES; INTERSTRAND CROSS-LINKING; BRAIN TUMOR-CELLS; ETHACRYNIC-ACID; ANTICANCER DRUGS; CYTO-TOXICITY; EXPRESSION; RESISTANCE; METABOLISM; INHIBITION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA-49248] NR 56 TC 27 Z9 28 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD DEC PY 1993 VL 307 IS 2 BP 369 EP 378 DI 10.1006/abbi.1993.1602 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MM266 UT WOS:A1993MM26600020 PM 8274024 ER PT J AU HELLMAN, P HELLMAN, B JUHLIN, C JUPPNER, H RASTAD, J RIDEFELT, P AKERSTROM, G AF HELLMAN, P HELLMAN, B JUHLIN, C JUPPNER, H RASTAD, J RIDEFELT, P AKERSTROM, G TI REGULATION OF PROLIFERATION IN JEG-3 CELLS BY A 500-KDA CA2+ SENSOR AND PARATHYROID HORMONE-RELATED PROTEIN SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID EMBRYONAL CARCINOMA-CELLS; ADENYLATE-CYCLASE; CYTOTROPHOBLAST CELLS; HUMORAL HYPERCALCEMIA; HUMAN CHORIOCARCINOMA; CYTOPLASMIC CA-2+; HUMAN PLACENTA; PEPTIDE; RECEPTOR; CALCIUM C1 UNIV UPPSALA,DEPT TOXICOL,S-75105 UPPSALA,SWEDEN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114. UNIV UPPSALA,DEPT SURG,S-75105 UPPSALA,SWEDEN. UNIV UPPSALA,DEPT OCCUPAT MED,S-75105 UPPSALA,SWEDEN. NR 34 TC 18 Z9 19 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD DEC PY 1993 VL 307 IS 2 BP 379 EP 385 DI 10.1006/abbi.1993.1603 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MM266 UT WOS:A1993MM26600021 PM 8274025 ER PT J AU PROSTAK, KS SEIFERT, P SKOBE, Z AF PROSTAK, KS SEIFERT, P SKOBE, Z TI ENAMELOID FORMATION IN 2 TETRAODONTIFORM FISH SPECIES WITH HIGH AND LOW FLUORIDE CONTENTS IN ENAMELOID SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE ODONTOGENESIS; ULTRASTRUCTURE; ENAMEL; FLUORIDE ID DENTAL EPITHELIUM; PHYLOGENETIC SIGNIFICANCE; TELEOST FISH; TEETH; ULTRASTRUCTURE; ORGAN; ODONTOBLASTS; RAT AB Forming teeth of parrotfish and pufferfish were viewed by transmission electron microscopy to correlate cytological features of the enameloid organ with the species' fluoride (F) content in mature enameloid. Secretory-stage inner dental epithelial cells (IDE) of parrotfish (high Fl and pufferfish (low F) secreted procollagen granules into the enameloid collagen matrix. The odontoblasts of both species, less numerous than IDE cells, also contained procollagen granules at the enameloid matrix formation stage. After the full thickness of enameloid matrix collagen had been deposited, enameloid crystallites formed parallel to the long axis of the enameloid collagen fibres. Concurrently, the plasma membranes of the outer dental epithelial cells (ODE) became invaginated in both species, but to a much greater extent in parrotfish. Highly undulating parrotfish ODE cells surrounded numerous fenestrated capillaries. In contrast, pufferfish ODE cells remained straight with few adjacent capillaries. Extensive tight junctions formed between ODE and IDE cells of both species, sealing the extracellular space. With increased mineralization, enameloid collagen fibres were no longer discernible. A thin layer of amorphous material, which subsequently mineralized, was secreted on to the enameloid surface by IDE cells in both species. Pufferfish odontoblasts secreted a mineralizing amorphous layer on the pulpal aspect of the enameloid. The results suggest that at the mineralization stage, a triad of cytostructural features, highly invaginated ODE cells, highly vascularized ODE cells, and extensive tight junctions are strongly correlated with high fluoride content of mature enameloid mineral. Species without any one of these features have lower fluoride in the enameloid. RP PROSTAK, KS (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. NR 35 TC 23 Z9 23 U1 2 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0003-9969 J9 ARCH ORAL BIOL JI Arch. Oral Biol. PD DEC PY 1993 VL 38 IS 12 BP 1031 EP 1044 DI 10.1016/0003-9969(93)90164-H PG 14 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MU994 UT WOS:A1993MU99400002 PM 8141664 ER PT J AU KHETARPAL, U MORTON, CC AF KHETARPAL, U MORTON, CC TI COL1A2 AND COL2A1 EXPRESSION IN TEMPORAL BONE OF LETHAL OSTEOGENESIS IMPERFECTA SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article ID II COLLAGEN DISTRIBUTION; INSITU HYBRIDIZATION; TRANSGENIC MICE; MESSENGER-RNAS; GENE COL2A1; OSTEOBLASTS; METABOLISM; MUTATION; EAR AB Objective: COL1A2 and COL2A1 genes are expressed al high levels in many cochlear cells of 16- to 23-week-old human fetuses. Given these prior observations and the rare opportunity to obtain temporal bones from a deceased neonate with osteogenesis imperfecta (OI) type II, we determined the cellular distribution and level of expression of COL1A2 mRNA in OI type II inner ear compared with the expression in second-trimester human fetal cochlea. Expression of COL2A1 mRNA was assessed for its normal role in OI type IL neonatal cochlea and to address potential spatial and temporal changes along with our observations in fetal cochlea. We describe our tissue in situ hybridization protocol and document its usefulness in assessing gene expression in human temporal bone obtained at autopsy. Design: RNA-RNA in situ hybridization was performed in formaldehyde-fixed, decalcified, paraffin-embedded temporal bone sections from a neonate with OI type II. Semi-quantitative assessment of gene expression was performed by visual inspection of grain densities. Results and Conclusions: COL1A2 and COL2A1 were e,expressed at moderate-to-high levels in many membranous cochlear cells, and no dramatic alterations in pattern or level of expression of these genes was noted compared with human fetal cochlea. Consistent with in vitro studies, expression of COL1A2 in osteoblasts lining enchondral and endosteal layers is less than that in identical cells of the fetal otic capsule undergoing osteoid deposition and mineralization. Expression of COL1A2 mRNA in osteoblasts lining the outer periosteum of otic capsule is markedly higher than osteoblasts lining enchondral and endosteal layers, suggesting that differential expression may exist between osteoblasts lining endosteal, enchondral, and periosteal surfaces of bone in OI type II. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. FU NIDCD NIH HHS [DC00871] NR 28 TC 5 Z9 5 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0886-4470 J9 ARCH OTOLARYNGOL JI Arch. Otolaryngol. Head Neck Surg. PD DEC PY 1993 VL 119 IS 12 BP 1305 EP 1314 PG 10 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA MW447 UT WOS:A1993MW44700006 PM 17431984 ER PT J AU ROBBINS, JA LEVINE, RL MASER, A ROSENBEK, JC KEMPSTER, GB AF ROBBINS, JA LEVINE, RL MASER, A ROSENBEK, JC KEMPSTER, GB TI SWALLOWING AFTER UNILATERAL STROKE OF THE CEREBRAL-CORTEX SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article ID RIGHT-HEMISPHERE STROKE; ASPIRATION; DYSPHAGIA C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV,MADISON,WI. GOVERNOR STATE UNIV,DIV COMMUN DISORDERS,UNIV PK,IL. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT SPEECH PATHOL & AUDIOL,MADISON,WI. UNIV WISCONSIN,HLTH SCI CTR,MADISON,WI 53706. RP ROBBINS, JA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,GRECC 11G,2500 OVERLOOK TERR,MADISON,WI 53705, USA. FU NINDS NIH HHS [NINDS NS24427] NR 34 TC 117 Z9 125 U1 0 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD DEC PY 1993 VL 74 IS 12 BP 1295 EP 1300 DI 10.1016/0003-9993(93)90082-L PG 6 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA ML134 UT WOS:A1993ML13400002 PM 8259895 ER PT J AU STEINER, LA HARRIS, BA KREBS, DE AF STEINER, LA HARRIS, BA KREBS, DE TI RELIABILITY OF ECCENTRIC ISOKINETIC KNEE FLEXION AND EXTENSION MEASUREMENTS SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,PROGRAM PHYS THERAPY,101 MERRIMAC ST,BOSTON,MA 02114. NR 28 TC 37 Z9 38 U1 0 U2 6 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD DEC PY 1993 VL 74 IS 12 BP 1327 EP 1335 DI 10.1016/0003-9993(93)90088-R PG 9 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA ML134 UT WOS:A1993ML13400008 PM 8259901 ER PT J AU KOHMURA, C GOLD, HK YASUDA, T HOLT, R NEDELMAN, MA GUERRERO, JL WEISMAN, HF COLLEN, D AF KOHMURA, C GOLD, HK YASUDA, T HOLT, R NEDELMAN, MA GUERRERO, JL WEISMAN, HF COLLEN, D TI A CHIMERIC MURINE/HUMAN ANTIBODY FAB FRAGMENT DIRECTED AGAINST THE PLATELET GPIIB/IIIA RECEPTOR ENHANCES AND SUSTAINS ARTERIAL THROMBOLYSIS WITH RECOMBINANT TISSUE-TYPE PLASMINOGEN-ACTIVATOR IN BABOONS SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Article DE CHIMERIC ANTIBODY; PLATELET GPIIB/IIIA ANTIBODY; THROMBOLYSIS; RECOMBINANT T-PA; BABOON ID GLYCOPROTEIN-IIB/IIIA RECEPTOR; ACUTE MYOCARDIAL-INFARCTION; COMBINED BOLUS INJECTION; MONOCLONAL-ANTIBODY; CORONARY THROMBOLYSIS; CANINE PREPARATION; F(AB')2 FRAGMENTS; UNSTABLE ANGINA; IIIA RECEPTOR; THROMBOSIS AB Inhibition of the platelet glycoprotein (GP) IIb/IIIa receptor with the murine monoclonal antibody 7E3 abolishes ex vivo platelet aggregation, reduces thrombogenicity, and sustains arterial recanalization with recombinant tissue-type plasminogen activator (rt-PA). A chimeric murine/human Fab fragment of 7E3 (c7E3-Fab) has a markedly reduced immunogenicity, but its potency as an adjunct for thrombolysis with rt-PA has not been evaluated. The effects of a single intravenous bolus injection of aspirin (17 mg/kg) or c7E3-Fab (0.45 mg/kg) on thrombolysis and reocclusion induced with rt-PA were studied in groups of six baboons with femoral arterial thrombosis and superimposed high-grade stenosis. This dose of c7E3-Fab blocked 96+/-1% of the platelet GPIIb/IIIa receptors and abolished ADP-induced platelet aggregation. Bolus intravenous injections of rt-PA (0.25 mg/kg) were repeated at 15-minute intervals until reperfusion occurred (maximum of four injections). In the aspirin group, reperfusion was obtained within 51+/-16 minutes (mean+/-SD) but was rapidly followed by reocclusion within 6+/-9 minutes and by cyclic reflow and reocclusion. In the c7E3-Fab group, reperfusion was obtained within 25+/-8 minutes (P<.01 versus aspirin group) and was associated with a delayed reocclusion of 63+/-63 minutes (P<.05 versus aspirin group). Template bleeding times remained unchanged in the aspirin/rt-PA group but were markedly prolonged (to >30 minutes) in the c7E3-Fab/rt-PA group. Bolus injection of 0.45 mg/kg of a chimeric murine/human Fab fragment of the monoclonal antibody 7E3 enhanced and sustained arterial recanalization with rt-PA and thus may constitute a less immunogenic alternative to the murine antibody for use in humans. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. CENTOCOR INC,MALVERN,PA. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 NR 31 TC 36 Z9 37 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD DEC PY 1993 VL 13 IS 12 BP 1837 EP 1842 PG 6 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MK852 UT WOS:A1993MK85200015 PM 8241105 ER PT J AU GABRIELI, JDE CORKIN, S MICKEL, SF GROWDON, JH AF GABRIELI, JDE CORKIN, S MICKEL, SF GROWDON, JH TI INTACT ACQUISITION AND LONG-TERM RETENTION OF MIRROR-TRACING SKILL IN ALZHEIMERS-DISEASE AND IN GLOBAL AMNESIA SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID CEREBELLAR MOTOR DISORDERS; ELBOW TRACKING MOVEMENT; CEREBRAL BLOOD-FLOW; HIPPOCAMPAL-FORMATION; HUNTINGTONS-DISEASE; MEMORY-SYSTEMS; IMPLICIT; DEMENTIA; DYSFUNCTION; DISSOCIATION AB The ability of patients with Alzheimer's disease (AD) or global amnesia (AMN) to acquire skill for tracing a pattern seen in mirror-reversed view and to retain that skill over 24-hr intervals was examined. Both patient groups had poor recall and recognition of their mirror-tracing experience, but they acquired and retained mirror-tracing skill as well as normal control subjects. One AMN patient (H.M.) retained the skill over a year-long interval. Furthermore, the patients transferred their skill normally to an alternate pattern. These results indicate that the memory system underlying mirror-tracing skill learning is separable from medial-temporal structures compromised in AMN and AD and from neocortical areas compromised in AD. Brain regions relatively spared in early AD, such as the basal ganglia or cerebellum, may mediate critical aspects of the learning of novel sensorimotor associations that underlie skilled mirror tracing. C1 MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. MIT,CLIN RECH INST,CAMBRIDGE,MA 02139. BOSTON UNIV,SCH MED,MEMORY DISORDERS RES CTR,BOSTON,MA 02118. BOSTON DEPT VET AFFAIRS,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. FU NCRR NIH HHS [M01RR00088]; NIA NIH HHS [5R37AG06605, 1P01AG06605] NR 59 TC 120 Z9 122 U1 2 U2 10 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7044 J9 BEHAV NEUROSCI JI Behav. Neurosci. PD DEC PY 1993 VL 107 IS 6 BP 899 EP 910 DI 10.1037/0735-7044.107.6.899 PG 12 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA MP936 UT WOS:A1993MP93600001 PM 8136066 ER PT J AU LEFKOPOULOU, M RYAN, L AF LEFKOPOULOU, M RYAN, L TI GLOBAL TESTS FOR MULTIPLE BINARY OUTCOMES SO BIOMETRICS LA English DT Article DE CLUSTERED DATA; DEVELOPMENTAL TOXICITY; EFFICIENCY; GENERAL ESTIMATING EQUATIONS; QUASI-LIKELIHOOD; SCORE TEST; TERATOLOGY ID LONGITUDINAL DATA-ANALYSIS; GENERALIZED LINEAR-MODELS; GLYCOL DIMETHYL ETHER; DEVELOPMENTAL TOXICITY; MICE; RATS; REGRESSION; ENDPOINTS AB The applied statistician often encounters the need to compare two or more groups with respect to more than one outcome or response. Several options are generally available, including reducing the dimension of the problem by averaging or summarizing the outcomes, using Bonferroni or other adjustments for multiple comparisons, or applying a global test based on a suitable multivariate model. For normally distributed data, it is well established that global tests tend to be significantly more sensitive than other procedures. While global tests have also been proposed for multiple binary outcomes, their properties have not been well studied nor have they been widely discussed in the context of clustered data. In this paper, we derive a class of quasi-likelihood score tests for multiple binary outcomes, and show that special cases of this class correspond to other tests that have been proposed. We discuss extensions to allow for clustered data, and compare the results to the simple approach of collapsing the data to a single binary outcome, indicating the presence or absence of at least one response. The asymptotic relative efficiencies of the tests are shown to depend not only on the correlation between the outcomes, but also on the response probabilities. Although global tests based on a multivariate model are generally recommended, our findings suggest that a test based on the collapsed data can maintain surprisingly high efficiency, especially when the outcomes of interest are rare. Data from several developmental toxicity studies illustrate our results. C1 DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 FU NCI NIH HHS [CA39640, CA48061]; NIAID NIH HHS [AI24643] NR 17 TC 70 Z9 70 U1 0 U2 4 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD DEC PY 1993 VL 49 IS 4 BP 975 EP 988 DI 10.2307/2532240 PG 14 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA MR636 UT WOS:A1993MR63600001 PM 8117908 ER PT J AU RYAN, L AF RYAN, L TI USING HISTORICAL CONTROLS IN THE ANALYSIS OF DEVELOPMENTAL TOXICITY DATA SO BIOMETRICS LA English DT Article DE CLUSTERED DATA; CORRELATED BINARY DATA; QUASI-LIKELIHOOD; SCORE TEST; TERATOLOGY ID LONGITUDINAL DATA-ANALYSIS; GENERALIZED LINEAR-MODELS; PROPORTIONS; REGRESSION; OUTCOMES; TRENDS AB Historical control data can often aid in the interpretation of the results from laboratory dose-response experiments. For example, formal statistical methods for using historical data are well established for carcinogenicity studies. In that case, a score test derived from a beta-binomial model yields a simple modification of the standard Cochran-Armitage test for trend. However, this test cannot be used for developmental toxicity studies since it does not allow for the additional correlation structure induced by the presence of litter effects. In this paper, quasi-likelihood methods are used to incorporate historical control information into a trend test for the types of correlated binary outcomes that typically arise in developmental toxicity studies. The proposed test is asymptotically equivalent to the beta-binomial score test in the special case when all the litter sizes are equal to 1. Malformation data from a series of developmental toxicity studies illustrate the results. C1 DANA FARBER CANC INST,BOSTON,MA 02115. RP RYAN, L (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 FU NCI NIH HHS [CA48061] NR 18 TC 19 Z9 19 U1 0 U2 1 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD DEC PY 1993 VL 49 IS 4 BP 1126 EP 1135 DI 10.2307/2532254 PG 10 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA MR636 UT WOS:A1993MR63600015 PM 8117906 ER PT J AU BERK, DA YUAN, F LEUNIG, M JAIN, RK AF BERK, DA YUAN, F LEUNIG, M JAIN, RK TI FLUORESCENCE PHOTOBLEACHING WITH SPATIAL FOURIER-ANALYSIS - MEASUREMENT OF DIFFUSION IN LIGHT-SCATTERING MEDIA SO BIOPHYSICAL JOURNAL LA English DT Article ID NEOPLASTIC TISSUES; TRANSPORT; RECOVERY; MACROMOLECULES; MICROSCOPY; CONVECTION; ANTIBODIES; MESENTERY; MOBILITY AB A new method for the measurement of diffusion in thick samples is introduced, based upon the spatial Fourier analysis of Tsay and Jacobson (Biophys. J. 60:360-368, 1991) for the video image analysis of fluorescence recovery after photobleaching (FRAP). In this approach, the diff usion coefficient is calculated from the decay of Fourier transform coefficients in successive fluorescence images. Previously, the application of FRAP in thick samples has been confounded by the optical effects of out-of-focus light and scattering and absorption by the sample. The theory of image formation is invoked to show that the decay rate is the same for both the observed fluorescence intensity and the true concentration distribution in the tissue. The method was tested in a series of macromolecular diff usion measurements in aqueous solution, in agarose gel, and in simulated tissue consisting of tumor cells (45% v/v) and blood cells (5% v/v) in an agarose gel. For a range of fluorescently labeled proteins (MW = 14 to 600 kD) and dextrans (MW = 4.4 to 147.8 kD), the diffusion coefficients in aqueous solution were comparable to previously published values. A comparison of the spatial Fourier analysis with a conventional direct photometric method revealed that even for the weakly scattering agarose sample, the conventional method gives a result that is inaccurate and dependent on sample thickness whereas the diff usion coefficient calculated by the spatial Fourier method agreed with published values and was independent of sample thickness. The diffusion coefficient of albumin in the simulated tissue samples, as determined by the spatial Fourier analysis, varied slightly with sample thickness. In contrast, when the same video images were analyzed by direct photometric analysis, the calculated diff usion coefficients were grossly inaccurate and highly dependent on sample thickness. No simple correction could be devised to ensure the accuracy of the direct photometric method of analysis. These in vitro experiments demonstrate the advantage of our new analysis for obtaining an accurate measure of the local diffusion coefficient in microscopic samples that are thick (thickness greater than the microscope depth of focus) and scatter light. RP BERK, DA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. RI Yuan, Fan/A-1287-2011; Berk, David/A-4863-2012; Leunig, Michael/E-7951-2017 OI Berk, David/0000-0002-3855-6886; Leunig, Michael/0000-0002-2036-5416 FU NCI NIH HHS [CA56591, CA59255] NR 32 TC 145 Z9 147 U1 1 U2 15 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD DEC PY 1993 VL 65 IS 6 BP 2428 EP 2436 PG 9 WC Biophysics SC Biophysics GA MM054 UT WOS:A1993MM05400017 PM 8312481 ER PT J AU KARLSSON, JOM CRAVALHO, EG RINKES, IHMB TOMPKINS, RG YARMUSH, ML TONER, M AF KARLSSON, JOM CRAVALHO, EG RINKES, IHMB TOMPKINS, RG YARMUSH, ML TONER, M TI NUCLEATION AND GROWTH OF ICE CRYSTALS INSIDE CULTURED-HEPATOCYTES DURING FREEZING IN THE PRESENCE OF DIMETHYL-SULFOXIDE SO BIOPHYSICAL JOURNAL LA English DT Article ID ISOLATED RAT HEPATOCYTES; CRYOPRESERVATION; TEMPERATURE; ADDITIVES; RECOVERY; KINETICS; STORAGE; EMBRYOS AB A three-part, coupled model of cell dehydration, nucleation, and crystal growth was used to study intracellular ice formation (IIF) in cultured hepatocytes frozen in the presence of dimethyl sulfoxide (DMSO). Heterogeneous nucleation temperatures were predicted as a function of DMSO concentration and were in good agreement with experimental data. Simulated freezing protocols correctly predicted and explained experimentally observed effects of cooling rate, warming rate, and storage temperature on hepatocyte function. For cells cooled to -40-degrees-C, no IIF occurred for cooling rates less than 10-degrees-C/min. IIF did occur at faster cooling rates, and the predicted volume of intracellular ice increased with increasing cooling rate. Cells cooled at 5-degrees-C/min to -80-degrees-C were shown to undergo nucleation at -46.8-degrees-C, with the consequence that storage temperatures above this value resulted in high viability independent of warming rate, whereas colder storage temperatures resulted in cell injury for slow warming rates. Cell damage correlated positively with predicted intracellular ice volume, and an upper limit for the critical ice content was estimated to be 3.7% of the isotonic water content. The power of the model was limited by difficulties in estimating the cytosol viscosity and membrane permeability as functions of DMSO concentration at low temperatures. C1 SHRINERS BURNS INST,RES CTR,1 KENDALL SQ,BLDG 1400 W,CAMBRIDGE,MA 02142. MASSACHUSETTS GEN HOSP,SURG RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. RUTGERS UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08885. FU NIDDK NIH HHS [1R29 DK46270] NR 36 TC 121 Z9 127 U1 3 U2 17 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD DEC PY 1993 VL 65 IS 6 BP 2524 EP 2536 PG 13 WC Biophysics SC Biophysics GA MM054 UT WOS:A1993MM05400029 PM 8312489 ER PT J AU WEISS, M YOKOYAMA, C SHIKAMA, Y NAUGLE, C DRUKER, B SIEFF, CA AF WEISS, M YOKOYAMA, C SHIKAMA, Y NAUGLE, C DRUKER, B SIEFF, CA TI HUMAN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR-RECEPTOR SIGNAL-TRANSDUCTION REQUIRES THE PROXIMAL CYTOPLASMIC DOMAINS OF THE ALPHA-SUBUNIT AND BETA-SUBUNIT SO BLOOD LA English DT Article ID HEMATOPOIETIC GROWTH-FACTORS; GM-CSF RECEPTOR; TYROSINE PHOSPHORYLATION; EXPRESSION CLONING; RECONSTITUTION; INTERLEUKIN-3; PROTEINS; CELLS; IL-3; CDNA C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT HEMATOL & ONCOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NR 24 TC 67 Z9 67 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 DEC 1 PY 1993 VL 82 IS 11 BP 3298 EP 3306 PG 9 WC Hematology SC Hematology GA MJ708 UT WOS:A1993MJ70800011 PM 8241501 ER PT J AU BURNSTINE, MA LEVIN, LA LOUIS, DN HEDLEYWHYTE, ET KUPSKY, WJ DOEPNER, D ALBERT, DM AF BURNSTINE, MA LEVIN, LA LOUIS, DN HEDLEYWHYTE, ET KUPSKY, WJ DOEPNER, D ALBERT, DM TI NUCLEOLAR ORGANIZER REGIONS IN OPTIC GLIOMAS SO BRAIN LA English DT Article ID LOW-GRADE GLIOMAS; LONG-TERM; PATHWAY TUMORS; NERVE GLIOMAS; SAN-FRANCISCO; BRAIN-TUMORS; MANAGEMENT; CHIASM; CHILDHOOD; ASTROCYTOMAS AB The biological nature of optic gliomas is controversial, with some considering them benign hamartomatous lesions, and others believing them to be true neoplasms. We evaluated the use of colloid silver impregnation of nucleolar organizer region-associated proteins (AgNORs) in making this distinction. Thirty-one optic gliomas, 14 optic nerve meningiomas, and a single case of giant cell glioblastoma multiforme (monstrocellular glioma) of the optic chasm were stained for AgNORs and counted in a masked fashion. The optic gliomas contained 2.01 +/-0.09 AgNORs per nucleus, similar to that of optic nerve meningiomas (2.15 +/-0.15) and our previously reported counts for diffuse fibrillary astrocytoma (2.22+/-0.10), and significantly more than that of reactive astrocytosis (1.18+/-0.02). Six of the seven optic gliomas examined had compound AgNORs, a feature associated with malignancy in other tumour types. AgNOR counts did not correlate with clinical features, including those seen during the post-operation course. These data suggest that optic gliomas may be true neoplasms, and not benign hamartomas. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA. CHILDRENS HOSP,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. UNIV MUNICH,HOSP EYE,MUNICH,GERMANY. NR 53 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 0006-8950 J9 BRAIN JI Brain PD DEC PY 1993 VL 116 BP 1465 EP 1476 DI 10.1093/brain/116.6.1465 PN 6 PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MW136 UT WOS:A1993MW13600010 PM 8293281 ER PT J AU HUBBARD, JW MIDHA, KK HAWES, EM MCKAY, G MARDER, SR ARAVAGIRI, M KORCHINSKI, ED AF HUBBARD, JW MIDHA, KK HAWES, EM MCKAY, G MARDER, SR ARAVAGIRI, M KORCHINSKI, ED TI METABOLISM OF PHENOTHIAZINE AND BUTYROPHENONE ANTIPSYCHOTIC-DRUGS - A REVIEW OF SOME RECENT RESEARCH FINDINGS AND CLINICAL IMPLICATIONS SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID HALOPERIDOL PLASMA-LEVELS; REDUCED HALOPERIDOL; SCHIZOPHRENIC-PATIENTS; FLUPHENAZINE; GLUCURONIDE; INTERCONVERSIONS; IDENTIFICATION; DOPAMINE; BRAIN AB Whereas some metabolites of antipsychotic drugs are psychoactive and contribute to clinical improvement, recent studies have provided evidence that certain metabolites contribute to side-effects which can be disabling enough to negate clinical improvement as regards the psychosis. The route of administration of the drug can determine the amount of metabolite produced in the body and affect how the patient feels in response to the treatment. C1 UNIV SASKATCHEWAN, COLL PHARM, SASKATOON S7N 0W0, SASKATCHEWAN, CANADA. UNIV CALIF LOS ANGELES, CLIN RES CTR SCHIZOPHRENIA & PSYCHIAT REHABIL, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, PSYCHOPHARMACOL LAB, LOS ANGELES, CA 90073 USA. UNIV SASKATCHEWAN, COLL MED, SASKATOON S7N 0W0, SASKATCHEWAN, CANADA. NR 18 TC 6 Z9 6 U1 0 U2 1 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON SW1X 8PG, ENGLAND SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD DEC PY 1993 VL 163 SU 22 BP 19 EP 24 PG 6 WC Psychiatry SC Psychiatry GA MN026 UT WOS:A1993MN02600003 ER PT J AU PEREZ, CA HANKS, GE LEIBEL, SA ZIETMAN, AL FUKS, Z LEE, WR AF PEREZ, CA HANKS, GE LEIBEL, SA ZIETMAN, AL FUKS, Z LEE, WR TI LOCALIZED CARCINOMA OF THE PROSTATE (STAGE-T1B, STAGE-T1C, STAGE-T2, AND STAGE-T3) - REVIEW OF MANAGEMENT WITH EXTERNAL-BEAM RADIATION-THERAPY SO CANCER LA English DT Review DE CARCINOMA OF THE PROSTATE; IRRADIATION; PROSTATE-SPECIFIC ANTIGEN; CLINICAL TRIALS ID TEMPORARY IR-192 IMPLANTATION; TREATMENT RELATED MORBIDITY; ANTIGEN LEVELS; DEFINITIVE RADIOTHERAPY; PELVIC LYMPHADENECTOMY; RADICAL PROSTATECTOMY; C ADENOCARCINOMA; TUMOR-CONTROL; INTERSTITIAL IMPLANTATION; DISTANT METASTASIS AB Background. Optimal treatment for patients with localized carcinoma of the prostate is controversial. Radiation therapy is an established modality in the management of these patients, and several reports indicate the results are comparable to those achieved with radical prostatectomy. Recently effectiveness of therapy for carcinoma of the prostate is being evaluated in light of post-treatment prostate-specific antigen (PSA) determinations. Methods. A review was performed of multiple publications and data from selected institutions with large experience in the management of carcinoma of the prostate. Survival and clinical incidence of local recurrence and distant metastases were analyzed as well as preliminary data on postirradiation PSA levels. Factors that affect the outcome of therapy and relevant clinical trials are discussed. Results. Reported differences in the age of patients treated with radical prostatectomy (59-63 years), irradiation (63-69 years), or observation (69-75.5 years) were identified. The effect of surgical staging on outcome of irradiation was significant. In multiple series of patients clinically and radiographically staged, the 5-year disease-free survival (DFS) with external irradiation was 95-100% for clinical stage T1a, 80-90% for Stage T1b,c, and 50-70% for clinical Stage T3. A correlation has been identified between the initial PSA levels and the probability from freedom of chemical failure (PSA elevation) after definitive irradiation. In five series comprising 814 patients with Stage Tlc and T2 tumors, the DFS (end point chemical failure) was 95%, with initial PSA of less than 4 ng/ml, 83-92% with 4.1-10 ng/ml, 35-85% with 10.1-20 ng/ml, and 10-63% with PSA higher than 20 ng/ml. In the various series, follow-up ranged from a median of 1.5 years to a minimum of 4 years. In two series of 225 and 201 patients receiving doses of 7500-8000 cGy, less morbidity has been observed with three-dimensional treatment planning conformal radiation therapy than with conventional irradiation. New directions for future clinical trials are discussed, including dose escalation studies; use of high linear energy transfer to improve locoregional tumor control; and combination of irradiation and androgen suppression to enhance local tumor control, decrease distant metastasis, and improve survival. Preliminary results of a randomized study recently reported by RTOG strongly suggest that the use of goserelin acetate and flutamide decreases the incidence of clinical local recurrence (12.4% in 225 patients) compared with a control group treated with irradiation alone (25.2% in 230 patients) and enhances disease-free survival. Conclusions. Although modern approaches to the management of patients with localized carcinoma of the prostate with irradiation are effective, investigators must continue to critically assess policies of treatment, develop appropriately designed prospective clinical trials, and define the optimal management of patients with localized carcinoma of the prostate. C1 FOX CHASE CANC CTR,DEPT RADIAT ONCOL,PHILADELPHIA,PA 19111. MEM SLOAN KETTERING CANC CTR,DEPT RADIAT ONCOL,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. RP PEREZ, CA (reprint author), WASHINGTON UNIV,SCH MED,MALLINCKRODT INST RADIOL,CTR RADIAT ONCOL,4511 FOREST PK,ST LOUIS,MO 63108, USA. NR 141 TC 69 Z9 70 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD DEC 1 PY 1993 VL 72 IS 11 BP 3156 EP 3173 DI 10.1002/1097-0142(19931201)72:11<3156::AID-CNCR2820721106>3.0.CO;2-G PG 18 WC Oncology SC Oncology GA MJ791 UT WOS:A1993MJ79100005 PM 7694785 ER PT J AU ANDREWS, CW JESSUP, JM GOLDMAN, H HAYES, DF KUFE, DW OHARA, CJ STEELE, GD AF ANDREWS, CW JESSUP, JM GOLDMAN, H HAYES, DF KUFE, DW OHARA, CJ STEELE, GD TI LOCALIZATION OF TUMOR-ASSOCIATED GLYCOPROTEIN DF3 IN NORMAL, INFLAMMATORY, AND NEOPLASTIC LESIONS OF THE COLON SO CANCER LA English DT Article DE GASTROINTESTINAL NEOPLASIA; ADENOMAS; ADENOCARCINOMA, COLON; ANTIBODIES, MONOCLONAL; ANTIGENS, NEOPLASM; HUMAN MILK FAT GLOBULE ID CARCINOMA-ASSOCIATED ANTIGEN; MONOCLONAL-ANTIBODY; ULCERATIVE-COLITIS; BREAST-CARCINOMA; CARCINOEMBRYONIC ANTIGEN; SUCRASE-ISOMALTASE; MOLECULAR-CLONING; CANCER; EXPRESSION; MUCIN AB Background. The expression of DF3 was assessed by a monoclonal antibody in normal, inflammatory, and neoplastic conditions in the large bowel. Methods. Using immunohistochemistry, expression was examined in formalin-fixed paraffin-embedded biopsy and resection samples of 19 normal colonic mucosal specimens, 49 inflammatory lesions, 34 adenomas, and 38 primary colonic adenocarcinomas. In addition, Western blots of normal colonic mucosa and adenocarcinoma were examined. Results. DF3 expression was detected in 84% of the adenocarcinomas with coarse membrane staining, intense positivity of luminal secretions, and focal cytoplasmic and intracytoplasmic vacuole staining. Nine of 32 areas of transitional mucosa revealed reactivity along apical membranes in crypt cells. Five adenomas containing carcinoma revealed DF3 positivity in the malignant areas Only, whereas the remaining 29 were negative. Staining was membrane, luminal, and intracytoplasmic. Two examples of active ulcerative colitis revealed focal reactivity along the apical membrane of crypt cells. No other areas of staining were noted, including 12 cases containing dysplasia. Four of 10 other inflammatory lesions also revealed similar membrane reactivity in crypt cells. Normal colonic mucosa was nonreactive. Examples of normal colonic mucosa were negative for DF3 by Western blot analysis, whereas two carcinoma samples that reacted immunohistochemically were positive. Conclusions. DF3 is not detectable in normal colonic tissues. It is expressed focally and predominantly along the apical membrane of crypt cells in some inflammatory lesions and in the transitional mucosa of primary adenocarcinomas. Most adenocarcinomas of the colon and adenomas with foci of invasive carcinoma demonstrate reactivity in the cytoplasm and luminal secretions. C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT PATHOL,CANC BIOL LAB,BOSTON,MA 02215. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [CA47041] NR 30 TC 25 Z9 25 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD DEC 1 PY 1993 VL 72 IS 11 BP 3185 EP 3190 DI 10.1002/1097-0142(19931201)72:11<3185::AID-CNCR2820721109>3.0.CO;2-7 PG 6 WC Oncology SC Oncology GA MJ791 UT WOS:A1993MJ79100008 PM 7694786 ER PT J AU DUKE, D CASTRESANA, J LUCCHINA, L LEE, TH SOBER, AJ CAREY, WP ELDER, DE BARNHILL, RL AF DUKE, D CASTRESANA, J LUCCHINA, L LEE, TH SOBER, AJ CAREY, WP ELDER, DE BARNHILL, RL TI FAMILIAL CUTANEOUS MELANOMA AND 2-MUTATIONAL-EVENT MODELING SO CANCER LA English DT Article DE MELANOMA; CUTANEOUS MELANOMA; HEREDITARY; GENETICS; MUTATION; SKIN CANCER ID DYSPLASTIC NEVUS SYNDROME; MALIGNANT-MELANOMA; RISK-FACTORS; CANCER; LOCUS; MUTATION; INDIVIDUALS AB Background. According to the Knudson two-mutational-event theory, two mutations at a genetic locus may be required for the development of some cancers. Persons who have inherited a defect in one chromosome and therefore require only one more mutation for cancer development are at a higher risk of manifesting cancer at a younger age than persons without an inherited mutation, who need two acquired ''hits.'' This difference allows one to distinguish familial and sporadic types of the same malignancy by evaluating age of disease onset. Methods. To study the role of inheritance in the etiology of familial cutaneous melanoma, characteristics of patients with familial versus nonfamilial melanoma were analyzed according to the Knudson two-mutational-event model. Results. The familial versus nonfamilial graphs, based on age of diagnosis, did not support this model. However, there was a statistically significant earlier age of diagnosis for patients with familial melanoma. Melanoma thickness was less (i.e., earlier cancer at possibly younger age) for patients with a positive versus a negative family history. Conversely, linear regression, after adjusting for tumor thickness, showed that patients with hereditary melanoma still manifested earlier ages of diagnosis of melanoma compared with sporadic patients. Conclusions. Genetic patterns other than the two-step model, additional family-related factors, patient-physician sensitization due to a family history, or a combination of these factors might explain this age difference. More complex multistep modeling of the data may be helpful in better characterizing the genetic patterns of cutaneous melanoma. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,MRB608,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL DERMATOPATHOL,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT CLIN EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HOSP UNIV PENN,DEPT DERMATOL,PHILADELPHIA,PA 19104. HOSP UNIV PENN,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. FU NCI NIH HHS [CA25298, CA25874] NR 26 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD DEC 1 PY 1993 VL 72 IS 11 BP 3239 EP 3243 DI 10.1002/1097-0142(19931201)72:11<3239::AID-CNCR2820721117>3.0.CO;2-2 PG 5 WC Oncology SC Oncology GA MJ791 UT WOS:A1993MJ79100016 PM 8242547 ER PT J AU JONES, M PHILIP, T PALMER, P VONDERMAASE, H VINKE, J ELSON, P FRANKS, CR SELBY, P AF JONES, M PHILIP, T PALMER, P VONDERMAASE, H VINKE, J ELSON, P FRANKS, CR SELBY, P TI THE IMPACT OF INTERLEUKIN-2 ON SURVIVAL IN RENAL-CANCER - A MULTIVARIATE-ANALYSIS SO CANCER BIOTHERAPY LA English DT Article ID ACTIVATED KILLER-CELLS; CONTINUOUS INFUSION INTERLEUKIN-2; RECOMBINANT HUMAN INTERLEUKIN-2; PHASE-II; ADOPTIVE IMMUNOTHERAPY; PROGNOSTIC FACTORS; CARCINOMA; INTERFERON; TRIAL; THERAPY AB The purpose of this analysis was to compare the survival of patients with advanced renal carcinoma treated with intravenous recombinant interleukin-2 to the survival of matched patients taken from the large and well characterised database of the Eastern Cooperative Oncology Group (ECOG). Recombinant interleukin-2 (rIL-2) given by continuous intravenous infusion was used to treat 387 patients with advanced adenocarcinoma of the kidney in five multi-centre studies and 327 of these patients fulfilled the study eligibility criteria and were evaluable for response, toxicity and survival The survival of patients treated with rIL-2 was compared in a multi-variate survival analysis taking account of all identified prognostic factors to 390 control patients receiving chemotherapy derived from the database. Thirteen patients treated with rIL-2 achieved a complete remission of their disease and 32 a partial remission giving an overall response rate of 14%. Remissions were durable with a median duration of 357 days for partial remissions and a median duration in excess of 926 days for complete remissions. Most patients experienced fever or mild to moderate hypotension and other toxicities are described. However, only 11 patients required admission to intensive care and in only five cases was this judged to be due to treatment toxicity. There were three deaths judged to be probably due to treatment toxicity. rIL-2 treatment was associated with significantly prolonged survival compared to the ECOG control patients. Patients with good prognostic features appeared to have a greater survival benefit from rIL-2 than those with poor prognostic features. This analysis provides the first evidence that rIL-2 prolongs survival in patients with advanced renal cancer but cannot provide proof which should be sought in randomised prospective trials drawing on the hypotheses generated herein. C1 UNIV LEEDS,ST JAMES HOSP,DEPT CLIN MED,IMPERIAL CANC RES FUND,CANC MED RES UNIT,BECKETT ST,LEEDS LS9 7TF,W YORKSHIRE,ENGLAND. CTR LEON BERARD,LYON,FRANCE. AARHUS UNIV HOSP,DK-8000 AARHUS,DENMARK. EUROCETUS BV,AMSTERDAM,NETHERLANDS. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. EASTERN COOPERAT ONCOL GRP,MADISON,WI. COOKRIDGE HOSP,YORKSHIRE REG CANC ORG,CLIN TRIALS OFF,LEEDS 16,ENGLAND. NR 25 TC 86 Z9 87 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1062-8401 J9 CANCER BIOTHERAPY JI Cancer Biother. PD WIN PY 1993 VL 8 IS 4 BP 275 EP 288 DI 10.1089/cbr.1993.8.275 PG 14 WC Oncology SC Oncology GA ML168 UT WOS:A1993ML16800002 PM 7804369 ER PT J AU TEICHER, BA SOTOMAYOR, EA HUANG, ZD ARA, G HOLDEN, S KHANDEKAR, V CHEN, YN AF TEICHER, BA SOTOMAYOR, EA HUANG, ZD ARA, G HOLDEN, S KHANDEKAR, V CHEN, YN TI BETA-CYCLODEXTRIN TETRADECASULFATE TETRAHYDROCORTISOL PLUS-OR-MINUS MINOCYCLINE AS MODULATORS OF CANCER THERAPIES IN-VITRO AND IN-VIVO AGAINST PRIMARY AND METASTATIC LEWIS LUNG-CARCINOMA SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE B-CYCLODEXTRIN; TETRADECASULFATE TETRAHYDROCORTISOL; MINOCYCLINE; LEWIS LUNG CARCINOMA ID 4 PLATINUM COMPLEXES; MOUSE MAMMARY-TUMOR; COLLAGENASE ACTIVITY; ANGIOGENESIS INHIBITION; ANGIOSTATIC STEROIDS; EXTRACELLULAR-MATRIX; BASEMENT-MEMBRANE; HEPARIN FRAGMENT; MESSENGER-RNA; RETINOIC ACID AB Tetrahydrocortisol, beta-cyclodextrin tetradecasulfate, and minocycline used alone or in combination are not very cytotoxic toward EMT-6 mouse mammary tumor cells growing in monolayer. Tetrahydrocortisol (100 muM, 24 h) and beta-cyclodextrin tetradecasulfate (100 muM, 24 h) protected EMT-6 cells from the cytotoxicity of CDDP, melphalan, 4-hydroperoxycyclophosphamide, BCNU, and X-rays under various conditions of oxygenation and pH. Minocycline (100 muM, 24 h) either had no effect upon or was additive with the antitumor alkylating agents or X-rays in cytotoxic activity toward the EMT-6 cells in culture. The combination of the three modulators either had no effect upon or was to a small degree protective against the cytotoxicity of the antitumor alkylating agents or X-rays. The Lewis lung carcinoma was chosen for primary tumor growth-delay studies and tumor lung-metastases studies. Tetrahydrocortisol and beta-cyclodextrin tetradecasulfate were given in a 1:1 molar ratio by continuous infusion over 14 days, and minocycline was given i.p. over 14 days, from day 4 to day 18 post tumor implantation. The combination of tetrahydrocortisol/beta-cyclodextrin tetradecasulfate diminished the tumor growth delay induced by CDDP and melphalan and produced modest increases in the tumor growth delay produced by cyclophosphamide and radiation. Minocycline co-treatment increased the tumor growth delay produced by CDDP, melphalan, radiation, bleomycin, and, especially cyclophosphamide, where 4 of 12 animals receiving minocycline (14 x 5 mg/kg, days 4-18) and cyclophosphamide (3 x 150 mg/kg, days 7, 9, 11) were long-term survivors. The 3 modulators given in combination produced further increases in tumor growth delay with all of the cytotoxic therapies, and 5 of 12 of the animals treated with the 3-modulator combination and cyclophosphamide were long-term survivors. Although neither tetrahydrocortisol/beta-cyclodextrin tetradecasulfate, minocycline, nor the three modulator combination impacted the number of lung metastases, there was a decrease in the number of large lung metastases. Treatment with the cytotoxic therapies alone reduced the number of lung metastases. Addition of the modulators to treatment with the cytotoxic therapies resulted in a further reduction in the number of lung metastases. These results indicate that agents that inhibit the breakdown of the extracellular matrix can be useful additions to the treatment of solid tumors. 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. FU NCI NIH HHS [P01-CA38493] NR 73 TC 17 Z9 18 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD DEC PY 1993 VL 33 IS 3 BP 229 EP 238 DI 10.1007/BF00686221 PG 10 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA MK006 UT WOS:A1993MK00600009 PM 8269604 ER PT J AU NAKAGOMI, H PETERSSON, M MAGNUSSON, I JUHLIN, C MATSUDA, M MELLSTEDT, H TAUPIN, JL VIVIER, E ANDERSON, P KIESSLING, R AF NAKAGOMI, H PETERSSON, M MAGNUSSON, I JUHLIN, C MATSUDA, M MELLSTEDT, H TAUPIN, JL VIVIER, E ANDERSON, P KIESSLING, R TI DECREASED EXPRESSION OF THE SIGNAL-TRANSDUCING ZETA-CHAINS IN TUMOR-INFILTRATING T-CELLS AND NK CELLS OF PATIENTS WITH COLORECTAL-CARCINOMA SO CANCER RESEARCH LA English DT Note ID NATURAL-KILLER-CELLS; GAMMA; CANCER AB An impaired immune response is frequently observed in cancer patients and tumor-bearing mice. T-cells from mice with an experimental colon carcinoma were recently shown to express T-cell receptors that completely lacked the signal-transducing molecule CD3 zeta. Here, we have investigated the expression of the signal-transducing molecule zeta on lymphocytes from 14 patients with colorectal carcinomas using flow cytometric analysis of permeabilized cells with a monoclonal antibody (TIA-2; IgG1) specific for the cytoplasmic domain of the zeta chain as well as with immunoprecipitation and analysis on diagonal gel electrophoresis. We demonstrate that T-cells isolated from the tumors of the patients express significantly less CD3 zeta than T-cells in the peripheral blood of the same patients and that the peripheral blood of the patients express decreased levels of zeta chains, as compared to the levels found in lymphocytes from healthy controls. This decreased expression was also observed on zeta chains associated with the low affinity Fc receptor for IgG found in tumor-infiltrating NK cells (FcgammaRIIIAalpha; CD16). C1 KAROLINSKA INST,IMMUNOL LAB,CTR MICROBIOL & TUMOR BIOL,S-10401 STOCKHOLM 60,SWEDEN. SODER SJUKHUSET,DEPT SURG,S-10064 STOCKHOLM,SWEDEN. KAROLINSKA HOSP,RADIUMHEMMET,S-10401 STOCKHOLM 60,SWEDEN. ACAD HOSP UPPSALA,DEPT SURG,S-75014 UPPSALA,SWEDEN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 7 TC 316 Z9 320 U1 1 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 1 PY 1993 VL 53 IS 23 BP 5610 EP 5612 PG 3 WC Oncology SC Oncology GA MJ268 UT WOS:A1993MJ26800008 PM 8242612 ER PT J AU CHANG, TKH WEBER, GF CRESPI, CL WAXMAN, DJ AF CHANG, TKH WEBER, GF CRESPI, CL WAXMAN, DJ TI DIFFERENTIAL ACTIVATION OF CYCLOPHOSPHAMIDE AND IFOSPHAMIDE BY CYTOCHROME-P-450-2B AND CYTOCHROME-P450-3A IN HUMAN LIVER-MICROSOMES SO CANCER RESEARCH LA English DT Article ID RAT HEPATIC CYTOCHROME-P-450; CYCLOSPORINE-A OXIDASE; CLINICAL PHARMACOKINETICS; HUMAN HEPATOCYTES; PRIMARY CULTURES; GENE-EXPRESSION; DRUG OXIDATION; METABOLISM; IDENTIFICATION; IFOSFAMIDE AB The present study identifies the specific human cytochrome P-450 (CYP) enzymes involved in hydroxylation leading to activation of the anticancer drug cyclophosphamide and its isomeric analogue, ifosphamide. Substantial interindividual variation (4-9-fold) was observed in the hydroxylation of these oxazaphosphorines by a panel of 12 human liver microsomes, and a significant correlation was obtained between these 2 activities (r = 0.85, P < 0.001). Enzyme kinetic analyses revealed that human liver microsomal cyclophosphamide 4-hydroxylation and ifosphamide 4-hydroxylation are best described by a 2-component Michaelis-Menten model composed of both low K(m) and high K(m) P-450 4-hydroxylases. To ascertain whether one or more human P-450 enzymes are catalytically competent in activating these oxazaphosphorines, microsomal fractions prepared from a panel of human B-lymphoblastoid cell lines stably transformed with individual P-450 complementary DNAs were assayed in vitro for oxazaphosphorine activation. Expressed CYP2A6, -2B6, -2C8, -2C9, and -3A4 were catalytically competent in hydroxylating cyclophosphamide and ifosphamide. Whereas CYP2C8 and CYP2C9 have the characteristics of low K(m) oxazaphosphorine 4-hydroxylases, CYP2A6, -2B6, and -3A4 are high K(m) forms. In contrast, CYP1A1, -1A2, -2D6, and -2E1 did not produce detectable activities. Furthermore, growth of cultured CYP2A6- and CYP2B6-expressing B-lymphoblastoid cells, but not of CYP-negative control cells, was inhibited by cyclophosphamide and ifosphamide as a consequence of prodrug activation to cytotoxic metabolites. Experiments with P-450 form-selective chemical inhibitors and inhibitory anti-P-450 antibodies were then performed to determine the contributions of individual P-450s to the activation of these drugs in human liver microsomes. Orphenadrine (a CYP2B6 inhibitor) and anti-CYP2B IgG inhibited microsomal cyclophosphamide hydroxylation to a greater extent than ifosphamide hydroxylation, consistent with the 8-fold higher activity of complementary DNA-expressed CYP2B6 with cyclophosphamide. In contrast, troleandomycin, a selective inhibitor of CYP3A3 and -3A4, and anti-CYP3A IgG substantially inhibited microsomal ifosphamide hydroxylation but had little or no effect on microsomal cyclophosphamide hydroxylation. By contrast, the CYP2D6-selective inhibitor quinidine did not affect either microsomal activity, while anti-CYP2A antibodies had only a modest inhibitory effect. Overall, the present study establishes that liver microsomal CYP2B and CYP3A preferentially catalyze cyclophosphamide and ifosphamide 4-hydroxylation, respectively, suggesting that liver P-450-inducing agents targeted at these enzymes might be used in cancer patients to enhance drug activation and therapeutic efficacy. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,ROOM JF-525,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC BIOL,BOSTON,MA 02115. GENTEST CORP,WOBURN,MA 01801. FU NCI NIH HHS [CA-49248] NR 65 TC 462 Z9 469 U1 1 U2 12 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 1 PY 1993 VL 53 IS 23 BP 5629 EP 5637 PG 9 WC Oncology SC Oncology GA MJ268 UT WOS:A1993MJ26800013 PM 8242617 ER PT J AU SINGER, S NEURINGER, LJ THILLY, WG CHEN, LB AF SINGER, S NEURINGER, LJ THILLY, WG CHEN, LB TI QUANTITATIVE DIFFERENTIAL-EFFECTS OF RHODAMINE-123 ON NORMAL-CELLS AND HUMAN COLON-CANCER CELLS BY MAGNETIC-RESONANCE SPECTROSCOPY SO CANCER RESEARCH LA English DT Article ID CARCINOMA-CELLS; NMR-SPECTROSCOPY; LIVING CELLS; MITOCHONDRIA; MAGNESIUM; INHIBITION; HEPATOCYTES; RETENTION; TRANSPORT; TOXICITY AB Rhodamine 123 is a lipophilic cationic compound that is selectively taken up by cancer cell mitochondria. This compound is toxic to epithelial cancer cells in vitro and displays significant anticancer activity in vivo. However, the mechanism of action of rhodamine 123 in intact, actively metabolizing cell preparations is unknown. We have used P-31- and C-13-nuclear magnetic resonance spectroscopy to quantitatively characterize how rhodamine 123 affects the energetics of human colon cancer cells (HCT-116) and spontaneously immortalized normal epithelial cells (CV-1). Rhodamine 123 differentially altered the phosphorus and glucose metabolism of HCT-116 and CV-1 cells. P-31-nuclear magnetic resonance detected mitochondrial poisoning in the HCT-116 human colon cancer cell line in its early stages after selective uptake of rhodamine 123. When we compared administration of rhodamine 123 and [1-C-13]glucose to administration of [1-C-13]glucose alone in the HCT-116 cells, we noted a marked decrease in intracellular pH to 6.7 +/- 0.06 (mean +/- SD) units, a 2.2-fold increase in lactate production, and a 1.8-fold increase in glucose consumption after 10 h. In addition, we found a 2-fold rise in intracellular free magnesium 12 h after rhodamine 123 administration. These results suggest that when rhodamine 123 inhibits mitochondrial ATP production, it initially stimulates cytoplasmic glycolysis in an attempt to maintain cellular energy demands. The marked fall in intracellular pH and rise in intracellular free magnesium after administration of rhodamine 123 may inhibit activity of several glycolytic enzymes: this effect would inhibit cytoplasmic ATP generation and interfere with multiple cell enzymatic processes, leading to cell death. The CV-1 cells showed no change in intracellular pH, intracellular free magnesium, or magnesium-bound ATP levels over the 24-h period following rhodamine 123 administration. Rhodamine 123 also failed to alter glucose utilization and lactate production levels significantly in the CV-1 cells. These results prove the usefulness of P-31- and C-13-nuclear magnetic resonance spectroscopy for quantifying differing effects of rhodamine 123 on the high energy phosphate metabolism and glucose metabolism of HCT-116 and CV-1 cells. C1 MIT,FRANCIS BITTER NATL MAGNET LAB,CAMBRIDGE,MA 02139. MIT,CTR ENVIRONM HLTH SCI,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP SINGER, S (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT SURG,DIV SURG ONCOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA09535-05, CA48096]; NCRR NIH HHS [RR-00995] NR 34 TC 14 Z9 14 U1 2 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 1 PY 1993 VL 53 IS 23 BP 5808 EP 5814 PG 7 WC Oncology SC Oncology GA MJ268 UT WOS:A1993MJ26800042 PM 8242640 ER PT J AU HAJJAR, RJ LIAO, RL YOUNG, JB FULEIHAN, F GLASS, M GWATHMEY, JK AF HAJJAR, RJ LIAO, RL YOUNG, JB FULEIHAN, F GLASS, M GWATHMEY, JK TI PATHOPHYSIOLOGICAL AND BIOCHEMICAL-CHARACTERIZATION OF AN AVIAN MODEL OF DILATED CARDIOMYOPATHY - COMPARISON TO FINDINGS IN HUMAN DILATED CARDIOMYOPATHY SO CARDIOVASCULAR RESEARCH LA English DT Article ID FURAZOLIDONE-INDUCED CARDIOMYOPATHY; CONGESTIVE HEART-FAILURE; INTRACELLULAR CALCIUM TRANSIENTS; HUMAN VENTRICULAR MYOCARDIUM; SYMPATHETIC NERVOUS-SYSTEM; HEREDITARY CARDIOMYOPATHY; CARDIAC-FUNCTION; MYOCYTE FUNCTION; SYRIAN-HAMSTER; CA-2+ AB Objective: With the recent availability of human myocardium, many animal models have been shown to be unsuitable as models of human heart failure. The aim of this study was to describe the pathophysiological changes in a model of dilated cardiomyopathy in turkey poults and to compare them to results obtained from failing human hearts. Methods: After receiving furazolidone for 2-3 weeks, animals developed cardiomyopathy (Fz-DCM) and were studied at the whole heart and isolated muscle level. Myofibrillar ATPase activity and noradrenaline turnover were determined in tissue homogenates in failing and non-failing control hearts. Results: Fz-DCM animals had greater heart weights, heart weight/body weight ratios, and end diastolic volumes. Fractional shortening of the left ventricle and systolic blood pressures were reduced (p<0.01) in myopathic animals. Isolated perfused hearts had lower peak developed pressures (p<0.01). Isolated muscle preparations showed no significant differences in peak twitch forces between control and Fz-DCM muscles at a 1 Hz stimulation rate. The relationship between force and frequency of stimulation was positive in control muscles up to 1.7 Hz, whereas in Fz-DCM muscles the relationship was sharply negative above 1 Hz. Time to 80% relaxation was markedly slower in the Fz-DCM muscles. Although [Ca2+](0) responsiveness was similar for Fz-DCM and normal animals, responsiveness to isoprenaline was significantly reduced in Fz-DCM hearts. Cardiomyopathic animals displayed diminished noradrenaline content in the left ventricle. Fractional noradrenaline turnover was higher (p<0.05) in the cardiomyopathic birds. In skinned fibre preparations from control and Fz-DCM hearts calcium activations were similar. Maximum myofibrillar ATPase activities were, however, significantly lower in myopathic animals and myofibrillar protein content was reduced by 25%. Conclusions: In this model of dilated cardiomyopathy: (1) relaxation is markedly prolonged; (2) the response to beta adrenergic stimulation is diminished; (3) Mg-ATPase activities and myofibrillar protein content are reduced; and (4) sympathetic activity in the heart is markedly increased with depletion of noradrenaline stores. Furthermore, a reduction in tissue noradrenaline content per se is a misleading index of the dynamic state of cardiac noradrenaline stores. With its similarities to human cardiomyopathy, this model promises to provide new insights into the pathophysiology and progression of dilated cardiomyopathy. C1 HARVARD UNIV,SCH MED,CARDIOVASC DIS & MUSCLE RES LABS,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. NORTHWESTERN UNIV,SCH MED,DEPT MED,CHICAGO,IL 60611. FU NHLBI NIH HHS [HL-36797, HL-39091]; NIDDK NIH HHS [DK 20378] NR 61 TC 23 Z9 26 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6363 J9 CARDIOVASC RES JI Cardiovasc. Res. PD DEC PY 1993 VL 27 IS 12 BP 2212 EP 2221 DI 10.1093/cvr/27.12.2212 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MM484 UT WOS:A1993MM48400023 PM 8313431 ER PT J AU ASSEY, ME ZILE, MR USHER, BW KARAVAN, MP CARABELLO, BA AF ASSEY, ME ZILE, MR USHER, BW KARAVAN, MP CARABELLO, BA TI EFFECT OF CATHETER POSITIONING ON THE VARIABILITY OF MEASURED GRADIENT IN AORTIC-STENOSIS SO CATHETERIZATION AND CARDIOVASCULAR DIAGNOSIS LA English DT Article DE AORTIC STENOSIS; INTRAVENTRICULAR PRESSURE GRADIENTS; AORTIC VALVE GRADIENTS ID RESISTANCE; PRESSURE AB The purpose of this study was to quantify the variation in measured aortic valve gradient and calculated aortic valve area when different techniques of cardiac catheterization were utilized. Hemodynamic assessment of aortic stenosis severity requires an accurately determined pressure gradient. In aortic stenosis, the presence of intraventricular pressure gradients and downstream pressure recovery within the aorta means that a range of aortic valve gradients could be measured in a given patient depending upon catheter position and measurement technique. To quantify the degree of variation in measured gradient and calculated aortic valve area, we generated transvalvular gradients by nine different techniques in 15 patients (11 men, 4 women; 29-86 years old). Patients were divided into those with severe aortic stenosis (aortic valve area less than or equal to 0.6 cm(2), n = 6) and those with moderately severe aortic stenosis (aortic valve area 0.61-0.90 cm(2), n = 9). Considerable variation in measured gradient and calculated aortic valve area was observed. The maximum variation in gradient was similar in severe and moderately severe aortic stenosis groups (33 mm Hg. vs. 32 mm Hg., p = NS). However, the variation in gradient as a percent of maximum gradient was greater (P<0.05) in the moderately severe aortic stenosis group. The maximum variation in calculated aortic valve area was 0.1 cm(2) in the severe group and 0.3 cm(2) in the moderately severe group (P<0.01). An intraventricular gradient, present in 13 of 15 (87%) patients, was partially responsible for the variation in pressure gradient measurement and calculated aortic valve area. We conclude that in patients with valvular aortic stenosis, catheterization technique has an important impact on the hemodynamic assessment of aortic stenosis severity. This is particularly true in patients with moderately severe aortic stenosis where any variation tends to represent a larger percentage of the total gradient. (c) 1993 Wiley-Liss, Inc. RP ASSEY, ME (reprint author), MED UNIV S CAROLINA,RALPH H JOHNSON VET ADM MED CTR,GAZES CARDIAC RES INST,DIV CARDIOL,CHARLESTON,SC 29425, USA. NR 12 TC 21 Z9 21 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0098-6569 J9 CATHETER CARDIO DIAG JI Catheter. Cardiovasc. Diagn. PD DEC PY 1993 VL 30 IS 4 BP 287 EP 292 DI 10.1002/ccd.1810300405 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MJ794 UT WOS:A1993MJ79400003 PM 8287452 ER PT J AU DONAHUE, DM WRIGHT, CD VIALE, G MATHISEN, DJ AF DONAHUE, DM WRIGHT, CD VIALE, G MATHISEN, DJ TI RESECTION OF PULMONARY BLEBS AND PLEURODESIS FOR SPONTANEOUS PNEUMOTHORAX SO CHEST LA English DT Article ID TETRACYCLINE; PLEURECTOMY AB Over a 20-year period, 83 patients underwent operative pleurodesis with resection of pulmonary blebs for spontaneous pneumothorax. Follow-up for all patients was between 5 and 25 years, with a mean of 9.1 years. There were five early (5.6 percent) and three late recurrences (3.6 percent). There were no deaths or need for blood transfusion in our series. There was a low incidence of postoperative fever (n = 8), minor wound infection (n = 6), air leak (n = 6), or pneumonia (n = 2). The low morbidity and recurrence rates compare favorably with published series of alternative treatment options for spontaneous pneumothorax. C1 MASSACHUSETTS GEN HOSP,THORAC SURG UNIT,WARREN 1109,BOSTON,MA 02114. NR 9 TC 42 Z9 43 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD DEC PY 1993 VL 104 IS 6 BP 1767 EP 1769 DI 10.1378/chest.104.6.1767 PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA ML308 UT WOS:A1993ML30800031 PM 8252960 ER PT J AU LERMAN, A WEBSTER, MWI CHESEBRO, JH EDWARDS, WD WEI, CM FUSTER, V BURNETT, JC AF LERMAN, A WEBSTER, MWI CHESEBRO, JH EDWARDS, WD WEI, CM FUSTER, V BURNETT, JC TI CIRCULATING AND TISSUE ENDOTHELIN IMMUNOREACTIVITY IN HYPERCHOLESTEROLEMIC PIGS SO CIRCULATION LA English DT Article DE ENDOTHELIN; CHOLESTEROL; RELAXING FACTORS; CORONARY ID CORONARY-ARTERY DISEASE; SMOOTH-MUSCLE CELLS; MESSENGER-RNA EXPRESSION; HEART-FAILURE; ATHEROSCLEROSIS; RELEASE; PEPTIDE; HUMANS; PATHOGENESIS; MODULATION AB Background. Hypercholesterolemia is characterized by a coronary vasoconstrictive response to the endothelium-dependent vasodilator acetylcholine. This abnormality may be due to reduced synthesis of endothelium-derived relaxing factor and/or enhanced synthesis and release of an endothelium-derived contracting factor. Endothelin is an endothelium-derived vasoconstrictor and mitogenic peptide that is present in normal plasma, and its circulating concentrations are elevated in disease states that are characterized by abnormal endothelium-dependent relaxation to acetylcholine. The current studies were designed to test the hypotheses that experimental hypercholesterolemia results in elevation of plasma and tissue endothelin immunoreactivity and that the abnormal acetylcholine-evoked coronary vasoconstriction in the hypercholesterolemic animals is associated with further elevation of plasma endothelin. Methods and Results. Plasma concentrations and molecular forms of endothelin immunoreactivity were determined following 2% cholesterol diet for 4 months in pigs and during intracoronary acetylcholine administration. Second, we assessed the presence of endothelin in the coronary vascular wall by using immunohistochemistry. Hypercholesterolemia elevated plasma endothelin concentration and enhanced coronary artery tissue endothelin immunoreactivity. The endothelium-dependent vasodilator acetylcholine further increases plasma endothelin in hypercholesterolemia in association with coronary vasoconstriction. The predominant molecular form of endothelin in hypercholesterolemia is the biological active endothelin-1. Conclusions. This study suggests a role for endothelin as an early participant and a marker for the endothelial dysfunction in hypercholesterolemia as well as a participant in the atherogenic process. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA. RP LERMAN, A (reprint author), MAYO CLIN & MAYO FDN,DEPT INTERNAL MED,DIV CARDIOVASC DIS,200 1ST ST SW,ROCHESTER,MN 55905, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 FU NHLBI NIH HHS [HL-0711, HL-36634] NR 33 TC 135 Z9 139 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD DEC PY 1993 VL 88 IS 6 BP 2923 EP 2928 PG 6 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ML699 UT WOS:A1993ML69900052 PM 8252706 ER PT J AU KIUCHI, K SATO, N SHANNON, RP VATNER, DE MORGAN, K VATNER, SF AF KIUCHI, K SATO, N SHANNON, RP VATNER, DE MORGAN, K VATNER, SF TI DEPRESSED BETA-ADRENERGIC RECEPTOR-MEDIATED AND ENDOTHELIUM-MEDIATED VASODILATION IN CONSCIOUS DOGS WITH HEART-FAILURE SO CIRCULATION RESEARCH LA English DT Article DE ILIAC BLOOD FLOW; ENDOTHELIUM-DERIVED RELAXING FACTOR; NITRIC OXIDE; VASCULAR BETA-RECEPTORS; TOTAL PERIPHERAL RESISTANCE ID PLASMA NOREPINEPHRINE; DILATED CARDIOMYOPATHY; EXPERIMENTAL-MODEL; DOWN-REGULATION; MUSCLE; VASOCONSTRICTION; DESENSITIZATION; DYSFUNCTION; STIMULATION; SYSTEMS AB Peripheral vasodilator responsiveness was examined in pacing-induced heart failure (HF) in 11 conscious dogs chronically instrumented for measurement of systemic (total peripheral resistance [TPR]) and local (iliac blood flow) vascular resistance. Dose responses to isoproterenol (ISO), acetylcholine (ACh), and nitroglycerin (NTG) were examined in the same dogs before pacing (control) and after 4 to 7 weeks of rapid ventricular pacing, which induced congestive HF, characterized by increased left ventricular end-diastolic pressure (6.7+/-0.4 [control] versus 28+/-1.5 [HF] mm Hg) and decreased cardiac output (-30+/-5%) and left ventricular dP/dt (-53+/-3%), as well as ascites and peripheral edema. In the control state, TPR fell by 57+/-2% in response to ISO (100 ng/kg), by 61+/-3% in response to ACh (3 mug/kg), and by 55+/-2% in response to NTG (10 mug/kg). In HF, smaller decreases (P<.05) in TPR were observed with the same doses of ISO (-50+/-2%) and ACh (-49+/-2%) but not with NTG (-58+/-3%). Depressed responses to systemic ISO and ACh, but not NTG, were observed in HF in the presence of ganglionic blockade and also after local administration of smaller doses of the drugs in the absence of ganglionic blockade, but where systemic effects were not elicited. Inhibition of nitric oxide synthase increased TPR to a greater degree before HF (+154+/-28% [control]) than after (+80+/-22% [HF]) and eliminated the depressed responses to ACh but not to ISO. Beta-Adrenergic receptor density, as determined by I-125-cyanopindolol binding in membrane preparations from mesenteric vessels was significantly decreased after HF (130+/-3 [control] versus 100+/-8 [HF] fmol/mg, P<.05) without any change in affinity. Thus, peripheral vascular beta-adrenergic receptor downregulation occurs in HF, independent of altered endothelium-mediated peripheral vasodilation. C1 NEW ENGLAND REG PRIMATE RES CTR,1 PINE HILL DR,POB 9102,SOUTHBOROUGH,MA 01772. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-37404, HL-38070, HL-33107] NR 45 TC 53 Z9 53 U1 0 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD DEC PY 1993 VL 73 IS 6 BP 1013 EP 1023 PG 11 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA MH644 UT WOS:A1993MH64400004 PM 7693360 ER PT J AU BOKEN, DJ SWINDELLS, S RINALDI, MG AF BOKEN, DJ SWINDELLS, S RINALDI, MG TI FLUCONAZOLE-RESISTANT CANDIDA-ALBICANS SO CLINICAL INFECTIOUS DISEASES LA English DT Article AB Mucocutaneous candidiasis caused by Candida albicans is a common complication of human immunodeficiency virus (HIV) infection. Recent reports of isolation of resistant strains of C. albicans raise the specter of more widespread resistance, but limited series are available to analyze situations in which the likelihood of resistance is greatest. We present our experience with fluconazole-resistant candidiasis in patients with HIV infection obtained from retrospective chart review and by testing strains of C. albicans isolated during relapse for susceptibility to antifungal agents. The possible reasons for failure of antifungal therapy are discussed, as well the correlation between in vivo and in vitro data. Resistant candidiasis in patients with HIV disease is an emerging problem of considerable concern that merits further study. C1 UNIV NEBRASKA,MED CTR,DEPT INTERNAL MED,INFECT DIS SECT,600 S 42ND ST,OMAHA,NE 68198. AUDIE L MURPHY MEM VET ADM MED CTR,VET ADM,SAN ANTONIO,TX 78284. NR 19 TC 136 Z9 137 U1 0 U2 0 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 DEC PY 1993 VL 17 IS 6 BP 1018 EP 1021 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA ML918 UT WOS:A1993ML91800011 PM 8110924 ER PT J AU BARKLEY, B LICHTENSTEIN, MJ GARZA, C HAZUDA, HP AF BARKLEY, B LICHTENSTEIN, MJ GARZA, C HAZUDA, HP TI VALIDATION OF THE WELCH-ALLYN PNEUMOCHECK(TM) SPIROMETER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. UTHSC,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A752 EP A752 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800200 ER PT J AU DENINO, LA SMITH, T PINKSTON, M WILLIAMS, JW MULROW, CD AGUILAR, C AF DENINO, LA SMITH, T PINKSTON, M WILLIAMS, JW MULROW, CD AGUILAR, C TI DEVELOPMENT OF A PICTORIAL DIARY OF HEALTH-CARE UTILIZATION SO CLINICAL 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 SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A750 EP A750 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800190 ER PT J AU FOUQUERAY, B KIYOMOTO, H GHOSHCHOUDHURY, G ABBOUD, HE AF FOUQUERAY, B KIYOMOTO, H GHOSHCHOUDHURY, G ABBOUD, HE TI GLUCOSE MODULATES TYROSINE PHOSPHATASE-ACTIVITY IN CULTURED MESANGIAL CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,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 SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A809 EP A809 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800510 ER PT J AU GIBSON, S GERETY, MB WILLIAMS, JW MULROW, CD CORNELL, JE AF GIBSON, S GERETY, MB WILLIAMS, JW MULROW, CD CORNELL, JE TI DEPRESSION SCREENING SCALES - EFFECT OF FUNCTION, COGNITION, DISEASE NUMBER ON OPERATING CHARACTERISTICS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A817 EP A817 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800541 ER PT J AU HOLLEMAN, DR WILLIAMS, JW SIMEL, DL AF HOLLEMAN, DR WILLIAMS, JW SIMEL, DL TI USUAL CARE OF PATIENTS WITH SINUS COMPLAINTS LACKING RADIOGRAPHIC SINUSITIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET AFFAIRS MED CTR,LEXINGTON,KY. VET AFFAIRS MED CTR,SAN ANTONIO,TX. VET AFFAIRS MED CTR,DURHAM,NC. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A818 EP A818 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800546 ER PT J AU HOWARD, JP DRAKE, TR KELLOGG, DL AF HOWARD, JP DRAKE, TR KELLOGG, DL TI DELIVERY OF HYDROXOCOBALAMIN BY LECTRO-PATCH(R) IONTOPHORESIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A758 EP A758 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800233 ER PT J AU KANTEN, DN MULROW, CD GERETY, MB CORNELL, JE ROSENBERG, J AF KANTEN, DN MULROW, CD GERETY, MB CORNELL, JE ROSENBERG, J TI PREDICTORS OF FALLS IN FRAIL NURSING-HOME RESIDENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A751 EP A751 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800194 ER PT J AU WAI, W LICHTENSTEIN, MJ MONTERROSA, A ESPINO, DV HAZUDA, HP AF WAI, W LICHTENSTEIN, MJ MONTERROSA, A ESPINO, DV HAZUDA, HP TI CORRELATION OF STATIC AND DYNAMIC MEASURES OF BALANCE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. UTHSC,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A752 EP A752 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800197 ER PT J AU WILLIAMS, JW HOLLEMAN, DR SAMSA, G SIMEL, DL AF WILLIAMS, JW HOLLEMAN, DR SAMSA, G SIMEL, DL TI RANDOMIZED DOUBLE-BLIND TRIAL OF 3 VERSUS 10 DAYS OF TRIMETHOPRIMSULFAMETHOXAZOLE FOR ACUTE SINUSITIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,SAN ANTONIO,TX. VET ADM MED CTR,LEXINGTON,KY 40511. VET ADM MED CTR,DURHAM,NC 27705. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1993 VL 41 IS 4 BP A752 EP A752 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA MN948 UT WOS:A1993MN94800201 ER PT J AU HUNT, LM AF HUNT, LM TI THE METASTASIS OF WITCHCRAFT - THE INTERRELATIONSHIP BETWEEN TRADITIONAL AND BIOMEDICAL CONCEPTS OF CANCER IN SOUTHERN MEXICO SO COLLEGIUM ANTROPOLOGICUM LA English DT Article ID ILLNESS; STRESS AB Patients receiving biomedical treatment for cancer in two provincial cities in Southern Mexico were observed in an ethnographic study, to rely primarily on biomedicine for diagnosis and treatment. However, close examination of their illness explanations and understandings revealed that they often incorporated traditional illness concepts (eg: witchcraft or susto) into these biomedically-based explanatory models. This paper explores their integration of traditional and biomedical models. It is proposed that, while biomedicine provides a basis for classifying illness and directing practical action, it leaves other needs unaddressed. An examination of case examples indicates that traditional illness models are incorporated with biomedical models because they address specific emotional, psychological, social and political-economic issues important to patients' experience of illness, but ignored by biomedical approaches. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP HUNT, LM (reprint author), UNIV N CAROLINA,DEPT SOCIOL ANTHROPOL & SOCIAL WORK,CHARLOTTE,NC 28223, USA. NR 32 TC 2 Z9 2 U1 1 U2 2 PU SCH BIOLOGICAL ANTHROPOLOGY PI ZAGREB PA MOSE PIJADE 158 P O BOX 291, 41001 ZAGREB, CROATIA SN 0350-6134 J9 COLLEGIUM ANTROPOL JI Coll. Anthropol. PD DEC PY 1993 VL 17 IS 2 BP 249 EP 256 PG 8 WC Anthropology SC Anthropology GA MP682 UT WOS:A1993MP68200008 ER PT J AU GELBER, RD GOLDHIRSCH, A COLE, BF AF GELBER, RD GOLDHIRSCH, A COLE, BF TI PARAMETRIC EXTRAPOLATION OF SURVIVAL ESTIMATES WITH APPLICATIONS TO QUALITY-OF-LIFE EVALUATION OF TREATMENTS SO CONTROLLED CLINICAL TRIALS LA English DT Article ID OF-LIFE; THERAPY AB Using parametric models, a procedure for projecting survival estimates beyond the follow-up limits of a clinical trial is developed. The methodology consists of fitting an appropriate parametric model to the tail of a survival curve and using the estimated model in conjunction with the Kaplan-Meier product-limit estimate to produce a composite survival-function estimator. This estimator is especially useful whenever a parametric model is more easily fit to the tail rather than to the entire survival curve. Probability plots are used to evaluate different parametric models as well as to determine appropriate values for the cut points that define the survival-function tail. The bootstrap method provides estimates of variation in the projected survival curve. The resulting projected survival estimates allow one to make inferences on long-term treatment effects in clinical trials. As a motivating application, we project survival curves to estimate long-term treatment effects on quality-of-life-adjusted survival. This represents an extension of a statistical procedure called Q-TWiST (Quality-adjusted Time Without Symptoms of disease and Toxicity of treatment), which evaluates treatments in terms of both quantity and quality of life. In a standard Q-TWiST analysis, the average time spent in each of a number of health states, which differ in quality of life, is estimated from clinical trial data. The health states are weighted according to the quality of life experienced, and the results are combined to produce an estimate of quality-adjusted survival. Such estimates, however, are restricted to the follow-up limit of the data. The way in which the extrapolation methodology provides longer range estimates of Q-TWiST is described. To illustrate the techniques, we apply the methodology to data from the International Breast Cancer Study Group Trial V, which compares long-duration adjuvant chemotherapy versus short-duration chemotherapy in the treatment of node-positive breast cancer. Five-year median follow-up data are used to predict 10-year results in terms of mean survival and mean Q-TWiST. The results indicate that patients continue to benefit greatly from the long-duration chemotherapy between 5 and 10 years following treatment. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. OSPED CIVICO,DEPT ONCOL,LUGANO,SWITZERLAND. RP GELBER, RD (reprint author), DANA FARBER CANC INST,DIV BIOSTAT,44 BINNEY ST,BOSTON,MA 02115, USA. RI Cole, Bernard/I-3775-2012 FU NCI NIH HHS [CA-06516] NR 14 TC 24 Z9 24 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD DEC PY 1993 VL 14 IS 6 BP 485 EP 499 DI 10.1016/0197-2456(93)90029-D PG 15 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MQ653 UT WOS:A1993MQ65300003 PM 8119064 ER PT J AU ROSENDORF, LL DAFNI, U AMATO, DA LUNGHOFER, B BARTLETT, JG LEEDOM, JM WARA, DW ARMSTRONG, JA GODFREY, E SUKKESTAD, E COUNTS, GW AF ROSENDORF, LL DAFNI, U AMATO, DA LUNGHOFER, B BARTLETT, JG LEEDOM, JM WARA, DW ARMSTRONG, JA GODFREY, E SUKKESTAD, E COUNTS, GW TI PERFORMANCE EVALUATION IN MULTICENTER CLINICAL-TRIALS - DEVELOPMENT OF A MODEL BY THE AIDS CLINICAL-TRIALS GROUP SO CONTROLLED CLINICAL TRIALS LA English DT Article DE PERFORMANCE MONITORING; PERFORMANCE EVALUATION; CLINICAL TRIAL; MODELING; AIDS; ACTG; PERFORMANCE SCORE ID ONCOLOGY-GROUP; PARTICIPATION; QUALITY AB The AIDS Clinical Trials Group (ACTG), supported by the National Institute of Allergy and Infectious Diseases (NIAID), is the largest federally funded program of AIDS clinical trials. It is a collaboration involving 59 institutions and affiliated clinical centers, known as AIDS Clinical Trials Units (ACTUs), NIAID staff, and a Statistical and Data Analysis Center (SDAC). An institutional evaluation tool was developed to evaluate ACTU performance, distinguish between clinical centers with superior performance and those not meeting standards, and assist NIAID in allocating funding based on performance. The evaluation tool was designed to reflect the many distinguishing features of ACTG study protocols and clinical trial centers in order to measure performance objectively. The evaluation focused on assessing the financial resources expended by the ACTU in recruiting, treating, and following study patients during the evaluation period; the number of women and minorities enrolled; and the ACTU's scientific contributions to the ACTG. To help quantify the ACTU's performance in enrolling study subjects, a formula was derived to assess the total effort required to screen, enroll, treat, and assess subjects participating in ACTG studies. A weighting system was developed for each study protocol to account for the variations in effort and resources required by the different protocols. Future directions in the ACTG evaluation process include strategies to evaluate performance in relation to quality of data and to determine ways in which the evaluation process can be used to enhance the achievement of programmatic goals. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. FRONTIER SCI & TECH RES FDN,AMHERST,NY. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. UNIV SO CALIF,LOS ANGELES,CA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. UNIV PITTSBURGH,PITTSBURGH,PA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP ROSENDORF, LL (reprint author), NIAID,POLICY ANAL & LEGISLAT BRANCH,BLDG 31,ROOM 7A51,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI-27662, AI-27673, AI-95030] NR 10 TC 6 Z9 6 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD DEC PY 1993 VL 14 IS 6 BP 523 EP 537 DI 10.1016/0197-2456(93)90032-9 PG 15 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MQ653 UT WOS:A1993MQ65300006 PM 8119067 ER PT J AU AKOVA, YA DUTT, J RODRIGUEZ, A JABBUR, N FOSTER, CS AF AKOVA, YA DUTT, J RODRIGUEZ, A JABBUR, N FOSTER, CS TI THE ROLE OF IGH-1 DISPARATE CONGENIC MOUSE T-LYMPHOCYTES IN THE PATHOGENESIS OF HERPETIC STROMAL KERATITIS SO CURRENT EYE RESEARCH LA English DT Article ID CORNEAL INFECTION; SIMPLEX KERATITIS; VIRUS; MICE; PROTECTS AB The corneal destruction associated with herpes simplex keratitis (HSK) is primarily the result of the host's immune response to herpes simplex virus type-1 (HSV-1) infection. We examined the role of T cells and T cell subsets in the pathogenesis of HSK. Naive and immune T cells and HSV-1 immune CD4+ and CD8+ subsets from Igh-1 disparate BALB/c congenic mice were adoptively transferred into athymic BALB/c nude mice, which normally do not develop HSK. The results demonstrated that while the transfer of naive T cells from either HSK-susceptible C.AL-20 (Igh-1(d)) or HSK-resistant C.B-17 (Igh-l(b)) mice had little influence on HSK development, transfer of either CD3+ or CD4+ HSV-1 immune T cells from C.AL-20 mice resulted in the development of severe HSK in all of the recipients. Transfer of the same cell populations from C.B-17 mice resulted in the development of only a mild keratitis in 50% of the recipients. Transfer of CD8+ cells from either donor strain did not result in stromal disease in any recipient mouse. These results clearly demonstrate the pivotal role of CD4+ T cells in the development of necrotizing herpes stromal keratitis, and further demonstrate that CD8+ T cells are not essential in HSK development in the BALB/c system. C1 MASSACHUSETTS EYE & EAR INFIRM,HARVARD MED SCH,HILLES IMMUNOL LAB,BOSTON,MA 02114. FU NEI NIH HHS [EY-06008] NR 22 TC 14 Z9 14 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD DEC PY 1993 VL 12 IS 12 BP 1093 EP 1101 DI 10.3109/02713689309033507 PG 9 WC Ophthalmology SC Ophthalmology GA MT627 UT WOS:A1993MT62700007 PM 7907969 ER PT J AU TSAI, LH TAKAHASHI, T CAVINESS, VS HARLOW, E AF TSAI, LH TAKAHASHI, T CAVINESS, VS HARLOW, E TI ACTIVITY AND EXPRESSION PATTERN OF CYCLIN-DEPENDENT KINASE-5 IN THE EMBRYONIC MOUSE NERVOUS-SYSTEM SO DEVELOPMENT LA English DT Article DE CYCLIN-DEPENDENT KINASES; CELL CYCLE; NEURONAL DIFFERENTIATION ID PROTEIN-KINASE; CELL-CYCLE; PHOSPHORYLATION SITES; CEREBRAL-CORTEX; CDC28 MUTATION; P34CDC2 KINASE; RAT-BRAIN; GROWTH; GAP-43; ACTIVATION AB Cyclin-dependent kinase 5 (cdk5) was originally isolated on the basis of its close primary sequence homology to the human cdc2 serine/threonine kinase, the prototype of the cyclin-dependent kinases. While kinase activities of both cdc2 and cdk2 are detected in proliferating cells and are essential for cells to progress through the key transition points of the cell cycle, cdk5 kinase activity has been observed only in lysates of adult brain. In this study, we compared the activity and expression of cdk5 with that of cdc2 and cdk2 in the embryonic mouse forebrain. The expression and activity of cdk5 increased progressively as increasing numbers of cells exited the proliferative cycle. In contrast, the expression and activity of cdc2 and cdk2 were maximum at gestational day 11 (Ell) when the majority of cells were proliferating and fell to barely detectable levels at E17 at the end of the cytogenetic period. Immunohistochemical studies showed that cdk5 is expressed in postmitotic neurons but not in glial cells or mitotically active cells. Expression of cdk5 was concentrated in fasciculated axons of postmitotic neurons. In contrast to other cell division cycle kinases to which it is closely related, cdk5 appears not to be expressed in dividing cells in the developing brain. These observations suggest that cdk5 may have a role in neuronal differentiation but not in the cell division cycle in the embryonic nervous system. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RP TSAI, LH (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 60 TC 381 Z9 392 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD DEC PY 1993 VL 119 IS 4 BP 1029 EP 1040 PG 12 WC Developmental Biology SC Developmental Biology GA MM509 UT WOS:A1993MM50900006 PM 8306873 ER PT J AU LUZI, L PETRIDES, AS DEFRONZO, RA AF LUZI, L PETRIDES, AS DEFRONZO, RA TI DIFFERENT SENSITIVITY OF GLUCOSE AND AMINO-ACID-METABOLISM TO INSULIN IN NIDDM SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; LEUCINE METABOLISM; PROTEIN-SYNTHESIS; SUBSTRATE AVAILABILITY; RESISTANCE; PATHOGENESIS; MUSCLE; OXIDATION; TURNOVER; DISPOSAL AB NIDDM subjects are characterized by impaired glucose tolerance and insulin resistance with respect to glucose metabolism. To examine whether the defect in glucose utilization extends to amino acid metabolism, 6 NIDDM subjects (64 +/- 4 yr of age; ideal body weight of 107 +/- 3%) and 7 control subjects (58 +/- 4 yr of age; ideal body weight of 105 +/- 2%) were studied with the euglycemic insulin clamp technique, in combination with [1-C-14]leucine and indirect calorimetry. All subjects participated in two studies. In study 1, after 3 h of tracer equilibration, a 3-h insulin clamp (40 mU.m-2.min-1) was performed to define the effect of insulin on leucine kinetics and glucose metabolism. In study 2, subjects received a repeat 3-h insulin clamp, and a balanced amino acid solution was infused to increase the plasma amino acid concentrations approximately 2-fold to examine the effect of combined physiological hyperinsulinemia-hyperaminoacidemia on the rate of leucine and glucose disposal, insulin-mediated total body glucose uptake was significantly reduced in NIDDM during both study 1 (5.6 +/- 0.4 vs. 6.9 +/- 0.6 mg.kg-1.min-1, P < 0.01) and study 2 (5.2 +/- 0.4 vs. 6.8 +/- 0.6, P < 0.01). Basal plasma leucine (120 +/- 10 vs. 123 +/- 11 muM) and alpha-ketoisocaproic acid concentrations (28 +/- 3 vs. 25 +/- 2 muM) were similar in NIDDM and control subjects, respectively. In contrast, the basal plasma glucose concentration (8.9 +/- 0.8 vs. 4.7 +/- 0.2 muM) and the HbA1c (8.5 +/- 0.2 vs. 5.7 +/- 0.2%) were significantly increased in NIDDM (P < 0.01). In the postabsorptive state, endogenous leucine flux, leucine oxidation, and nonoxidative leucine disposal were similar in NIDDM and control subjects. When insulin was infused without amino acids (study 1), the decrement in plasma leucine (53 +/- 5 vs. 48 +/- 4 muM), endogenous leucine flux (13 +/- 2 vs. 11 +/-1 mumol.m-2.min-1), leucine oxidation (1.6 +/- 0.2 vs. 1.3 +/- 0.1 mumol.m-2.min-1), and nonoxidative leucine disposal (10 +/- 1 vs. 8 +/- 1 mumol.m-2.min-1) was comparable in both groups. During combined insulin and amino acid infusion (study 2), plasma leucine concentration (185 +/- 20 vs. 190 +/- 15 muM) rose similarly in NIDDM and control subjects. In NIDDM, the increment in leucine oxidation (9.0 +/- 0.7 vs. 8.5 +/- 0.6 mumol.m-2.min-1) and nonoxidative leucine disposal (9.3 +/- 0.7 vs. 10.5 +/- 0.9 mumol.m-2.min-1) was similar to that observed in control subjects; the decrement in endogenous leucine flux (22.3 +/- 2.1 vs. 20.2 +/- 1.9 mumol.m-2.min-1) was comparable in both groups. We conclude that 1) insulin-mediated glucose disposal is significantly impaired in NIDDM and 2) the effect of insulin on endogenous leucine flux (protein degradation), nonoxidative leucine disposal (protein synthesis), and leucine oxidation is similar in NIDDM and control subjects. These results indicate a clear-cut dissociation between the effect of insulin on glucose and protein metabolism in NIDDM. C1 UNIV TEXAS,HLTH SCI CTR,DEPT INTERNAL MED,DIV DIABET,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP LUZI, L (reprint author), UNIV MILAN,S RAPHAEL SCI INST,DEPT MED,RADIOACT & STABLE ISOTOPES LAB,I-20132 MILAN,ITALY. RI Luzi, Livio/M-2696-2016 OI Luzi, Livio/0000-0003-3183-0552 FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK-24092] NR 36 TC 62 Z9 63 U1 0 U2 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD DEC PY 1993 VL 42 IS 12 BP 1868 EP 1877 DI 10.2337/diabetes.42.12.1868 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MJ775 UT WOS:A1993MJ77500023 PM 8243833 ER PT J AU STJAMES, PJ YOUNGER, MD HAMILTON, BD WAISBREN, SE AF STJAMES, PJ YOUNGER, MD HAMILTON, BD WAISBREN, SE TI UNPLANNED PREGNANCIES IN YOUNG-WOMEN WITH DIABETES - AN ANALYSIS OF PSYCHOSOCIAL FACTORS SO DIABETES CARE LA English DT Article ID CONTRACEPTIVE BEHAVIOR; MATERNAL PHENYLKETONURIA; MELLITUS; MANAGEMENT; PREVENTION AB OBJECTIVE- To assess psychosocial factors related to preventing birth defects in children born to diabetic women. Diabetic women are at high risk for bearing children with congenital anomalies associated with teratogenic effects early in pregnancy. This study focuses on factors related to the family planning behavior of diabetic women. RESEARCH DESIGN AND METHODS- Sixty-six diabetic women were included in a 5-yr, prospective, longitudinal study along with 69 phenylketonuric women, who also face a high risk of bearing children with birth defects, and 68 healthy women. Annual interviews and questionnaires were administered. Women who did not want a pregnancy completed measures related to contraceptive behavior and quality of life. Areas assessed were knowledge, personality, attitudes, and social support. RESULTS- Diabetic women were more likely to be sexually active than women with phenylketonuria. Use and type of birth control were comparable among the groups except that diabetic women used condoms more often. For diabetic women, social support and positive attitudes towards birth control were associated with consistent birth control use. Of the diabetic women, 23 became pregnant, and only 6 (26%) were planned pregnancies. CONCLUSIONS- Birth control use by diabetic women needs to be addressed by health professionals. Attitudes about birth control of the women and those close to them appear to be important factors in consistent birth control use. Suggestions are made for addressing these factors. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP STJAMES, PJ (reprint author), CHILDRENS HOSP MED CTR,DIV GENET,BIOCHEM GENET UNIT,GARDNER 817,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU PHS HHS [MCJ-25059] NR 39 TC 41 Z9 41 U1 1 U2 5 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD DEC PY 1993 VL 16 IS 12 BP 1572 EP 1578 DI 10.2337/diacare.16.12.1572 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MJ773 UT WOS:A1993MJ77300005 PM 8299452 ER PT J AU JACOBSON, AM AF JACOBSON, AM TI DEPRESSION AND DIABETES SO DIABETES CARE LA English DT Editorial Material ID PSYCHIATRIC-DISORDERS; MELLITUS RP JACOBSON, AM (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 14 TC 37 Z9 37 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD DEC PY 1993 VL 16 IS 12 BP 1621 EP 1623 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MJ773 UT WOS:A1993MJ77300014 PM 8299460 ER PT J AU KIERS, L CROS, D CHIAPPA, KH FANG, J AF KIERS, L CROS, D CHIAPPA, KH FANG, J TI VARIABILITY OF MOTOR POTENTIALS-EVOKED BY TRANSCRANIAL MAGNETIC STIMULATION SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE TRANSCRANIAL MAGNETIC STIMULATION; VARIABILITY; STIMULUS INTENSITY ID ELECTRICAL-STIMULATION; MULTIPLE-SCLEROSIS; BRAIN-STIMULATION; HAND MUSCLES; RESPONSES; CORTEX; COIL; MOTONEURONS; UNITS AB We studied the effect of stimulus intensity, coil size, mental alertness and prestimulus muscle contraction on the variability of motor evoked potentials (MEPs) produced by magnetic cortical stimulation (MCS). In 5 healthy subjects we delivered MCS either with a circular coil centered at the vertex or a figure-8 coil centered over the motor cortex hand area, recording from first dorsal interosseous. With the subject at rest or exerting 5% maximum voluntary contraction, 30 consecutive stimuli were given at 4 stimulus intensities (SIs) in 10% increments above resting motor threshold. Concurrent mental arithmetic constituted mental alertness. Spectral analysis was performed on data from 300 consecutive stimuli. The variability of MEP response size was inversely related to stimulus intensity, prestimulus voluntary muscle contraction, the recruitment of motoneurons and the size of the field generated by the magnetic coil. The MEP variability was larger than and not correlated with the variability of the H-reflex. Fast Fourier transformation and cross-correlation analysis did not identify a consistent dominant frequency, suggesting that the variability in MEP size is essentially random. We suggest that the variability in MEP response is caused by constant, rapid, spontaneous fluctuations in corticospinal and segmental motoneuron excitability levels. Any maneuver that raises this level or increases the probability of motoneuron firing will decrease MEP variability. C1 MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LABS,EMG LAB,BIGELOW 12,BOSTON,MA 02114. NR 30 TC 205 Z9 205 U1 2 U2 8 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD DEC PY 1993 VL 89 IS 6 BP 415 EP 423 DI 10.1016/0168-5597(93)90115-6 PG 9 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA MR557 UT WOS:A1993MR55700007 PM 7507428 ER PT J AU KEARSE, LA KOSKI, G HUSAIN, MV PHILBIN, DM MCPECK, K AF KEARSE, LA KOSKI, G HUSAIN, MV PHILBIN, DM MCPECK, K TI EPILEPTIFORM ACTIVITY DURING OPIOID ANESTHESIA SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE ELECTROENCEPHALOGRAPHY; EPILEPTIFORM; SEIZURES; OPIOID RECEPTORS; OPIOID; CONVULSANTS ID POSITRON EMISSION TOMOGRAPHY; TEMPORAL-LOBE EPILEPSY; MU-OPIATE RECEPTORS; HIGH-DOSE FENTANYL; INDUCED SEIZURES; ELECTROENCEPHALOGRAM; SUFENTANIL; ALFENTANIL; ENKEPHALIN; INDUCTION AB The proconvulsant properties of exogenously administered opioids in man are not established. We prospectively evaluated relationships between epileptiform activity and opioid dose in 20 patients undergoing coronary artery revascularization. Baseline electroencephalograms were performed before surgery. Ten subjects were given fentanyl and 10 sufentanil, at 100 mu g/kg and 10 mu g/kg, respectively, in 4 divided doses, 3 min apart. Midazolam (4 mg) was given 3 min after the last dose of narcotic. Serum opioid concentrations were measured by radioimmunoassay. Within 3 min of the first opioid dose, 19 of 20 patilnts developed epileptiform activity, characterized by generalized single and multiphasic, low-to-moderate voltage spike discharges, similar in appearance to benign epileptiform transients of sleep (BETS). Despite continuously increasing serum concentrations of opioid, the number of spike discharges initially increased during the first and second dose intervals and then declined during the third and fourth dose intervals. This dissociation between epileptiform discharges and measured serum opioid concentration was unexpected and remained unexplained. Spike activity was consistently attenuated (P = 0.000003) within 20 sec of midazolam administration. Abrupt cessation of discharges after administration of the anticonvulsant, midazolam, suggests an epileptogenic mechanism for the opioid-induced activity. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RP KEARSE, LA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 29 TC 31 Z9 31 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD DEC PY 1993 VL 87 IS 6 BP 374 EP 379 DI 10.1016/0013-4694(93)90150-T PG 6 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA MR140 UT WOS:A1993MR14000004 PM 7508369 ER PT J AU LEUCHTER, AF COOK, IA NEWTON, TF DUNKIN, J WALTER, DO ROSENBERGTHOMPSON, S LACHENBRUCH, PA WEINER, H AF LEUCHTER, AF COOK, IA NEWTON, TF DUNKIN, J WALTER, DO ROSENBERGTHOMPSON, S LACHENBRUCH, PA WEINER, H TI REGIONAL DIFFERENCES IN BRAIN ELECTRICAL-ACTIVITY IN DEMENTIA - USE OF SPECTRAL POWER AND SPECTRAL RATIO MEASURES SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE QUANTITATIVE EEG; ALZHEIMERS DISEASE; MULTIINFARCT DEMENTIA; REGIONAL DIFFERENCES ID EMISSION COMPUTED-TOMOGRAPHY; MULTI-INFARCT DEMENTIA; ALZHEIMERS-DISEASE; SENILE DEMENTIA; VASCULAR DEMENTIA; DEPRESSED SUBJECTS; FREQUENCY-ANALYSIS; EEG ANALYSIS; DIAGNOSIS; DISTRIBUTIONS AB The pathologic changes in dementia of the Alzheimer's type (DAT) commonly affect selected brain regions. The cortical areas affected in multi-infarct dementia (MID) are less predictable and may be secondary to subcortical gray or white matter damage that is widespread in MID, We compared several types of quantitative EEG power measures (absolute and relative power, and ratios of power) to determine their regional distribution, and their association with changes in cognitive status and age. We examined 49 subjects with clinically diagnosed mild-to-moderate DAT, 29 with mild-to-moderate MID, and 38 elderly controls (CON). We used discriminant analysis to identify, for each parameter type, the brain region and frequency band where the parameter best distinguished between groups of subjects. The parameters showed regional differences in distinguishing between DAT and MID subjects, and in their association with age and cognitive status. All parameters were useful for detecting differences between normal and demented subjects and correctly identified comparable proportions of subjects as having dementia. Subjects who were abnormal on several parameters were much more likely to have dementia. The additive effects of these parameters in correct classification suggest that they may be monitoring different physiologic processes. Combinations of several types of parameters may be more useful than individual parameters for distinguishing demented from non-demented subjects. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,DEPT BIOSTAT,LOS ANGELES,CA 90024. RP LEUCHTER, AF (reprint author), UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,QUANTITAT EEG LAB,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. OI newton, thomas/0000-0002-3198-5901 FU NIMH NIH HHS [NIMH MH 17140, NIMH MH 40705, NIMH MH 00665] NR 45 TC 137 Z9 142 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD DEC PY 1993 VL 87 IS 6 BP 385 EP 393 DI 10.1016/0013-4694(93)90152-L PG 9 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA MR140 UT WOS:A1993MR14000006 PM 7508371 ER PT J AU CHEN, JZ YOUNG, F BOTTARO, A STEWART, V SMITH, RK ALT, FW AF CHEN, JZ YOUNG, F BOTTARO, A STEWART, V SMITH, RK ALT, FW TI MUTATIONS OF THE INTRONIC IGH ENHANCER AND ITS FLANKING SEQUENCES DIFFERENTIALLY AFFECT ACCESSIBILITY OF THE J(H)-LOCUS SO EMBO JOURNAL LA English DT Article DE E-MU ENHANCER; GENE TARGETING; METHYLATION; REARRANGEMENT; TRANSCRIPTION ID IMMUNOGLOBULIN GENE REARRANGEMENT; VARIABLE REGION GENE; HEAVY-CHAIN GENES; PRE-B-CELLS; NUCLEOTIDE-SEQUENCE; V(D)J RECOMBINATION; DNA METHYLATION; TRANSCRIPTION; SEGMENTS; EXPRESSION AB To investigate the role of intronic immunoglobulin heavy chain (IgH) enhancer (Emu) in generating accessibility of the J(H) locus for VDJ recombination, we generated ES cells in which Eu or its flanking sequences were mutated by replacement with or insertion of an expressed neo(r) gene. Heterozygous mutant ES cells were used to generate chimeric mice from which pre-B cell tines were derived by transformation of bone marrow cells with Abelson murine leukemia virus (A-MuLV). Comparison of the rearrangement status of the normal and mutated alleles in individual pre-B cell lines allowed us to assay for cis-acting effects of the mutations. Replacement of a 700 bp region immediately downstream from the core Emu [which includes part of the 3' matrix associated region (MAR) and the Imu exon] had no obvious effect on rearrangement of the targeted allele, indicating that insertion of a transcribed neo(r) gene into the J(H)-Cmu intron does not affect J(H) accessibility. In contrast, replacement of an overlapping 1 kb DNA fragment that contains the Emu resulted in a dramatic cis-acting inhibition of rearrangement, demethylation and germline transcription of the associated J(H) locus. Surprisingly, insertion of the neo(r) gene into the 5' MAR sequence approximately 100 bp upstream of the core Emu also dramatically decreased recombination of the linked J(H) locus; but, in many lines, did not prevent demethylation of this locus. We conclude that integrity of the Emu and upstream flanking sequences is required for efficient rearrangement of the J(H) locus and that demethylation of this locus, per se, does not necessarily make it a good substrate for VDJ recombination. C1 HARVARD UNIV,CHILDRENS HOSP,HOWARD HUGHES MED INST,SCH MED,320 LONGWOOD AVE,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. FU NIAID NIH HHS [AI20047, U01 AI31541] NR 43 TC 167 Z9 167 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD DEC 1 PY 1993 VL 12 IS 12 BP 4635 EP 4645 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MF994 UT WOS:A1993MF99400018 PM 8223473 ER PT J AU WU, SX PIROLA, CJ GREEN, J YAMAGUCHI, DT OKANO, K JUEPPNER, H FORRESTER, JS FAGIN, JA CLEMENS, TL AF WU, SX PIROLA, CJ GREEN, J YAMAGUCHI, DT OKANO, K JUEPPNER, H FORRESTER, JS FAGIN, JA CLEMENS, TL TI EFFECTS OF N-TERMINAL, MIDREGION, AND C-TERMINAL PARATHYROID HORMONE-RELATED PEPTIDES ON ADENOSINE-3',5'-MONOPHOSPHATE AND CYTOPLASMIC FREE CALCIUM IN RAT AORTIC SMOOTH-MUSCLE CELLS AND UMR-106 OSTEOBLAST-LIKE CELLS SO ENDOCRINOLOGY LA English DT Article ID BONE-RESORPTION; HUMORAL HYPERCALCEMIA; SYNTHETIC PEPTIDE; COMMON RECEPTOR; HUMAN-TUMOR; PROTEIN; EXPRESSION; GENE; MALIGNANCY; FRAGMENTS AB N-Terminal analogs of PTH-related protein (PTHrP) and PTH bind to a common receptor and exhibit similar biological properties. However, recent studies suggest that certain midregion and C-terminal PTHrP peptides have activities distinct from those of PTH in the placenta and in osteoclasts, respectively. In this study we determined the biological activities of full-length recombinant PTHrP-(1-141) and several synthetic N-terminal, midregion, and C-terminal PTHrP fragments in two PTHrP-producing cell types. Peptides were tested for their ability to stimulate CAMP production and raise intracellular free calcium ([Ca2+]i) in primary rat aortic smooth muscle cells (VSMC) and UMR-106 rat osteoblast-like (UMR) cells. In UMR cells PTHrP-(1-34)NH2, PTHrP-(1-141), and bovine PTH-(1-34) all increased CAMP (approximately 50 fold) and [Ca2+]i (180 nm). By contrast, in VSMC, these N-terminal peptides increased CAMP (3-fold) but had no detectable effect on [Ca2+]i. PTHrP-(1-34) and PTHrP-(1-141) significantly blunted the angiotensin 11-induced rise in CAMP (but not the calcium signal) consistent with the concept that PTHrP opposes angiotensin II activity in VSMC. PTHrP-(67-86)NH2, PTHrP-(107-138)NH2, and PTHrP-(107-111)NH2 had no effect on either CAMP or [Ca2+]i in either cell type. VSMC and UMR-106 cells both expressed a 2.5-kilobase PTH/PTHrP receptor messenger RNA (MRNA) transcript. However, high affinity specific binding of I-125-labeled [Tyr36]PTHrP-(1-36)NH2 was detected in UMR cells but not in VSMC. We conclude that the PTH-like, N terminus of the PTHrP molecule is critical in induction of CAMP and [Ca2+]i pathways in UMR cells, and for CAMP stimulation in VSMC. In addition, PTHrP, like other established vasodilators, signals in VSMC mainly (if not exclusively) by increasing the production of CAMP. C1 W LOS ANGELES VET ADM HOSP,GRECC LAB,LOS ANGELES,CA 90048. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. CEDARS SINAI MED CTR,CEDARS SINAI RES INST,DEPT MED,DIV ENDOCRINOL,LOS ANGELES,CA 90048. CEDARS SINAI MED CTR,CEDARS SINAI RES INST,DEPT MED,DIV CARDIOL,LOS ANGELES,CA 90048. CEDARS SINAI MED CTR,CEDARS SINAI RES INST,DEPT MED,DIV NEPHROL,LOS ANGELES,CA 90048. OI Pirola, Carlos/0000-0001-8234-4058 FU NCI NIH HHS [CA-50706, CA-50906]; NHLBI NIH HHS [HL-47811] NR 39 TC 52 Z9 52 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 DEC PY 1993 VL 133 IS 6 BP 2437 EP 2444 DI 10.1210/en.133.6.2437 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MK151 UT WOS:A1993MK15100005 PM 8243262 ER PT J AU CATLIN, EA EZZELL, RM DONAHOE, PK GUSTAFSON, ML SON, EV MACLAUGHLIN, DT AF CATLIN, EA EZZELL, RM DONAHOE, PK GUSTAFSON, ML SON, EV MACLAUGHLIN, DT TI IDENTIFICATION OF A RECEPTOR FOR HUMAN MULLERIAN-INHIBITING SUBSTANCE SO ENDOCRINOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; FETAL-RAT LUNG; EXPRESSION CLONING; ACTIVIN RECEPTOR; CELLS; BINDING; KINASE; PURIFICATION; PROTEINS AB Mullerian inhibiting substance (MIS), a Sertoli cell-derived glycoprotein and member of the transforming growth factor-beta supergene family, plays a key down-stream role in mammalian sex determination. Identification of a receptor for MIS has now been achieved in a MIS-responsive human vulvar carcinoma cell line, A431, using fluorescein isothiocyanate labeling of recombinant human MIS (FITC-rhMIS) and RRAs with iodinated carboxy-terminal rhMIS. Confocal fluorescence microscopy of A431 cells incubated on ice with 30-nm concentrations of covalently bound FITC-rhMIS reveals specific punctate cell surface fluorescent signal. Cytosolic fluorescent signal is seen after incubation at 37 C for 1 h as well as occasional apparent perinuclear accumulation. FITC-rhMIS coincubated with molar excesses of unlabeled rhMIS in A431 cells eliminates cell surface and cytosolic fluorescent uptake. Double label experiments with FITC-rhMIS and tetramethyl rhodamine isothiocyanate epidermal growth factor establish separate binding of each ligand, displaceable, respectively, by large molar excesses of unlabeled rhMIS or epidermal growth factor. RRAs reveal a single, high affinity (K(d), 5.8 nm), saturable, low abundance binding species for carboxy-terminal rhMIS. Solubilized supernatants of A431 whole cells cross-linked with I-125-carboxy-terminal rhMIS identify a band with a mol wt of 88,000 on electrophoresis and autoradiography. This identification of a MIS receptor in A431 cells now permits the design of affinity purification protocols using rhMIS, followed by direct protein microsequencing. C1 MASSACHUSETTS GEN HOSP, PEDIAT SURG SERV, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, PEDIAT SURG RES LAB, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT SURG, BOSTON, MA 02114 USA. RP MASSACHUSETTS GEN HOSP, CHILDRENS SERV, NEONATOL UNIT, 32 FRUIT ST, BOSTON, MA 02114 USA. FU NHLBI NIH HHS [R29-HL-46198]; NICHD NIH HHS [P30-HD-28138] NR 28 TC 12 Z9 12 U1 0 U2 0 PU ENDOCRINE SOC PI WASHINGTON PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD DEC PY 1993 VL 133 IS 6 BP 3007 EP 3013 DI 10.1210/en.133.6.3007 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MK151 UT WOS:A1993MK15100083 PM 8243329 ER PT J AU RYAN, L AF RYAN, L TI POTENCY MEASURES FOR DEVELOPMENTAL TOXICITY SO ENVIRONMETRICS LA English DT Article; Proceedings Paper CT International Conference on Environmental Biometrics CY DEC 14-15, 1992 CL UNIV SYDNEY, WOMENS COLL, SYDNEY, AUSTRALIA SP SSA, SYDNEY WATER BOARD, BIOMETR SOC, ASA, SECT STAT & ENVIRONM, INT ENVIRONM SOC HO UNIV SYDNEY, WOMENS COLL DE GENERALIZED ESTIMATING EQUATIONS; CLUSTERED DATA; TERATOLOGY AB Potency measures provide a useful means of ranking chemicals, drugs and other substances with respect to the danger they pose to humans. While several authors have proposed estimators of carcinogenic potency, the task of ranking developmental toxicants has received little attention. The purpose of this paper is to develop a quantitative measure of developmental potency, based on a correlated multinominal model that allows for dose effects on foetal death, variation and malformation rates. The proposed estimator is illustrated with data from several studies conducted through the National Toxicology Program. RP RYAN, L (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 NR 0 TC 1 Z9 1 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 1180-4009 J9 ENVIRONMETRICS JI Environmetrics PD DEC PY 1993 VL 4 IS 4 BP 507 EP 518 DI 10.1002/env.3170040409 PG 12 WC Environmental Sciences; Mathematics, Interdisciplinary Applications; Statistics & Probability SC Environmental Sciences & Ecology; Mathematics GA NB339 UT WOS:A1993NB33900008 ER PT J AU JANG, IK LASSILA, R FUSTER, V AF JANG, IK LASSILA, R FUSTER, V TI ATHEROGENESIS AND INFLAMMATION SO EUROPEAN HEART JOURNAL LA English DT Article; Proceedings Paper CT 10th Paavo Nurmi Symposium on Role of Infection and Inflammation in Vascular Disease CY AUG, 1992 CL HELSINKI, FINLAND SP PAAVO NURMI FDN DE ATHEROGENESIS; MACROPHAGE; MONOCYTE; SMOOTH MUSCLE CELLS; VASCULAR INJURY ID SMOOTH-MUSCLE CELLS; LOW-DENSITY LIPOPROTEIN; ATHEROSCLEROTIC PLAQUE; ARTERIAL INJURY; TISSUE FACTOR; MACROPHAGE; PATHOGENESIS; MECHANISMS; THROMBOSIS; WALL C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. WIHURI RES INST,HELSINKI,FINLAND. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 38 TC 51 Z9 52 U1 0 U2 1 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0195-668X J9 EUR HEART J JI Eur. Heart J. PD DEC PY 1993 VL 14 SU K BP 2 EP 6 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MU105 UT WOS:A1993MU10500002 PM 8131783 ER PT J AU PAKZABAN, P DEACON, TW BURNS, LH ISACSON, O AF PAKZABAN, P DEACON, TW BURNS, LH ISACSON, O TI INCREASED PROPORTION OF ACETYLCHOLINESTERASE-RICH ZONES AND IMPROVED MORPHOLOGICAL INTEGRATION IN HOST STRIATUM OF FETAL GRAFTS DERIVED FROM THE LATERAL BUT NOT THE MEDIAL GANGLIONIC EMINENCE SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE NEURAL TRANSPLANTATION; FETAL GRAFTS; HUNTINGTON DISEASE; NEURAL REGENERATION; NEURAL DEVELOPMENT; RAT ID ACID-LESIONED STRIATUM; RAT NEOSTRIATAL GRAFTS; ELECTRON-MICROSCOPIC ANALYSIS; HUNTINGTONS-DISEASE; EFFERENT PROJECTIONS; BEHAVIORAL RECOVERY; PRIMATE MODEL; NEURONS; ORGANIZATION; CONNECTIVITY AB Fetal striatal grafts are found to have a modular organization revealed by acetylcholinesterase (AChE) histochemistry. The AChE-rich zones represent the only portions of these grafts that are anatomically and functionally integrated into the host brain. In this study, the medial and lateral ganglionic eminences (MGEs and LGEs) were selectively dissected from the basal telencephalon of embryonic-day-14 (E14) rat fetuses to compare their relative contributions to the AChE-rich fraction of intrastriatal grafts. Separate cell suspensions prepared from either eminence were stereotaxically implanted into excitotoxically lesioned neostriatum of adult rats. Eight weeks after transplantation, grafts of the MGE were compared with those of the LGE with respect to the proportion of AChE-rich zones, graft size, graft morphology, and afferent dopaminergic innervation as revealed by tyrosine hydroxylase (TH) immunostaining. The mean AChE-rich fraction in LGE grafts (87% +/- 4%) was markedly greater than the AChE-rich fraction in MGE grafts (25% +/- 10%). The LGE grafts were also morphologically better incorporated into the lesioned host striatum, partially reconstituting the striatal morphology. There was no statistically significant difference in graft size between the two groups. The AChE-rich LGE grafts were TH immunoreactive, whereas the AChE-poor MGE grafts were not. We conclude that grafts derived exclusively from the fetal LGE reconstitute the striatal morphology and consist almost entirely of AChE-rich zones. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROSURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02114. RP PAKZABAN, P (reprint author), MCLEAN HOSP,MRC 119,NEUROREGENERAT LAB,BELMONT,MA 02178, USA. FU NINDS NIH HHS [NINDS 5T32 NS07340, NS29178, NS30064] NR 43 TC 117 Z9 120 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PD DEC PY 1993 VL 97 IS 1 BP 13 EP 22 PG 10 WC Neurosciences SC Neurosciences & Neurology GA MM145 UT WOS:A1993MM14500002 PM 7907548 ER PT J AU ROBERTS, RC AHN, A SWARTZ, KJ BEAL, MF DIFIGLIA, M AF ROBERTS, RC AHN, A SWARTZ, KJ BEAL, MF DIFIGLIA, M TI INTRASTRIATAL INJECTIONS OF QUINOLINIC ACID OR KAINIC ACID - DIFFERENTIAL PATTERNS OF CELL-SURVIVAL AND THE EFFECTS OF DATA-ANALYSIS ON OUTCOME SO EXPERIMENTAL NEUROLOGY LA English DT Article ID STRIATAL NEUROPEPTIDE-Y; RAT CAUDATE-NUCLEUS; HUNTINGTONS-DISEASE; CHOLINERGIC NEURONS; NADPH-DIAPHORASE; BASAL GANGLIA; SUBSTANCE-P; HUMAN-BRAIN; CHOREA; SOMATOSTATIN C1 MASSACHUSETTS GEN HOSP,CELLULAR NEUROBIOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP ROBERTS, RC (reprint author), UNIV MARYLAND,SCH MED,MARYLAND PSYCHIAT RES CTR,DEPT PSYCHIAT,POB 21247,BALTIMORE,MD 21228, USA. NR 39 TC 78 Z9 80 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 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD DEC PY 1993 VL 124 IS 2 BP 274 EP 282 DI 10.1006/exnr.1993.1197 PG 9 WC Neurosciences SC Neurosciences & Neurology GA MR569 UT WOS:A1993MR56900011 PM 8287926 ER PT J AU RACHMILEWITZ, D STAMLER, JS KARMELI, F MULLINS, ME SINGEL, DJ LOSCALZO, J XAVIER, RJ PODOLSKY, DK AF RACHMILEWITZ, D STAMLER, JS KARMELI, F MULLINS, ME SINGEL, DJ LOSCALZO, J XAVIER, RJ PODOLSKY, DK TI PEROXYNITRITE-INDUCED RAT COLITIS - A NEW MODEL OF COLONIC INFLAMMATION SO GASTROENTEROLOGY LA English DT Article ID NITRIC-OXIDE; ULCERATIVE-COLITIS; SUPEROXIDE; OXIDATION C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. BRIGHAM & WOMENS HOSP, DIV RESP & CARDIOVASC, BOSTON, MA 02115 USA. HARVARD UNIV, DEPT CHEM, CAMBRIDGE, MA 02138 USA. FU NIDDK NIH HHS [5P30 DK 43351] NR 25 TC 236 Z9 237 U1 0 U2 2 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 EI 1528-0012 J9 GASTROENTEROLOGY JI Gastroenterology PD DEC PY 1993 VL 105 IS 6 BP 1681 EP 1688 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ML100 UT WOS:A1993ML10000011 PM 8253344 ER PT J AU FRIEDMAN, LS MARTIN, P AF FRIEDMAN, LS MARTIN, P TI THE PROBLEM OF GASTROINTESTINAL-BLEEDING SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA LA English DT Article ID HEMORRHAGE; MANAGEMENT; ULCER C1 HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. UNIV CALIF LOS ANGELES, MED CTR, DIV GASTROENTEROL, LOS ANGELES, CA USA. RP FRIEDMAN, LS (reprint author), MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BULFINCH 127, 32 FRUIT ST, BOSTON, MA 02114 USA. NR 17 TC 42 Z9 42 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0889-8553 J9 GASTROENTEROL CLIN N JI Gastroenterol. Clin. North Am. PD DEC PY 1993 VL 22 IS 4 BP 717 EP 721 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MG990 UT WOS:A1993MG99000002 PM 8307639 ER PT J AU FRIEDMAN, LS AF FRIEDMAN, LS TI GASTROINTESTINAL BLEEDING-I - PREFACE SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA LA English DT Editorial Material RP FRIEDMAN, LS (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BULFINCH 127,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8553 J9 GASTROENTEROL CLIN N JI Gastroenterol. Clin. North Am. PD DEC PY 1993 VL 22 IS 4 BP R11 EP R12 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MG990 UT WOS:A1993MG99000001 ER PT J AU MCCORMICK, MK BUCKLER, A BRUNO, W CAMPBELL, E SHERA, K TORNEY, D DEAVEN, L MOYZIS, R AF MCCORMICK, MK BUCKLER, A BRUNO, W CAMPBELL, E SHERA, K TORNEY, D DEAVEN, L MOYZIS, R TI CONSTRUCTION AND CHARACTERIZATION OF A YAC LIBRARY WITH A LOW-FREQUENCY OF CHIMERIC CLONES FROM FLOW-SORTED HUMAN-CHROMOSOME-9 SO GENOMICS LA English DT Article ID YEAST ARTIFICIAL CHROMOSOMES; TUBEROUS SCLEROSIS; DNA; MANIPULATION; SEQUENCES; STRATEGY; VECTORS; FUSION; PROBE; LOCUS C1 LOS ALAMOS NATL LAB,CTR HUMAN GENOME STUDIES,LOS ALAMOS,NM 87545. LOS ALAMOS NATL LAB,DIV LIFE SCI,LOS ALAMOS,NM 87545. LOS ALAMOS NATL LAB,DIV THEORET,LOS ALAMOS,NM 87545. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. RP MCCORMICK, MK (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 27 TC 23 Z9 23 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD DEC PY 1993 VL 18 IS 3 BP 553 EP 558 DI 10.1016/S0888-7543(05)80355-6 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA MP480 UT WOS:A1993MP48000012 PM 8307565 ER PT J AU GOODMAN, A BELL, DA RICE, LW AF GOODMAN, A BELL, DA RICE, LW TI DNA-PLOIDY STATUS - ITS IMPACT ON EARLY-STAGE ENDOMETRIAL ADENOCARCINOMA SO GYNECOLOGIC ONCOLOGY LA English DT Article ID FLOW CYTOMETRIC DNA; STEROID-RECEPTOR CONCENTRATION; PROGNOSTIC-SIGNIFICANCE; MYOMETRIAL INVASION; SOLID TUMORS; RISK-FACTORS; CARCINOMA; CANCER; RECURRENCE; SURVIVAL C1 TUFTS UNIV,SCH MED,NEW ENGLAND MED CTR,BOSTON,MA 02114. RP GOODMAN, A (reprint author), MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT GYNECOL,FRUIT ST,BOSTON,MA 02114, USA. NR 32 TC 11 Z9 11 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD DEC PY 1993 VL 51 IS 3 BP 355 EP 361 DI 10.1006/gyno.1993.1303 PG 7 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA MW768 UT WOS:A1993MW76800012 PM 8112645 ER PT J AU JACOBY, AF FULLER, AF THOR, AD MUNTZ, HG AF JACOBY, AF FULLER, AF THOR, AD MUNTZ, HG TI PRIMARY LEIOMYOSARCOMA OF THE FALLOPIAN-TUBE SO GYNECOLOGIC ONCOLOGY LA English DT Note ID MIXED MULLERIAN TUMORS; UTERINE SARCOMAS; CHEMOTHERAPY; CARCINOMA; ADRIAMYCIN; IFOSFAMIDE; CISPLATIN; TRIAL C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,VINCENT MEM GYNECOL SERV,BOSTON,MA 02114. NR 23 TC 10 Z9 10 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 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD DEC PY 1993 VL 51 IS 3 BP 404 EP 407 DI 10.1006/gyno.1993.1312 PG 4 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA MW768 UT WOS:A1993MW76800021 PM 8112653 ER PT J AU GOFF, BA AF GOFF, BA TI UNTITLED SO GYNECOLOGIC ONCOLOGY LA English DT Letter ID SMEARS RP GOFF, BA (reprint author), MASSACHUSETTS GEN HOSP,DEPT GYNECOL ONCOL,BOSTON,MA 02114, USA. NR 5 TC 0 Z9 0 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 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD DEC PY 1993 VL 51 IS 3 BP 425 EP 426 PG 2 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA MW768 UT WOS:A1993MW76800028 ER PT J AU LIANG, TJ JEFFERS, LJ REDDY, KR DEMEDINA, M PARKER, IT CHEINQUER, H IDROVO, V RABASSA, A SCHIFF, ER AF LIANG, TJ JEFFERS, LJ REDDY, KR DEMEDINA, M PARKER, IT CHEINQUER, H IDROVO, V RABASSA, A SCHIFF, ER TI VIRAL PATHOGENESIS OF HEPATOCELLULAR-CARCINOMA IN THE UNITED-STATES SO HEPATOLOGY LA English DT Article ID HEPATITIS-B VIRUS; POLYMERASE CHAIN-REACTION; CHRONIC LIVER-DISEASE; RECOMBINANT IMMUNOBLOT ASSAY; NON-A-HEPATITIS; C VIRUS; CHRONIC CARRIERS; SURFACE-ANTIGEN; DNA SEQUENCES; INFECTION AB Chronic hepatitis B virus infection is closely associated with the development of hepatocellular carcinoma, which is a major cause of cancer death worldwide. Recent studies have implicated hepatitis C virus infection as a major pathogenic agent of HBsAg-negative hepatocellular carcinoma. The significance of hepatitis C virus and hepatitis B virus infections in the occurrence of HBsAg-negative hepatocellular carcinoma has not been well established in the United States. We studied 91 HBsAg-negative American patients with hepatocellular carcinoma for evidence of hepatitis C virus or hepatitis B virus infection. These patients had no other predisposing factors to hepatocellular carcinoma. A sensitive polymerase chain reaction was employed to detect hepatitis C virus RNA and hepatitis B virus DNA in serum and liver. Three sets of hepatitis C virus and hepatitis B virus primers were used to optimize the detection of viral genomes. Hepatitis C virus antibodies were measured with second-generation immunoassays. Twenty-six (29%) of these patients carried low levels of hepatitis B virus DNA in either serum, liver/tumor tissue or both. On the basis of the results from serological and polymerase chain reaction analyses of serum and liver, we found that 53 of 91 patients (58%) exhibited evidence of hepatitis C virus infection. When data were combined, 14 patients (15%) had evidence of hepatitis B virus/hepatitis C virus coinfection, whereas 12 (13%) were infected with hepatitis B virus alone and 39 (43%) had hepatitis C virus only. Twenty-six (29%) had no markers of hepatitis B virus or hepatitis C virus infection. All patients with identifiable viral markers had coexisting chronic liver disease. Our study suggests that hepatitis C virus and occult hepatitis B virus infections account for most (71%) hepatocellular carcinoma cases of unknown pathogenesis in the United States. However, in some patients with hepatocellular carcinoma no defined pathogenesis is associated with development of disease. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MED SERV,GASTROINTESTINAL UNIT,JACKSON 812,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV MIAMI,SCH MED,CTR LIVER DIS,MIAMI,FL 33136. VET AFFAIRS MED CTR,MIAMI,FL 33136. FU NCI NIH HHS [CA-54524]; NIDDK NIH HHS [DK-01952] NR 56 TC 150 Z9 153 U1 0 U2 5 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 DEC PY 1993 VL 18 IS 6 BP 1326 EP 1333 DI 10.1016/0270-9139(93)90219-D PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MJ626 UT WOS:A1993MJ62600006 PM 8244256 ER PT J AU WENZEL, SL GELBERG, L BAKHTIAR, L CASKEY, N HARDIE, E REDFORD, C SADLER, N AF WENZEL, SL GELBERG, L BAKHTIAR, L CASKEY, N HARDIE, E REDFORD, C SADLER, N TI INDICATORS OF CHRONIC HOMELESSNESS AMONG VETERANS SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article ID MENTAL-HEALTH; ADULTS; PROGRAM; SHELTER; OLDER; CITY AB Objective: This study sought to develop a set of indicators of chronic homelessness as a basis for better understanding and treatment of the homeless veteran population. Methods: Chi square analysis and the t test or Mann-Whitney U test were used to compare characteristics of veterans who reported long-term homelessness (more than 12 months total since age 18) with those of veterans who reported short-term homelessness (12 months or less). Subjects were 343 homeless male veterans receiving treatment for physical, mental, or substance abuse disorders at the West Los Angeles site of the Domiciliary Care for Homeless Veterans Program. Variables included history of homelessness, employment history, physical and mental health, substance abuse history, social and financial support, criminal history, age, ethnic group, education, military service, and program discharge status. Results: Veterans experiencing long-term homelessness were more likely to be white, to have had a longer period of recent homelessness and a greater number of homeless episodes, to have a poor employment history, to have symptoms of mental and substance abuse disorders, and to have weaker social support. Conclusions: Results show that variables besides duration of lifetime homelessness are important indicators of chronic homelessness. C1 W LOS ANGELES VET AFFAIRS MED CTR,DOMICILIARY CARE HOMELESS VET PROGRAM,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT SOCIOL,10833 LECONTE AVE,ROOM 50-071 CHS,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DIV FAMILY MED,LOS ANGELES,CA 90024. NR 42 TC 18 Z9 18 U1 2 U2 6 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD DEC PY 1993 VL 44 IS 12 BP 1172 EP 1176 PG 5 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA MK091 UT WOS:A1993MK09100009 PM 8132190 ER PT J AU CANCHIS, PW BHAN, AK LANDAU, SB YANG, L BALK, SP BLUMBERG, RS AF CANCHIS, PW BHAN, AK LANDAU, SB YANG, L BALK, SP BLUMBERG, RS TI TISSUE DISTRIBUTION OF THE NON-POLYMORPHIC MAJOR HISTOCOMPATIBILITY COMPLEX CLASS I-LIKE MOLECULE, CD1D SO IMMUNOLOGY LA English DT Article ID INTESTINAL EPITHELIAL-CELLS; THYMIC DIFFERENTIATION; MONOCLONAL-ANTIBODY; EXPRESSION; ANTIGENS; LYMPHOCYTES; CDNA; BETA-2-MICROGLOBULIN; IDENTIFICATION; THYMOCYTES AB The CD1 gene family is composed of five distinct molecules: CD1a, b, c, d and e. CD1a, b and c are primarily expressed thymically with limited extrathymic expression. Preliminary studies have shown that CD1d is primarily expressed extrathymically in gastrointestinal epithelial cells, renal tubular epithelial cells and B cells. This report characterizes the expression of CD1d in a variety of human tissues by immunohistochemistry using two anti-human CD1d monoclonal antibodies (mAb). CD1d was found in a wide range of tissues including the intestine, liver, pancreas, skin, kidney, uterus, conjunctiva, epididymis, thymus and tonsil. Within those tissues CD1d was mainly present in epithelial cells, vascular smooth muscle cells and parenchymal cells. Therefore, the tissue distribution of CD1d is distinct from CD1a-c and classical major histocompatibility complex (MHC) proteins implicating a unique role for CD1d in the immune system. C1 BRIGHAM & WOMENS HOSP,DIV GASTROENTEROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,BOSTON,MA 02114. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02215. FU NIDDK NIH HHS [2P01-DK33506, P30-DK4351, DK44319-01] NR 27 TC 120 Z9 122 U1 1 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD DEC PY 1993 VL 80 IS 4 BP 561 EP 565 PG 5 WC Immunology SC Immunology GA ML181 UT WOS:A1993ML18100008 PM 7508419 ER PT J AU BLAKE, DC RUSSELL, RG AF BLAKE, DC RUSSELL, RG TI DEMONSTRATION OF LIPOPOLYSACCHARIDE WITH O-POLYSACCHARIDE CHAINS AMONG DIFFERENT HEAT-STABLE SEROTYPES OF CAMPYLOBACTER-JEJUNI BY SILVER STAINING OF POLYACRYLAMIDE GELS SO INFECTION AND IMMUNITY LA English DT Note ID PASSIVE HEMAGGLUTINATION; PSEUDOMONAS-AERUGINOSA; NEISSERIA-MENINGITIDIS; THERMOSTABLE ANTIGENS; MACACA-NEMESTRINA; COLI; STRAINS; HETEROGENEITY AB Lipopolysaccharide (LPS) from three human and four monkey isolates of Campylobacter jejuni was extracted in high yields that revealed ladder-like structures in polyacrylamide gels by direct silver staining. These observations demonstrate that C. jejuni possesses LPS with O-chain repeating units typical of the family Enterobacteriaceae. The isolates showed differences in the number and electrophoretic mobility of bands in silver-stained gels. C1 US DEPT VET AFFAIRS,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,PROGRAM COMPARAT MED,BALTIMORE,MD 21201. FU NCRR NIH HHS [RR03123] NR 35 TC 9 Z9 9 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD DEC PY 1993 VL 61 IS 12 BP 5384 EP 5387 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MH823 UT WOS:A1993MH82300060 PM 7693600 ER PT J AU TAYLOR, CR ANDERSON, RR AF TAYLOR, CR ANDERSON, RR TI TREATMENT OF BENIGN PIGMENTED EPIDERMAL LESIONS BY Q-SWITCHED RUBY-LASER SO INTERNATIONAL JOURNAL OF DERMATOLOGY LA English DT Article ID GUINEA-PIG SKIN; ARGON-LASER; TATTOOS; IRRADIATION AB Background. Disorders of cutaneous pigmentation are a common problem, which can cause substantial cosmetic morbidity. Traditional treatments are often ineffective and sometimes associated with further hyperpigmentation, hypopigmentation, or scarring. Because the Q-switched ruby laser has proven useful for the treatment of tattoos and, in a small number of cases, benign disorders of the epidermal melanin, we decided to apply this modality systematically to additional benign pigmented lesions. Methods. Thirty-four benign pigmented epidermal lesions including lentigines, cafe-au-lait macules, and nevi spill in nine white patients were exposed to single pulses of a Q-switched ruby laser (694 nm, 40 ns pulse duration) at 4.5 and/or 7.5 J/cm(2). Results. After one treatment, substantial clearing occurred at each fluence in all lentigines and cafe-au-lait macules. Initial improvement was achieved in a small nevus spilus after two treatments at 4.5 J/cm(2) and a larger nevus spilus after one treatment at 7.5 J/cm(2) with complete removal of the junctional or compound nevi portion but no improvement in the cafe-au-lait portion. Complete return of the background pigment was observed by 1 year. There was no scarring. Immediately after treatment, histology revealed vacuolizaton of keratinocytes and melanocytes, and occasional subepidermal blisters. Conclusions. These findings show that while the Q-switched ruby laser may not be entirely useful for treating nevi spill, it does provide an effective treatment for lentigines and cafe-au-lait macules. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. FU NIAMS NIH HHS [1R3AR38992] NR 25 TC 64 Z9 64 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0011-9059 J9 INT J DERMATOL JI Int. J. Dermatol. PD DEC PY 1993 VL 32 IS 12 BP 908 EP 912 DI 10.1111/j.1365-4362.1993.tb01417.x PG 5 WC Dermatology SC Dermatology GA MJ771 UT WOS:A1993MJ77100021 PM 8125702 ER PT J AU AWWAD, JT AF AWWAD, JT TI FEMUR FRACTURE DURING CESAREAN BREECH DELIVERY SO INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS LA English DT Letter DE FEMUR; FRACTURE; CESAREAN SECTION; BREECH; BIRTH TRAUMA ID SECTION RP AWWAD, JT (reprint author), MASSACHUSETTS GEN HOSP,VINCENT MEM GYNECOL SERV,GURNHAM BLDG,RM 127,BOSTON,MA 02114, USA. NR 4 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0020-7292 J9 INT J GYNECOL OBSTET JI Int. J. Gynecol. Obstet. PD DEC PY 1993 VL 43 IS 3 BP 324 EP 326 DI 10.1016/0020-7292(93)90524-Z PG 3 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA MP633 UT WOS:A1993MP63300014 PM 7907046 ER PT J AU VENTURA, J GREEN, MF SHANER, A LIBERMAN, RP AF VENTURA, J GREEN, MF SHANER, A LIBERMAN, RP TI TRAINING AND QUALITY ASSURANCE WITH THE BRIEF PSYCHIATRIC RATING-SCALE - THE DRIFT BUSTERS SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH LA English DT Article DE BPRS; BPRS TRAINING; BPRS QUALITY ASSURANCE; PSYCHIATRIC SYMPTOM ASSESSMENT; BPRS RELIABILITY ID SCHIZOPHRENIA; RELIABILITY; SYMPTOMS AB Despite the prominence of the Brief Psychiatric Rating Scale (BPRS) in psychiatric research, relatively little has been published about training methods and procedures used to maintain consistency over time of interviewer style and inter-rater reliability. A training and quality assurance program, developed at the UCLA Clinical Research Center for Schizophrenia and Psychiatric Rehabilitation, has relied on an expanded manual with behavioral anchor points that are used when trainees view a series of videotaped BPRSs or conduct live BPRS interviews. Trainees with both advanced and predoctoral degrees were able to achieve and maintain high levels of reliability. RP VENTURA, J (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VET ADM MED CTR, LOS ANGELES, CA 90073 USA. NR 30 TC 560 Z9 563 U1 3 U2 11 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1049-8931 J9 INT J METH PSYCH RES JI Int. J. Methods Psychiatr. Res. PD DEC PY 1993 VL 3 IS 4 BP 221 EP 244 PG 24 WC Psychiatry SC Psychiatry GA MX331 UT WOS:A1993MX33100003 ER PT J AU LEE, SJ LI, ZH SHERMAN, B FOSTER, CS AF LEE, SJ LI, ZH SHERMAN, B FOSTER, CS TI SERUM LEVELS OF TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-6 IN OCULAR CICATRICIAL PEMPHIGOID SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE TUMOR NECROSIS FACTOR; INTERLEUKIN-6; CICATRICIAL PEMPHIGOID; OCULAR IMMUNOLOGY; CYTOKINES ID DISEASES AB Purpose. These studies examined regulation of the cytokines interleukin-6 and tumor necrosis factor-alpha in ocular cicatricial pemphigoid (OCP), a systemic autoimmune disease. Methods. Serum levels of interleukin-6 and tumor necrosis factor-alpha in sera collected from 35 patients with OCP, 29 normal persons and 17 patients with ocular inflammatory diseases were determined using an enzyme-linked immunosorbent assay. Results. Levels of interleukin-6 were significantly decreased in sera of patients with OCP (median, 28.9; range, 7.5 to 136.7 pg/ml, P < 0.001) compared with sera from normal subjects (median, 65.2; range, 21.1 to 303.9 pg/ml). Sera from patients with non-OCP, extraocular inflammatory diseases and uveitis, showed no such decrease. In contrast, tumor necrosis factor-alpha levels were significantly elevated in OCP patients (median, 22.5; range, 8.3 to 44.4 pg/ml, P < 0.001), whereas no such increase was observed in sera from patients with extraocular inflammatory disease or uveitis, compared to normal sera controls (median, 17.4; range, 5 to 27.2 pg/ml). Conclusions. These results suggest that elevated serum tumor necrosis factor-alpha levels and decreased serum interleukin-6 levels can be added to the increasing list of systemic immunologic correlates of active OCP, again emphasizing that OCP is a systemic disease whose primary manifestation is ocular. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,RHODES MOLEC IMMUNOL LAB,BOSTON,MA 02114. NR 10 TC 44 Z9 47 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD DEC PY 1993 VL 34 IS 13 BP 3522 EP 3525 PG 4 WC Ophthalmology SC Ophthalmology GA MN579 UT WOS:A1993MN57900007 PM 8258509 ER PT J AU ANDO, H TWINING, SS YUE, BYJT ZHOU, XY FINI, ME KAIYA, T HIGGINBOTHAM, EJ SUGAR, J AF ANDO, H TWINING, SS YUE, BYJT ZHOU, XY FINI, ME KAIYA, T HIGGINBOTHAM, EJ SUGAR, J TI MMPS AND PROTEINASE-INHIBITORS IN THE HUMAN AQUEOUS-HUMOR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE AQUEOUS HUMOR; GELATINASE; CASEINASE; ZYMOGRAPHY; PROTEINASE INHIBITOR ID HUMAN TRABECULAR MESHWORK; GROWTH-FACTOR-BETA; ALPHA-1-PROTEINASE INHIBITOR; MATRIX METALLOPROTEINASES; PLASMINOGEN-ACTIVATOR; CORNEA; COLLAGENASE; EXPRESSION; ALPHA-2-MACROGLOBULIN; ALPHA2-MACROGLOBULIN AB Purpose. This study was performed to examine the gelatinolytic and caseinolytic activities and the levels of two proteinase inhibitors, alpha1-proteinase inhibitor (alpha1-antitrypsin) and alpha2-macroglobulin, in the human aqueous humor. Methods. Aqueous humor samples were collected during elective surgery in patients with cataracts. Zymography with gelatin- and casein-containing gels was performed. The inhibitors were examined by Western blot analyses, enzyme-linked immunosorbent assay, and dot blot assays. Results. The aqueous humor contained a major band of gelatinolytic activity at a molecular weight of 66 kD and minor bands at 125, 95, and 62 kD. These gelatinases were inhibited by 10 mM ethylenediaminetetraacetic acid (EDTA) or 1,10-phenanthroline. After extended incubation (48 hours), zymography on casein-containing gels showed proteinase bands with molecular weights in the 80- to 84-kD range. Additional bands at 68 and 48 kD also were observed. All the caseinase activities were inhibited by 10 mM phenylmethylsulfonyl fluoride and 1 mug/ml aprotinin. No inhibition was observed with 5 mM EDTA, 5 muM E-64, or 1 muM pepstatin. These results indicated that the caseinases are serine proteinases. Western blot analysis showed a 53-kD alpha1-proteinase inhibitor band in the aqueous humor. the concentration was 32.2 +/- 9.9 mug/ml, constituting approximately 15% of the total protein. A 360-kD protein band immunoreactive to anti-alpha2-macroglobulin also was detected. Its level in the aqueous humor was 3.2 +/- 1.3 mug/ml. Conclusions. The gelatinases, serine-like proteinases, and proteinase inhibitors found in the aqueous humor may participate in the remodeling of extracellular matrices in the trabecular meshwork and other tissues bordering the anterior chamber. C1 UNIV ILLINOIS,COLL MED,DEPT OPHTHALMOL & VISUAL SCI,CHICAGO,IL 60680. MED COLL WISCONSIN,DEPT BIOCHEM,MILWAUKEE,WI 53226. MED COLL WISCONSIN,DEPT OPHTHALMOL,MILWAUKEE,WI 53226. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. SEIREI HAMAMATSU GEN HOSP,DEPT OPHTHALMOL,HAMAMATSU,JAPAN. UNIV MICHIGAN,DEPT OPHTHALMOL,ANN ARBOR,MI 48109. FU NEI NIH HHS [EY05628, EY06663, EY03890] NR 49 TC 63 Z9 65 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD DEC PY 1993 VL 34 IS 13 BP 3541 EP 3548 PG 8 WC Ophthalmology SC Ophthalmology GA MN579 UT WOS:A1993MN57900010 PM 7505006 ER PT J AU CAI, XX FOSTER, CS LIU, JJ KUPFERMAN, AE FILIPEC, M COLVIN, RB LEE, SJ AF CAI, XX FOSTER, CS LIU, JJ KUPFERMAN, AE FILIPEC, M COLVIN, RB LEE, SJ TI ALTERNATIVELY SPLICED FIBRONECTIN MOLECULES IN THE WOUNDED CORNEA - ANALYSIS BY PCR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE FIBRONECTIN ISOFORMS; CORNEA; WOUND HEALING; EPITHELIAL WOUNDS ID GROWTH-FACTOR-BETA; AUTOLOGOUS FIBRONECTIN; RABBIT CORNEA; RAT; MIGRATION; CELLS AB Purpose. To determine whether certain fibronectin isoforms participate in corneal epithelial wound healing, the authors used the polymerase chain reaction to detect different splicing patterns of the EIIIA segment of fibronectin mRNA in epithelial scrape-wounded cornea of rats. Methods. Specific fibronectin cDNA sequences synthesized from rat cornea with total RNA were amplified with various sets of synthetic oligonucleotidc primers. Results. The authors detected both the EIIIA+ and EIIIA- fibronectin mRNA isoforms during corneal wound healing. The kinetics of corneal expression of both total fibronectin mRNA and the EIIIA- fibronectin mRNA isoform was polyphasic; an initial decrease was followed by an increase at 45 minutes, a second increase at 2 hours, and a third increase at 4 days after wounding. EIIIA+ fibronectin mRNA, not found in normal cornea, also was detected during healing. Conclusions. The expression of total fibronectin mRNA and both the EIIIA+ and EIIIA- fibronectin mRNA is upregulated during corneal epithelial wound healing. The expression of EIIIA+ fibronectin mRNA during wound healing, a fibronectin isoform that was highly expressed in embryonic tissue, suggests that this fibronectin isoform is involved functionally in corneal wound healing. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,RHOADS MOLEC IMMUNOL LAB,BOSTON,MA 02114. FU NCI NIH HHS [R37CA208822] NR 31 TC 31 Z9 31 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD DEC PY 1993 VL 34 IS 13 BP 3585 EP 3592 PG 8 WC Ophthalmology SC Ophthalmology GA MN579 UT WOS:A1993MN57900016 PM 8258516 ER PT J AU WEISSLEDER, R BOGDANOV, A FRANK, H NOSSIFF, N BOGDANOVA, A SCHAFFER, BK BRADY, T WITTENBERG, J AF WEISSLEDER, R BOGDANOV, A FRANK, H NOSSIFF, N BOGDANOVA, A SCHAFFER, BK BRADY, T WITTENBERG, J TI A DRUG SYSTEM (PDH) FOR INTERVENTIONAL RADIOLOGY SYNTHESIS, PROPERTIES, AND EFFICACY SO INVESTIGATIVE RADIOLOGY LA English DT Article DE INTERVENTIONAL RADIOLOGY; ANGIOGRAPHY; PHARMACEUTICALS; EMBOLIZATION; POLYETHYLENEGLYCOL; HYDROGEL; MAGNETIC RESONANCE IMAGING ID MICROSPHERES; RELEASE; EMBOLIZATION; DOXORUBICIN; CARCINOMA; DELIVERY; ALBUMIN; ACID; OIL AB RATIONALE AND OBJECTIVES. The authors synthesized and tested a novel hydrogel system proposed for use in extra- and intravascular radiologic interventions, such as chemoembolizations and embolizations, and as a vehicle for sustained drug release. MATERIALS. The material was specifically designed to meet the prerequisites of biodegradation, biocompatibility, low immunogenicity, low toxicity, and easy use. The material consists of a protein backbone cross-linked with activated bifunctional polyethyleneglycol (PEG) derivatives (PEG-derivatized hydrogel, [PDH]) to which are attached therapeutic (e.g., doxorubicin, a chemotherapeutic agent = PDH-dx) or diagnostic labels (e.g. Gd-DTPA). RESULTS. PDH-dx effectively reduced the risk of local tumor recurrence in a rat model when implanted locally after surgical tumor removal. After administration, PDH is degraded by proteases released from macrophages; implantations of 1 mL samples into paraspinal muscles of rats were completely absorbed within 4 weeks and its constituents were metabolized. Antibody titers (total Ig response) against the PDH were not detectable 1 week after implantation, whereas protein control substances elicited a strong response. CONCLUSIONS. PDH and its derivatives are relatively nontoxic, biodegradable materials for use in radiologic interventions and as a vehicle for sustained drug release. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP WEISSLEDER, R (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,MRPP,BOSTON,MA 02114, USA. NR 19 TC 2 Z9 2 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD DEC PY 1993 VL 28 IS 12 BP 1083 EP 1089 DI 10.1097/00004424-199312000-00001 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MU843 UT WOS:A1993MU84300001 PM 8307710 ER PT J AU BENNETT, RL GILMAN, SC GEORGE, L GUZE, PA BENNETT, CL AF BENNETT, RL GILMAN, SC GEORGE, L GUZE, PA BENNETT, CL TI IMPROVED OUTCOMES IN INTENSIVE-CARE UNITS FOR AIDS-RELATED PNEUMOCYSTIS-CARINII PNEUMONIA - 1987-1991 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Article DE PNEUMOCYSTIS-CARINII PNEUMONIA; INTENSIVE CARE UNIT; OUTCOME; SURVIVAL RATE ID ACQUIRED IMMUNODEFICIENCY SYNDROME; RESPIRATORY-FAILURE; SURVIVAL AB Respiratory failure due to Pneumocystis carinii pneumonia (PCP) is the most common complication requiring an intensive care unit (ICU) for persons with AIDS. In this study, we evaluated patterns of ICU use for ICU patients with first-episode PCP in 15 Veterans Administration Medical Centers from 1987 to 1991. Twelve percent of all patients with PCP received care in the ICU. The survival rates improved steadily during these years. Although there was little variation in the relative frequency of ICU use, the effectiveness of ICU use appeared to improve over time. In the more recent years, relatively more survivors and relatively fewer nonsurvivors received care in an ICU. Changes in medical practice such as adjunctive use of steroids for severe cases of PCP and more effective use of scarce resources may account for the improved survival rates for patients with PCP who are treated in an ICU. C1 DURHAM VET AFFAIRS, DIV HLTH SERV RES & DEV 152, 508 FULTON ST, DURHAM, NC 27705 USA. VET AFFAIRS WESTERN REG SPECIAL STUDIES GRP, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS HOSP, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. UNIV CALIF IRVINE, SCH MED, IRVINE, CA 92717 USA. DUKE UNIV, DURHAM, NC 27706 USA. FU AHRQ HHS [1R01HS06494-01] NR 12 TC 15 Z9 15 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. PD DEC PY 1993 VL 6 IS 12 BP 1319 EP 1321 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MM128 UT WOS:A1993MM12800006 PM 8254469 ER PT J AU COTTON, DJ FINKELSTEIN, DM HE, WL FEINBERG, J AF COTTON, DJ FINKELSTEIN, DM HE, WL FEINBERG, J TI DETERMINANTS OF ACCRUAL OF WOMEN TO A LARGE, MULTICENTER CLINICAL-TRIALS PROGRAM OF HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Article DE WOMEN; CLINICAL TRIALS; HIV INFECTION; AIDS ID EPIDEMIC; DRUG; AIDS; AGE AB To determine factors influencing the enrollment of women in a large multicenter human immunodeficiency virus (HIV) clinical trials program in the United States, we analyzed enrollment and demographic data of the AIDS Clinical Trials Group (ACTG) during the period 1987-90. Women comprised 6.7% of 11,909 ACTG participants enrolled in 1987-90. Women entering ACTG trials were significantly more likely to be white (48.5%) and less likely to have ever used i.v. drugs (22.6%) than U.S. women reported to have AIDS (26.5% were white; 51.0% had ever used i.v. drugs, p < 0.0001). In a multiple logistic regression model, specific attributes of individual trials did not influence enrollment of women with the exception that trials that targeted asymptomatic persons had greater enrollment of women. There was wide variation among research units in the percentage of women enrolled (1.0-37.5%), and evidence of significant regional variation in the ability of units to recruit available women. Units with female principal or coprincipal investigators had more than twice the percentage of female enrollment as units headed by men (10.8 vs. 5.3%, p < 0.001). Enrollment of women in a large HIV clinical trials program was low and appeared to be influenced more by demographic and geographic factors that attributes of specific trials. An apparent positive influence of female leadership on the enrollment of women warrants further study. C1 BETH ISRAEL HOSP, DEPT MED, DIV INFECT DIS, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH PUBL HLTH, CTR STAT & DATA ANAL, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, CTR BIOSTAT, BOSTON, MA 02114 USA. JOHNS HOPKINS UNIV, BALTIMORE, MD 21218 USA. FU NIAID NIH HHS [2-UO1-AI-27668, N0-AI-95030] NR 20 TC 38 Z9 38 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. PD DEC PY 1993 VL 6 IS 12 BP 1322 EP 1328 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA MM128 UT WOS:A1993MM12800007 PM 8254470 ER PT J AU ARSTILA, T JACOBY, GA HUOVINEN, P AF ARSTILA, T JACOBY, GA HUOVINEN, P TI EVALUATION OF 5 DIFFERENT METHODS TO PREPARE BACTERIAL EXTRACTS FOR THE IDENTIFICATION OF BETA-LACTAMASES BY ISOLECTRIC FOCUSING SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID GRAM-NEGATIVE BACTERIA; SONICATION C1 TURKU UNIV,DEPT MED MICROBIOL,SF-20520 TURKU,FINLAND. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. RP ARSTILA, T (reprint author), NATL PUBL HLTH INST,ANTIMICROBIAL RES UNIT,SF-20520 TURKU,FINLAND. RI Huovinen, Pentti/C-1917-2009 FU NIAID NIH HHS [AI20415] NR 18 TC 8 Z9 8 U1 1 U2 2 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD DEC PY 1993 VL 32 IS 6 BP 809 EP 816 DI 10.1093/jac/32.6.809 PG 8 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA MQ600 UT WOS:A1993MQ60000004 PM 8144421 ER PT J AU GUTTMANN, D SCHMALZRIED, TP JASTY, M HARRIS, WH AF GUTTMANN, D SCHMALZRIED, TP JASTY, M HARRIS, WH TI LIGHT-MICROSCOPIC IDENTIFICATION OF SUBMICRON POLYETHYLENE WEAR DEBRIS SO JOURNAL OF APPLIED BIOMATERIALS LA English DT Article AB A simple, yet specific, means to identify submicron polyethylene (PE) particles in routine histologic sections would be practically useful. We have previously reported a very fine, diffuse, birefringence (when viewed under polarized light) in the cytoplasm of phagocytic cells from around total hip replacements (THRs) with a PE acetabular bearing and proposed that this finding was caused by multiple submicron PE particles. In order to determine the specificity of this light microscopic finding, we have analyzed a wide range of specimens (N = 27), characterized by a foreign-body inflammatory response to both biologic and prosthetic material, that do not contain PE. In no case was there any suggestion of the diffuse cytoplasmic birefringence that is characteristic of specimens from THRs with a PE acetabular bearing surface. This study indicates that, within the range of orthopedic implant materials and designs currently in use, this diffuse birefringence is a specific finding and it represents a simple, practical, and useful method for light microscopic identification of submicron PE. (C) 1993 John Wiley & Sons, Inc. C1 UNIV CALIF LOS ANGELES, HARBOR MED CTR, 1000 W CARSON ST, TORRANCE, CA 90509 USA. ORTHOPED HOSP, INST JOINT REPLACEMENT, LOS ANGELES, CA 90007 USA. MASSACHUSETTS GEN HOSP, ORTHOPAED BIOMECH LAB, BOSTON, MA 02114 USA. NR 7 TC 30 Z9 30 U1 0 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1045-4861 J9 J APPL BIOMATER JI J. Appl. Biomater. PD WIN PY 1993 VL 4 IS 4 BP 303 EP 307 DI 10.1002/jab.770040404 PG 5 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA MH534 UT WOS:A1993MH53400003 ER PT J AU SCHMALZRIED, TP JASTY, M ROSENBERG, A HARRIS, WH AF SCHMALZRIED, TP JASTY, M ROSENBERG, A HARRIS, WH TI HISTOLOGIC IDENTIFICATION OF POLYETHYLENE WEAR DEBRIS USING OIL RED O-STAIN (VOL 4, PG 119, 1993) SO JOURNAL OF APPLIED BIOMATERIALS LA English DT Correction, Addition C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SCHMALZRIED, TP (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,DEPT ORTHOPAED SURG,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1045-4861 J9 J APPL BIOMATER JI J. Appl. Biomater. PD WIN PY 1993 VL 4 IS 4 BP 363 EP 363 PG 1 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA MH534 UT WOS:A1993MH53400012 ER PT J AU MORALES, CF ANZUETO, A ANDRADE, F LEVINE, SM MAXWELL, LC LAWRENCE, RA JENKINSON, SG AF MORALES, CF ANZUETO, A ANDRADE, F LEVINE, SM MAXWELL, LC LAWRENCE, RA JENKINSON, SG TI DIETHYLMALEATE PRODUCES DIAPHRAGMATIC IMPAIRMENT AFTER RESISTIVE BREATHING SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE RESPIRATORY MUSCLES; DIAPHRAGM; FREE RADICALS; EXERTION; GLUTATHIONE; ANTIOXIDANT; MUSCLE FATIGUE; CONTRACTILE PROPERTIES; OXIDIZED GLUTATHIONE; GLUTATHIONE REDOX CYCLE ID EXHAUSTIVE EXERCISE; SKELETAL-MUSCLE; RAT DIAPHRAGM; GLUTATHIONE; METABOLISM; ACETYLCYSTEINE; PERFORMANCE; DAMAGE; CYCLE AB Formation of oxygen-derived free radicals and activation of the glutathione (GSH) redox cycle has been associated with impaired rat diaphragm performance. Diethylmaleate (DEM) given intraperitoneally irreversibly conjugates with GSH, resulting in marked decreases in tissue concentrations of GSH. We have investigated the effects of acute GSH depletion by DEM on diaphragmatic function during resistive breathing (RB) in the rat. The experimental groups were 1) control, 2) DEM alone, 3) RB, and 4) DEM with RB (DEM + RB). RB was obtained by inspiratory RB until the rats were unable to sustain 70% of maximum airway opening pressure. A portion of the diaphragm was frozen for biochemical assays, and the rest of the diaphragm was prepared for measurement of in vitro contractile properties, including maximum tetanic tension, twitch tension, force-frequency curves, and contraction times. DEM treatment produced a profound depletion of GSH in the DEM and DEM + RB groups. Neither DEM nor RB alone significantly altered diaphragm contractile properties. In DEM + RB rats, however, there was a significant decrease in maximum tetanic tension, twitch tension, and tetanic tension. These data reveal that DEM produced an acute depletion of GSH in the diaphragm without impairment of the muscle in nonstressed rats. In the presence of DEM-induced GSH depletion, RB did result in marked diaphragm impairment. The depletion of GSH and the subsequent impairment in diaphragm contractility after RB suggest that GSH may play an important role in protecting the diaphragm against oxidative stress associated with RB. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. WILFORD HALL USAF MED CTR,SAN ANTONIO,TX 78236. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 FU NHLBI NIH HHS [HL-32824] NR 32 TC 21 Z9 21 U1 0 U2 0 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 DEC PY 1993 VL 75 IS 6 BP 2406 EP 2411 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA MN705 UT WOS:A1993MN70500010 PM 8125857 ER PT J AU OCONNELL, JX ROSENTHAL, DI MANKIN, HJ ROSENBERG, AE AF OCONNELL, JX ROSENTHAL, DI MANKIN, HJ ROSENBERG, AE TI SOLITARY OSTEOMA OF A LONG-BONE - A CASE-REPORT SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. RP OCONNELL, JX (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 18 TC 8 Z9 8 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD DEC PY 1993 VL 75A IS 12 BP 1830 EP 1834 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MN144 UT WOS:A1993MN14400014 PM 8258555 ER PT J AU GELBERMAN, RH EATON, R URBANIAK, JR AF GELBERMAN, RH EATON, R URBANIAK, JR TI PERIPHERAL-NERVE COMPRESSION SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID CARPAL-TUNNEL SYNDROME; FAST AXONAL-TRANSPORT; RABBIT VAGUS NERVE; COMPLICATIONS; ENTRAPMENT; PRESSURES; FIBERS C1 ST LUKES ROOSEVELT HOSP,CTR HAND SURG,NEW YORK,NY 10019. DUKE UNIV,MED CTR,DURHAM,NC 27710. RP GELBERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,WACC-527,BOSTON,MA 02114, USA. NR 97 TC 32 Z9 32 U1 0 U2 2 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD DEC PY 1993 VL 75A IS 12 BP 1854 EP 1878 PG 25 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MN144 UT WOS:A1993MN14400018 ER PT J AU SPRINGFIELD, D AF SPRINGFIELD, D TI UNTITLED SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Letter RP SPRINGFIELD, D (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 2 Z9 2 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD DEC PY 1993 VL 75A IS 12 BP 1880 EP 1880 PG 1 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MN144 UT WOS:A1993MN14400022 PM 8258559 ER PT J AU DEALMEIDA, JB DOHERTY, J AUSIELLO, DA STOW, JL AF DEALMEIDA, JB DOHERTY, J AUSIELLO, DA STOW, JL TI BINDING OF THE CYTOSOLIC P200 PROTEIN TO GOLGI MEMBRANES IS REGULATED BY HETEROTRIMERIC G-PROTEINS SO JOURNAL OF CELL SCIENCE LA English DT Article DE GOLGI; G PROTEIN; P200 ID BREFELDIN-A; PERTUSSIS-TOXIN; BETA-COP; GUANINE-NUCLEOTIDE; CELLS; ARF; MASTOPARAN; TRANSPORT; SECRETION; EXCHANGE AB The formation of vesicles for protein trafficking requires the dynamic binding of cytosolic coat proteins onto Golgi membranes and this binding is regulated by a variety of GTPases, including heterotrimeric G proteins. We have previously shown the presence of the pertussis toxin-sensitive Galpha(i-3) protein on Golgi membranes and demonstrated a functional role for Galpha(i-3) in the trafficking of secretory proteins through the Golgi complex. We have also described a brefeldin A-sensitive phosphoprotein, p200, which is found in the cytoplasm and on Golgi membranes. The present study investigations the role of heterotrimeric G proteins in the regulation of p200 binding to Golgi membranes. An in vitro binding assay was used to measure the binding of cytosolic p200 to LLC-PK1 cell microsomal membranes and to purified rat liver Golgi membranes in the presence of specific activators of G proteins. The binding of p200 to Golgi membranes was compared to that of the coatomer protein beta-COP, for which G protein-dependent membrane binding has previously been established. Membrane binding of both p200 and beta-COP was induced maximally by activation of all G proteins in the presence of GTPgammaS. More selective activation of the heterotrimeric G proteins, with AlFn or mastoparan, also induced membrane binding of p200 and beta-COP. Pertussis toxin pretreatment of Golgi membranes, to selectively inactivate Galpha(i-3), reduced the AlFn and mastoparan-induced binding of p200 to Golgi membranes, whereas no significant effect of pertussis toxin on beta-COP binding was found in this assay. The effect of pertussis toxin thus implicates Galpha(i-3), as one component of a regulatory pathway, in the binding of cytosolic p200 to Golgi membranes. The effects of AlFn and pertussis toxin on p200 membrane binding were also shown in intact cells by immunofluorescence staining. AlFn treatment of cells induced translocation of p200 from the cytoplasm onto the Golgi complex, resulting in a conformational change in some Golgi membranes. The translocation of p200 was blocked by pretreatment of intact NRK cells with pertussis toxin. The data presented here support the conclusion that the binding of the p200 protein to Golgi membranes involves regulation by the pertussis toxin-sensitive heterotrimeric G proteins, specifically the Galpha(i-3) protein. C1 MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02129 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02129 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02129 USA. OI Stow, Jennifer/0000-0002-5409-9101 FU NIDDK NIH HHS [P0DK38452] NR 35 TC 29 Z9 29 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 DEC PY 1993 VL 106 BP 1239 EP 1248 PN 4 PG 10 WC Cell Biology SC Cell Biology GA MP529 UT WOS:A1993MP52900022 PM 8126104 ER PT J AU PUGLIESE, A SOLIMENA, M AWDEH, ZL ALPER, CA BUGAWAN, T ERLICH, HA DECAMILLI, P EISENBARTH, GS AF PUGLIESE, A SOLIMENA, M AWDEH, ZL ALPER, CA BUGAWAN, T ERLICH, HA DECAMILLI, P EISENBARTH, GS TI ASSOCIATION OF HLA-DQB1-ASTERISK-0201 WITH STIFF-MAN SYNDROME SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID ISLET CELL ANTIBODIES; GLUTAMIC-ACID DECARBOXYLASE; DEPENDENT DIABETES-MELLITUS; AUTOANTIBODIES; POLYMORPHISM AB Stiff-man syndrome (SMS) is a rare disorder of the central nervous system of probable autoimmune origin. Patients with SMS often have other autoimmune diseases, in particular type I (insulin-dependent) diabetes mellitus (IDDM). Approximately 60% of patients with SMS have high titers of autoantibodies against the enzyme glutamic acid decarboxylase, Similar to SMS, the majority of patients with IDDM have autoantibodies against glutamic acid decarboxylase at or before diabetes onset, although usually at a lower titer and with a different reaction pattern than patients with SMS. To investigate the immunogenetic basis of SMS, we HLA-typed 18 patients with the disease. Seventy-two percent carried the DQB1*0201 allele (13 of 18, P = 0.02 vs. 18 of 48 controls), indicating that SMS is associated with this allele. DQB1*0201 is also a susceptibility allele for IDDM and other autoimmune diseases. Patients with SMS carried the IDDM-protective DQB1*0602 allele and other sequence-related DQB1*06 alleles with the same frequency observed in controls. In contrast, these alleles are rarely found in IDDM. Five of 8 (62.5%) SMS patients lacking a DQB1*06 allele were diabetic in contrast to only 2 of 10 (20%) with a DQB1*06 allele (P = 0.08), suggesting that the presence of DQB1*0602 or other DQB1*06 alleles may be associated with a reduced prevalence of diabetes among patients with SMS. C1 UNIV COLORADO, HLTH SCI CTR, BARBARA DAVIS CTR CHILDHOOD DIABET, DENVER, CO 80262 USA. YALE UNIV, SCH MED,HOWARD HUGHES MED INST,DEPT CELL BIOL, RES LABS, NEW HAVEN, CT USA. HARVARD UNIV, SCH MED, CTR BLOOD RES, BOSTON, MA USA. ROCHE MOLEC SYST INC, DEPT HUMAN GENET, ALAMEDA, CA USA. RI Solimena, Michele/E-1275-2011 FU NIDDK NIH HHS [DK-33790, DK-39233, DK-32083] NR 19 TC 33 Z9 33 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 DEC PY 1993 VL 77 IS 6 BP 1550 EP 1553 DI 10.1210/jc.77.6.1550 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MM202 UT WOS:A1993MM20200021 PM 8263140 ER PT J AU HAFFNER, SM MYKKANEN, L VALDEZ, RA KATZ, MS AF HAFFNER, SM MYKKANEN, L VALDEZ, RA KATZ, MS TI RELATIONSHIP OF SEX-HORMONES TO LIPIDS AND LIPOPROTEINS IN NONDIABETIC MEN SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID CARDIOVASCULAR RISK-FACTORS; HEPATIC TRIGLYCERIDE LIPASE; ANABOLIC-STEROID THERAPY; POST-MENOPAUSAL WOMEN; BODY-FAT DISTRIBUTION; HEALTHY ADULT MEN; BINDING GLOBULIN; DEHYDROEPIANDROSTERONE SULFATE; INSULIN-RESISTANCE; POSTMENOPAUSAL WOMEN AB Although many studies show that increased androgenicity is associated with increased triglyceride (TG) and decreased high density lipoprotein cholesterol in both pre- and postmenopausal women, relatively few data are available on the association of sex hormones to lipids and lipoproteins in men. We examined the association of sex hormone-binding globulin (SHBG), total and free testosterone, dehydroepiandrosterone sulfate (DHEA-SO4), and estradiol with lipids and lipoproteins in 178 nondiabetic men from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. The TG concentration was significantly inversely related to SHBG (r = -0.22), free testosterone (r = -0.15), total testosterone (r = -0.22), and DHEA-SO4 (r = -0.16). High density lipoprotein (HDL) cholesterol was significantly positively correlated to SHBG (r = 0.21), free testosterone (r = 0.15), total testosterone (I = 0.17), and DHEA-SO4 (r = 0.16). Total testosterone was significantly related to total cholesterol (r = -0.17) and low density lipoprotein cholesterol (r = -0.15). After adjustment for age, body mass index, waist to hip ratio, and glucose and insulin concentrations, TG concentrations remained significantly related to SHBG (r = -0.20), free testosterone (r = -0.15), and DHEA-SO4 (r = -0.18), and HDL cholesterol remained significantly associated with SHBG (r = 0.17), free testosterone (r = 0.15), total testosterone (r = 0.14), and DHEA-SO4 (r = 0.16). In conclusion, we observed a less atherogenic lipid and lipoprotein profile with increased testosterone concentrations. This was not explained by differences in glucose or insulin concentrations. However, sex hormones explained only a small percentage of the variation in total TG and HDL cholesterol concentrations. These findings are in striking contrast to data from women, in whom increased androgenicity is strongly associated with increased TG and decreased HDL cholesterol levels. C1 AUDIE L MURPHY MEM VET ADM MED CTR, CTR GERIATR RES EDUC & CLIN, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV CLIN EPIDEMIOL, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV GERIATR & GERONTOL, SAN ANTONIO, TX 78284 USA. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X FU NHLBI NIH HHS [NHLBI R01-HL-24799, NHLBI R37-HL-36820] NR 50 TC 150 Z9 155 U1 0 U2 1 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 DEC PY 1993 VL 77 IS 6 BP 1610 EP 1615 DI 10.1210/jc.77.6.1610 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MM202 UT WOS:A1993MM20200031 PM 8263149 ER PT J AU GANZINI, L LEE, MA HEINTZ, RT BLOOM, JD AF GANZINI, L LEE, MA HEINTZ, RT BLOOM, JD TI DEPRESSION, SUICIDE, AND THE RIGHT TO REFUSE LIFE-SUSTAINING TREATMENT SO JOURNAL OF CLINICAL ETHICS LA English DT Note C1 OREGON HLTH SCI UNIV,DEPT PSYCHIAT,PORTLAND,OR 97201. DAMMASCH STATE HOSP,WILSONVILLE,OR. RP GANZINI, L (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR, USA. NR 12 TC 5 Z9 5 U1 0 U2 0 PU UNIV PUBL GROUP, INC PI FREDERICK PA 12 SOUTH MARKET ST, STE 301, FREDERICK, MD 21701 SN 1046-7890 J9 J CLIN ETHIC JI J. Clin. Ethics PD WIN PY 1993 VL 4 IS 4 BP 337 EP 340 PG 4 WC Ethics; Social Sciences, Biomedical SC Social Sciences - Other Topics; Biomedical Social Sciences GA MM314 UT WOS:A1993MM31400012 PM 7803833 ER PT J AU HALVORSEN, YDC BURSELL, SE WILKISON, WO CLERMONT, AC BRITTIS, M MCGOVERN, TJ SPIEGELMAN, BM AF HALVORSEN, YDC BURSELL, SE WILKISON, WO CLERMONT, AC BRITTIS, M MCGOVERN, TJ SPIEGELMAN, BM TI VASODILATION OF RAT RETINAL MICROVESSELS INDUCED BY MONOBUTYRIN - DYSREGULATION IN DIABETES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ADIPOCYTE; ANGIOGENESIS; DIABETES; LIPID; VASODILATION ID 3T3 ADIPOCYTES; BLOOD-FLOW; MELLITUS; MICROCIRCULATION; ANGIOGENESIS; STIMULATION; CIRCULATION AB 1-Butyryl-glycerol (monobutyrin) is a simple lipid product of adipocytes with angiogenic activity. Recent studies have shown that the biosynthesis of this compound is tightly linked to lipolysis, a process associated with changes in blood flow. We now present data indicating that monobutyrin is an effective vasodilator of rodent blood vessels using a fluorescent retinal angiogram assay. The vasodilatory activity of monobutyrin is potent (ED50 = 3.3 x 10(-7) M), dose dependent, and stereospecific. Because diabetes represents a catabolic, lipolytic state with numerous vascular complications, we examined the action and regulation of monobutyrin in insulin-deficient diabetic rats. Serum levels of monobutyrin in streptozotocin-induced diabetic rats were greatly elevated compared to normal animals. At the same time, the retinal vessels of the diabetic animals develop a resistance to the vasodilatory activity of monobutyrin. These results demonstrate a role for monobutyrin in the control of vascular tone and suggest a possible involvement in the pathology of diabetes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BEETHAM EYE INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. FU NIDDK NIH HHS [5F32DK08277] NR 25 TC 16 Z9 16 U1 0 U2 1 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 DEC PY 1993 VL 92 IS 6 BP 2872 EP 2876 DI 10.1172/JCI116908 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA ML643 UT WOS:A1993ML64300043 PM 8254042 ER PT J AU LENCER, WI DEALMEIDA, JB MOE, S STOW, JL AUSIELLO, DA MADARA, JL AF LENCER, WI DEALMEIDA, JB MOE, S STOW, JL AUSIELLO, DA MADARA, JL TI ENTRY OF CHOLERA-TOXIN INTO POLARIZED HUMAN INTESTINAL EPITHELIAL-CELLS - IDENTIFICATION OF AN EARLY BREFELDIN-A SENSITIVE EVENT REQUIRED FOR A(1)-PEPTIDE GENERATION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CHOLERA TOXIN; BREFELDIN-A; VESICULAR TRANSPORT; CELL POLARITY; CL- SECRETION ID ADP-RIBOSYLATION FACTOR; PERIPHERAL MEMBRANE-PROTEIN; TRANS-GOLGI NETWORK; ADENYLATE-CYCLASE; MDCK CELLS; ENDOPLASMIC-RETICULUM; SELECTIVE-INHIBITION; PERMEABILIZED CELLS; ORGANELLE STRUCTURE; SECRETORY PROTEINS AB The effect of brefeldin-A (BFA), a reversible inhibitor of vesicular transport, on cholera toxin (CT)-induced Cl secretion (I(sc)) was examined in the polarized human intestinal cell line, T84. Pretreatment of T84 monolayers with 5 muM BFA reversibly inhibited I(sc) in response to apical or basolateral addition of 120 nM CT (2.4+/-0.5 vs. 68+/-3 muA/cm2, n = 5). In contrast, BFA did not inhibit I(sc) responses to the cAMP agonist VIP (63+/-7 muA/cm2). BFA had no effect on cell surface binding and endocytosis of a functional fluorescent CT analog or on the dose dependency of CT induced P-32-NAD ribosylation of Gsalpha in vitro. In contrast, BFA completely inhibited (> 95%) the ability of T84 cells to reduce CT to the enzymatically active A1-peptide. BFA had to be added within the first 10 min of CT exposure to inhibit Cr-elicited I(sc). The early BFA-sensitive step occurred before a temperature-sensitive step essential for apical CT action. These studies show that sequential steps are required for a biological response to apical CT: (a) binding to cell surfaces and rapid endocytosis; (b) early, BFA-sensitive vesicular transport essential for reduction of the A1-peptide; and (c) subsequent temperature-sensitive translocation of a signal (the A1-peptide or possibly ADP-ribose-Gsalpha) to the basolateral domain. C1 MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, CTR DIGEST DIS, BOSTON, MA 02115 USA. RP CHILDRENS HOSP MED CTR, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA 02115 USA. OI Stow, Jennifer/0000-0002-5409-9101 FU NIDDK NIH HHS [DK35932, DK48106, DK33506] NR 72 TC 72 Z9 72 U1 0 U2 0 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 EI 1558-8238 J9 J CLIN INVEST JI J. Clin. Invest. PD DEC PY 1993 VL 92 IS 6 BP 2941 EP 2951 DI 10.1172/JCI116917 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA ML643 UT WOS:A1993ML64300052 PM 8254049 ER PT J AU AISENBERG, AC AF AISENBERG, AC TI PRIMARY LARGE-CELL LYMPHOMA OF THE MEDIASTINUM SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID DIFFUSE LARGE-CELL; NON-HODGKINS LYMPHOMA; B-CELLS; SCLEROSIS; HYPERPLASIA; ENTITY; SUBSET; THYMUS; TUMOR RP AISENBERG, AC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 37 TC 21 Z9 21 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 DEC PY 1993 VL 11 IS 12 BP 2291 EP 2294 PG 4 WC Oncology SC Oncology GA MK118 UT WOS:A1993MK11800001 PM 8246017 ER PT J AU PONTIUS, AA AF PONTIUS, AA TI SPATIAL REPRESENTATION, MODIFIED BY ECOLOGY - FROM HUNTER-GATHERERS TO CITY DWELLERS IN INDONESIA SO JOURNAL OF CROSS-CULTURAL PSYCHOLOGY LA English DT Article ID FACE; LITERACY; PHASES AB Performance with the Kohs Block Design and Face Drawing Tests were assessed in two ecologically distinct groups of healthy Indonesians: 196 urbanized subjects and 130 near ''hunter-gatherers'' (Dani and Asmat from inland West New Guinea). Analysis of subjects' error patterns on the block design construction tasks revealed disproportionally and significantly higher percentages of ''nonrandom'' configuration-preserving errors by Dani and Asmat subjects (22.18%) than by urbanized subjects, whose errors were fewer but significantly more random and unrelated to the target design. Relations, ratios, and orientation among features within a design pattern tended to be neglected by the Dani and Asmat but rarely by the urbanized subjects (9.78%). On the face drawing task, 81% of Asmat and Dani subjects drew schematized versions (the ''neolithic'' face pattern), whereas only 39% of urbanized subjects did so. Results suggest that the impact of ecological context on neuropsychologic functioning is profound, influencing even basic visuospatial cognitive processing. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP PONTIUS, AA (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 32 TC 4 Z9 5 U1 0 U2 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0022-0221 J9 J CROSS CULT PSYCHOL JI J. Cross-Cult. Psychol. PD DEC PY 1993 VL 24 IS 4 BP 399 EP 413 DI 10.1177/0022022193244002 PG 15 WC Psychology, Social SC Psychology GA MG090 UT WOS:A1993MG09000002 ER PT J AU VIVIER, E SORRELL, JM ACKERLY, M ROBERTSON, MJ RASMUSSEN, RA LEVINE, H ANDERSON, P AF VIVIER, E SORRELL, JM ACKERLY, M ROBERTSON, MJ RASMUSSEN, RA LEVINE, H ANDERSON, P TI DEVELOPMENTAL REGULATION OF A MUCIN-LIKE GLYCOPROTEIN SELECTIVELY EXPRESSED ON NATURAL-KILLER-CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID KERATAN SULFATE PROTEOGLYCAN; MONOCLONAL-ANTIBODIES; TYROSINE PHOSPHORYLATION; NK CELLS; B-CELLS; RECEPTOR; COMPLEX; CORNEAL; FC-GAMMA-RIII(CD16); CYTOTOXICITY AB Natural killer (NK) cells are CD3:TCR-, CD16+, CD56+ large granular lymphocytes capable of recognizing and eliminating a variety of virus-infected, malignant, and antibody-coated target cells. Two functionally distinct populations of peripheral blood NK cells can be differentiated by their surface expression of an isoform of the neural cell adhesion molecule (CD56). CD56bright NK cells have the attributes of an undifferentiated cell, in that they proliferate in response to exogenous cytokines, but exert poor cytolytic activity. CD56dim NK cells have the attributes of a more differentiated cell, in that they proliferate poorly in response to exogenous cytokines, but are potent cytolytic effector cells. Here we describe the molecular characterization of a NK cell restricted epitope (PEN5) that is selectively expressed on the functionally differentiated CD56dim NK cells. PEN5+ NK cells proliferate poorly in response to interleukin 2 (IL-2), but are potent cytolytic effectors, whereas PEN5- NK cells proliferate in response to IL-2, but are poor cytolytic effectors. Biochemical and immunochemical analyses reveal the PEN5 epitope to be an unusual sulfated poly-N-lactosamine carbohydrate related to keratan sulfate glycosaminoglycans. Immunoprecipitates prepared using a monoclonal antibody reactive with PEN5 include two polydisperse membrane-bound glycoproteins, PEN5alpha (120-170 kD) and PEN5beta (210-245 kD). Enzymatic deglycosylation reduces the apparent molecular weight of both PEN5 isoforms by 80-90%, and classifies PEN5beta as a mucinlike glycoprotein. The surface expression of the PEN5 epitope is downmodulated by stimuli that induce NK cell proliferation, and it is absent from leukemic NK cells of patients with granular lymphocyte proliferative disorder. Taken together, these results indicate that PEN5 is a developmentally regulated poly-N-lactosamine epitope associated with a mucin-type glycoprotein, whose expression is restricted to the population of nonproliferative NK cells fully committed to cytolytic effector function. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. CASE WESTERN RESERVE UNIV,DEPT BIOL,CLEVELAND,OH 44106. FU NCI NIH HHS [CA-53595] NR 39 TC 30 Z9 31 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD DEC 1 PY 1993 VL 178 IS 6 BP 2023 EP 2033 DI 10.1084/jem.178.6.2023 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MJ267 UT WOS:A1993MJ26700016 PM 7504054 ER PT J AU AHMED, AR YUNIS, JJ MARCUSBAGLEY, D YUNIS, EJ SALAZAR, M KATZ, AJ AWDEH, Z ALPER, CA AF AHMED, AR YUNIS, JJ MARCUSBAGLEY, D YUNIS, EJ SALAZAR, M KATZ, AJ AWDEH, Z ALPER, CA TI MAJOR HISTOCOMPATIBILITY COMPLEX SUSCEPTIBILITY GENES FOR DERMATITIS-HERPETIFORMIS COMPARED WITH THOSE FOR GLUTEN-SENSITIVE ENTEROPATHY SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID INHERITED STRUCTURAL POLYMORPHISM; CELIAC-DISEASE; HLA-DP; PEMPHIGUS-VULGARIS; JEWISH PATIENTS; HAPLOTYPES; DQ; LINKAGE; HLA-DR3; ALLELES AB Dermatitis herpetiformis (DH) shares some clinical features and major histocompatibility complex (MHC) markers with gluten-sensitive enteropathy (GSE). We compared MHC haplotypes in 27 patients with DH, 35 patients with GSE, and normal controls. As in GSE, the frequencies of two extended haplotypes, [HLA-B8, SC01, DR3] and [HLA-B44, FC31, DR7], were increased in patients with DH. Distributions of fragments of extended haplotypes, consisting of some but not all of the elements of complete extended haplotypes, were analyzed to attempt to localize a susceptibility gene. Besides complete extended susceptibility haplotypes, (DR3, DQ2) and (DR7, DQ2) fragments were most common in GSE. In contrast, DH showed only a few such fragments but many instances of the fragment (SC01). The differences in distribution of these fragments in the two diseases were highly significant (P <0.002). HLA-DQ2 and DR3 had the highest odds ratios for GSE, but the highest odds ratio for DH was for the complotype SC01. These findings suggest that the MHC susceptibility gene for DH is between class II and complotype regions, closest to the complotype, whereas that for GSE is in the class II region. C1 CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,DEPT ORAL PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. NEWTON WELLESLEY HOSP,NEWTON LOWER FALLS,MA 02162. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. AMER RED CROSS,BLOOD SERV,NE REG,DEDHAM,MA 02026. FU NHLBI NIH HHS [HL-29583]; NICHD NIH HHS [HD-17461]; NIDDK NIH HHS [DK-26844] NR 37 TC 21 Z9 21 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD DEC 1 PY 1993 VL 178 IS 6 BP 2067 EP 2075 DI 10.1084/jem.178.6.2067 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MJ267 UT WOS:A1993MJ26700020 PM 8245782 ER PT J AU DASILVA, AJ JANSSEN, O RUDD, CE AF DASILVA, AJ JANSSEN, O RUDD, CE TI T-CELL RECEPTOR-ZETA CD3-P59(FYN(T))-ASSOCIATED P120/130 BINDS TO THE SH2 DOMAIN OF P59(FYN(T)) SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID PROTEIN-TYROSINE KINASE; GROWTH-FACTOR RECEPTOR; ANTIGEN RECEPTOR; SIGNAL TRANSDUCTION; SRC FAMILY; ASSOCIATION; ACTIVATION; P56LCK; CD4; PHOSPHORYLATION AB Intracellular signaling from the T cell receptor (TCR)zeta/CD3 complex is likely to be mediated by associated protein tyrosine kinases such as p59fyn(T), ZAP-70, and the CD4:p56lck and CD8:p56lck coreceptors. The nature of the signaling cascade initiated by these kinases, their specificities, and downstream targets remain to be elucidated. The TCR-zeta/CD3:p59fyn(T) complex has previously been noted to coprecipitate a 120/130-kD doublet (p120/130). This intracellular protein of unknown identity associates directly with p59fyn(T) within the receptor complex. In this study, we have shown that this interaction with p120/130 is specifically mediated by the SH2 domain (not the fyn-SH3 domain) of p59fyn(T). Further, based on the results of in vitro kinase assays, p120/130 appears to be preferentially associated with p59fyn(T) in T cells, and not with p56lck. Antibody reprecipitation studies identified p120/130 as a previously described 130-kD substrate of pp60v-src whose function and structure is unknown. TCR-zeta/CD3 induced activation of T cells augmented the tyrosine phosphorylation of p120/130 in vivo as detected by antibody and GST:fyn-SH2 fusion proteins. p120/130 represents the first identified p59fyn(T):SH2 binding substrate in T cells, and as such is likely to play a key role in the early events of T cell activation. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RI Janssen, Ottmar/E-9735-2010 FU PHS HHS [R01 12069] NR 42 TC 53 Z9 53 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD DEC 1 PY 1993 VL 178 IS 6 BP 2107 EP 2113 DI 10.1084/jem.178.6.2107 PG 7 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MJ267 UT WOS:A1993MJ26700024 PM 7504057 ER PT J AU FREEMAN, GJ BORRIELLO, F HODES, RJ REISER, H GRIBBEN, JG NG, JW KIM, J GOLDBERG, JM HATHCOCK, K LASZLO, G LOMBARD, LA WANG, S GRAY, GS NADLER, LM SHARPE, AH AF FREEMAN, GJ BORRIELLO, F HODES, RJ REISER, H GRIBBEN, JG NG, JW KIM, J GOLDBERG, JM HATHCOCK, K LASZLO, G LOMBARD, LA WANG, S GRAY, GS NADLER, LM SHARPE, AH TI MURINE B7-2, AN ALTERNATIVE CTLA4 COUNTER-RECEPTOR THAT COSTIMULATES T-CELL PROLIFERATION AND INTERLEUKIN-2 PRODUCTION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID ACTIVATION ANTIGEN-B7; MOLECULAR-CLONING; B-CELLS; EXPRESSION; SIGNAL; SUPERFAMILY; INDUCTION; PROVIDES; CLONES; ANERGY AB The B7-1 molecule, expressed on antigen presenting cells (APC), provides a crucial costimulatory signal for T cell activation. Recent studies demonstrate the existence of alternative, non-B7-1 CTLA4 counter-receptors in mice and humans. Here, we describe the molecular cloning and demonstrate costimulatory function of the murine B7-2 (mB7-2) gene. Murine B7-2 cDNA encodes a member of the Ig supergene family that binds CTLA4-Ig and stains with the GL1 but not anti-mB7-1 mAb. Murine B7-2 costimulates the proliferation and interleukin 2 production of CD4+ T cells and this costimulation can be inhibited by either CTLA4-Ig or GL1 mAb. Identification of the B7-2 molecule will permit further manipulation of the B7:CD28/CTLA4 costimulatory pathway which has been shown to be involved in the prevention of tolerance, induction of tumor immunity, and most recently, in the pathogenesis of autoimmunity. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. REPLIGEN CORP,CAMBRIDGE,MA 02139. BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV IMMUNOL RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NIA,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. RP FREEMAN, GJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV HEMATOL MALIGNANCIES,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-40216]; NHLBI NIH HHS [5T33 HL07627]; NIAID NIH HHS [AI-33679] NR 32 TC 351 Z9 358 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD DEC 1 PY 1993 VL 178 IS 6 BP 2185 EP 2192 DI 10.1084/jem.178.6.2185 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MJ267 UT WOS:A1993MJ26700033 PM 7504059 ER PT J AU KOLAKOWSKI, LF RICE, K AF KOLAKOWSKI, LF RICE, K TI EVOLUTIONARY HISTORY OF G-PROTEIN-COUPLED RECEPTORS IS A FUNCTIONAL CLASSIFICATION SO JOURNAL OF GENERAL PHYSIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,DEPT ORGANISM & EVOLUT BIOL,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1295 J9 J GEN PHYSIOL JI J. Gen. Physiol. PD DEC PY 1993 VL 102 IS 6 BP A14 EP A14 PG 1 WC Physiology SC Physiology GA MN163 UT WOS:A1993MN16300043 ER PT J AU LAWRENCE, MB SPRINGER, TA AF LAWRENCE, MB SPRINGER, TA TI NEUTROPHILS ROLL ON E-SELECTIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LEUKOCYTE ADHESION MOLECULE-1; ENDOTHELIAL CELL RECOGNITION; CHEMOTACTIC FACTORS; SOLUBLE FORM; T-CELLS; EXPRESSION; GMP-140; INVIVO; ELAM-1; MAC-1 AB Using flow conditions that simulate those in post capillary venules, we have found that neutrophils attach and roll on a substrate bearing purified E-selectin. E-selectin resembles P-selectin (CD62) with regard to the dependence of attachment efficiency on wall shear stress and selectin density. In contrast, once attached, neutrophils form rolling adhesionson E-selectin that are much stronger than those on P-selectin. Rolling velocities on E-selectin are slower and have less variance than on P-selectin. With increasing shear stress, rolling velocities reach a plateau level that is dependent on E-selectin density, suggesting that the number of receptor-ligand bonds and the bond dissociation rate limit rolling velocity, and that the bonds are not broken by the applied force. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,200 LONGWOOD AVE,ROOM 250,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA31799]; NHLBI NIH HHS [P01-HL48675] NR 38 TC 294 Z9 296 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 DEC 1 PY 1993 VL 151 IS 11 BP 6338 EP 6346 PG 9 WC Immunology SC Immunology GA MH756 UT WOS:A1993MH75600047 PM 7504018 ER PT J AU CAREY, K AF CAREY, K TI RESERVATION PRICE ANNOUNCEMENT IN SEALED BID AUCTIONS SO JOURNAL OF INDUSTRIAL ECONOMICS LA English DT Article AB This article compares the strategic announcement of a reservation price by a bid-taking buyer in a first-price sealed bid auction with the strategy of no announcement. Simulation results indicate that an operative ceiling price that is unknown to bidders will yield lower supply costs to the buyer than when the latter announces the reservation price truthfully. However, given enough bidders, the buyer can achieve an even lower expected cost of supply by announcing a falsely low reservation price. RP CAREY, K (reprint author), US DEPT VET AFFAIRS,MANAGEMENT SCI GRP,200 SPRINGS RD,BEDFORD,MA 01730, USA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0022-1821 J9 J IND ECON JI J. Indust. Econ. PD DEC PY 1993 VL 41 IS 4 BP 421 EP 429 DI 10.2307/2950601 PG 9 WC Business, Finance; Economics SC Business & Economics GA MJ198 UT WOS:A1993MJ19800006 ER PT J AU MACDONALD, ME BARNES, G SRINIDHI, J DUYAO, MP AMBROSE, CM MYERS, RH GRAY, J CONNEALLY, PM YOUNG, A PENNEY, J SHOULSON, I HOLLINGSWORTH, Z KOROSHETZ, W BIRD, E VONSATTEL, JP BONILLA, E MOSCOWITZ, C PENCHASZADEH, G BRZUSTOWICZ, L ALVIR, J CONDE, JB CHA, JH DURE, L GOMEZ, F RAMOSARROYO, M SANCHEZRAMOS, J SNODGRASS, SR DEYOUNG, M WEXLER, NS MACFARLANE, H ANDERSON, MA JENKINS, B GUSELLA, JF AF MACDONALD, ME BARNES, G SRINIDHI, J DUYAO, MP AMBROSE, CM MYERS, RH GRAY, J CONNEALLY, PM YOUNG, A PENNEY, J SHOULSON, I HOLLINGSWORTH, Z KOROSHETZ, W BIRD, E VONSATTEL, JP BONILLA, E MOSCOWITZ, C PENCHASZADEH, G BRZUSTOWICZ, L ALVIR, J CONDE, JB CHA, JH DURE, L GOMEZ, F RAMOSARROYO, M SANCHEZRAMOS, J SNODGRASS, SR DEYOUNG, M WEXLER, NS MACFARLANE, H ANDERSON, MA JENKINS, B GUSELLA, JF TI GAMETIC BUT NOT SOMATIC INSTABILITY OF CAG REPEAT LENGTH IN HUNTINGTONS-DISEASE SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID BULBAR MUSCULAR-ATROPHY; MYOTONIC-DYSTROPHY; TRINUCLEOTIDE REPEAT; FRAGILE-X; TRIPLET REPEAT; CTG REPEAT; GENE; MUTATIONS; EXPANSION; SEQUENCE AB Instability of a CAG repeat in 4p16.3 has been found in Huntington's disease (HD) chromosomes. Unlike a similar repeat in the fragile X syndrome, the expanded HD repeat showed no evidence of somatic instability in a comparison of blood, lymphoblast, and brain DNA from the same persons. Four pairs of monozygotic HD twins displayed identical CAG repeat lengths suggesting that repeat size is determined in gametogenesis. In contrast with the fragile X syndrome and with HD somatic tissue, mosaicism was readily detected as a diffuse spread of repeat lengths in DNA from HD sperm samples. Typically, the modal repeat size was larger in the sperm DNA than in corresponding lymphoblast DNA, with the greatest degree of gametic mosaicism coinciding with the longest somatic CAG repeats. These data indicate that the developmental timing of repeat instability appears to differ between HD and fragile X syndrome, and that the fundamental mechanisms leading to repeat expansion may therefore be distinct. C1 BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. INDIANA UNIV,MED CTR,DEPT MED GENET,INDIANAPOLIS,IN 46202. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. UNIV ROCHESTER,MED CTR,DEPT NEUROL,ROCHESTER,NY 14642. MCLEAN HOSP,BRAIN TISSUE RESOURCE CTR,BELMONT,MA 02178. HARVARD UNIV,SCH MED,DEPT NEUROPATHOL,BELMONT,MA 02178. BAYLOR UNIV,COLL MED,HOUSTON,TX 77009. HOSP VIRGEN CAMINO,SERV GENET,E-31008 PAMPLONA,SPAIN. UNIV MIAMI,DEPT NEUROL,MIAMI,FL 33136. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,MOLEC NEUROPATHOL LAB,BOSTON,MA 02129. UNIV ZULIA,MARACAIBO,VENEZUELA. COLUMBIA UNIV COLL PHYS & SURG,DEPT NEUROL,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT PSYCHIAT,NEW YORK,NY 10032. HEREDITARY DIS FDN,SANTA MONICA,CA 90401. LONG ISL JEWISH MED CTR,GLEN OAKS,NY 11004. RP MACDONALD, ME (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02129, USA. RI Dure, Leon/B-3243-2008; Sanchez-Ramos, Juan/A-1188-2009 OI Sanchez-Ramos, Juan/0000-0002-3391-7857 FU NINDS NIH HHS [NS02385, NS16367, NS31862] NR 25 TC 115 Z9 118 U1 1 U2 6 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD DEC PY 1993 VL 30 IS 12 BP 982 EP 986 DI 10.1136/jmg.30.12.982 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA ML547 UT WOS:A1993ML54700003 PM 8133508 ER PT J AU BOWLING, AC SCHULZ, JB BROWN, RH BEAL, MF AF BOWLING, AC SCHULZ, JB BROWN, RH BEAL, MF TI SUPEROXIDE-DISMUTASE ACTIVITY, OXIDATIVE DAMAGE, AND MITOCHONDRIAL ENERGY-METABOLISM IN FAMILIAL AND SPORADIC AMYOTROPHIC-LATERAL-SCLEROSIS SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE AMYOTROPHIC LATERAL SCLEROSIS; NEURODEGENERATION; FREE RADICALS; OXIDATIVE DAMAGE; SUPEROXIDE DISMUTASE; OXIDATIVE PHOSPHORYLATION ID MOTOR NEURON DISEASE; DEGENERATIVE DISEASES; CEREBROSPINAL-FLUID; BRAIN; SENSITIVITY; DYSFUNCTION; SYSTEM; DNA AB The cause of neuronal death in amyotrophic lateral sclerosis (ALS) is unknown. Recently, it was found that some patients with autosomal-dominant familial ALS (FALS) have point mutations in the gene that encodes Cu/Zn superoxide dismutase (SOD1). In this study of postmortem brain tissue, we examined SOD activity and quantified protein carbonyl groups, a marker of oxidative damage, in samples of frontal cortex (Brodmann area 6) from 10 control patients, three FALS patients with known SOD1 mutations (FALS-1), one autosomal-dominant FALS patient with no identifiable SOD1 mutations (FALS-0), and 11 sporadic ALS (SALS) patients. Also, we determined the activities of components of the electron transport chain (complexes I, II-III, and IV) in these samples. The cytosolic SOD activity, which is primarily SOD1 activity, was reduced by 38.8% (p < 0.05) in the FALS-1 patients and not significantly altered in the SALS patients or the FALS-0 patient relative to the control patients. The mitochondrial SOD activity, which is primarily SOD2 activity, was not significantly altered in the FALS-1, FALS-0, or SALS patients. The protein carbonyl content was elevated by 84.8% (p < 0.01) in the SALS patients relative to the control patients. Finally, the complex I activity was increased by 55.3% (p < 0.001) in the FALS-1 patients relative to the control patients. These results from cortical tissue demonstrate that SOD1 activity is reduced and complex I activity is increased in FALS-1 patients and that oxidative damage to proteins is increased in SALS patients. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,DAY NEUROMUSCULAR RES CTR,WARREN 408,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Schulz, Jorg/D-9786-2012 OI Schulz, Jorg/0000-0002-8903-0593 FU NIA NIH HHS [AG05134]; NINDS NIH HHS [NS16367, NS10828] NR 31 TC 483 Z9 487 U1 2 U2 17 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD DEC PY 1993 VL 61 IS 6 BP 2322 EP 2325 DI 10.1111/j.1471-4159.1993.tb07478.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MH022 UT WOS:A1993MH02200045 PM 8245985 ER PT J AU GABUZDA, D BUSCIGLIO, J YANKNER, BA AF GABUZDA, D BUSCIGLIO, J YANKNER, BA TI INHIBITION OF BETA-AMYLOID PRODUCTION BY ACTIVATION OF PROTEIN-KINASE-C SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE BETA-AMYLOID PRODUCTION; AMYLOID PRECURSOR PROTEIN; PROTEIN KINASE-C; ALZHEIMERS DISEASE ID ALZHEIMERS-DISEASE; PRECURSOR PROTEIN; PHOSPHORYLATION; QUANTIFICATION; PEPTIDE AB The cellular factors regulating the generation of beta-amyloid from the amyloid precursor protein (APP) are unknown. Activation of protein kinase C (PKC) by phorbol ester treatment inhibited the generation of the 4-kDa beta-amyloid peptide in transfected COS cells, a human glioma cell line, and human cortical astrocytes. An analogue of diacylglycerol, the endogenous cellular activator of PKC, also inhibited the generation of beta-amyloid. Activation of PKC increased the level of secreted APP in transfected COS cells but did not significantly affect the level of secreted APP in primary human astrocytes or in the glioma cell line. Cell-associated APP and the secreted APP derivative, but not beta-amyloid, were phosphorylated on serine residues. Activation of PKC did not increase the level of APP phosphorylation, suggesting that PKC modulates the proteolytic cleavage of APP indirectly by phosphorylation of other substrates. These results indicate that PKC activation inhibits beta-amyloid production by altering APP processing and suggest that beta-amyloid production can be regulated by the phospholipase C-diacylglycerol signal transduction pathway. C1 CHILDRENS HOSP MED CTR,DEPT NEUROL,ENDERS 260,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NIA NIH HHS [AG09229]; NINDS NIH HHS [NS30352] NR 16 TC 129 Z9 131 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD DEC PY 1993 VL 61 IS 6 BP 2326 EP 2329 DI 10.1111/j.1471-4159.1993.tb07479.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MH022 UT WOS:A1993MH02200046 PM 8245986 ER PT J AU TAKAHASHI, T CAVINESS, VS AF TAKAHASHI, T CAVINESS, VS TI PCNA-BINDING TO DNA AT THE G1/S TRANSITION IN PROLIFERATING CELLS OF THE DEVELOPING CEREBRAL WALL SO JOURNAL OF NEUROCYTOLOGY LA English DT Article ID NUCLEAR ANTIGEN; CONFOCAL MICROSCOPY; REPLICATION INVITRO; S-PHASE; CYCLE; MECHANISM; SITES AB Proliferating cell nuclear antigen is a nuclear protein essential to DNA synthesis in eukaryotic cells. It is known to form part of a multi-protein complex which binds to DNA from the outset of S-phase of the cell cycle. We define in this analysis the interval of proliferating cell nuclear antigen binding to DNA (strictly speaking, the interval through which proliferating cell nuclear antigen is stained immunohistochemically after ethanol fixation) with respect to the stages of the cell cycle in the intact mammalian brain. The epithelium of the developing cerebral wall is favourable for such an analysis because nuclei at the same stage of the cell division cycle are spatially aligned with each other at the same depth of the epithelium. Therefore spatial location of a nucleus within the epithelium is a reliable indicator of the stage of the cell cycle for that nucleus. Proliferating cell nuclear antigen-DNA binding in this epithelium is initiated in the final 5% (26 min) of G1-phase and continues through the initial 35% (1.3 h) of S-phase. This phasic pattern of proliferating cell nuclear antigen-DNA binding, as revealed for the first time in the intact cerebral wall, approximates closely the phasic pattern as it has been characterized until now only in vitro in vertebrate cell lines. This analysis illustrates the potential of the cerebral proliferative epithelium for study of the molecular events of the cell cycle under in vivo conditions of histogenetic regulation. RP TAKAHASHI, T (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,25 FRUIT ST,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS12005] NR 31 TC 64 Z9 65 U1 0 U2 1 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0300-4864 J9 J NEUROCYTOL JI J. Neurocytol. PD DEC PY 1993 VL 22 IS 12 BP 1096 EP 1102 DI 10.1007/BF01235751 PG 7 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA ML532 UT WOS:A1993ML53200007 PM 7906297 ER PT J AU KAWASE, T LIBERMAN, MC AF KAWASE, T LIBERMAN, MC TI ANTIMASKING EFFECTS OF THE OLIVOCOCHLEAR REFLEX .1. ENHANCEMENT OF COMPOUND ACTION-POTENTIALS TO MASKED TONES SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID AUDITORY-NERVE FIBERS; GUINEA-PIG COCHLEA; ELECTRICAL-STIMULATION; EFFERENT NEURONS; CONTRALATERAL SOUND; RESPONSE PROPERTIES; CAT; BUNDLE; NOISE; SUPPRESSION AB 1. The effects of olivocochlear (OC) feedback on signal processing in the cochlea were studied by comparing responses seen with and without a contralateral noise or by comparing responses seen before and after cutting the OC bundle (OCB). Adding and subtracting a contralateral noise is a convenient, reversible way of changing the level of OC feedback; however, it fully reveals only the contribution of the contralaterally responsive efferent fibers. Cutting the OCB can reveal the full contribution of all fibers in the OCB; however, the manipulation can only be performed once per experiment. 2. The amplitude of the compound action potential (CAP), recorded from anesthetized or decerebrate cats in response to tone pips, could be increased by addition of contralateral noise at moderate sound pressure levels. These enhancement phenomena were most easily demonstrable when the tone pips were masked by ipsilateral broadband noise; however, in some animals CAP enhancement was seen in the absence of ipsilateral maskers. Enhancement-in-quiet may arise because of internal masking from animal-generated noise. All contralateral-noise enhancement disappeared when the OCB was cut. 3. Enhancement effects of contralateral noise could be seen in both simultaneous and forward-masking paradigms. Enhancement was largest for high-frequency tone pips (8-16 kHz) and could be demonstrated over a wide range of tone-pip levels and ipsilateral-masker levels. Suppression of CAP by the contralateral noise was often seen for lower tone-pip frequencies (2-8 kHz) and lower tone-pip intensities. These trends may be understood in the context of known properties of OC peripheral effects and known properties of physiological masking. 4. Cutting the OCB resulted in a decrease in CAP amplitudes to masked tone pips. When CAP was measured to tone pips presented in equilevel, binaural noise, OCB section resulted in a decrease in CAP amplitudes equivalent to at least a 6-dB decrease in signal-to-noise ratio. Such antimasking effects of an intact OCB were seen in both simultaneous and forward-masking paradigms. 5. Present evidence suggests that all these antimasking effects can be explained on the basis of activation of the medial OC fibers to the outer hair cells. By suppressing responses to continuous noise backgrounds, the OC reflex may enhance responses to transient masked stimuli by decreasing the level of adaptation in auditory nerve fibers. Such effects of the OC reflex should improve discrimination of transient signals presented in a continuous noise background. C1 MASSACHUSETTS GEN HOSP,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114. TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,SENDAI,MIYAGI 980,JAPAN. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. MIT,DW HLTH SCI TECHNOL,CAMBRIDGE,MA 02139. FU NIDCD NIH HHS [P01 DC-00119, R01 DC-00188] NR 43 TC 118 Z9 119 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD DEC PY 1993 VL 70 IS 6 BP 2519 EP 2532 PG 14 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA MN613 UT WOS:A1993MN61300028 PM 8120596 ER PT J AU KAWASE, T DELGUTTE, B LIBERMAN, MC AF KAWASE, T DELGUTTE, B LIBERMAN, MC TI ANTIMASKING EFFECTS OF THE OLIVOCOCHLEAR REFLEX .2. ENHANCEMENT OF AUDITORY-NERVE RESPONSE TO MASKED TONES SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID GUINEA-PIG COCHLEA; ELECTRICAL-STIMULATION; INTENSITY DISCRIMINATION; EFFERENT INNERVATION; CONTRALATERAL SOUND; TUNING CURVES; FIBERS; NOISE; CAT; NEURONS AB 1. The antimasking effects of olivocochlear (OC) efferent feedback were studied in anesthetized or decerebrate cats by comparing responses of single auditory-nerve fibers (ANFs) to tone bursts in continuous masking noise seen with and without addition of a moderate-level contralateral noise known to activate the OC reflex. Responses were measured as a function of tone-burst intensity, tone-burst frequency, and masker intensity and were analyzed so as to allow quantitative estimates of the detectability of the tone bursts against the noise background. 2. Addition of the contralateral OC elicitor both increased the maximum discharge rates to the masked tone bursts and decreased the rates to the ipsilateral masker. The rate increases to the tone bursts could be explained on the basis of a decrease in adaptation caused by decreasing the steady response to the masker. The result is a steepening of the rate-versus-level function for masked tone bursts and a concomitant increase in the estimated discriminability of small increments of tone-burst intensity. 3. For tone bursts at the fiber's characteristic frequency (CF), the OC effects on detection threshold for the masked tone bursts depended on masker level, with small increases in threshold for low masker levels and somewhat larger decreases in threshold for higher masker levels. For tone bursts below CF, OC effects, when present, always decreased the detection threshold. 4. The largest antimasking effects were seen for fibers with CFs between 6 and 12 kHz and for masker levels within 20 dB of the fiber's threshold to the masker. These trends appeared to hold for fibers of all spontaneous rates (SRs). .5. Enhancement of the response to unmasked tone bursts and concomitant decrease in the ''spontaneous rate'' was elicited by OC activation in fibers if threshold sensitivity approached - 10 dB SPL. This ''enhancement-in-quiet'' appears to arise when an animal-generated noise produces a continuous response (in the absence of purposely applied sound) that is suppressed by OC activity. This finding raises questions as to the range of ''true'' spontaneous rates in the cat. 6. The results highlight two important distinctions between the effects of OC feedback in quiet versus those in noise. In quiet, the effects are predominately suppressive and are restricted to stimuli at frequencies near a fiber's CF and at intensities within its dynamic range. In continuous background noise, the OC reflex can enhance the responses to transient stimuli. Such effects are seen throughout the fiber's response area. Because true quiet is only conceivable under artificial laboratory conditions, the predominant effect of the OC reflex in a natural sound environment is to enhance the response to transient stimuli as it suppresses the responses to steady backgrounds. C1 MASSACHUSETTS GEN HOSP,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114. TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,SENDAI,MIYAGI 980,JAPAN. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MIT,DIV HLTH SCI TECHNOL,CAMBRIDGE,MA 02139. FU NIDCD NIH HHS [P01 DC-00119, R01 DC-00188] NR 67 TC 157 Z9 158 U1 0 U2 5 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD DEC PY 1993 VL 70 IS 6 BP 2533 EP 2549 PG 17 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA MN613 UT WOS:A1993MN61300029 PM 8120597 ER PT J AU GORMAN, DG CUMMINGS, JL AF GORMAN, DG CUMMINGS, JL TI NEUROBEHAVIORAL PRESENTATIONS OF THE ANTIPHOSPHOLIPID ANTIBODY SYNDROME SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; ANTICARDIOLIPIN ANTIBODIES; ANTICOAGULANT; DISEASE; PREVALENCE; DISORDERS; STANDARDIZATION; AUTOANTIBODIES; CARDIOLIPIN; COAGULATION AB Antiphospholipid antibodies, including lupus anticoagulant and anticardiolipin antibodies, are increasingly recognized as a cause of neurological morbidity. They may occur with or without evidence of systemic lupus erythematosus and have been associated with stroke, migraine, and confusional states. Their role as etiologic or contributing factors in neurobehavioral and neuro-psychiatric syndromes of obscure etiology has not been emphasized. The cases of 7 patients who were referred for evaluation of behavior abnormalities and had antiphospholipid antibodies are presented, and the potential relationships of the anti-phospholipid antibody syndrome to behavioral alterations are discussed. C1 W LOS ANGELES VAMC, PSYCHIAT SERV,BEHAV NEUROSCI SECT,NEUROBEHAV UNIT, BLDG 256B, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL & PSYCHIAT, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT BIOBEHAV SCI, LOS ANGELES, CA USA. NR 28 TC 21 Z9 21 U1 0 U2 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD WIN PY 1993 VL 5 IS 1 BP 37 EP 42 PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KK041 UT WOS:A1993KK04100006 PM 8094019 ER PT J AU WEILBURG, JB SCHACHTER, S SACHS, GS WORTH, J POLLACK, MH IVES, JR SCHOMER, DL AF WEILBURG, JB SCHACHTER, S SACHS, GS WORTH, J POLLACK, MH IVES, JR SCHOMER, DL TI FOCAL PAROXYSMAL EEG CHANGES DURING ATYPICAL PANIC ATTACKS SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID STATUS EPILEPTICUS; DISORDER; FEAR; SEIZURES; EPILEPSY; ABNORMALITIES; ANXIETY AB Atypical panic attacks include features such as focal paresthesias or sensory distortions, but attempts to demonstrate a relationship to partial seizures have been unsuccessful. Two patients with atypical panic attacks had attacks during EEG monitoring: one during a routine EEG in the EEG laboratory, the other at home during ambulatory monitoring. Focal paroxysms of sharp wave activity appeared on both patients' EEGs coincident with the spontaneous onset of panic attack symptoms. Both patients remained conscious. The correlation of focal paroxysmal EEG changes with panic attack symptoms suggests that these attacks were produced by partial seizure activity. Further study of the relationship between panic attacks and seizures is indicated. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. BETH ISRAEL HOSP,ELECTROENCEPHALOG LAB,BOSTON,MA 02215. RP WEILBURG, JB (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,ACC 815,BOSTON,MA 02115, USA. NR 32 TC 16 Z9 17 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD WIN PY 1993 VL 5 IS 1 BP 50 EP 55 PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KK041 UT WOS:A1993KK04100008 PM 8428135 ER PT J AU KAOUTZANIS, M YOKOTA, M SIBILIA, R PETERSON, JW AF KAOUTZANIS, M YOKOTA, M SIBILIA, R PETERSON, JW TI NEUROLOGIC EVALUATION IN A CANINE MODEL OF SINGLE AND DOUBLE SUBARACHNOID HEMORRHAGE SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE CANINE MODEL; EXPERIMENTAL SUBARACHNOID HEMORRHAGE; NEUROLOGIC EVALUATION; COMA SCORE ID DELAYED CEREBRAL VASOSPASM; GENE-RELATED PEPTIDE; VASOACTIVE INTESTINAL POLYPEPTIDE; CEREBROVASCULAR NERVE-FIBERS; HIGH-DOSE METHYLPREDNISOLONE; BASILAR ARTERIES; INTRACRANIAL PROSTAGLANDINS; CEREBROSPINAL-FLUID; THERAPEUTIC VALUE; DOGS AB The pathophysiology of cerebral vasospasm is complex and multifactorial. The present study sought to identify the degree of correlation between cerebral vasospasm as observed angiographically and clinical evaluation of an animal's neurologic status in the canine model following a single and double experimental subarachnoid hemorrhage (SAH) protocol. Nineteen mongrel dogs underwent single or double experimental SAH by percutaneous needle puncture of the cisterna magna and placement of a subarachnoid blood clot in the basal cistern on day 1 and day 4, respectively. At 72 h after each experimental SAH, vertebral angiography was performed and compared to control angiography. Basilar artery diameter measured at multiple positions was expressed as percentage of control diameter. Clinical evaluation of the animals was performed every day throughout the experiments. To assess the degree of neurologic impairment we developed a coma scale that efficiently estimated motor ability, eye response and eating habits of the animals. Vasoconstriction after experimental SAH reduced mean basilar artery diameter to 79.1% (+/-5.4) of control diameter following single SAH and to 69.0% (+/-2.1) of control diameter following double SAH. No changes were observed in the neurologic behavior of the animals throughout the experiment. Since a principal characteristic of human cerebral vasospasm is the close correlation between arterial constriction and neurological deficit, we believe that the canine model of SAH, although good in creating cerebral arterial vasoconstriction, does not fully represent the best model of human cerebral vasospasm. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,CEREBROVASC BIOPHYS LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02114. FU NHLBI NIH HHS [NHLBI HL44554-01] NR 51 TC 15 Z9 19 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 J9 J NEUROSCI METH JI J. Neurosci. Methods PD DEC PY 1993 VL 50 IS 3 BP 301 EP 307 DI 10.1016/0165-0270(93)90037-R PG 7 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MR111 UT WOS:A1993MR11100005 PM 8152241 ER PT J AU STONE, JL LICHTOR, T CROWELL, RM AF STONE, JL LICHTOR, T CROWELL, RM TI MICROVASCULAR SLING DECOMPRESSION FOR TRIGEMINAL NEURALGIA SECONDARY TO ECTATIC VERTEBROBASILAR COMPRESSION - CASE-REPORT SO JOURNAL OF NEUROSURGERY LA English DT Note DE TRIGEMINAL NEURALGIA; VERTEBROBASILAR ARTERY; MICROVASCULAR DECOMPRESSION ID HEMIFACIAL SPASM; BASILAR ARTERY; TIC CONVULSIF; ECTASIA; SYSTEM; NERVE AB A patient with trigeminal neuralgia caused by a tortuous and ectatic vertebrobasilar artery is presented. He was treated with microvascular decompression using a fine silicone sling sutured to the dura over the petrous pyramid. The technical details are described. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP STONE, JL (reprint author), LOYOLA UNIV,COOK CTY HOSP,SCH MED,DIV NEUROSURG,1835 W HARRISON ST,CHICAGO,IL 60612, USA. NR 18 TC 27 Z9 29 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD DEC PY 1993 VL 79 IS 6 BP 943 EP 945 DI 10.3171/jns.1993.79.6.0943 PG 3 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA MJ274 UT WOS:A1993MJ27400022 PM 8246064 ER PT J AU ZERVAS, NT AF ZERVAS, NT TI THE MASSACHUSETTS-GENERAL-HOSPITAL - THE SEQUEL SO JOURNAL OF NEUROSURGERY LA English DT Article RP ZERVAS, NT (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114, USA. NR 27 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD DEC PY 1993 VL 79 IS 6 BP 958 EP 959 DI 10.3171/jns.1993.79.6.0958 PG 2 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA MJ274 UT WOS:A1993MJ27400025 ER PT J AU FISCHMAN, AJ RAUH, D SOLOMON, H BABICH, JW TOMPKINS, RG KROON, D STRAUSS, HW RUBIN, RH AF FISCHMAN, AJ RAUH, D SOLOMON, H BABICH, JW TOMPKINS, RG KROON, D STRAUSS, HW RUBIN, RH TI IN-VIVO BIOACTIVITY AND BIODISTRIBUTION OF CHEMOTACTIC PEPTIDE ANALOGS IN NONHUMAN-PRIMATES SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; IMAGING FOCAL SITES; CHEMOATTRACTANT RECEPTORS; INFECTION; PROTEIN; RATS AB The dose dependence of the effect of chemotactic peptide on peripheral leukocyte levels was measured in normal Rhesus monkeys. A Tc-99m-labeled hydrazino nicotinamide (HYNIC) derivatized chemotactic peptide analog was used to study biodistribution and inflammation imaging in Rhesus monkeys. In normal animals the studies demonstrated that chemotactic peptide induced a clear dose-dependent reduction in peripheral leukocyte levels. The decrease in leukocyte number occurred almost immediately after injection and rapidly returned to baseline. Significant effects on differential WBC count, blood pressure, pulse rate or respiration rate were not detected. The lowest dose of peptide tested (10 ng/kg) had minimal effect on leukocyte level. The HYNIC derivatized peptide was prepared in excellent yield and purity, had biological activity similar to the native peptide and was readily labeled at specific activity of >20,000 mCi/mu mole. When similar to 0.5 mCi (<2.0 ng/kg) of radiolabeled peptide was injected in monkeys with focal sites of mild sterile inflammation, a pattern of biodistribution similar to radiolabeled WBCs was observed and reductions in leukocyte levels were not detected. At 3 hr after injection, the site of inflammation was readily apparent with a target-to-background ratio of similar to 3:1. These studies demonstrate that radiolabeled chemotactic peptide analogs are effective agents for imaging sites of inflammation in monkeys. By radiolabeling at high specific activity, the effect of these reagents on peripheral leukocyte levels can be avoided. C1 HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. SHRINERS BURN INST,BOSTON,MA 02114. RW JOHNSON PHARMACEUT RES INST,SPRING HOUSE,PA. MASSACHUSETTS GEN HOSP,MED SERV,CLIN INVEST PROGRAM,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SURG SERV,TRAUMA UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 20 TC 71 Z9 72 U1 0 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1993 VL 34 IS 12 BP 2130 EP 2134 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MK579 UT WOS:A1993MK57900023 PM 8254400 ER PT J AU NICOL, PD MATSUEDA, GR HABER, E KHAW, BA AF NICOL, PD MATSUEDA, GR HABER, E KHAW, BA TI SYNTHETIC PEPTIDE IMMUNOGENS FOR THE DEVELOPMENT OF A CARDIAC MYOSIN LIGHT CHAIN-1 SPECIFIC RADIOIMMUNOASSAY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID EXPERIMENTAL MYOCARDIAL-INFARCTION; CDNA CLONES; SERUM; PROTEINS AB To determine if the presence of cardiac light chains in blood could be used to detect acute myocardial infarction, we developed a specific light chain immunoassay. A synthetic peptide sequence specific for human cardiac ventricular myosin light chain 1 (VLC1) was synthesized and designated P348. This peptide coupled to keyhole limpet hemocyanin was used as an immunogen to obtain murine monoclonal antibodies specific for VLC1. Five monoclonal antibodies were obtained. One of these designated Mab-8E3 reacted equally well with both the synthetic peptide and VLC1. Although the 8E3 antibody is specific for VLC1, the use of HPLC purification of skeletal muscle myosin light chain 1 demonstrated that VLC1 is present in human skeletal muscle. The clinical utility of the assay was tested in 18 patients with creatine kinase (CK) and ECG documented acute myocardial infarction. VLC1 was below the limit of detection (<1 ng/ml) in sera obtained from healthy volunteers and patients without myocardial infarction or chest pain. In contrast VLC1 was elevated in the serum of all 18 patients with acute myocardial infarction. Combining the two test results at the time of admission resulted in 83% of patients having detectable serum levels of one or both markers. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. WELLESLEY COLL HOSP,TORONTO,ON,CANADA. NR 31 TC 8 Z9 8 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1993 VL 34 IS 12 BP 2144 EP 2151 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MK579 UT WOS:A1993MK57900025 PM 8254402 ER PT J AU BABICH, JW GRAHAM, W BARROW, SA DRAGOTAKES, SC TOMPKINS, RG RUBIN, RH FISCHMAN, AJ AF BABICH, JW GRAHAM, W BARROW, SA DRAGOTAKES, SC TOMPKINS, RG RUBIN, RH FISCHMAN, AJ TI TC-99M-LABELED CHEMOTACTIC PEPTIDES - COMPARISON WITH INDIUM-111-LABELED WHITE BLOOD-CELLS FOR LOCALIZING ACUTE BACTERIAL-INFECTION IN THE RABBIT SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID TC-99M-HMPAO LABELED LEUKOCYTES; IMAGING FOCAL SITES; POLYCLONAL IGG; INFLAMMATION; RATS AB The biodistribution and infection imaging properties of (TC)-T-99m-labeled formyl-methionyl-leucyl-phenylalanyl-lysyl-hydrazinonic-otinamide (Tc-99m-HP) were compared with In-111-labeled leukocytes (In-111-WBCs) in rabbits with E. coli infections. Groups of six animals were co-injected with 1 mCi of Tc-99m-HP plus 0.05 mCi of In-111-WBCs and serial scintigrams were acquired from 3 to 6 hr and 18 hr postinjection. After acquiring the final images, the animals were killed and biodistribution was determined. At all imaging times, the distributions of Tc-99m-HP and In-111-WBCs were similar and the sites of infection were well visualized with both radiopharmaceuticals. The target (infected muscle) to background (contralateral normal muscle) ratios (T/B) were: 3.38 +/- 0.46, 3.80 +/- 0.37 and 10.87 +/- 1.44 for Tc-99m-Hp and 1.71 +/- 0.04, 1.81 +/- 0.26 and 3.79 +/- 0.83, for In-111-WBCs at 3, 6 and 18 hr postinjection, respectively. The average ratio of T/B ratios (Tc-99m-HP-to-In-111-WBCs) was 2.99 +/- 1.88, with no value less than unity. T/B ratios calculated from direct tissue sampling were significantly higher for Tc-99m-Hp than for In-111-WBCs (33.6:1 versus 8.1:1, p < 0.01). These differences were primarily due to increased absolute accumulation of (TC)-T-99m-Hp (0.102 %ID/g versus 0.024 %ID/g, p < 0.01) in infected muscle rather than a difference in accumulation in normal skeletal muscle. These results indicate that (TC)-T-99m-Hp yields target-to-background ratios greater than or equal to those achievable with In-111-WBCs probably as a result of an increase in absolute accumulation at the site of infection. C1 MASSACHUSETTS GEN HOSP, DEPT RADIOL, DIV NUCL MED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, MED SERV, CLIN INVEST UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, SURG SERV, BOSTON, MA 02114 USA. SHRINERS BURN INST, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT RADIOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA USA. NR 23 TC 86 Z9 86 U1 0 U2 2 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 EI 1535-5667 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1993 VL 34 IS 12 BP 2176 EP 2181 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MK579 UT WOS:A1993MK57900030 PM 8254406 ER PT J AU YASUDA, T MATSUURA, H AF YASUDA, T MATSUURA, H TI HYPERTROPHIC CARDIOMYOPATHY COMPLICATED WITH VENTRICULAR ANEURYSM AND MYOCARDIAL NECROSIS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID EMISSION COMPUTED-TOMOGRAPHY; MONOCLONAL ANTIMYOSIN FAB; CORONARY-ARTERY DISEASE; MYOSIN-SPECIFIC ANTIBODY; CONGESTIVE CARDIOMYOPATHY; STANNOUS PYROPHOSPHATE; TL-201 SCINTIGRAPHY; SUBAORTIC STENOSIS; CLINICAL COURSE; N-13 AMMONIA C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP YASUDA, T (reprint author), MASSACHUSETTS GEN HOSP,DIV NUCL MED,32 FRUIT ST,TILTON 2,BOSTON,MA 02114, USA. NR 56 TC 2 Z9 2 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1993 VL 34 IS 12 BP 2227 EP 2235 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MK579 UT WOS:A1993MK57900040 PM 8254416 ER PT J AU FISCHMAN, AJ BABICH, JW STRAUSS, HW AF FISCHMAN, AJ BABICH, JW STRAUSS, HW TI A TICKET TO RIDE - PEPTIDE RADIOPHARMACEUTICALS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID SINGLE-CHAIN-FV; RADIOIODINATED SOMATOSTATIN ANALOG; POSITRON EMISSION TOMOGRAPHY; RECEPTOR-POSITIVE TUMORS; IMAGING FOCAL SITES; MONOCLONAL-ANTIBODIES; LABELED INSULIN; INVIVO; PROTEINS; BINDING AB Over the past three decades, biospecific imaging agents have evolved from large proteins (i.e., antibodies) to antibody fragments (i.e., F(ab')(2) and Fab fragments) to smaller ''molecular recognition units'' such as Fv fragments, antigen binding domain fragments and small biologically active peptides. The smaller size of these molecules confers desirable pharmacokinetic properties, such as higher target-to-background ratios and faster blood clearance, that are favorable for imaging. Molecular engineering techniques now permit the peptide to carry the radionuclide-binding group in its structure while maintaining high-affinity binding to the receptor site. An important component to this system is the ability to radiolabel these agents with high specific activity using short-lived radionuclides, particularly Tc-99m. Recently, the application of small radiolabeled biologically active peptides for external imaging of a variety of biological processes has received considerable interest. These applications have ranged from the current widespread use of somatostatin analogs for imaging numerous types of tumors to the development of radiolabeled chemotactic peptides for infection imaging. In this review, we will describe many of the parameters for the rational development of peptide-based imaging agents, including: classes of peptides for imaging, methods for radiolabeling peptides, current biologically active peptide-based radiopharmaceuticals and future prospects for this new technology. C1 HARVARD UNIV, SCH MED, BOSTON, MA USA. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP, DEPT RADIOL, DIV NUCL MED, 32 FRUIT ST, BOSTON, MA 02114 USA. NR 86 TC 178 Z9 179 U1 0 U2 4 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 EI 1535-5667 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1993 VL 34 IS 12 BP 2253 EP 2263 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MK579 UT WOS:A1993MK57900044 PM 8254420 ER PT J AU SCOTT, JA AF SCOTT, JA TI THOUGHTS AT COMPLINE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material RP SCOTT, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1993 VL 34 IS 12 BP 2272 EP 2273 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MK579 UT WOS:A1993MK57900047 PM 8254423 ER PT J AU RABITO, CA MOORE, RH BOUGAS, C DRAGOTAKES, SC AF RABITO, CA MOORE, RH BOUGAS, C DRAGOTAKES, SC TI THE AMBULATORY RENAL MONITOR - REPLY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Letter RP RABITO, CA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1993 VL 34 IS 12 BP 2277 EP 2277 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MK579 UT WOS:A1993MK57900051 ER PT J AU YANUSHPOLSKY, EH OZTURK, M POLGAR, K BERKOWITZ, RS HILL, JA AF YANUSHPOLSKY, EH OZTURK, M POLGAR, K BERKOWITZ, RS HILL, JA TI THE EFFECTS OF CYTOKINES ON HUMAN CHORIONIC-GONADOTROPIN (HCG) PRODUCTION BY A TROPHOBLAST CELL-LINE SO JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Article DE CYTOKINES; TROPHOBLAST; HUMAN CHORIONIC GONADOTROPIN; PROTEIN SYNTHESIS ID NECROSIS-FACTOR-ALPHA; MONOCLONAL-ANTIBODIES; INTERLEUKIN-6 IL-6; SYNTHETIC PEPTIDE; BETA-HCG; RELEASE; MACROPHAGES; LEUKOCYTES; PLACENTAS; SECRETION AB The present study was conducted to investigate the effects of cytokines on human chorionic gonadotropin (hCG) and its alpha- and beta-subunit release as well as protein synthesis in a trophoblast cell line. The human choriocarcinoma cell line, Jar, was used as a trophoblast model. Jar cells were incubated for 24 h with varying concentrations(5 x 10(-4)-40 mu g/ml) of the following cytokines: Il-1, Il-2, Il-3, Il-4, Il-5, Il-6, IFN-gamma, tumor necrosis factor (TNF)-alpha, M-CSF and GM-CSF. Supernatants were assayed for hCG and its alpha- and beta-subunits by immunoradiometric methods. Cytotoxic effects were assessed by trypan blue staining. Protein synthesis was measured by [H-3]leucine incorporation. The cytokines Il-1 and TNF-alpha significantly stimulated hCG release. The other cytokines had no significant effect on hCG production. Protein synthesis by the Jar cells was not significantly affected by either IL-1 or TNF-alpha. However, IFN-gamma (40 mu g/ml) significantly suppressed protein synthesis by the Jar cells. Trophoblast viability in the presence of TNF-alpha (10 mu g/ml) and IFN-gamma (40 mu g/ml) was only 40% and 50%, respectively. These results suggest that cytokines may be important regulators of trophoblast function. Il-1 appears to have a stimulatory effect on trophoblast hCG release, while TNF-alpha and IFN-gamma appear to have cytotoxic effects on trophoblast cells. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET GYNECOL & REPROD BIOL,DIV REPROD IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA. RI ozturk, mehmet/G-3330-2014 FU NICHD NIH HHS [HD-23547, HD-000815] NR 26 TC 38 Z9 38 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-0378 J9 J REPROD IMMUNOL JI J. Reprod. Immunol. PD DEC PY 1993 VL 25 IS 3 BP 235 EP 247 DI 10.1016/0165-0378(93)90066-Q PG 13 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA NC770 UT WOS:A1993NC77000004 PM 8207712 ER PT J AU DEPAUL, R BROOKS, BR AF DEPAUL, R BROOKS, BR TI MULTIPLE OROFACIAL INDEXES IN AMYOTROPHIC-LATERAL-SCLEROSIS SO JOURNAL OF SPEECH AND HEARING RESEARCH LA English DT Article DE AMYOTROPHIC LATERAL SCLEROSIS (ALS); DYSARTHRIA; SPEECH; WEAKNESS; TONGUE; LIP; JAW ID PRIMARY MOTOR CORTEX; TRAINED TONGUE-PROTRUSION; FUNCTIONAL-PROPERTIES; SINGLE NEURONS; MOTONEURON INVOLVEMENT; SPEECH-INTELLIGIBILITY; CLINICAL-FEATURES; DYSARTHRIA; PERFORMANCE; DISEASE AB Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by significant speech and swallowing problems resulting from upper and lower motor neuron loss. Weakness is the primary ALS disease-related sign, and measures of muscle strength have revealed nonuniform patterns of muscle weakness in orofacial muscles. To a large extent, muscle strength measures in these studies have not been evaluated in terms of functional significance, and few researchers have addressed the relation between weakness and motor neuron loss. This study addressed whether multiple measures, including static isometric maximum voluntary contraction (MVC), a dynamic measure of the peak rate of change of force (PRCF), an upper motor neuron (UMN) index, and a functional disability score (FDS) might enhance understanding of speech dysfunction in ALS. Ten males diagnosed with sporadic ALS showing mild speech impairment and an equal number of matched controls were studied. Tongue MVC and PRCF were more impaired than those of the lip and jaw, irrespective of the time post onset and site of initial symptoms. Results also suggested that disproportionate tongue impairment may be related to UMN deficits. However, impairments in the rate of contraction did not appear to be related to UMN deficits. Tongue weakness and tongue and lower lip PRCF were related to the degree of speech severity, but none of the measures was related to speech intelligibility. The value of a functional outcome measure like speech intelligibility and its role in characterizing orofacial involvement in the early stages of ALS bulbar impairment are discussed. C1 UNIV WISCONSIN,WHITEWATER,WI 53190. WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV,MADISON,WI 53705. RP DEPAUL, R (reprint author), UNIV WISCONSIN,WAISMAN CTR,RM 579,1500 HIGHLAND AVE,MADISON,WI 53705, USA. FU NIDCD NIH HHS [R29DC00921-01] NR 87 TC 34 Z9 36 U1 0 U2 3 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE RD, ROCKVILLE, MD 20852-3279 SN 0022-4685 J9 J SPEECH HEAR RES JI J. Speech Hear. Res. PD DEC PY 1993 VL 36 IS 6 BP 1158 EP 1167 PG 10 WC Language & Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA MK809 UT WOS:A1993MK80900005 PM 8114482 ER PT J AU BROOKS, R GARAN, H TORCHIANA, D VLAHAKES, GJ JACKSON, G NEWELL, J MCGOVERN, BA RUSKIN, JN AF BROOKS, R GARAN, H TORCHIANA, D VLAHAKES, GJ JACKSON, G NEWELL, J MCGOVERN, BA RUSKIN, JN TI DETERMINANTS OF SUCCESSFUL NONTHORACOTOMY CARDIOVERTER-DEFIBRILLATOR IMPLANTATION - EXPERIENCE IN 101 PATIENTS USING 2 DIFFERENT LEAD SYSTEMS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID MALIGNANT VENTRICULAR ARRHYTHMIAS; HOSPITAL CARDIAC-ARREST; THRESHOLD; EFFICACY; SURVIVAL AB Objectives. This study was conducted to identify the determinants of successful nonthoracotomy cardioverter-defibrillator implantation. Background. Until recently, either median sternotomy or thoracotomy was necessary to implant the electrodes used for internal cardioverter-defibrillator systems. A number of manufacturers have developed nonthoracotomy lead systems comprising two transvenous coil electrodes and a subcutaneous patch electrode. At present, the factors associated with the success or failure of a nonthoracotomy approach are unknown. Methods. A total of 101 consecutive patients requiring a cardioverter-defibrillator underwent an initial nonthoracotomy approach. Factors associated with successful nonthoracotomy implantation were prospectively determined. Results. A nonthoracotomy system was implanted in 72 (71%) of 101 patients. Twenty-nine patients (29%) required thoracotomy. Univariate predictors of successful nonthoracotomy implantation included smaller cardiac size (p < 0.0001), smaller cardiothoracic ratio (p < 0.0002), QRS duration < 120 ms (p = 0.003), female gender (p = 0.006), ventricular fibrillation as the presenting arrhythmia (p = 0.03) and smaller echocardiographic left ventricular size (p = 0.04). Multivariate predictors included smaller cardiac size (p < 0.002) and female gender (p < 0.007). Total actuarial survival over a mean (+/- SD) follow-up interval of 12 +/- 7 months was 91 +/- 0.03% and was not different in the thoracotomy and nonthoracotomy groups. Conclusions. A nonthoracotomy cardioverter-defibrillator system can be implanted in a majority of patients. Smaller cardiac size and female gender are associated with a high probability of successful implantation. RP BROOKS, R (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BULFINCH 019,BOSTON,MA 02114, USA. NR 16 TC 62 Z9 62 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 DEC PY 1993 VL 22 IS 7 BP 1835 EP 1842 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MQ366 UT WOS:A1993MQ36600013 PM 8245336 ER PT J AU SHIMAKAWA, T WARRAM, JH HERRERAACENA, MG KROLEWSKI, AS AF SHIMAKAWA, T WARRAM, JH HERRERAACENA, MG KROLEWSKI, AS TI USUAL DIETARY-INTAKE AND HEMOGLOBIN A(1) LEVEL IN PATIENTS WITH INSULIN-DEPENDENT DIABETES SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID FOOD FREQUENCY QUESTIONNAIRE; HIGH-CARBOHYDRATE DIET; HIGH-FIBER DIET; GLUCOSE CONTROL; BINDING; COMPLICATIONS; RETINOPATHY; ADIPOCYTES; MELLITUS; RISK AB Objective To explore epidemiologic evidence for the relation ship between dietary intake and glycemic control. Design/subjects We examined usual dietary intake, assessed by a food frequency questionnaire, from a random sample (n=136) of patients who had had insulin-dependent diabetes mellitus for 15 to 21 years. Results In men, absolute intakes of energy, carbohydrate, protein, fat, and dietary fiber were positively correlated with hemoglobin A(1) (HbA(1)) (P<.05); Spearman correlation coefficients (gamma(s)) were .28,.22,.28,.34, and.25, respectively. In women, the correlations were weaker and not significant; gamma(s) values were .18,.13,.17,.19, and .16, respectively. When these nutrients were expressed as a percentage of energy or as an amount per 1,000 kcal, only percentage of energy from fat showed a significant association with HbA(1)-but only in men (gamma(s)=.23 for ren and.02 for women). Adjustment for body weight, insulin dose, and physical activity using multiple regression analysis did not change the relationship between HbA(1) and intakes of energy and fat. Sucrose and alcohol intakes did not show any association with HbA,. Conclusions Among men with insulin-dependent diabetes mellitus, the major dietary correlates of poor glycemic control were high intake of energy and percentage of energy from fat. Further investigation is needed to confirm this relationship of energy, fat, and glycemic control. C1 JOSLIN DIABET CTR,DIV RES,EPIDEMIOL & GENET SECT,BOSTON,MA 02215. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-41526] NR 33 TC 10 Z9 10 U1 0 U2 1 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 DEC PY 1993 VL 93 IS 12 BP 1409 EP & DI 10.1016/0002-8223(93)92243-Q PG 0 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MM037 UT WOS:A1993MM03700012 PM 8245375 ER PT J AU GERETY, MB CORNELL, JE PLICHTA, DT EIMER, M AF GERETY, MB CORNELL, JE PLICHTA, DT EIMER, M TI ADVERSE EVENTS RELATED TO DRUGS AND DRUG-WITHDRAWAL IN NURSING-HOME RESIDENTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ELDERLY POPULATION; HIP FRACTURE; LONG; SERVICES; ILLNESS; THERAPY; TRIAL; RISK AB Objective: To (1) develop and standardize explicit criteria to link clinical adverse events to drug withdrawal, (2) determine the incidence and severity of Adverse Drug Events (ADEs) and Adverse Drug Withdrawal Events (ADWEs) in a nursing home population, and (3) establish the contribution of demographic, clinical, and functional characteristics to ADEs and ADWEs. Design: Retrospective record review of an admission cohort. Setting and Subjects: Consecutive admissions of residents of an academic Veterans Affairs nursing home with available records and lengths of stay >30 days (n = 175). Subjects were 96% men, aged 70 +/- 12 years, and took 7.0 +/- 3.4 medications. Methods: We applied standardized algorithms to determine incidence, probability, and severity of ADEs and ADWEs. Multiple regression techniques were used to identify factors associated with frequency and risk of events. Results: Ninety five residents experienced 201 ADEs. Twelve required hospitalization or prolonged hospitalization, and one resident died. Sixty two persons had 94 ADWEs. None were associated with death and one with hospitalization. The four most commonly prescribed drug classes accounted for 72% of ADEs and 80% of ADWEs. Results of multivariate analyses showed common risk factors for both ADEs and ADWEs: number of diagnoses, number of medications, and hospitalization during the nursing home stay. Conclusions: ADEs and ADWEs were common in nursing home residents in this Veteran's Affairs setting. Explicit criteria developed and applied in this study should be applied prospectively in other settings, both to further define risk of drug discontinuation and to assist in development of specific drug discontinuation guidelines. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712. RP GERETY, MB (reprint author), AUDIE L MURPHY VET MEM HOSP,GRECC 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 39 TC 64 Z9 64 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD DEC PY 1993 VL 41 IS 12 BP 1326 EP 1332 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA MK559 UT WOS:A1993MK55900007 PM 8227915 ER PT J AU ALLAM, A GIOIOSO, D TAGHIAN, A DUFFY, M FIDLER, IJ SUIT, HD AF ALLAM, A GIOIOSO, D TAGHIAN, A DUFFY, M FIDLER, IJ SUIT, HD TI INTRINSIC RADIATION SENSITIVITY - NO CORRELATION WITH THE METASTATIC POTENTIAL OF HUMAN AND MURINE TUMOR-CELL LINES SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Note ID LOCAL-CONTROL; CARCINOMA; DISSEMINATION; HETEROGENEITY; RADIOTHERAPY; IMPLANTATION; PROSTATE; THERAPY; SURGERY; CLONES C1 UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX 77025. RP ALLAM, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,RADIAT BIOL LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA13311] NR 24 TC 7 Z9 7 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD DEC 1 PY 1993 VL 85 IS 23 BP 1954 EP 1957 DI 10.1093/jnci/85.23.1954 PG 4 WC Oncology SC Oncology GA MJ838 UT WOS:A1993MJ83800017 PM 8230288 ER PT J AU DRETLER, SP YOUNG, RH AF DRETLER, SP YOUNG, RH TI STONE GRANULOMA - A CAUSE OF URETERAL STRICTURE SO JOURNAL OF UROLOGY LA English DT Article DE URETERAL CALCULI; GRANULOMA ID MANAGEMENT AB Ureteral stricture is a recognized complication of ureteroscopy and ureteral stone fragmentation. Although most strictures are either asymptomatic or easily dilated, there are some strictures that result in progressive ureteral obstruction, do not respond to ureteral dilation and require operative intervention. A review of 125 percutaneous nephrostolithotomies for staghorn stone disease and 652 ureteroscopic stone fragmentations revealed 5 cases in which refractory ureteral strictures developed, requiring operative intervention. In 4 patients a ''stone granuloma,'' embedded particles of calcium oxalate associated with macrophages and foreign body giant cells, was found with surrounding fibrosis and ureteral obstruction. In the remaining patient a suture granuloma from a recent ureterolithotomy was the source of the stricture. In each instance of stone granuloma the particles of calcium oxalate had become embedded in the wall as a consequence of ureteroscopic stone fragmentation and partial ureteral wall disruption. During ureteroscopy and intracorporeal lithotripsy every effort should be made to prevent calcium oxalate particles from becoming embedded in the ureteral wall. They are not inert and may cause irreversible stricture formation. To our knowledge, stone granuloma is a previously undescribed phenomenon and should be suspected when ureteral strictures that occur following ureteroscopy do not respond to endourological methods of management. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DRETLER, SP (reprint author), MASSACHUSETTS GEN HOSP,CTR KIDNEY STONE,BOSTON,MA 02114, USA. NR 8 TC 28 Z9 29 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD DEC PY 1993 VL 150 IS 6 BP 1800 EP 1802 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA MG321 UT WOS:A1993MG32100014 PM 8230508 ER PT J AU GERTLER, JP PERRY, L LITALIEN, G CHUNGWELCH, N CAMBRIA, RP ORKIN, R ABBOTT, WM AF GERTLER, JP PERRY, L LITALIEN, G CHUNGWELCH, N CAMBRIA, RP ORKIN, R ABBOTT, WM TI AMBIENT OXYGEN-TENSION MODULATES ENDOTHELIAL FIBRINOLYSIS SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 7th Annual Meeting of the Eastern-Vascular-Society CY APR 29-MAY 02, 1993 CL PHILADELPHIA, PA SP E VASC SOC ID CELLS; SYSTEM AB Purpose: Vascular procedures reoxygenate ischemic endothelial cells (EC) and arterialize saphenous vein (HSV) EC. The balance between the EC-derived fibrinolytic components, plasminogen activator (tPA), and plasminogen inhibitor (PAZ-I) contributes to maintaining thromboresistance. This balance also affects proteolysis through plasmin generation, mediating matrix metabolism endothelial migration, angiogenesis, and theoretically affecting the development of intimal hyperplasia. Methods: To explore the impact of varying oxygen tensions on EC fibrinolysis, HSV and human umbilical vein (HUV) were subjected to PO2 of 40 mm Hg for 24 hours with restoration of Po, to 150 mm Hg for 24 hours. The tPA and PAI-1 antigen and tPA/PAI-1 antigen ratio in conditioned media (CM), expressed as up arrow or down arrow % change, normalized for cell count, versus controls, were analyzed by enzyme-linked immunosorbent assay. Cellular tPA and PAI-I mRNAs were assessed by Northern analysis. Results: The tPA but not PAT-1 was significantly decreased after the first 24 hows in HSVEC and significantly decreased after 48 hours in both HUVEC and HSVEC when compared with controls. Messenger RNA for tPA was unchanged but PAI-1 mRNA increased significantly for HSVEC and HUVEC after 24 hours of Po, of 40 mm Hg, returning to baseline within 24 hours of Po-2 to 150 mm Hg restoration. Conclusions: These data support the hypothesis of a fibrinolytic shift after altered ambient O-2 tensions exposure in endothelium and demonstrate that HSVEC are more sensitive to altered O-2 tension than HUVEC. Altered O-2 tensions depress EC fibrinolysis in this model. RP GERTLER, JP (reprint author), MASSACHUSETTS GEN HOSP,DIV VASC SURG,15 PARKMAN ST,SUITE 464,BOSTON,MA 02114, USA. NR 17 TC 65 Z9 68 U1 0 U2 0 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 DEC PY 1993 VL 18 IS 6 BP 939 EP 946 PG 8 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA MM412 UT WOS:A1993MM41200006 PM 8264050 ER PT J AU PETERSEN, MJ ABBOTT, WM HDOUBLER, PB LITALIEN, GJ HOPPEL, BE ROSEN, BR FALLON, JT ORKIN, RW AF PETERSEN, MJ ABBOTT, WM HDOUBLER, PB LITALIEN, GJ HOPPEL, BE ROSEN, BR FALLON, JT ORKIN, RW TI HEMODYNAMICS AND ANEURYSM DEVELOPMENT IN VASCULAR ALLOGRAFTS SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID ABDOMINAL AORTIC-ANEURYSMS; HUMAN PERIPHERAL-BLOOD; WISTAR-KYOTO RATS; COLLAGENASE AB Purpose: Mechanical and immunologic factors may play a role in the development of native arterial and biologic graft aneurysms. We developed an experimental rat aortic allograft aneurysm model in which segments of infrarenal aorta were transplanted between hypertensive and normotensive rats to study these factors in this model. Methods: Aortic allografts and autografts were inserted into spontaneously hypertensive (SHR) and normotensive Wistar. Kyoto (WKY) rats. Effects of immunologic and antihypertensive therapy were evaluated. Graft diameters were followed up with magnetic resonance imaging and at harvest. Direct-pressure measurements were taken and dp/dt(max) (force of ventricular contractions) was calculated before harvest. Results: Autografts remained isodiametric and maintained their histologic architecture. Aneurysmal dilation of transplanted segments occurred in SHR host allografts but not in WKY host allografts. Histologic examination of ah allograft specimens noted a rejection reaction characterized by inflammatory cell infiltration and medial smooth muscle cell loss. Antigenic enhancement accelerated aneurysm development in SHR hosts but had no significant effect on WKY hosts. Rates of allograft enlargement and final allograft diameters were similar in antihypertensive treated and untreated SHR hosts. The dp/dt(max) in untreated SHR hosts was greatest and differed significantly from that in the WKY rats but only marginally from that in treated SHR hosts. Conclusions: Immunologic rejection but not abnormal hemodynamics is necessary for development of allograft aneurysm in this model. C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. FU NCI NIH HHS [CA40303]; NHLBI NIH HHS [HL34780, HL39810] NR 25 TC 9 Z9 9 U1 1 U2 3 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD DEC PY 1993 VL 18 IS 6 BP 955 EP 964 PG 10 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA MM412 UT WOS:A1993MM41200008 PM 8264052 ER PT J AU COHEN, SN HOBSON, RW WEISS, DG CHIMOWITZ, M JARRETT, F RILES, T CALLIGARO, K THIELE, BL SCHECHTER, DC SMITH, RB AMMONS, J GIANNETTI, R VOLLMAN, RW JOHNSON, W BUTLER, R KASE, C HAMILTON, J WALKER, N GAGE, A POWELL, CS SORIA, E OLSZEWSKI, WA GUTIERREZ, I YOUNG, DE BURCH, K LYNCH, TG PADBERG, F SHANAWANI, S JOHNSON, DA ROGERS, C HIRATZKA, LF CORSON, J TALMAN, WT MARTIN, C GRIMTH, VB YUTZY, J LUTES, B THOMPSON, BW MORGAN, D MCDONALD, C BAKER, JD METTER, EJ RABEY, N DIX, D TOWNE, JB BANDYK, D SAXENA, VK NAVINE, J CATAROZOLI, K LANZA, D PARSON, P KRUPSKI, WC RAPP, J SHARP, F PEREZ, S GOLDSTONE, J BERNHARD, V LABADIE, E NASH, M PHELPS, B VANCE, J ANDERSON, G ZIERLER, RE STABILE, B WILSON, S EMMA, L HUBBERT, C HAAKENSON, CI TOUSSAINT, D YOUNG, L COLLING, C FIELDS, WS MOORE, WS WRIGHT, CB ROSSOS, S GEORGE, A CALLOW, AD FLORA, RE GROTTA, JC IMPARATO, A CRIGLER, C BEARD, W CAESAR, SL COVI, L GAUVEY, SK LIPMAN, RS KURZ, R BLOCK, K LEVITON, SP RASKIN, A MOORE, M SAFER, D FELDBUSH, MW PEREZ, E WEISS, R ARTHUR, MM HOBBINS, TE SONG, IS CAPLAN, LR WRIGHT, C KLETT, CJ COLLINS, JF JACKSON, P MORSON, D CARTER, BD MCMULLEN, B KUHN, R MILLER, B LEE, M PRESTON, D DAVIS, D LINZY, L LUCAS, C DEYKIN, D GOLD, J HUANG, P AF COHEN, SN HOBSON, RW WEISS, DG CHIMOWITZ, M JARRETT, F RILES, T CALLIGARO, K THIELE, BL SCHECHTER, DC SMITH, RB AMMONS, J GIANNETTI, R VOLLMAN, RW JOHNSON, W BUTLER, R KASE, C HAMILTON, J WALKER, N GAGE, A POWELL, CS SORIA, E OLSZEWSKI, WA GUTIERREZ, I YOUNG, DE BURCH, K LYNCH, TG PADBERG, F SHANAWANI, S JOHNSON, DA ROGERS, C HIRATZKA, LF CORSON, J TALMAN, WT MARTIN, C GRIMTH, VB YUTZY, J LUTES, B THOMPSON, BW MORGAN, D MCDONALD, C BAKER, JD METTER, EJ RABEY, N DIX, D TOWNE, JB BANDYK, D SAXENA, VK NAVINE, J CATAROZOLI, K LANZA, D PARSON, P KRUPSKI, WC RAPP, J SHARP, F PEREZ, S GOLDSTONE, J BERNHARD, V LABADIE, E NASH, M PHELPS, B VANCE, J ANDERSON, G ZIERLER, RE STABILE, B WILSON, S EMMA, L HUBBERT, C HAAKENSON, CI TOUSSAINT, D YOUNG, L COLLING, C FIELDS, WS MOORE, WS WRIGHT, CB ROSSOS, S GEORGE, A CALLOW, AD FLORA, RE GROTTA, JC IMPARATO, A CRIGLER, C BEARD, W CAESAR, SL COVI, L GAUVEY, SK LIPMAN, RS KURZ, R BLOCK, K LEVITON, SP RASKIN, A MOORE, M SAFER, D FELDBUSH, MW PEREZ, E WEISS, R ARTHUR, MM HOBBINS, TE SONG, IS CAPLAN, LR WRIGHT, C KLETT, CJ COLLINS, JF JACKSON, P MORSON, D CARTER, BD MCMULLEN, B KUHN, R MILLER, B LEE, M PRESTON, D DAVIS, D LINZY, L LUCAS, C DEYKIN, D GOLD, J HUANG, P TI DEATH ASSOCIATED WITH ASYMPTOMATIC CAROTID-ARTERY STENOSIS - LONG-TERM CLINICAL-EVALUATION SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID ENDARTERECTOMY; BRUIT; MANAGEMENT AB Purpose: As part of a prospective clinical trial on the efficacy of carotid endarterectomy in patients with asymptomatic carotid artery stenosis, we studied the risk factors for death in 444 male patients. Methods: At entry to the trial, patients were judged to be healthy enough to be randomized to operative intervention and were judged to be free of any disease that would preclude a minimal 5-year life expectancy after randomization. Results: Patients were treated with aspirin and optimal medical care and were monitored for an average of 4 years. Combined mortality rate was 37% (9% per year) for the medical group (38%) and surgical group (35%). Eight factors were identified that were significantly associated with increased mortality rates: coronary artery disease (p = 0.044), history of angina (p = 0.047), congestive heart failure (CHP) (P = 0.012), abnormal electrocardiography results at entry (p = 0.005), peripheral vascular disease (p = 0.019), claudication (p = 0.044), diabetes (p = 0.008), and history of hypertension (p = 0.044). The increase in risk indicated by the odds ratios (OR) were moderate (OR < 2.00) for each of the clinical risk factors except for CHP. Sixteen of 27 patients (59%) with a history of CHF at entry to the study died during follow-up (OR = 2.67). Arteriographic predictors of increased mortality rates included bilateral carotid artery stenosis and intracranial vascular disease (ICVD). With bilateral stenosis, 42% (80 of 190 patients) died compared with 33% (83 of 252 patients) with unilateral stenosis (p = 0.062). With ICVD, 43% (56 of 130 patients) died compared with 34% (107 of 314 patients) of those without ICVD (p = 0.073). Multivariate analysis demonstrated that three risk factors were significantly associated with an increased risk of death: diabetes, abnormal electrocardiography results, and claudication. Patients with two or three of these risk factors demonstrated annual mortality rates of 11.3% and 13%, respectively. This was significantly higher than patients with none of these risks (OR = 2.95 and OR = 4.06, respectively). Conclusion: Adult male patients with high-grade asymptomatic carotid artery stenosis demonstrate a mortality rate of 37% at a mean follow-up of 4 years. Although age was not a risk for increased mortality rates in this population, diabetes, abnormal electrocardiography results, and claudication were significant. Patients with two or three of these risk factors were at high risk of death and may require aggressive treatment of their concurrent medical diseases. C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. E ORANGE VET AFFAIRS MED CTR, NEWARK, NJ USA. UNIV MED & DENT NEW JERSEY, NEWARK, NJ USA. US DEPT VET AFFAIRS, COOPERAT STUDIES PROGRAM, PERRY POINT, MD USA. UNIV MICHIGAN, ANN ARBOR, MI 48109 USA. VET AFFAIRS MED CTR, ANN ARBOR, MI USA. RP COHEN, SN (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, NEUROL SERV W127, LOS ANGELES, CA 90073 USA. NR 26 TC 27 Z9 27 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD DEC PY 1993 VL 18 IS 6 BP 1002 EP 1011 PG 10 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA MM412 UT WOS:A1993MM41200013 PM 8264028 ER PT J AU YEH, L SCHAFFER, PA AF YEH, L SCHAFFER, PA TI A NOVEL CLASS OF TRANSCRIPTS EXPRESSED WITH LATE KINETICS IN THE ABSENCE OF ICP4 SPANS THE JUNCTION BETWEEN THE LONG AND SHORT SEGMENTS OF THE HERPES-SIMPLEX VIRUS TYPE-1 GENOME SO JOURNAL OF VIROLOGY LA English DT Article ID TEMPERATURE-SENSITIVE MUTANTS; SITE-SPECIFIC CLEAVAGE; THYMIDINE KINASE GENE; TRIGEMINAL GANGLIA; MACROMOLECULAR-SYNTHESIS; DELETION MUTANTS; A-SEQUENCE; VIRAL-DNA; REGULATORY PROTEIN-ICP4; NUCLEOTIDE-SEQUENCES AB A novel family of transcripts that span the junction between the long and short segments of the herpes simplex virus type 1 genome has been identified. These transcripts, designated L/S junction-spanning transcripts (L/STs), are synthesized in abundance in a variety of cells infected with mutant viruses defective in the gene for ICP4, the major transcriptional regulatory protein of the virus. Transcription of abundant 2.3- and 8.5-kb series of L/STs was shown to initiate within the same sequences as less abundant 4.2-, 7.3-, and >9.5-kb transcripts by Northern (RNA) blot analysis. S1 nuclease analysis revealed a single 5' terminus 28 bp downstream of a TATA box and 6 bp downstream of a consensus ICP4 binding site. The location of the transcriptional start site indicates that the promoter of the L/STs likely corresponds to the bidirectional promoter described by Bohenzky et al. (R. A. Bohenzky, A. G. Papavassiliou, I. H. Gelman, and S. Silverstein, J. Virol. 67:632-642, 1993). The L/STs accumulate with late kinetics in ICP4 mutant-infected cells and are polyadenylated. Mutant viruses encoding forms of ICP4 unable to bind the consensus site, ATCGTC, exhibited abundant expression of the L/STs, whereas mutants encoding forms of ICP4 able to bind this site expressed no detectable L/STs, suggesting that ICP4 plays a critical role in repressing L/ST expression. Their synthesis in ICP4 mutant-infected cells is inhibited by the protein synthesis inhibitor cycloheximide, indicating that they are induced either by an immediate-early viral protein other than ICP4 or by a virus-induced cellular protein. Preliminary evidence indicates that the L/STs are not present in latently infected ganglia. The abundant expression of the L/STs with late kinetics only in the absence of functional ICP4 and the sensitivity of their synthesis to cycloheximide indicate that they are not members of any of the recognized kinetic classes of herpes simplex virus type 1 transcripts but constitute a new class of viral transcript. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [R37CA20260]; NIAID NIH HHS [P01AI24010] NR 61 TC 69 Z9 70 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 DEC PY 1993 VL 67 IS 12 BP 7373 EP 7382 PG 10 WC Virology SC Virology GA MG307 UT WOS:A1993MG30700054 PM 7901428 ER PT J AU CAI, WH ASTOR, TL LIPTAK, LM CHO, C COEN, DM SCHAFFER, PA AF CAI, WH ASTOR, TL LIPTAK, LM CHO, C COEN, DM SCHAFFER, PA TI THE HERPES-SIMPLEX VIRUS TYPE-1 REGULATORY PROTEIN ICP0 ENHANCES VIRUS-REPLICATION DURING ACUTE INFECTION AND REACTIVATION FROM LATENCY SO JOURNAL OF VIROLOGY LA English DT Article ID TEMPERATURE-SENSITIVE MUTANTS; IMMEDIATE EARLY GENE-1; COMPLETE DNA-SEQUENCE; LONG UNIQUE REGION; MESSENGER-RNA; DELETION MUTANTS; REPEAT REGION; EXPRESSION; TRANSCRIPT; GENOME AB ICP0 is a potent activator of herpes simplex virus type 1 gene expression in transient assays and in productive infection. A role for ICP0 in reactivation from latency in vivo has also been suggested on the basis of the observation that viruses with mutations in both copies of the diploid gene for ICP0 reactivate less efficiently than wild-type virus. Because the ICP0 gene is contained entirely within the coding sequences for the latency-associated transcripts (LATs), ICP0 mutants also contain mutations in LAT coding sequences. This overlap raises the question of whether mutations in ICP0 or the LATs, which have also been implicated in reactivation, are responsible for the reduced reactivation frequencies characteristic of ICP0 mutants. Two approaches were taken to examine more definitively the role of ICP0 in the establishment and reactivation of latency. First, a series of ICP0 nonsense, insertion, and deletion mutant viruses that exhibit graded levels of ICP0-specific transactivating activity were tested for parameters of the establishment and reactivation of latency in a mouse ocular model. Although these mutants are ICP0 LAT double mutants, all nonsense mutants induced the synthesis of near-wild-type levels of the 2-kb LAT, demonstrating that the nonsense linker did not disrupt the synthesis of this LAT species. All mutants replicated less efficiently than the wild-type virus in mouse eyes and ganglia during the acute phase of infection. The replication efficiencies of the mutants at these sites corresponded well with the ICP0 transactivating activities of individual mutant peptides in transient expression assays. All mutants exhibited reduced reactivation frequencies relative to those of wild-type virus, and reactivation frequencies, like replication efficiencies in eyes and ganglia, correlated well with the level of ICP0 transactivating activity exhibited by individual mutant peptides. The amount of DNA of the different mutants varied in latently infected ganglia, as demonstrated by polymerase chain reaction analysis. No correlation was evident between reactivation frequencies and the levels of viral DNA in latently infected ganglia. Thus, replication and reactivation efficiencies of ICP0 mutant viruses correlated well with the transactivating efficiency of the corresponding mutant peptides. In a second approach to examining the role of ICP0 in latency, a single copy of the wild-type gene for ICP0 was inserted into the genome of an ICP0- LAT-double mutant, 7134, which exhibits a marked impairment in its ability to replicate in the mouse eye and reactivate from latency. Insertion of one copy of the ICP0 gene into 7134 restored the ability of the mutant to replicate in the eye and reactivate from latency to approximately one-half of wild-type level. Together, these results demonstrate a role for ICP0 distinct from the role of the LATs in the establishment and reactivation of latency. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC GENET,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. FU NCI NIH HHS [R37 CA 20260]; NIAID NIH HHS [P01 AI 24010] NR 58 TC 170 Z9 174 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 DEC PY 1993 VL 67 IS 12 BP 7501 EP 7512 PG 12 WC Virology SC Virology GA MG307 UT WOS:A1993MG30700069 PM 8230470 ER PT J AU KOZIEL, MJ DUDLEY, D AFDHAL, N CHOO, QL HOUGHTON, M RALSTON, R WALKER, BD AF KOZIEL, MJ DUDLEY, D AFDHAL, N CHOO, QL HOUGHTON, M RALSTON, R WALKER, BD TI HEPATITIS-C VIRUS (HCV)-SPECIFIC CYTOTOXIC T-LYMPHOCYTES RECOGNIZE EPITOPES IN THE CORE AND ENVELOPE PROTEINS OF HCV SO JOURNAL OF VIROLOGY LA English DT Article ID NON-B-HEPATITIS; HIV-1 NEF PROTEIN; NON-A; FINE SPECIFICITY; CHORIOMENINGITIS VIRUS; PEPTIDE ANTIGENS; CELL RESPONSE; LONG-TERM; IMMUNODEFICIENCY; INFECTION AB Hepatitis C virus (HCV) is a major cause of posttransfusion and community-acquired hepatitis, and a majority of individuals infected with this virus will subsequently develop chronic hepatitis. Characterization of the host immune response to this infection is an important first step that should facilitate the development of immunomodulatory agents and vaccines. Cellular immune responses, especially those mediated by cytotoxic T lymphocytes (CTL), are important in the control of many viral diseases. In this study, liver-infiltrating lymphocytes from persons with chronic HCV hepatitis were examined for evidence of HCV-specific CTL by using target cells infected with recombinant vaccinia viruses expressing the HCV core, E1, E2, and part of the NS2 proteins. Bulk expansion of liver-derived CD8+ lymphocytes resulted in the detection of HCV-specific CTL activity, whereas activity could not be found in CD8+ lymphocytes expanded from peripheral blood. Epitopes recognized by these CTL were defined by using CTL clones obtained by limiting dilution and target cells sensitized with synthetic HCV peptides. Four distinct HLA class I-restricted epitopes were identified, including two epitopes in the amino-terminal portion of the core protein. These studies provide evidence that the highly conserved core protein is a target for HCV-specific CTL and identify CTL epitopes within the more highly variable E2 envelope protein. Our studies also suggest that HCV-specific CTL are localized at the site of tissue injury in infected persons with chronic hepatitis. Identification of the epitopes recognized by HCV-specific CTL will facilitate exploration of their role in disease pathogenesis and may provide information useful in development of therapeutic interventions or vaccines. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. BOSTON CITY HOSP,DIV GASTROENTEROL,BOSTON,MA 02118. CHIRON CORP,EMERYVILLE,CA 94608. RP KOZIEL, MJ (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. RI Ralston, Robert/A-6924-2009; Yang, Chen/G-1379-2010 FU NIAID NIH HHS [AI31563] NR 82 TC 280 Z9 288 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 DEC PY 1993 VL 67 IS 12 BP 7522 EP 7532 PG 11 WC Virology SC Virology GA MG307 UT WOS:A1993MG30700071 PM 7693974 ER PT J AU DYSON, N DEMBSKI, M FATTAEY, A NGWU, C EWEN, M HELIN, K AF DYSON, N DEMBSKI, M FATTAEY, A NGWU, C EWEN, M HELIN, K TI ANALYSIS OF P107-ASSOCIATED PROTEINS - P107 ASSOCIATES WITH A FORM OF E2F THAT DIFFERS FROM PRB-ASSOCIATED E2F-1 SO JOURNAL OF VIROLOGY LA English DT Note ID RETINOBLASTOMA GENE-PRODUCT; TRANSCRIPTION FACTOR E2F; ADENOVIRUS E1A PROTEINS; CELL-CYCLE REGULATION; REGION 1A PROTEINS; BINDING PROTEIN; VIRAL ONCOPROTEINS; MOLECULAR-CLONING; COMPLEX-FORMATION; T-ANTIGEN AB The binding of viral oncogenes to cellular proteins is thought to modulate the activities of these cellular targets. The p107 protein is targeted by many viral proteins, including adenovirus EIA, simian virus 40 large T antigen, and human papillomavirus type 16 E7 protein. A panel of monoclonal antibodies against p107 was raised and used to identify cellular proteins that interact with the p107 protein in vivo. p107-associated proteins included cyclin A, cyclin E, and cdk2. In addition, p107 was found to associate with 62- to 65- and 50-kDa phosphoproteins in ML-1 cells, a human myeloid leukemia cell line. The 62- to 65-kDa proteins have many of the properties of the transcription factor E2F but were distinguished from pRB-associated E2F-1 by both immunologic and biochemical properties. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP DYSON, N (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 52 TC 110 Z9 112 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 DEC PY 1993 VL 67 IS 12 BP 7641 EP 7647 PG 7 WC Virology SC Virology GA MG307 UT WOS:A1993MG30700086 PM 8230483 ER PT J AU LOEKEN, MR AF LOEKEN, MR TI MULTIPLE, DISTINCT TRANSACTIVATION FUNCTIONS ARE ENCODED BY THE SIMIAN VIRUS-40 LARGE-T AND SMALL-T ANTIGENS, ONLY SOME OF WHICH REQUIRE THE 82-RESIDUE AMINO-TERMINAL COMMON DOMAIN SO JOURNAL OF VIROLOGY LA English DT Note ID LARGE TUMOR-ANTIGEN; TRANSFORMATION-GOVERNING SEQUENCE; TRANSCRIPTION FACTOR E2F; SV40 LARGE-T; PROTEIN PHOSPHATASE-2A; RETINOBLASTOMA PRODUCT; BINDING-ACTIVITY; CYCLIN-A; GENE; TRANSACTIVATION AB Simian virus 40 (SV40) small t and large T antigens can each trans activate the adenovirus (Ad) E2A and the Ad VA-1 promoters. The first 82 amino acids of large T and small t are identical. However, this large T-small t common domain between residues 1 and 82 does not trans activate, suggesting that large T and small t each encode separate trans-activation functions. To determine whether the large T or small t unique domains, which are required for trans activation of the E2A promoter, are sufficient for this activity, we have employed expression plasmids separately encoding the common and unique domains of large T and small t. Cotransfection of a large T unique domain expression plasmid efficiently trans activated the E2A promoter. Optimal trans activation by large T required the motif that binds cellular proteins such as the retinoblastoma gene product, which is located in the large T unique domain, and additional large T structures outside this motif. In contrast, the small t unique domain did not trans activate the E2A promoter. Experiments utilizing E2A promoter mutants containing only the ATF- or EIIF-binding sites demonstrated that trans activation by small t involves only the EIIF transcription factor and that this function requires both the common (residues 1 to 82) and the small t unique domains expressed as a colinear protein. trans activation by large T, in contrast, involves at least three mechanisms. There appear to be at least two mechanisms that involve the EIIF transcription factor, at least one of which does not require the common domain (residues 1 to 82) and one mechanism that involves the ATF factor and does require both the common and the large T unique domains. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02215. RP LOEKEN, MR (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NCI NIH HHS [CA50599] NR 37 TC 13 Z9 13 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 DEC PY 1993 VL 67 IS 12 BP 7684 EP 7689 PG 6 WC Virology SC Virology GA MG307 UT WOS:A1993MG30700095 PM 8230491 ER PT J AU KRADIN, RL BHAN, AK AF KRADIN, RL BHAN, AK TI TUMOR-INFILTRATING LYMPHOCYTES SO LABORATORY INVESTIGATION LA English DT Editorial Material ID MAJOR HISTOCOMPATIBILITY ANTIGENS; INFLAMMATORY CELLULAR INFILTRATE; GROWTH FACTOR-BETA; T-CELLS; CLASS-I; ADVANCED CANCER; BREAST-CANCER; KILLER CELLS; EXPRESSION; INTERLEUKIN-2 C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP KRADIN, RL (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,BOSTON,MA 02114, USA. NR 45 TC 14 Z9 14 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 DEC PY 1993 VL 69 IS 6 BP 635 EP 638 PG 4 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA MP637 UT WOS:A1993MP63700001 PM 8264226 ER PT J AU MIZUTANI, T LAMURAGLIA, GM AF MIZUTANI, T LAMURAGLIA, GM TI TRANSMISSION OF LASER ENERGY AND ASSESSMENT OF TARGET TEMPERATURE IN AN EXPERIMENTAL-MODEL OF LASER BALLOON ANGIOPLASTY SO LASERS IN MEDICAL SCIENCE LA English DT Article DE DIODE LASER; INDOCYANINE GREEN; LASER BALLOON ANGIOPLASTY; POLYETHYLENE TEREPHTHALATE; THERMAL DIFFUSIVITY C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,GEN SURG SERV,DIV VASC SURG,BOSTON,MA 02114. NR 11 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 0268-8921 J9 LASER MED SCI JI Lasers Med. Sci. PD DEC PY 1993 VL 8 IS 4 BP 247 EP 252 DI 10.1007/BF02547847 PG 6 WC Engineering, Biomedical; Surgery SC Engineering; Surgery GA NC525 UT WOS:A1993NC52500003 ER PT J AU HOPPEL, BE WEISSKOFF, RM THULBORN, KR MOORE, JB KWONG, KK ROSEN, BR AF HOPPEL, BE WEISSKOFF, RM THULBORN, KR MOORE, JB KWONG, KK ROSEN, BR TI MEASUREMENT OF REGIONAL BLOOD OXYGENATION AND CEREBRAL HEMODYNAMICS SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE MAGNETIC RESONANCE IMAGING; BLOOD OXYGENATION; INTRAVASCULAR SUSCEPTIBILITY ID MAGNETIC-SUSCEPTIBILITY; TRANSVERSE RELAXATION; CAPILLARY RECRUITMENT; HYPOXIC HYPOXIA; CONTRAST AGENT; MR CONTRAST; CAT BRAIN; FLOW; TIME; RAT AB An echo planar linewidth mapping technique, Shufflebutt, has allowed temporal measurements of changes in linewidth caused by static inhomogeneities (DELTALWSI) and transverse relaxation rate (DELTAR2) in models of hypoxia and hypercapnia. We demonstrate these changes are due to intravascular susceptibility differences/(DELTA(chi)) between the blood and tissue. Contrast agent injections at a DELTA(chi) equivalent to that of deoxygenated blood showed a twofold difference between the contrast agent and physiological anoxia values. Hypercapnia decreased both DELTALWSI and DELTAR2 consistent with an increase in blood oxygenation. We attribute these findings to constant oxygen extraction during an increase in blood flow, resulting in less deoxygenated venous blood and thus reduced DELTA(chi). For in vivo perturbations we found that DELTAR2/DELTAR2' almost-equal-to 0.33, a ratio much different from that measured in whole blood phantoms (DELTAR2/DELTAR2' almost-equal-to 2). This demonstrates that signal changes in these studies are produced predominantly by dephasing of extravascular protons due to field inhomogeneities produced by intravascular deoxygenated hemoglobin (deoxyHb). C1 MIT,CAMBRIDGE,MA 02139. RP HOPPEL, BE (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,MGH NMR CTR,BLDG 149,BOSTON,MA 02129, USA. RI Thulborn, Keith/D-9183-2015 OI Thulborn, Keith/0000-0001-6197-4296 FU NCI NIH HHS [R01-CA-40303, P01-CA-48729]; NHLBI NIH HHS [R01-HL-39810] NR 42 TC 93 Z9 93 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD DEC PY 1993 VL 30 IS 6 BP 715 EP 723 DI 10.1002/mrm.1910300609 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MK175 UT WOS:A1993MK17500008 PM 8139453 ER PT J AU HELTON, RA HARRISON, WA KELLEY, K KANE, MA AF HELTON, RA HARRISON, WA KELLEY, K KANE, MA TI MELATONIN INTERACTIONS WITH CULTURED MURINE B16 MELANOMA-CELLS SO MELANOMA RESEARCH LA English DT Article DE CANCER; MELANOMA; MELATONIN; RECEPTOR; TAMOXIFEN AB Both in vitro and in vivo observations have suggested that melatonin modulates malignant cell growth. The present studies aimed to characterize the interactions of melatonin with cultured murine B16 melanoma cells. Time- and temperature-dependent specific melatonin accumulation by B16 murine melanoma cells was observed. B16 cells possessed a high affinity binding site (K-D = 1.4 nM) which exhibited structural specificity in its affinity for analogues of melatonin (melatonin > 6-hydroxymelatonin = N-acetyl-5-hydroxytryptamine > 5-methoxytryptamine >> 5-hydroxytryptamine). Evidence for a lower affinity uptake system without structural specificity was also observed. Ninety-five per cent of the specific cell-associated melatonin in B16 cells was present in the soluble subcellular fraction of lysed cells; more than 97% of the cell-associated radioactivity was authentic melatonin. When the solubilized cell extracts from the binding assay were analysed by gel filtration Immediately, all of the bound counts eluted at the void volume. Continuous exposure to melatonin for 48-120 h did not affect B16 cell proliferation as determined by cell counts, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay or [H-3]thymidine incorporation. After 8-h pulse exposures to melatonin daily for 3 days, a 15% stimulation of B16 cell proliferation (p < 0.02) was observed at melatonin concentrations of 0.1 and 1 nM. The anti-oestrogen, tamoxifen, Inhibited B16 cell growth and increased specific melatonin accumulation by B16 cells at 1 x 10(-6) M (p < 0.02). Cultured 816 murine melanoma cells possessed a specific, high affinity uptake system for melatonin which appeared to be altered by anti-oestrogen exposure. C1 DENVER VET AFFAIRS MED CTR,MED ONCOL SECT,DENVER,CO 80220. NR 0 TC 20 Z9 20 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0960-8931 J9 MELANOMA RES JI Melanoma Res. PD DEC PY 1993 VL 3 IS 6 BP 403 EP 413 DI 10.1097/00008390-199311000-00003 PG 11 WC Oncology; Dermatology; Medicine, Research & Experimental SC Oncology; Dermatology; Research & Experimental Medicine GA MU244 UT WOS:A1993MU24400003 PM 8161880 ER PT J AU YOSHINAGA, IG VINK, J DEKKER, SK MIHM, MC BYERS, HR AF YOSHINAGA, IG VINK, J DEKKER, SK MIHM, MC BYERS, HR TI ROLE OF ALPHA(3)BETA(1) AND ALPHA(2)BETA(1) INTEGRINS IN MELANOMA CELL-MIGRATION SO MELANOMA RESEARCH LA English DT Article DE CELL MIGRATION; COLLAGEN; INTEGRINS LAMININ; MELANOMA AB Recent findings indicate that variable expression of a integrins may play a role in differential melanoma cell motility. Primary melanoma (PM) and metastatic melanoma (MM) cultures, derived from the same patient, were tested for their beta(1), alpha(2), alpha(3) and alpha(6) integrin subunit expression and cell migration on type IV collagen (CN IV) or laminin (LN). The MM cell line expressed markedly increased levels of the beta(1), alpha(2) and alpha(3), but not alpha(6) subunit compared to the PM cell line. The MM cell migration rate was significantly higher than that of the PM cell line on LN- or CN IV-coated substrates. Furthermore, the cell migration rate of both lines was significantly higher (p < 0.001) on these substrates than on the control substrates. The MM and PM cell migration was significantly Inhibited by function-blocking anti-beta(1) and anti-alpha(3) MAbs, but not by the anti-alpha(6), MAb tested. In contrast, the anti-alpha(2) MAb significantly Inhibited MM but not PM cell migration. These data show that the alpha(3) subunit plays a significant role In melanoma cell motility on CN IV and LN and that. the alpha(2) subunit has a significant contribution to the motility of the MM cell line. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. FU NCI NIH HHS [CA-45587] NR 0 TC 50 Z9 53 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0960-8931 J9 MELANOMA RES JI Melanoma Res. PD DEC PY 1993 VL 3 IS 6 BP 435 EP 441 DI 10.1097/00008390-199311000-00006 PG 7 WC Oncology; Dermatology; Medicine, Research & Experimental SC Oncology; Dermatology; Research & Experimental Medicine GA MU244 UT WOS:A1993MU24400006 PM 7512849 ER PT J AU TOMERA, JF LILFORD, K HARAKAL, C AF TOMERA, JF LILFORD, K HARAKAL, C TI VECTORIAL ANALYSIS OF HYPERTROPHY, CALCIUM AND CADMIUM DEPENDENCE IN NORMOTENSIVE AND HYPERTENSIVE RABBITS SO METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY LA English DT Article DE CALCIUM; CADMIUM; CADMIUM-INDUCED HYPERTENSION; HYPERTROPHY; MULTIPLE LINEAR REGRESSION; RENAL HYPERTENSION; VECTORIAL ANALYSIS ID HEART AB Hypertension is the most common disease in the United States and its development has been linked to a wide number of factors. This report examines the relationship between calcium and cadmium accumulation and hypertrophy using a two-dimensional vector model. The dependence of calcium, cadmium and hypertrophy was examined in controls and in two hypertensive groups. Calcium and cadmium levels were measured using flame atomic absorption spectrophotometry. Numerous relationships were found based on multiple linear regression. These relationships were further examined using two-dimensional vectorial analysis. Through this analysis, the relationship of calcium and cadmium accumulation to the development of heart disease can be clearly examined. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIOL,BOSTON,MA 02115. TEMPLE UNIV,HLTH SCI CTR,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19140. RP TOMERA, JF (reprint author), SHRINERS BURNS RES CTR,ANESTHESIA SERV,CLIN PHARMACOL LAB,1 KENDALL SQ,BLDG 1400W,CAMBRIDGE,MA 02142, USA. NR 28 TC 9 Z9 9 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. PD DEC PY 1993 VL 15 IS 10 BP 669 EP 688 PG 20 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MP820 UT WOS:A1993MP82000001 ER PT J AU SHAMAH, SM STILES, CD GUHA, A AF SHAMAH, SM STILES, CD GUHA, A TI DOMINANT-NEGATIVE MUTANTS OF PLATELET-DERIVED GROWTH-FACTOR REVERT THE TRANSFORMED PHENOTYPE OF HUMAN ASTROCYTOMA-CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SIS GENE-PRODUCT; FACTOR RECEPTORS; FACTOR PDGF; MESSENGER-RNA; HUMAN GLIOMAS; BRAIN-TUMOR; AUTOCRINE STIMULATION; KINASE ACTIVATION; B-CHAIN; EXPRESSION AB Malignant astrocytoma is the most common primary human brain tumor. Most astrocytomas express a combination of platelet-derived growth factor (PDGF) and PDGF receptor which could close an autocrine loop. It is not known whether these autocrine loops contribute to the transformed phenotype of astrocytoma cells or are incidental to that phenotype. Here we show that dominant-negative mutants of the PDGF ligand break the autocrine loop and revert the phenotype of BALB/c 3T3 cells transformed by the PDGF-A or PDGF-B (c-sis) gene. Then, we show that these mutants are selective in that they do not alter the phenotype of 3T3 cells transformed by an activated Ha-ras or v-src gene or by simian virus 40. Finally, we show that these mutants revert the transformed phenotype of two independent human astrocytoma cell lines. They have no effect on the growth of human medulloblastoma, bladder carcinoma, or colon carcinoma cell lines. These observations are consistent with the view that PDGF autocrine loops contribute to the transformed phenotype of at least some human astrocytomas. C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV TORONTO,DIV NEUROSURG & SURG ONCOL,TORONTO M5S 1A1,ONTARIO,CANADA. FU NIGMS NIH HHS [GM 31489] NR 48 TC 136 Z9 138 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7203 EP 7212 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100001 PM 8246942 ER PT J AU LIU, VF WEAVER, DT AF LIU, VF WEAVER, DT TI THE IONIZING RADIATION-INDUCED REPLICATION PROTEIN-A PHOSPHORYLATION RESPONSE DIFFERS BETWEEN ATAXIA-TELANGIECTASIA AND NORMAL HUMAN-CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID VIRUS-40 DNA-REPLICATION; DOUBLE-STRAND BREAKS; SACCHAROMYCES-CEREVISIAE; SCID MUTATION; BINDING-PROTEIN; FISSION YEAST; HELA-CELLS; CYCLE; REPAIR; KINASE AB Replication protein A (RPA), the trimeric single-stranded DNA-binding protein complex of eukaryotic cells, is important to DNA replication and repair. Phosphorylation of the p34 subunit of RPA is modulated by the cell cycle, occurring during S and G2 but not during G1. The function of phosphorylated p34 remains unknown. We show that RPA p34 phosphorylation is significantly induced by ionizing radiation. The phosphorylated form, p36, is similar if not identical to the phosphorylated S/G2 form. Gamma-Irradiation-induced phosphorylation occurs without new protein synthesis and in cells in G1. Mutation of cdc2-type protein kinase phosphorylation sites in p34 eliminates the ionizing radiation response. The gamma-irradiation-induced phosphorylation of RPA p34 is delayed in cells from ataxia telangiectasia, a human inherited disease conferring DNA repair defects and early-onset tumorigenesis. UV-induced phosphorylation of RPA p34 occurs less rapidly than gamma-irradiation-induced phosphorylation but is kinetically similar between ataxia telangiectasia and normal cells. This is the first time that modification of a repair protein, RPA, has been linked with a DNA damage response and suggests that phosphorylation may play a role in regulating DNA repair pathways. C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 64 TC 181 Z9 182 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7222 EP 7231 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100003 PM 8246944 ER PT J AU FATTAEY, AR HARLOW, E HELIN, K AF FATTAEY, AR HARLOW, E HELIN, K TI INDEPENDENT REGIONS OF ADENOVIRUS E1A ARE REQUIRED FOR BINDING TO AND DISSOCIATION OF E2F-PROTEIN COMPLEXES SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RETINOBLASTOMA GENE-PRODUCT; TRANSCRIPTION FACTOR E2F; HUMAN MYC PROMOTER; LARGE T-ANTIGEN; HUMAN CYCLIN-A; TRANS-ACTIVATION; DNA-BINDING; TRANSFORMING REGION; VIRAL ONCOPROTEINS; MOLECULAR-CLONING AB The transcription factor E2F is present in independent complexes with the product of the retinoblastoma susceptibility gene, pRB, and a related gene product, p107, in association with the cyclin A-cdk2 or the cyclin E-cdk2 kinase complex. pRB and p107 can negatively regulate E2F activity, since overexpression of pRB or p107 in cells lacking a functional pRB leads to the repression of E2F activity. The products of the adenovirus EIA gene can disrupt E2F complexes and result in free and presumably active E2F transcription factor. The regions of EIA required for this function are also essential for binding to a number of cellular proteins, including pRB and p107. Through the use of a number of glutathione S-transferase fusion proteins representing different regions of EIA, as well as in vivo expression of EIA proteins containing deletions of either conserved region 1 (CRI) or CR2, we find that CR2 of EIA can form stable complexes with E2F. EIA proteins containing both CRI and CR2 also associate with E2F, although the presence of these proteins results in the release of free E2F from its complexes. In vitro reconstitution experiments indicate that EIA-E2F interactions are not direct and that pRB can serve to facilitate these interactions. Complexes containing E1A, p107, cyclin A, and E2F were identified in vivo, which indicates that EIA may associate with E2F through either p107 or pRB. Peptide competition experiments demonstrate that the pRB-binding domain of the human E2F-1 protein can compete with the CR1 but not CR2 domain of EIA for binding to pRB. These results indicate that EIA CRI and E2F-1 may bind to the same or overlapping sites on pRB and that EIA CR2 binds to an independent region. On the basis of our results, we propose a two-step model for the release of E2F from pRB and p107 cellular proteins. RP FATTAEY, AR (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 82 TC 116 Z9 117 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7267 EP 7277 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100008 PM 8246949 ER PT J AU ROSENWALD, IB LAZARISKARATZAS, A SONENBERG, N SCHMIDT, EV AF ROSENWALD, IB LAZARISKARATZAS, A SONENBERG, N SCHMIDT, EV TI ELEVATED LEVELS OF CYCLIN D1 PROTEIN IN RESPONSE TO INCREASED EXPRESSION OF EUKARYOTIC INITIATION-FACTOR 4E SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RNA 5' CAP; MESSENGER-RNA; MALIGNANT TRANSFORMATION; TRANSLATIONAL CONTROL; SECONDARY STRUCTURE; CELL-CYCLE; FACTOR-EIF-4E; ONCOGENE; GENES; MYC AB Cyclin D1 is a G1-specific cyclin that has been linked to lymphoid, parathyroid, and breast tumors. Recent studies suggested that high protein levels of cyclin Dl are not always produced when cyclin D1 mRNA is overexpressed in transfected cells, suggesting that posttranscriptional events may be important in cyclin D1 regulation. The mRNA cap-binding protein (eukaryotic initiation factor 4E [eIF-4E]) is a potential regulator of several posttranscriptional events, and it can itself induce neoplastic transformation. Consequently, we examined eIF-4E as a potential regulator of cyclin D1. Overexpression of cyclin D1 mRNA in NIH 3T3 cells did not increase cyclin D1 protein. In contrast, overexpression of eIF-4E markedly increased the amount of cyclin D1 protein in NIH 3T3 cells. This increase was specific to cyclin D1 in comparison with the retinoblastoma gene product, c-Myc, actin, and eukaryotic initiation factor 2alpha. We also examined cyclin Dl protein in cells expressing an estrogen receptor-Myc fusion protein because we previously found that eIF-4E increases after induction of c-myc function. In these cells, increased levels of eIF-4E protein were closely followed by increases in levels of cyclin D1 protein, but the level of cyclin D1 mRNA was not increased. We conclude that increases in cyclin D1 levels may result from increased expression of eIF-4E, and this regulation may be one determinant of cyclin D1 levels in the cell. C1 MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129. MCGILL UNIV,DEPT BIOCHEM,MONTREAL H3G 1Y6,QUEBEC,CANADA. NR 37 TC 246 Z9 250 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7358 EP 7363 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100017 PM 8246956 ER PT J AU SUN, XJ CRIMMINS, DL MYERS, MG MIRALPEIX, M WHITE, MF AF SUN, XJ CRIMMINS, DL MYERS, MG MIRALPEIX, M WHITE, MF TI PLEIOTROPIC INSULIN SIGNALS ARE ENGAGED BY MULTISITE PHOSPHORYLATION OF IRS-1 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SRC HOMOLOGY-2 DOMAINS; PHOSPHATIDYLINOSITOL 3'-KINASE; PROTEIN; TRANSDUCTION; EXPRESSION; SUBSTRATE; SH2; IDENTIFICATION; PURIFICATION; ASSOCIATION AB IRS-1 (insulin receptor substrate 1) is a principal insulin receptor substrate that undergoes tyrosine phosphorylation during insulin stimulation. It contains over 20 potential tyrosine phosphorylation sites, and we suspect that multiple insulin signals are enabled when the activated insulin receptor kinase phosphorylates several of them. Tyrosine-phosphorylated IRS-1 binds specifically to various cellular proteins containing Src homology 2 (SH2) domains (SH2 proteins). We identified some of the tyrosine residues of IRS-1 that undergo insulin-stimulated phosphorylation by the purified insulin receptor and in intact cells during insulin stimulation. Automated sequencing and manual radiosequencing revealed the phosphorylation of tyrosine residues 460, 608, 628, 895, 939, 987, 1172, and 1222; additional sites remain to be identified. Immobilized SH2 domains from the 85-kDa regulatory subunit (p85alpha) of the phosphatidylinositol 3'-kinase bind preferentially to tryptic phosphopeptides containing Tyr(P)-608 and Tyr(P)-939. By contrast, the SH2 domain in GRB2 and the amino-terminal SH2 domain in SHPTP2 (Syp) specifically bind to Tyr(P)-895 and Tyr(P)-1172, respectively. These results confirm that p85alpha recognizes YMXM motifs and suggest that GRB2 prefers a phosphorylated YVNI motif, whereas SHPTP2 (Syp) binds to a phosphorylated YIDL motif. These results extend the notion that IRS-1 is a multisite docking protein that engages various downstream regulatory elements during insulin signal transmission. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM CELLULAR & DEV BIOL,BOSTON,MA 02115. WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,ST LOUIS,MO 63110. FU NIDDK NIH HHS [DK43808, DK38721] NR 42 TC 410 Z9 417 U1 0 U2 11 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7418 EP 7428 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100024 PM 7504175 ER PT J AU HUANG, JK LIANG, TJ AF HUANG, JK LIANG, TJ TI A NOVEL HEPATITIS-B VIRUS (HBV) GENETIC ELEMENT WITH REV RESPONSE ELEMENT-LIKE PROPERTIES THAT IS ESSENTIAL FOR EXPRESSION OF HBV GENE-PRODUCTS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; VIRAL MESSENGER-RNA; X-PROTEIN; BINDING-PROTEIN; ENHANCER; TRANSACTIVATION; SEQUENCES; PROMOTER; REGION; CELLS AB Many viruses possess complex mechanisms involving multiple gene products and cis-regulatory elements in order to achieve a fine control of their gene expression at both transcriptional and posttranscriptional levels. Hepatitis B virus (HBV) and retroviruses share many structural and functional similarities. in this study, by genetic and biochemical analyses, we have demonstrated the existence of a novel genetic element within the HBV genome which is essential for high-level expression of viral gene products. This element is located 3' to the envelope coding region. We have shown that this genetic element is cis acting at the posttranscriptional level and that its function is exerted at the level of RNA processing as part of transcribed sequences. This RNA element is also functional in the context of a heterologous gene. Similar to the function of Rev-Rev response element interaction of human immunodeficiency virus type 1, this element appears to inhibit the splicing process and facilitate the transport and utilization of HBV transcripts. C1 MASSACHUSETTS GEN HOSP,MED SERV,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NCI NIH HHS [CA-54524]; NIDDK NIH HHS [DK-01952] NR 50 TC 121 Z9 129 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7476 EP 7486 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100030 PM 8246965 ER PT J AU CAI, H ERHARDT, P TROPPMAIR, J DIAZMECO, MT SITHANANDAM, G RAPP, UR MOSCAT, J COOPER, GM AF CAI, H ERHARDT, P TROPPMAIR, J DIAZMECO, MT SITHANANDAM, G RAPP, UR MOSCAT, J COOPER, GM TI HYDROLYSIS OF PHOSPHATIDYLCHOLINE COUPLES RAS TO ACTIVATION OF RAF PROTEIN-KINASE DURING MITOGENIC SIGNAL-TRANSDUCTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MOLECULAR-SPECIES ANALYSIS; EPIDERMAL GROWTH-FACTOR; NIH 3T3 CELLS; ALPHA-THROMBIN; PHOSPHOLIPASE-C; MAP KINASE; TYROSINE KINASE; FACTOR RECEPTOR; PC12 CELLS; FIBROBLASTS AB We have investigated the relationship between hydrolysis of phosphatidylcholine (PC) and activation of the Raf-I protein kinase in Ras-mediated transduction of mitogenic signals. As previously reported, cotransfection of a PC-specific phospholipase C (PC-PLC) expression plasmid bypassed the block to cell proliferation resulting from expression of the dominant inhibitory mutant Ras N-17. In contrast, PC-PLC failed to bypass the inhibitory effect of dominant negative Raf mutants, suggesting that PC-PLC functions downstream of Ras but upstream of Raf. Consistent with this hypothesis, treatment of quiescent cells with exogenous PC-PLC induced Raf activation, even when normal Ras function was blocked by Ras N-17 expression. Further, activation of Raf in response to mitogenic growth factors was blocked by inhibition of endogenous PC-PLC. Taken together, these results indicate that hydrolysis of PC mediates Raf activation in response to mitogenic growth factors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NCI,FREDERICK CANC RES CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV AUTONOMA MADRID,CSIC,CTR BIOL MOLEC,E-28049 MADRID,SPAIN. RI Moscat, Jorge/A-7011-2009 FU NCI NIH HHS [R01 CA18689] NR 47 TC 128 Z9 128 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7645 EP 7651 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100047 PM 8246981 ER PT J AU PRASAD, KVS KAPELLER, R JANSSEN, O REPKE, H DUKECOHAN, JS CANTLEY, LC RUDD, CE AF PRASAD, KVS KAPELLER, R JANSSEN, O REPKE, H DUKECOHAN, JS CANTLEY, LC RUDD, CE TI PHOSPHATIDYLINOSITOL (PI) 3-KINASE AND PI 4-KINASE BINDING TO THE CD4-P56(LCK) COMPLEX - THE P56(LCK) SH3 DOMAIN BINDS TO PI 3-KINASE BUT NOT PI 4-KINASE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID TYROSINE-PROTEIN-KINASE; T-CELL RECEPTOR; HUMAN-IMMUNODEFICIENCY-VIRUS; GROWTH-FACTOR RECEPTOR; HUMAN LYMPHOCYTES-T; SIGNAL TRANSDUCTION; ANTIGEN RECEPTOR; CROSS-LINKING; CD3 COMPLEX; MIDDLE-T AB CD4 serves as a receptor for major histocompatibility complex class II antigens and as a receptor for the human immunodeficiency virus type 1 (HIV-1) viral coat protein gp120. It is coupled to the protein-tyrosine kinase p56lck, an interaction necessary for an optimal response of certain T cells to antigen. In addition to the protein-tyrosine kinase domain, p56lck possesses Src homology 2 and 3 (SH2 and SH3) domains as well as a unique N-terminal region. The mechanism by which p56lck generates intracellular signals is unclear, although it has the potential to interact with various downstream molecules. One such downstream target is the lipid kinase phosphatidylinositol 3-kinase (PI 3-kinase), which has been found to bind to activated pp60src and receptor-tyrosine kinases. In this study, we verified that PI 3-kinase associates with the CD4:p56lck complex as judged by the presence of PI 3-phosphate generated from anti-CD4 immunoprecipitates and detected by high-pressure liquid chromatographic analysis. However, surprisingly, CD4-p56lck was also found to associate with another lipid kinase, phosphatidylinositol 4-kinase (PI 4-kinase). The level of associated PI 4-kinase was generally higher than PI 3-kinase activity. HIV-1 gp120 and antibody-mediated cross-linking induced a 5- to 10-fold increase in the level of CD4-associated PI 4- and PI 3-kinases. The use of glutathione S-transferase fusion proteins carrying Lck-SH2, Lck-SH3, and Lck-SH2/SH3 domains showed PI 3-kinase binding to the SH3 domain of p56lck, an interaction facilitated by the presence of an adjacent SH2 domain. PI 4-kinase bound to neither the SH2 nor the SH3 domain of p56lck. CD4-p56lck contributes PI 3-and PI 4-kinases to the activation process of T cells and may play a role in HIV-1-induced immune defects. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. BETH ISRAEL HOSP,DIV SIGNAL TRANSDUCT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV RETROVIROL,BOSTON,MA 02115. RI Janssen, Ottmar/E-9735-2010; Cantley, Lewis/D-1800-2014; Duke-Cohan, Jonathan/A-5812-2010 OI Cantley, Lewis/0000-0002-1298-7653; Duke-Cohan, Jonathan/0000-0002-9478-9609 FU NCI NIH HHS [NCI CA51887-02]; NIGMS NIH HHS [R01 GM041890, GM 36624, GM 41890] NR 83 TC 152 Z9 152 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7708 EP 7717 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100053 PM 8246987 ER PT J AU LEES, JA SAITO, M VIDAL, M VALENTINE, M LOOK, T HARLOW, E DYSON, N HELIN, K AF LEES, JA SAITO, M VIDAL, M VALENTINE, M LOOK, T HARLOW, E DYSON, N HELIN, K TI THE RETINOBLASTOMA PROTEIN BINDS TO A FAMILY OF E2F TRANSCRIPTION FACTORS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HUMAN MYC PROMOTER; TRANS-ACTIVATION; CYCLIN-A; RB GENE; TUMOR SUPPRESSOR; CARCINOMA-CELLS; DNA; PRODUCT; EXPRESSION; IDENTIFICATION AB E2F is a transcription factor that helps regulate the expression of a number of genes that are important in cell proliferation. Recently, several laboratories have isolated a cDNA clone that encodes an E2F-like protein, known as E2F-1. Subsequent characterization of this protein showed that it had the properties of E2F, but it was difficult to account for all of the suggested E2F activities through the function of this one protein. Using low-stringency hybridization, we have isolated cDNA clones that encode two additional E2F-like proteins, called E2F-2 and E2F-3. The chromosomal locations of the genes for E2F-2 and E2F-3 were mapped to 1p36 and 6q22, respectfully, confirming their independence from E2F-1. However, the E2F-2 and E2F-3 proteins are closely related to E2F-1. Both E2F-2 and E2F-3 bound to wild-type but not mutant E2F recognition sites, and they bound specifically to the retinoblastoma protein in vivo. Finally, E2F-2 and E2F-3 were able to activate transcription of E2F-responsive genes in a manner that was dependent upon the presence of at least one functional E2F binding site. These observations suggest that the E2F activities described previously result from the combined action of a family of proteins. C1 ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. RP LEES, JA (reprint author), MASSACHUSETTS GEN HOSP, CTR CANC, BLDG 149, 13TH ST, BOSTON, MA 02129 USA. NR 61 TC 389 Z9 394 U1 2 U2 8 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1993 VL 13 IS 12 BP 7813 EP 7825 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MJ341 UT WOS:A1993MJ34100064 PM 8246996 ER PT J AU PARISSENTI, AM SU, LH RIEDEL, H AF PARISSENTI, AM SU, LH RIEDEL, H TI RECONSTITUTION OF PROTEIN-KINASE-C ALPHA-FUNCTION BY THE PROTEIN-KINASE-C BETA-I CARBOXY-TERMINUS SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE PROTEIN KINASE C; CHIMERA; C-TERMINUS; CDNA EXPRESSION; DOMAIN SWAPPING; SACCHAROMYCES CEREVISIAE ID PHORBOL ESTER BINDING; SACCHAROMYCES-CEREVISIAE; SUBSTRATE-SPECIFICITY; REGULATORY DOMAIN; ENDOTHELIAL-CELLS; GENE-EXPRESSION; GROWTH-FACTOR; CA-2+ INFLUX; YEAST; ISOZYMES AB The Ca2+ - and phospholipid-dependent Ser/Thr kinase protein kinase C (PKC) plays important roles in the transduction of cellular signals. Various PKC isoforms exist in mammalian cells which share conserved and variable regions as defined by cDNA sequence comparisons. To test whether carboxyl (C) terminal sequences of distinct isoforms can complement each other to yield functional chimeric molecules, we have constructed a PKC chimera in which amino acids 595-672 at the C-terminus of bovine PKC alpha (a) were replaced with the corresponding C-terminal amino acids (598-671) of rat PKC beta-I (b) to yield the chimera alpha/beta-I (ab). The chimera was then characterized biochemically and functionally, and compared with the parental isoforms. Since structure/ function analysis of PKC in mammalian experimental systems is complicated by multiple PKC isoforms and by cellular complexity, we stably introduced the PKC constructs into the yeast Saccharomyces cerevisiae, a simple, lower eukaryote with a short doubling time and well established molecular genetics. In yeast, the faithfully expressed PKCab chimera and normal PKC isoforms bound radiolabelled phorbol ester and were recognized on immunoblots by PKC-specific antibodies. The chimera phosphorylated substrate peptides in a PMA- and Ca2+-dependent manner, and, upon activation, increased the cell doubling time and the rate of Ca2+ uptake into cells. In addition, PKCab displayed characteristics distinct from normal PKCb, but virtually indistinguishable from normal PKCa. Our findings indicate the reconstitution of PKCa function by the PKCb carboxyl terminus. C1 HARVARD UNIV, SCH MED, JOSLIN DIABET CTR, MOLEC BIOL SECT, BOSTON, MA USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DEPT MED, BOSTON, MA USA. NR 69 TC 8 Z9 8 U1 0 U2 1 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0303-7207 J9 MOL CELL ENDOCRINOL JI Mol. Cell. Endocrinol. PD DEC PY 1993 VL 98 IS 1 BP 9 EP 16 DI 10.1016/0303-7207(93)90230-H PG 8 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA MR584 UT WOS:A1993MR58400002 PM 8143918 ER PT J AU WEAVER, DR AF WEAVER, DR TI A(2A) ADENOSINE RECEPTOR GENE-EXPRESSION IN DEVELOPING RAT-BRAIN SO MOLECULAR BRAIN RESEARCH LA English DT Article DE ADENOSINE RECEPTOR; GENE EXPRESSION; STRIATUM; IN-SITU HYBRIDIZATION; ONTOGENY; BRAIN ID INSITU HYBRIDIZATION HISTOCHEMISTRY; TERM RESERPINIZED MICE; DOPAMINE RECEPTOR; MOLECULAR-CLONING; NERVOUS-SYSTEM; BINDING-SITES; EARLY LOCALIZATION; CHRONIC CAFFEINE; BASAL GANGLIA; MESSENGER-RNA AB Adenosine is a neuromodulator in the adult central nervous system. Membrane-bound receptors for adenosine have been identified and cDNAs for A1, A2a, A2b and A3 adenosine receptor subtypes have been cloned recently. The present study documents the developmental appearance of A2a adenosine receptor gene expression in the rat brain. In situ hybridization using S-35-labeled RNA probes generated from the rat A2a adenosine receptor cDNA revealed receptor gene expression in the striatum on gestational day (GD) 14. Developmental alterations in the pattern of receptor gene expression within the striatum suggest that this receptor mRNA is expressed by striatal neurons soon after they complete neurogenesis. Transient expression of the A2a adenosine receptor mRNA was observed in cerebral cortex, subiculum, parafascicularis nucleus of the thalamus, facial nucleus, trigeminal nucleus, locus coeruleus, area postrema, anterior pituitary gland and in the fetal cerebral vasculature. The ganglia of cranial nerves V, VII, VIII, IX and X expressed A2a adenosine receptor mRNA in fetuses; adults have not been examined. A2a adenosine receptor mRNA was expressed in the carotid body and intermediate lobe of the pituitary during development and also in adult rats. Northern blot analysis revealed that the A2a adenosine receptor transcript is consistent in size (ca 2.5 kb) across the developmental period examined (GD 14 through adult). Previous studies in adult rats have reported that A2a adenosine receptor gene expression is limited to a population of striatal medium spiny neurons. This study documents early developmental expression of the A2a adenosine receptor gene in the striatum and its transient expression elsewhere in the brain and cerebral vasculature. If the A2a adenosine receptor mRNA is translated into receptor protein shortly after the mRNA is expressed, adenosine could influence neuronal differentiation, migration, synaptogenesis, and angiogenesis. Expression of A2a adenosine receptor mRNA in cranial ganglia, carotid body, and intermediate lobe of the pituitary gland similarly suggests novel sites of adenosine action during development and in the adult. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP WEAVER, DR (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DEV CHRONOBIOL LAB,JACKSON 1226,BOSTON,MA 02114, USA. OI Weaver, David/0000-0001-7941-6719 NR 69 TC 106 Z9 106 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD DEC PY 1993 VL 20 IS 4 BP 313 EP 327 DI 10.1016/0169-328X(93)90058-W PG 15 WC Neurosciences SC Neurosciences & Neurology GA MJ737 UT WOS:A1993MJ73700004 ER PT J AU CHOI, HS MOORE, DD AF CHOI, HS MOORE, DD TI INDUCTION OF C-FOS AND C-JUN GENE-EXPRESSION BY PHENOLIC ANTIOXIDANTS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID YA-SUBUNIT GENE; DNA-BINDING ACTIVITY; CONTROLLING INDUCIBLE EXPRESSION; ELECTROPHILE-RESPONSIVE ELEMENT; PLANAR AROMATIC-COMPOUNDS; FACTOR KAPPA-B; TRANSCRIPTION FACTOR; OXIDATIVE STRESS; GROWTH-HORMONE; IDENTIFICATION AB We have found that phenolic antioxidants specifically induce expression of the c-fos and c-jun protooncogenes. After treatment of quiescent human hepatoma HepG2 cells with butylated hydroxytoluene, butylated hydroxyanisole, or other phenolic antoxidants, the levels of c-fos and c-jun mRNAs are substantially increased. This response is antioxidant specific, dose dependent, and transient, with maximal levels at 3-6 h. The antioxidant-specific induction of c-fos/CAT promoter constructs in transient transfections indicates that at least a portion of this response is transcriptional. Deletions and point mutations map sequences required for the antioxidant response of the c-fos promoter to the serum response element. The antioxidant-specific induction of expression directed by a reporter plasmid containing four AP-1 sites and the induction of AP-1 DNA-binding activity confirm previous results indicating that antioxidant treatment increases AP-1 activity. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 39 TC 70 Z9 71 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD DEC PY 1993 VL 7 IS 12 BP 1596 EP 1602 DI 10.1210/me.7.12.1596 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ853 UT WOS:A1993MQ85300009 PM 8145765 ER PT J AU SHIRLEY, BW GOODMAN, HM AF SHIRLEY, BW GOODMAN, HM TI AN ARABIDOPSIS GENE HOMOLOGOUS TO MAMMALIAN AND INSECT GENES ENCODING THE LARGEST PROTEASOME SUBUNIT SO MOLECULAR & GENERAL GENETICS LA English DT Article DE PROTEASOME; ARABIDOPSIS; DELETION MUTATION; GENE EXPRESSION; EVOLUTION ID MULTICATALYTIC PROTEINASE COMPLEX; MOLECULAR-CLONING; SEQUENCE-ANALYSIS; THERMOPLASMA-ACIDOPHILUM; MAJOR SUBUNITS; ALPHA-SUBUNIT; CDNA CLONING; CELLS; DROSOPHILA; EXPRESSION AB A gene encoding a protein with extensive homology to the largest subunit of the multicatalytic proteinase complex (proteasome) has been identified in Arabidopsis thaliana. This gene, referred to as AtPSM30, is entirely encompassed within a previously characterized radiation-induced deletion, which may thus provide the first example of a proteasome null mutation in a higher eukaryote. However, the growth rate and fertility of Arabidopsis plants do not appear to be significantly affected by this mutation, even though disruption experiments in yeast have shown that most proteasome subunits are essential. Analysis of mRNA levels in developing seedlings and mature plants indicates that expression of AtPSM30 is differentially regulated during development and is slightly induced in response to stress, as has been observed for proteasome genes in yeast, Drosophila, and mammals. Southern blot analysis indicates that the Arabidopsis genome contains numerous sequences closely related to AtPSM30, consistent with recent reports of at least two other proteasome genes in Arabidopsis. A comparison of the deduced amino acid sequences for all proteasome genes reported to date suggests that multiple proteasome subunits evolved in eukaryotes prior to the divergence of plants and animals. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. VIRGINIA POLYTECH INST & STATE UNIV,DEPT BIOL,BLACKSBURG,VA 24061. RP SHIRLEY, BW (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114, USA. RI Winkel, Brenda/A-6602-2008 OI Winkel, Brenda/0000-0003-3481-024X NR 39 TC 24 Z9 25 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD DEC PY 1993 VL 241 IS 5-6 BP 586 EP 594 DI 10.1007/BF00279901 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA ML714 UT WOS:A1993ML71400013 PM 8264533 ER PT J AU WOOD, SC HILL, WA MILLER, KW AF WOOD, SC HILL, WA MILLER, KW TI CYCLOALKANEMETHANOLS DISCRIMINATE BETWEEN VOLUME-DEPENDENT AND LENGTH-DEPENDENT LOSS OF ACTIVITY OF ALKANOLS AT THE TORPEDO NICOTINIC ACETYLCHOLINE-RECEPTOR SO MOLECULAR PHARMACOLOGY LA English DT Article ID ANESTHETIC TARGET SITES; MOLECULAR DIMENSIONS; GENERAL-ANESTHESIA; ALCOHOLS; CHANNELS; MEMBRANES; INHIBITION; ETHANOL; MODEL AB Primary normal alcohols (1-n-alkanols) exert two effects on the nicotinic acetylcholine receptor when added simultaneously with agonist. First, propanol through decanol inhibit the open channel. Second, methanol through butanol, but not higher homologs, increase the apparent affinity of the agonist for inducing cation flux. To test the hypothesis that the length or volume of the alcohols might account for the fact that some members of the 1-n-alkanol homologous series lack activity, we have studied in parallel 11 members of another homologous series, i.e., the cycloalkanemethanols, c(CnH(2n-1))CH2OH. With steadily increasing potency, agents from cyclopropanemethanol to cyclodecanemethanol completely inhibited carbachol-stimulated Rb-86+ efflux from nicotinic acetylcholine receptor-rich postsynaptic vesicles from the electroplaques of Torpedo nobiliana, but even 90% saturated solutions of cycloundecanemethanol inhibited only part of the flux and neither cyclododecanemethanol nor cyclotetradecanemethanol caused any inhibition. Comparison of these results with those previously obtained for 1-n-alkanols indicates that as both series are ascended the cut-off in the inhibitory action on the channel occurs when the volume of the compounds exceeds approximately 340 angstrom3. The apparent affinity for carbachol-induced flux was enhanced only by cyclopropanemethanol through cyclooctanemethanol, consistent with the hypothesis that a critical length of approximately 6.3 angstrom cannot be exceeded. Thus, the sites mediating the two effects have different steric requirements and may be physically distinct. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIAAA NIH HHS [AA07040]; NIGMS NIH HHS [GM15904] NR 26 TC 17 Z9 17 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD DEC PY 1993 VL 44 IS 6 BP 1219 EP 1226 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MN466 UT WOS:A1993MN46600018 PM 8264559 ER PT J AU BOOTH, RG WYRICK, SD BALDESSARINI, RJ KULA, NS MYERS, AM MAILMAN, RB AF BOOTH, RG WYRICK, SD BALDESSARINI, RJ KULA, NS MYERS, AM MAILMAN, RB TI NEW SIGMA-LIKE RECEPTOR RECOGNIZED BY NOVEL PHENYLAMINOTETRALINS - LIGAND-BINDING AND FUNCTIONAL-STUDIES SO MOLECULAR PHARMACOLOGY LA English DT Article ID RAT STRIATAL TISSUE; POTENTIAL ANTIPSYCHOTIC DRUG; GUINEA-PIG BRAIN; DOPAMINE SYNTHESIS; TYROSINE-HYDROXYLASE; CORPUS STRIATUM; SITES; BMY-14802; NEURONS; OPIATES AB Several novel phenylaminotetralins (PATs) cause functional changes in brain that are associated with binding to saturable, high affinity sites that are not identical to any known central nervous system receptor. These PATs were tested for their ability to cause receptor-mediated functional effects on tyrosine hydroxylase activity in corpus striatum from rat and guinea pig brain. (+/-)-(trans)-1-Phenyl-3-dimethylamino-6-chloro-7-hydroxy-1,2,3,4-tetrahydronaphthalene (Cl,OH-PAT) increased tyrosine hydroxylase activity (by approximately 30-40%) at 0.1 mum. Higher concentrations inhibited enzyme activity by indirect mechanisms that may include displacement of intraneuronal dopamine. The 6,7-unsubstituted congener (+/-)-(trans)-1-phenyl-3-di-methylamino-1,2,3,4-tetrahydronaphthalene stimulated tyrosine hydroxylase by as much as 50-60% over basal activity, without displacement of dopamine. Similarly to certain (+)-benzomorphan sigma receptor ligands, the effects of both PATs to activate tyrosine hydroxylase were blocked competitively by the putative sigma antagonist BMY-14802. Radiolabeled [H-3]Cl,OH-PAT bound saturably and with high affinity to guinea pig brain membranes (K(d) = 31 pm, B(max) = 6.5 fmol/mg of protein). The pharmacological profile of these binding sites was inconsistent with those of known sigma1, sigma2, dopaminergic, serotonergic, adrenergic, opioid, N-methyl-D-aspartate, or several other characterized central nervous system recognition sites. Together, these data suggest that these PATs may be agonists at a novel sigma-like site that has neuromodulatory activity that results in increases of brain catecholamine synthesis via activation of tyrosine hydroxylase. C1 UNIV N CAROLINA,BRAIN & DEV RES CTR,CHAPEL HILL,NC 27599. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,MCLEAN DIV,BELMONT,MA 02178. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MCLEAN DIV,NEUROSCI PROGRAM,BELMONT,MA 02178. HARVARD UNIV,MASSACHUSETTS GEN HOSP,MAILMAN RES CTR,MCLEAN DIV,BELMONT,MA 02178. RP BOOTH, RG (reprint author), UNIV N CAROLINA,SCH PHARM,DIV MED CHEM & NAT PROD,CHAPEL HILL,NC 27599, USA. FU NIMH NIH HHS [MH40537, MH34006, MH47370] NR 49 TC 38 Z9 39 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD DEC PY 1993 VL 44 IS 6 BP 1232 EP 1239 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MN466 UT WOS:A1993MN46600020 PM 8264560 ER PT J AU HALEYZITLIN, V RICHARDSON, A AF HALEYZITLIN, V RICHARDSON, A TI EFFECT OF DIETARY RESTRICTION ON DNA-REPAIR AND DNA-DAMAGE SO MUTATION RESEARCH LA English DT Article DE DNA REPAIR; DIETARY RESTRICTION; DNA DAMAGE ID DRUG-METABOLIZING-ENZYMES; CALORIC RESTRICTION; FEED RESTRICTION; RATS; RODENTS; MICE; AGE; LONGEVITY; KIDNEY; CANCER AB Dietary restriction is the only experimental manipulation known to extend lifespan and retard aging in mammals. Therefore, it is a powerful tool for identifying cellular processes that are involved in aging and senescence. Recently, several laboratories have begun to examine the effects of dietary restriction on the integrity of the genome and the ability of cells to repair DNA. In most studies, it was found that the repair of DNA damage, as measured by unscheduled DNA synthesis, was significantly higher in cells isolated from rodents fed calorie-restricted diets compared to cells isolated from rodents fed ad libitum. Dietary restriction also was observed to be associated with a reduction of the levels of certain types of DNA damage; however, preliminary experiments suggest that the effect of dietary restriction on the age-related accumulation of DNA damage depends on the type of DNA damage studied. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG-0188, AG-0548] NR 32 TC 39 Z9 40 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD DEC PY 1993 VL 295 IS 4-6 BP 237 EP 245 DI 10.1016/0921-8734(93)90023-V PG 9 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA MV034 UT WOS:A1993MV03400008 PM 7507560 ER PT J AU TANZI, RE PETRUKHIN, K CHERNOV, I PELLEQUER, JL WASCO, W ROSS, B ROMANO, DM PARANO, E PAVONE, L BRZUSTOWICZ, LM DEVOTO, M PEPPERCORN, J BUSH, AI STERNLIEB, I PIRASTU, M GUSELLA, JF EVGRAFOV, O PENCHASZADEH, GK HONIG, B EDELMAN, IS SOARES, MB SCHEINBERG, IH GILLIAM, TC AF TANZI, RE PETRUKHIN, K CHERNOV, I PELLEQUER, JL WASCO, W ROSS, B ROMANO, DM PARANO, E PAVONE, L BRZUSTOWICZ, LM DEVOTO, M PEPPERCORN, J BUSH, AI STERNLIEB, I PIRASTU, M GUSELLA, JF EVGRAFOV, O PENCHASZADEH, GK HONIG, B EDELMAN, IS SOARES, MB SCHEINBERG, IH GILLIAM, TC TI THE WILSON DISEASE GENE IS A COPPER TRANSPORTING ATPASE WITH HOMOLOGY TO THE MENKES DISEASE GENE SO NATURE GENETICS LA English DT Article ID ESTERASE-D; PROTEIN; LINKAGE; HYDROPHOBICITY; CHROMOSOME-13; RESISTANCE; MARKERS; LOCUS AB Wilson disease (WD) is an autosomal recessive disorder characterized by the toxic accumulation of copper in a number of organs, particularly the liver and brain. As shown in the accompanying paper, linkage disequilibrium & haplotype analysis confirmed the disease locus to a single marker interval at 13q14.3. Here we describe a partial cDNA clone (pWD) which maps to this region and shows a particular 76% amino acid homology to th Menkes disease gene, Mc1. The predicted functional properties of the pWD gene together with its strong homology to Mc1, genetic mapping data and identification of four independent disease-specific mutations, provide convincing evidence that pWD is the Wilson disease gene. C1 COLUMBIA UNIV,DEPT GENET & DEV,NEW YORK,NY 10032. COLUMBIA UNIV,DEPT PSYCHIAT,NEW YORK,NY 10032. COLUMBIA UNIV,DEPT BIOCHEM & MOLEC BIOPHYS,NEW YORK,NY 10032. COLUMBIA UNIV,DEPT MED,NEW YORK,NY 10032. COLUMBIA UNIV,CTR REPROD SCI,NEW YORK,NY 10032. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CATANIA,PEDIAT CLIN,CATANIA,ITALY. NATL CTR STUDY WILSONS DIS,NEW YORK,NY 10019. ST LUKES ROOSEVELT HOSP,NEW YORK,NY 10019. CNR,INST RIC TALASSEMIE & ANEMIE MEDITERRANEE,CAGLIARI,ITALY. MOSCOW MED GENET RES CTR,MOSCOW,RUSSIA. RI Bush, Ashley/A-1186-2007; Pellequer, Jean-Luc/L-6855-2013 OI Bush, Ashley/0000-0001-8259-9069; FU NHGRI NIH HHS [HG00462]; NIDDK NIH HHS [DK34668]; NINDS NIH HHS [NS28877] NR 37 TC 888 Z9 910 U1 3 U2 22 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD DEC PY 1993 VL 5 IS 4 BP 344 EP 350 DI 10.1038/ng1293-344 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA ML145 UT WOS:A1993ML14500009 PM 8298641 ER PT J AU PARK, S BERNARD, A BOVE, KE SENS, DA HAZENMARTIN, DJ GARVIN, AJ HABER, DA AF PARK, S BERNARD, A BOVE, KE SENS, DA HAZENMARTIN, DJ GARVIN, AJ HABER, DA TI INACTIVATION OF WT1 IN NEPHROGENIC RESTS, GENETIC PRECURSORS TO WILMS-TUMOR SO NATURE GENETICS LA English DT Article ID ZINC-FINGER GENE; DELETION; KIDNEY; MUTATIONS; ASSOCIATION; DISEASE; CANCER; MODEL; LOCUS; CELLS AB Nephrogenic rests consist of foci of primitive renal cells, typically microscopic, that are found within the normal kidney tissue of children with Wilms' tumour. To study the relationship between nephrogenic rests and the associated tumours, we screened these lesions for mutations in the 11p13 Wilms' tumour suppressor gene, WT1. In two cases in which the Wilms' tumour contained a somatic WT1 mutation, the nephrogenic rest had the identical mutation. Nephrogenic rests and Wilms' tumours are therefore topographically distinct lesions that are clonally derived from an early renal stem cell. Inactivation of WT1 appears to be an early genetic event which can lead to the formation of nephrogenic rests, enhancing the probability that additional genetic hits will lead to Wilms' tumour. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC GENET LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. CHILDRENS HOSP MED CTR,DEPT PATHOL,CINCINNATI,OH 45229. MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. FU NCI NIH HHS [CA58596, CA37887] NR 31 TC 114 Z9 116 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD DEC PY 1993 VL 5 IS 4 BP 363 EP 367 DI 10.1038/ng1293-363 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA ML145 UT WOS:A1993ML14500012 PM 8298644 ER PT J AU MEYER, JS OBARA, K MURAMATSU, K AF MEYER, JS OBARA, K MURAMATSU, K TI DIASCHISIS SO NEUROLOGICAL RESEARCH LA English DT Review DE DIASCHISIS; STROKE; CEREBRAL BLOOD FLOW; METABOLISM; NEUROLOGICAL RECOVERY ID CROSSED CEREBELLAR DIASCHISIS; EMISSION COMPUTED-TOMOGRAPHY; TEMPORARY BALLOON OCCLUSION; CEREBRAL BLOOD-FLOW; CORTICAL DIASCHISIS; STROKE; INFARCTION; METABOLISM; LESIONS; HUMANS AB Following acute, localized lesions of the central nervous system, arising from any cause, there are immediate depressions of neuronal synaptic functions in other areas of the central nervous system remote from the lesion. These remote effects result from deafferentation, a phenomenon known as ''diaschisis''. After an interval of time, which will vary directly with the severity of the lesion, functional recovery occurs due to synaptic reactivation of neurones. This is favourably influenced by rehabilitation. Diaschisis most commonly manifests itself by such neurological signs as impaired consciousness or cognitive impairments including dementia, dyspraxias, dystaxias, dysphasias, incoordination and sensory neglect. The nature of diaschisis has been demonstrated by widespread depressions of local cerebral blood flow and metabolism extending far beyond the anatomical lesion. Recovery of function is associated with recovery of local perfusion and metabolism. C1 BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. RP MEYER, JS (reprint author), BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,CEREBROVASC RES LAB,BLDG 100,ROOM 225,HOUSTON,TX 77030, USA. NR 41 TC 83 Z9 83 U1 1 U2 3 PU FOREFRONT PUBL GROUP PI LONDON PA MONOMARK HOUSE 27 OLD GLOUCESTER STREET, LONDON, ENGLAND WC1N 3XX SN 0161-6412 J9 NEUROL RES JI Neurol. Res. PD DEC PY 1993 VL 15 IS 6 BP 362 EP 366 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MK401 UT WOS:A1993MK40100001 PM 7907401 ER PT J AU DOBYNS, WB OZELIUS, LJ KRAMER, PL BRASHEAR, A FARLOW, MR PERRY, TR WALSH, LE KASARSKIS, EJ BUTLER, IJ BREAKEFIELD, XO AF DOBYNS, WB OZELIUS, LJ KRAMER, PL BRASHEAR, A FARLOW, MR PERRY, TR WALSH, LE KASARSKIS, EJ BUTLER, IJ BREAKEFIELD, XO TI RAPID-ONSET DYSTONIA-PARKINSONISM SO NEUROLOGY LA English DT Article ID MARKED DIURNAL FLUCTUATION; DOPA-RESPONSIVE DYSTONIA; TORSION DYSTONIA; LINKAGE ANALYSIS; JUVENILE-ONSET; GENE; EXCLUSION; SYMPTOMS; FAMILY; LOCUS AB We studied a large family with a previously undescribed, autosomal dominant dystonia-parkinsonism syndrome. We chose to call the disorder ''rapid-onset dystonia-parkinsonism'' (RDP) based on the unusually rapid evolution of signs and symptoms. Affected individuals developed dystonia and parkinsonism between 14 and 45 years of age. The onset was acute in six individuals with the abrupt onset of symptoms over the course of several hours, and subacute in four others who had evolution over several days or weeks. Thereafter, progression of symptoms was usually very slow. Two had intermittent focal dystonia without parkinsonism, and one obligate gene carrier was asymptomatic at 68 years. CSF levels of homovanillic acid were decreased in the two individuals tested, but dopaminergic therapy provided only slight benefit. The DYT1 gene responsible for early-onset, generalized idiopathic torsion dystonia in Jewish and some non-Jewish families has been mapped to chromosome 9q34. Linkage analysis with three markers near the DYT1 gene showed several obligate recombinations, excluding DYT1 as a candidate gene for RDP. We believe RDP is unique and should be classified separately from other forms of hereditary dystonia-parkinsonism. C1 MASSACHUSETTS GEN HOSP,NEUROSCI CTR NEUROL,MOLEC NEUROGENET UNIT,BOSTON,MA. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. INDIANA UNIV,SCH MED,DEPT NEUROL,INDIANAPOLIS,IN 46202. UNIV KENTUCKY,SCH MED,DEPT NEUROL,LEXINGTON,KY 40506. UNIV TEXAS,SCH MED,DEPT NEUROL,HOUSTON,TX 77025. RP DOBYNS, WB (reprint author), UNIV MINNESOTA,SCH MED,DEPT PEDIAT,DIV PEDIAT NEUROL,BOX 486 UMHC,420 DELAWARE ST SE,MINNEAPOLIS,MN 55455, USA. OI Dobyns, William/0000-0002-7681-2844 FU NCRR NIH HHS [RR02558]; NINDS NIH HHS [NINDS NS28384] NR 38 TC 105 Z9 108 U1 0 U2 3 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD DEC PY 1993 VL 43 IS 12 BP 2596 EP 2602 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA MM324 UT WOS:A1993MM32400031 PM 8255463 ER PT J AU TRIGGS, WJ KIERS, L CROS, D FANG, J CHIAPPA, KH AF TRIGGS, WJ KIERS, L CROS, D FANG, J CHIAPPA, KH TI FACILITATION OF MAGNETIC MOTOR EVOKED-POTENTIALS DURING THE CORTICAL STIMULATION SILENT PERIOD SO NEUROLOGY LA English DT Article ID VOLUNTARY CONTRACTION; CORTEX STIMULATION; BRAIN-STIMULATION; INTACT MAN; ELECTRICAL-STIMULATION; CORTICOSPINAL NEURONS; UNIT RESPONSES; MUSCLE; EXCITABILITY; REFLEXES AB We investigated the relationship between stimulus intensity and magnetic motor evoked potentials (MEPs) elicited 100 msec after a conditioning stimulus that was 25% of stimulator output above resting motor threshold (RMT) during tonic contraction of abductor pollicis brevis. In five subjects, MEPs elicited with stimuli less than 25% above RMT were inhibited during the EMG cortical stimulation silent period (CSSP) produced by the conditioning stimulus, relative to MEPs elicited with the test stimulus given at rest. However, increasing the intensity of the test stimulus increased the amplitude of MEPs elicited during the CSSP relative to MEPs elicited at rest, such that MEPs elicited with stimuli 30 to 45% above RMT were facilitated during the CSSP. Increasing the intensity of the test stimulus also increased the amplitude of MEPs elicited with paired stimulation at rest, and caused facilitation in one subject. Since facilitation of MEPs was never accompanied by shortening of MEP latency, our observations point to supraspinal facilitory mechanisms. We suggest that facilitation of MEPs during the CSSP reflects temporal and spatial summation of conditioning and test stimuli. C1 MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LABS,BOSTON,MA 02114. RP TRIGGS, WJ (reprint author), UNIV FLORIDA,DEPT NEUROL,BOX 100236 JHMHC,GAINESVILLE,FL 32610, USA. NR 36 TC 24 Z9 24 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD DEC PY 1993 VL 43 IS 12 BP 2615 EP 2620 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA MM324 UT WOS:A1993MM32400034 PM 8255466 ER PT J AU JENKINS, BG KOROSHETZ, WJ BEAL, MF ROSEN, BR AF JENKINS, BG KOROSHETZ, WJ BEAL, MF ROSEN, BR TI EVIDENCE FOR IMPAIRMENT OF ENERGY-METABOLISM IN-VIVO IN HUNTINGTONS-DISEASE USING LOCALIZED H-1-NMR SPECTROSCOPY SO NEUROLOGY LA English DT Article ID MAGNETIC-RESONANCE SPECTROSCOPY; HUMAN-BRAIN; GLUCOSE CONSUMPTION; H-1-NMR; PET; FEATURES; FERRITIN; LACTATE; LESIONS; CORTEX AB The Huntington's disease (HD) gene mutation has recently been found; however, the biochemical defect that leads to neurodegeneration is still unknown. A progressive impairment of neuronal energy metabolism is a possible etiologic factor. We tested this possibility using localized proton nuclear magnetic resonance (NMR) spectroscopy in 18 patients at high risk for, or suffering from, HD as compared with normal controls. Lactate concentrations were increased in the occipital cortex of symptomatic HD patients when compared with normal controls, and the lactate level correlated with duration of illness. In addition, several patients showed highly elevated lactate levels in the basal ganglia. Basal ganglia levels of N-acetylaspartate were lowered and choline dramatically elevated, relative to creatine, reflecting neuronal loss and gliosis in this brain region. These findings are consistent with a possible defect in energy metabolism in HD, which could contribute to the pathogenesis of the disease. The presence of elevated lactate in HD brains may provide a simple marker that can be followed over time noninvasively and repeatedly to aid in devising and monitoring possible therapies for HD patients. C1 MGH,CTR NMR,DEPT RADIOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA40303-07] NR 39 TC 335 Z9 345 U1 3 U2 3 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD DEC PY 1993 VL 43 IS 12 BP 2689 EP 2695 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA MM324 UT WOS:A1993MM32400049 PM 8255479 ER PT J AU SIMONIAN, NA GILLIAM, FG CHIAPPA, KH AF SIMONIAN, NA GILLIAM, FG CHIAPPA, KH TI IFOSFAMIDE CAUSES A DIAZEPAM-SENSITIVE ENCEPHALOPATHY SO NEUROLOGY LA English DT Note ID MESNA AB An encephalopathy characterized by confusion, stupor, and mutism frequently occurs during administration of the chemotherapeutic drug ifosfamide (IFX). We investigated two patients who developed encephalopathy during IFX infusion. Both exhibited a rapid and near-complete restoration of baseline mental status functioning concurrent with EEG improvement after administration of intravenous diazepam. We recommend an EEG and trial of benzodiazepines in patients with IFX encephalopathy. RP SIMONIAN, NA (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,WARREN 407,FRUIT ST,BOSTON,MA 02114, USA. NR 10 TC 26 Z9 26 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD DEC PY 1993 VL 43 IS 12 BP 2700 EP 2702 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA MM324 UT WOS:A1993MM32400052 PM 8255482 ER PT J AU VONDEIMLING, A BENDER, B LOUIS, DN WIESTLER, OD AF VONDEIMLING, A BENDER, B LOUIS, DN WIESTLER, OD TI A RAPID AND NONRADIOACTIVE PCR BASED ASSAY FOR THE DETECTION OF ALLELIC LOSS IN HUMAN GLIOMAS SO NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY LA English DT Article DE LOH; ALLELIC; TUMOR SUPPRESSOR GENES; GLIOMA; MICROSATELLITES; CA-DINUCLEOTIDE REPEATS; SILVER STAINING ID POLYMERASE CHAIN-REACTION; SHORT ARM; HETEROZYGOSITY; DELETIONS; RETINOBLASTOMA; TUMORIGENESIS; RECOMBINATION; POLYMORPHISMS; ASTROCYTOMA; MECHANISMS AB Studies of the loss of allelic heterozygosity (LOH) in tumour tissues have evolved as an important tool for the identification of chromosomal regions which are likely to harbour tumour suppressor genes. The classical procedure to determine LOH has been restriction fragment length polymorphism (RFLP) analysis and Southern blotting, a time consuming method requiring radioisotopes and several micrograms of DNA. Recently, the use of highly polymorphic microsatellites of the CA-dinucleotide repeat class and polymerase chain reaction (PCR) has considerably advanced and facilitated the detection of LOH in tumour tissues. We here describe a strategy to identify LOH based on PCR amplification of CA-dinucleotide repeats, denaturing polyacrylamide gel electrophoresis (PAGE) and nucleic acid detection with a sensitive silver staining protocol. In a comparative study of 20 astrocytomas, this rapid technique was able to identify all cases of LOH on chromosome 17p that had previously been found in these tumours by RFLP analysis and Southern blotting. This non-radioactive PCR based assay has a great potential for LOH studies in human tumours. C1 UNIV BONN,MED CTR,DEPT NEUROPATHOL,BONN,GERMANY. MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X NR 25 TC 73 Z9 73 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0305-1846 J9 NEUROPATH APPL NEURO JI Neuropathol. Appl. Neurobiol. PD DEC PY 1993 VL 19 IS 6 BP 524 EP 529 PG 6 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA MP320 UT WOS:A1993MP32000008 PM 7510049 ER PT J AU AKOVA, YA JABBUR, NS FOSTER, CS AF AKOVA, YA JABBUR, NS FOSTER, CS TI OCULAR PRESENTATION OF POLYARTERITIS-NODOSA - CLINICAL COURSE AND MANAGEMENT WITH STEROID AND CYTOTOXIC THERAPY SO OPHTHALMOLOGY LA English DT Article ID ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES; WEGENERS GRANULOMATOSIS; AUTOANTIBODIES; VASCULITIS; CLASSIFICATION; ASSOCIATION; PROGNOSIS; CRITERIA AB Background: Polyarteritis nodosa is a necrotizing vasculitis affecting medium and small-sized arteries throughout the body, including ocular tissues. Untreated polyarteritis nodosa carries a very poor prognosis. Treatment with steroids increases the 5-year survival to 48%, whereas addition of cytotoxic immunosuppressive treatment improves the outcome dramatically. Methods: The authors reviewed five cases of polyarteritis nodosa with a spectrum of ocular findings which preceded and contributed to its diagnosis. Results: The ophthalmic manifestations of polyarteritis nodosa in these patients included scleritis, peripheral ulcerative keratitis, nongranulomatous uveitis, retinal vasculitis, pseudotumor of the orbit, and central retinal artery occlusion associated with temporal arteritis. In four patients, cytotoxic immunosuppressive therapy was begun promptly, and elimination of inflammation was achieved. Conclusions: The authors' presentation of these cases is intended to emphasize the fact that ocular inflammation can be the earliest presenting manifestation of polyarteritis nodosa and that its recognition may lead to the early institution of therapy, which can decrease morbidity and mortality in this disease. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,IMMUNOL SERV,243 CHARLES ST,BOSTON,MA 02114. NR 35 TC 53 Z9 54 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD DEC PY 1993 VL 100 IS 12 BP 1775 EP 1781 PG 7 WC Ophthalmology SC Ophthalmology GA MM544 UT WOS:A1993MM54400009 PM 7903120 ER PT J AU JUNG, FF BOUYOUNES, B BARRIO, R TANG, SS DIAMANT, D INGELFINGER, JR AF JUNG, FF BOUYOUNES, B BARRIO, R TANG, SS DIAMANT, D INGELFINGER, JR TI ANGIOTENSIN-CONVERTING ENZYME IN RENAL ONTOGENY - HYPOTHESIS FOR MULTIPLE ROLES SO PEDIATRIC NEPHROLOGY LA English DT Article; Proceedings Paper CT 5th International Workshop on Developmental Renal Physiology CY AUG 26-28, 1992 CL TREMEZZO, ITALY DE RENIN ANGIOTENSIN SYSTEM; ANGIOTENSIN CONVERTING ENZYME; DEVELOPMENT AB Angiotensin converting enzyme (ACE) has multiple effects both as the enzyme which cleaves angiotensin II from angiotensin I and as that which breaks down bradykinin. The present study examines ACE mRNA and protein expression in the rat kidney during development. Changes in distribution and expression during development are consistent with suggestions that the renin angiotensin system is important in growth modulation, vascular development and regulation, and protein reabsorption. C1 MASSACHUSETTS GEN HOSP,PEDIAT RENAL RES LAB,BOSTON,MA 02114. FU NHLBI NIH HHS [HL 40210, HL 43131, HL 48455] NR 0 TC 24 Z9 24 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0931-041X J9 PEDIATR NEPHROL JI Pediatr. Nephrol. PD DEC PY 1993 VL 7 IS 6 BP 834 EP 840 PG 7 WC Pediatrics; Urology & Nephrology SC Pediatrics; Urology & Nephrology GA MP183 UT WOS:A1993MP18300036 PM 8130118 ER PT J AU GATTONICELLI, S BYERS, RH CALORINI, L FERRONE, S AF GATTONICELLI, S BYERS, RH CALORINI, L FERRONE, S TI ORGAN-SPECIFIC METASTASES IN MELANOMA - EXPERIMENTAL ANIMAL-MODELS SO PIGMENT CELL RESEARCH LA English DT Review DE MELANOMA; METASTASIS; IMMUNODEFICIENT MICE ID TUMOR-METASTASIS; NUDE-MICE; CHOROIDAL MELANOMA; MALIGNANT-CELLS; GROWTH; EXPRESSION; SUPPRESSION; PATTERNS; SPREAD; TISSUE AB Metastases from certain primary tumors frequently exhibit specific organ preference. Animal models have been developed to induce in a reproducible fashion the formation of organ-specific metastases by malignant melanoma cells. Some of these models rely on the use of immunodeficient mice, which can support the growth of murine as well as human malignant melanomas. Moreover, immunodeficient mice, because of their diminished ability to mount an effective immune response, allow the expression of malignant properties (e.g., preferential colonization of certain organs), which are intrinsic to transplanted melanoma cells. This review discusses the relevant factors (and limitations) of some of the animal models used to study the in vivo properties of melanoma cells. C1 NEW YORK MED COLL,DEPT MICROBIOL & IMMUNOL,VALHALLA,NY 10595. TUFTS UNIV NEW ENGLAND MED CTR,DEPT RADIAT ONCOL,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. FU NCI NIH HHS [CA37959, CA39559] NR 28 TC 7 Z9 7 U1 0 U2 2 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0893-5785 J9 PIGM CELL RES JI Pigm. Cell. Res. PD DEC PY 1993 VL 6 IS 6 BP 381 EP 384 DI 10.1111/j.1600-0749.1993.tb00619.x PG 4 WC Cell Biology; Dermatology SC Cell Biology; Dermatology GA MV087 UT WOS:A1993MV08700001 PM 8146087 ER PT J AU DEWDNEY, J CONLEY, TR SHIH, MC GOODMAN, HM AF DEWDNEY, J CONLEY, TR SHIH, MC GOODMAN, HM TI EFFECTS OF BLUE AND RED-LIGHT ON EXPRESSION OF NUCLEAR GENES ENCODING CHLOROPLAST GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE OF ARABIDOPSIS-THALIANA SO PLANT PHYSIOLOGY LA English DT Article ID NICOTIANA-TABACUM; PHYTOCHROME-B; SMALL SUBUNIT; PEA; CARBOXYLASE; PLANTS; RNA; PHOTORECEPTORS; ACCUMULATION; INDUCTION AB We have characterized the effects of different light spectra on expression of the nuclear genes (GapA and GapB) encoding chloroplast glyceraldehyde-3-phosphate dehydrogenase in Arabidopsis thaliana. Steady-state mRNA levels for both genes in etiolated seedlings increased after a short exposure to red or blue light. However, these increases could not be reversed by immediate farred light following the initial light treatment. In mature plants, a short light pulse, regardless of its spectrum, had no apparent effect on GapA or GapB mRNA levels in dark-adapted plants. In contrast, continuous exposure to red, blue, or white light resulted in increases of GapA and GapB mRNA levels, with blue and white light being far more efficient than red light. Similarly, continuous exposure of etiolated seedlings to red, blue, or white light also resulted in increased GapA and GapB mRNA levels. In addition, we show that illumination of red light-saturated Arabidopsis plants with continuous blue light results in further increases of GapA and GapB mRNA levels. Based on these results, we conclude that both blue light photoreceptor- and phytochrome-mediated pathways are involved in light regulation of GapA and GapB genes in Arabidopsis, with blue light acting as the dominant regulator. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. UNIV IOWA,DEPT BIOL SCI,IOWA CITY,IA 52242. FU NIGMS NIH HHS [GM41669] NR 28 TC 28 Z9 28 U1 0 U2 2 PU AMER SOC PLANT PHYSIOLOGISTS PI ROCKVILLE PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 SN 0032-0889 J9 PLANT PHYSIOL JI Plant Physiol. PD DEC PY 1993 VL 103 IS 4 BP 1115 EP 1121 DI 10.1104/pp.103.4.1115 PG 7 WC Plant Sciences SC Plant Sciences GA ML412 UT WOS:A1993ML41200011 PM 8290625 ER PT J AU FIALA, TGS NOVELLINE, RA YAREMCHUK, MJ AF FIALA, TGS NOVELLINE, RA YAREMCHUK, MJ TI COMPARISON OF CT IMAGING ARTIFACTS FROM CRANIOMAXILLOFACIAL INTERNAL-FIXATION DEVICES SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID CLIP ARTIFACTS; SURGICAL CLIPS; IMPLANTS; REDUCTION AB This study compares the artifacts caused by craniomaxillofacial internal fixation devices in CT images. Mandibular reconstruction and ''mini'' titanium, Vitallium, and stainless steel systems, ''micro'' titanium and Vitallium systems, and stainless steel wires were evaluated. The hardware was placed on a nylon grid and submerged in water. CT images were obtained with both bone and soft-tissue window settings. All artifacts were compared and graded after a minimum of five observations each. The severity of ''starburst'' artifact was found to be related to the physical size of the fixation hardware and its composition. Titanium hardware caused the least amount of artifact. Vitallium and stainless steel fixation devices, with the exception of interfragmentary wiring, produced significantly more artifact. These results agree with theoretical predictions; The data indicate that when postoperative imaging is an important clinical consideration, (1) the least amount of implant material necessary to achieve stable fixation should be used, (2) the proximity of implant material to the area of interest should be considered, and (3) titanium implants produce less artifact than Vitallium or stainless steel implants. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV PLAST SURG,WACC,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. NR 15 TC 56 Z9 56 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD DEC PY 1993 VL 92 IS 7 BP 1227 EP 1232 PG 6 WC Surgery SC Surgery GA MK869 UT WOS:A1993MK86900003 PM 8248397 ER PT J AU CHEN, NT HONG, HZ HOOPER, DC MAY, JW AF CHEN, NT HONG, HZ HOOPER, DC MAY, JW TI EFFECT OF SYSTEMIC ANTIBIOTIC AND ANTIBIOTIC-IMPREGNATED POLYMETHYLMETHACRYLATE BEADS ON THE BACTERIAL CLEARANCE IN WOUNDS CONTAINING CONTAMINATED DEAD BONE SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID FREE TISSUE; INOCULATION; MUSCLE; FLAPS AB A dorsal muscular wound model was used in 40 New Zealand White rabbits to study the effect of systemic and local antibiotics on the bacterial clearance of contaminated dead bone. Devitalized iliac crest bone preincubated with Staphylococcus aureus was implanted in each deep muscular wound with or without tobramycin-impregnated polymethylmethacrylate beads. Either systemic tobramycin or cefazolin was administered for 7 days. Animals were sacrificed at 7 and 14 days. The wounds containing tobramycin beads had significantly fewer bacteria than those without antibiotic beads (2.0 x 10(2) versus 1.3 X 10(6); p < 0.008). The reduction in bacteria due to the tobramycin beads did not differ significantly with respect to the concurrent systemic antibiotics or to the duration of incubation. We conclude that tobramycin-impregnated beads are effective in reducing bacterial count in contaminated bony wounds treated with systemic antibiotics. Furthermore, the bactericidal effect of the antibiotic beads is independent of and additive to the systemic antibiotic delivered to the wounds by well-perfused muscles. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV PLAST SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 18 TC 6 Z9 9 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD DEC PY 1993 VL 92 IS 7 BP 1305 EP 1311 PG 7 WC Surgery SC Surgery GA MK869 UT WOS:A1993MK86900016 PM 8248406 ER PT J AU MAY, JW AF MAY, JW TI PLASTIC-SURGERY BOARD REVIEW COURSES - TO REVIEW OR TO REVEAL ... THAT IS THE QUESTION SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Editorial Material RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,ACC-453,15 PARKMAN ST,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 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD DEC PY 1993 VL 92 IS 7 BP 1362 EP 1363 PG 2 WC Surgery SC Surgery GA MK869 UT WOS:A1993MK86900026 PM 8248412 ER PT J AU DULIC, V DRULLINGER, LF LEES, E REED, SI STEIN, GH AF DULIC, V DRULLINGER, LF LEES, E REED, SI STEIN, GH TI ALTERED REGULATION OF G(1)-CYCLINS IN SENESCENT HUMAN-DIPLOID FIBROBLASTS - ACCUMULATION OF INACTIVE CYCLIN-E-CDK2 AND CYCLIN-D1-CDK2 COMPLEXES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CELL CYCLE; CELLULAR AGING; RETINOBLASTOMA PROTEIN; PHOSPHORYLATION ID CYCLE-DEPENDENT GENES; CELL-CYCLE; PROTEIN-KINASES; S-PHASE; EXPRESSION; G1; PHOSPHATASE; TRANSITION; GROWTH; YEAST AB Senescent human diploid fibroblasts are unable lo enter S phase in response to mitogenic stimulation. One of the key deficiencies in mitogen-stimulated senescent cells is their failure to phosphorylate the retinoblastoma protein, which acts as an inhibitor of entry into S phase in its unphosphorylated form. Recent data suggest that cyclin-dependent kinases (Cdks) regulated by G1 cyclins (D type and E) are responsible for the primary phosphorylation of the retinoblastoma protein prior to the G1/S boundary. Surprisingly, we found 10- to 15-fold higher constitutive amounts of both cyclin E and cyclin DI in senescent cells compared to quiescent early-passage cells. Nevertheless, cyclin E-associated kinase activity in senescent cells was very low and did not increase significantly upon mitogenic stimulation even though cyclin E-Cdk2 complexes were abundant. In contrast to early-passage cells in late G1 phase, senescent cells contained mainly underphosphorylated cyclin E and proportionally more unphosphorylated and inactive Cdk2, perhaps accounting for the low kinase activity. We also show that a majority of the Cdk2 in senescent cells, but not in early-passage cells, was complexed with cyclin Dl. Cyclin D1-Cdk2 complexes, severalfold enriched in senescent cells, contained exclusively unphosphorylated Cdk2. Amounts of cyclin A, which ordinarily accumulates in S and G2 phases, were extremely low in stimulated senescent cells. We suggest that the failure to activate cyclin E-Cdk2 kinase activity in senescent cells may account for the inability of these cells to phosphorylate the retinoblastoma protein in late G1 phase, which in turn may block the expression of late G1 genes such as cyclin A that are required for entry into S phase. C1 MASSACHUSETTS GEN HOSP, CTR CANC, BOSTON, MA 02129 USA. UNIV COLORADO, DEPT MOLEC CELLULAR & DEV BIOL, BOULDER, CO 80309 USA. RP DULIC, V (reprint author), SCRIPPS RES INST, LA JOLLA, CA 92037 USA. OI Dulic, Vjekoslav/0000-0003-1201-3901 FU NIA NIH HHS [AG00947]; NIGMS NIH HHS [GM46006] NR 36 TC 274 Z9 277 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 1 PY 1993 VL 90 IS 23 BP 11034 EP 11038 DI 10.1073/pnas.90.23.11034 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK094 UT WOS:A1993MK09400032 PM 8248208 ER PT J AU BISWAS, DK AHLERS, CM DEZUBE, BJ PARDEE, AB AF BISWAS, DK AHLERS, CM DEZUBE, BJ PARDEE, AB TI COOPERATIVE INHIBITION OF NF-KAPPA-B AND TAT-INDUCED SUPERACTIVATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 LONG TERMINAL REPEAT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE PENTOXIFYLLINE; RO24-7429; TRANSCRIPTION; JURKAT ID GENE-EXPRESSION; T-CELLS; TRANSCRIPTION; ACTIVATION; BINDING; REPLICATION; MECHANISM; ENHANCER; CYSTEINE; PROTEIN AB Human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR)-regulated gene expression is stimulated independently by the cellular trans-activator NF-kappaB and the viral protein Tat. Noncytotoxic concentrations of the drug pentoxifylline (PTX) inhibited interaction of NF-kappaB with its motif and the stimulation of HIV-1 LTR-driven gene expression in Jurkat cells. Tat protein (from a cotransfected Tat-expression vector) also induced activation of HIV-1 LTR-driven gene expression. This activation was unaffected by PTX when NF-kappaB sites in the HIV-1 LTR were mutated, suggesting that this drug does not directly influence Tat function, which, however, was inhibited by the Tat-inhibitor Ro 24-7429. Transient reporter gene expression regulated by HIV-1 LTR with wild-type NF-kappaB motifs in the presence of Tat protein was 10- to 60-fold higher than in the presence of either of the trans-activators alone, demonstrating superactivation of HIV-1 LTR by the concerted action of both the transactivators. Treatment of cells with either PTX or Ro 24-7429 inhibited this superactivation of the HIV-1 LTR. The inhibitory effect of these two drugs in combination, at concentrations that alone did not significantly influence viral promoter activity, was far more than additive. A cooperative action of PTX (NF-kappaB inhibitor) and Ro 24-7429 (Tat inhibitor) on HIV-1 LTR-regulated gene expression is suggested. Concentrations of the drugs that induced maximum inhibition of HIV-1 LTR through their cooperative action are far below cytotoxic levels. Thus, the combination of these two inhibitors could be very effective for anti-HIV therapy. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP BISWAS, DK (reprint author), HARVARD UNIV, SCH MED,DANA FARBER CANC INST, DIV CELL GROWTH & REGULAT,DANA 810, 44 BINNEY ST, BOSTON, MA 02115 USA. NR 28 TC 48 Z9 48 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 1 PY 1993 VL 90 IS 23 BP 11044 EP 11048 DI 10.1073/pnas.90.23.11044 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK094 UT WOS:A1993MK09400034 PM 8248210 ER PT J AU BOUSSIOTIS, VA FREEMAN, GJ GRIBBEN, JG DALEY, J GRAY, G NADLER, LM AF BOUSSIOTIS, VA FREEMAN, GJ GRIBBEN, JG DALEY, J GRAY, G NADLER, LM TI ACTIVATED HUMAN B-LYMPHOCYTES EXPRESS 3 CTLA-4 COUNTERRECEPTORS THAT COSTIMULATE T-CELL ACTIVATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ANTIGEN B7; CD28; PROVIDES; RECEPTOR; SIGNAL; INTERLEUKIN-2; SUPERFAMILY; BINDING; ANERGY; LIGAND AB Signaling via the T-cell receptor complex is necessary but not sufficient to induce antigen-specific T lymphocytes to expand clonally. To proliferate, T cells must receive one or more costimulatory signals provided by antigen presenting cells (APCs). One such critical costimulatory signal is delivered by the CD28/CTLA-4 counterreceptor, B7, expressed on APCs. B7 costimulation induces CD28 signaling, resulting in interleukin 2 (IL-2) secretion, and T-cell proliferation. Conversely, T-cell receptor signaling in the absence of B7 costimulation results in induction of antigen-specific tolerance. Here, we show that activated human B lymphocytes express two additional CTLA-4 counterreceptors also capable of providing T-cell costimulation. At 24 hr postactivation, B cells express a CTLA-4 counterreceptor not recognized by anti-B7 or -BB-1 monoclonal antibodies (mAbs), which induces detectable IL-2 secretion and T-cell proliferation. At 48 and 72 hr postactivation, B cells express both B7 and a third CTLA-4 counterreceptor identified by the anti-BB-1 mAb. BB-1 appears to be a molecule distinct from B7 by its expression on B7-cells and its capacity to induce T cells to proliferate without significant accumulation of IL-2. As observed for B7, costimulatory signals mediated by these alternative CTLA-4/CD28 counterreceptors are likely to be essential for generation of an immune response and their absence may result in antigen-specific tolerance. We propose the following terminology for these CTLA-4 counterreceptors: (i) B7, B7-1; (ii) early CTLA-4 binding counterreceptor, B7-2; and (iii) BB-1, B7-3. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. REPLIGEN CORP,CAMBRIDGE,MA 02139. RP BOUSSIOTIS, VA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 40216] NR 30 TC 240 Z9 244 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 1 PY 1993 VL 90 IS 23 BP 11059 EP 11063 DI 10.1073/pnas.90.23.11059 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK094 UT WOS:A1993MK09400037 PM 7504293 ER PT J AU RAZIWOLF, Z GALVIN, F GRAY, G REISER, H AF RAZIWOLF, Z GALVIN, F GRAY, G REISER, H TI EVIDENCE FOR AN ADDITIONAL LIGAND, DISTINCT FROM B7, FOR THE CTLA-4 RECEPTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID T-CELL ACTIVATION; COSTIMULATORY SIGNAL; LYMPHOCYTES-T; IL-2 PRODUCTION; MURINE LYMPHOCYTES; ANTIGEN PROVIDES; MESSENGER-RNA; CD28 LIGAND; EXPRESSION; MOLECULE AB Activation of T lymphocytes requires the recognition of peptide-major histocompatibility complex complexes and costimulatory signals provided by antigen-presenting cells (APCs). The best-characterized costimulatory molecule to date is the B7 antigen, a member of the immunoglobulin family that binds two receptors, CD28 and CTLA-4, expressed on the T-cell surface. Using the anti-mouse B7 (mB7) monoclonal antibody (mAb) 16-10A1, which we recently developed, we found that mB7 is indeed an important costimulatory ligand for the antigen-specific activation of murine T cells by B lymphocytes. Three lines of evidence suggest, however, the existence of at least one additional ligand for the CTLA-4 receptor. First, a soluble fusion protein of human CTLA-4 and the IgG1 Fc region, termed CTLA4Ig, blocks better than the anti-mB7 mAb the allogeneic stimulation of T cells by unfractionated splenic APCs. Second, saturating amounts of anti-mB7 mAb do not significantly block binding of fluorescein isothiocyanate-conjugated CTLA4Ig to activated splenic APCs. Furthermore, CTLA4Ig but not the anti-mB7 mAb reacts with the M12 and M12.C3 cell lines. The identification of an additional ligand for CTLA-4 may have applications to the treatment of autoimmune disease and transplant-associated disorders. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. REPLIGEN CORP,CAMBRIDGE,MA 02139. FU NIAID NIH HHS [AI-33679] NR 41 TC 66 Z9 66 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 1 PY 1993 VL 90 IS 23 BP 11182 EP 11186 DI 10.1073/pnas.90.23.11182 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK094 UT WOS:A1993MK09400062 PM 7504299 ER PT J AU LIBOI, E CARROLL, M DANDREA, AD MATHEYPREVOT, B AF LIBOI, E CARROLL, M DANDREA, AD MATHEYPREVOT, B TI ERYTHROPOIETIN RECEPTOR SIGNALS BOTH PROLIFERATION AND ERYTHROID-SPECIFIC DIFFERENTIATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HEMATOPOIETIC GROWTH FACTOR RECEPTOR; BETA-GLOBIN ID VIRUS GP55 GLYCOPROTEIN; PROTEIN TYROSINE PHOSPHORYLATION; CYTOPLASMIC REGION; GENE-TRANSFER; BETA-CHAIN; CELL-LINE; EXPRESSION; ACTIVATION; GROWTH; INTERLEUKIN-3 AB Ectopic expression of the erythropoietin receptor (EPO-R) in Ba/F3, an interleukin 3-dependent progenitor cell line, confers EPO-dependent cell growth. To examine whether the introduced EPO-R could affect differentiation, we isolated Ba/F3-EPO-R subclones in interleukin 3 and assayed for the induction of beta-globin mRNA synthesis after exposure to EPO. Detection of beta-globin mRNA was observed within 3 days of EPO treatment, with peak levels accumulating after 10 days. When EPO was withdrawn, expression of beta-globin mRNA persisted in most clones, suggesting that commitment to erythroid differentiation had occurred. Although EPO-R expression also supports EPO-dependent proliferation of CTLL-2, a mature T-cell line, those cells did not produce globin transcripts, presumably because they lack requisite cellular factors involved in erythrocyte differentiation. We conclude that the EPO-R transmits signals important for both proliferation and differentiation along the erythroid lineage. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115. FU NHLBI NIH HHS [5PO1 HL32262] NR 26 TC 83 Z9 85 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 1 PY 1993 VL 90 IS 23 BP 11351 EP 11355 DI 10.1073/pnas.90.23.11351 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK094 UT WOS:A1993MK09400096 PM 8248252 ER PT J AU LICHT, JD RO, M ENGLISH, MA GROSSEL, M HANSEN, U AF LICHT, JD RO, M ENGLISH, MA GROSSEL, M HANSEN, U TI SELECTIVE REPRESSION OF TRANSCRIPTIONAL ACTIVATORS AT A DISTANCE BY THE DROSOPHILA KRUPPEL PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE TRANSCRIPTION; RNA POLYMERASE-II; TRANSCRIPTION FACTOR-SP1 ID DNA-BINDING PROTEINS; GENE-EXPRESSION; MAMMALIAN-CELLS; DIFFERENTIAL REGULATION; EUKARYOTIC PROMOTERS; BASAL TRANSCRIPTION; NEGATIVE REGULATION; SEGMENTATION GENES; GAP; HUNCHBACK AB The Kruppel (Kr) protein, bound at kilobase distances from the start site of transcription, represses transcription by RNA polymerase 11 in mammalian cells. Repression is monotonically dependent on the dose of Kr protein and the presence of Kr binding site(s) on the DNA. These data suggest an inhibitory protein-protein interaction between the Kr protein and proximal transcription factors. Repression by Kr depends on the specific activator protein driving transcription. In particular, Kr protein selectively represses transcription mediated by the Spl glutamine-rich activation domain, tethered to the promoter by a GAL4 DNA-binding domain, but does not repress transcription stimulated by the acidic GAL4 activator. We believe this represents repression by a quenching interaction between DNA-bound Kr protein and the activation region of Spl, rather than competition between Spl and Kr for a limiting transcriptional component. Selective, context-related repression affords an added layer of combinatorial control of gene expression by sequence-specific transcription factors. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LICHT, JD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,EUKARYOT TRANSCRIPT LAB,ROOM B411,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [K11CA01272] NR 59 TC 49 Z9 49 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC 1 PY 1993 VL 90 IS 23 BP 11361 EP 11365 DI 10.1073/pnas.90.23.11361 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MK094 UT WOS:A1993MK09400098 PM 8248254 ER PT J AU PONTIUS, AA AF PONTIUS, AA TI NEUROPSYCHIATRIC UPDATE OF THE CRIME PROFILE AND SIGNATURE IN SINGLE OR SERIAL HOMICIDES - RULE OUT LIMBIC PSYCHOTIC TRIGGER REACTION SO PSYCHOLOGICAL REPORTS LA English DT Article ID TEMPORAL-LOBE EPILEPSY; FRONTAL-LOBE; QUESTIONABLE ASPECTS; SYSTEM DYSFUNCTION; NARRATIVES; SEIZURES; STIMULI; MODEL AB A neuropsychiatric and -psychological update of the crime ''profile'' and ''signature'' is a necessary addition to the traditional sociopsychological model likely to miss limbic system dysfunctioning. Thus, occurrence of a brief (c. 20 minutes) limbic seizure has been proposed based on behaviors of 12 white male homicidal loners, who showed a dozen symptoms and signs: Limbic Psychotic Trigger Reaction. Readily overlooked can be (a) a transient psychosis (hallucinations and/or delusions), (b) autonomic hyperactivation (e.g., loss of bladder control, nausea, ejaculation), (c) motiveless, out-of-character, unplanned, and well-remembered homicidal acts, (d) committed with a flat affect (not emotionally or impulsively provoked), (e) typically involving a stranger who happened to provide an objectively harmless and only subjectively important stimulus. (f) Such an individualized stimulus triggered the memory revival of mild to moderate but repeatedly experienced hurts. Such a specific sequence of events implicates the specific mechanism of limbic seizure, ''kindling,'' which does not necessarily involve motor convulsions. Repetition of such limbic episodes with ''criminal acts'' is conceivable under specific circumstances including cases in which the triggering stimulus is associated with pleasurable delusions (e.g., of grandiose power or wealth) or constitutes a specific aspect of a basic drive motive. For example, eating or sexual activities might be planned but degenerate into a limbic episode with a specific core symptomatology. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. RP PONTIUS, AA (reprint author), HARVARD UNIV,SCH MED,DEPT PSYCHIAT,FRUIT ST,BOSTON,MA 02115, USA. NR 35 TC 9 Z9 9 U1 1 U2 7 PU PSYCHOLOGICAL REPORTS PI MISSOULA PA P O BOX 9229, MISSOULA, MT 59807 SN 0033-2941 J9 PSYCHOL REP JI Psychol. Rep. PD DEC PY 1993 VL 73 IS 3 BP 875 EP 892 PN 1 PG 18 WC Psychology, Multidisciplinary SC Psychology GA MJ034 UT WOS:A1993MJ03400025 PM 8302991 ER PT J AU LANGLEY, RE PALAYOOR, ST COLEMAN, CN BUMP, EA AF LANGLEY, RE PALAYOOR, ST COLEMAN, CN BUMP, EA TI MODIFIERS OF RADIATION-INDUCED APOPTOSIS SO RADIATION RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Apoptosis/Programmed Cell Death at the 41st Annual Meeting of the Radiation-Research-Society CY MAR 20-25, 1993 CL DALLAS, TX SP RADIAT RES SOC ID TERATOCARCINOMA STEM-CELLS; HAMSTER OVARY CELLS; DNA FRAGMENTATION; IONIZING-RADIATION; GAMMA-IRRADIATION; MAMMALIAN-CELLS; RETINOIC ACID; POLY(ADP-RIBOSE); INDUCTION; DAMAGE C1 DANA FARBER CANC INST,BOSTON,MA 02115. RP LANGLEY, RE (reprint author), HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115, USA. NR 53 TC 48 Z9 49 U1 0 U2 1 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD DEC PY 1993 VL 136 IS 3 BP 320 EP 326 DI 10.2307/3578543 PG 7 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA MQ741 UT WOS:A1993MQ74100003 PM 8278572 ER PT J AU KOPANS, DB AF KOPANS, DB TI REVIEW OF STEREOTAXIC LARGE-CORE NEEDLE-BIOPSY AND SURGICAL BIOPSY RESULTS IN NONPALPABLE BREAST-LESIONS SO RADIOLOGY LA English DT Editorial Material DE BREAST, BIOPSY; BREAST NEOPLASMS, DIAGNOSIS C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,AMBULATORY CARE BLDG,STE 219,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 5 TC 37 Z9 37 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD DEC PY 1993 VL 189 IS 3 BP 665 EP 666 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MH586 UT WOS:A1993MH58600006 PM 8234687 ER PT J AU SHEA, SA ANDRES, LP PAYDARFAR, D BANZETT, RB SHANNON, DC AF SHEA, SA ANDRES, LP PAYDARFAR, D BANZETT, RB SHANNON, DC TI EFFECT OF MENTAL ACTIVITY ON BREATHING IN CONGENITAL CENTRAL HYPOVENTILATION SYNDROME SO RESPIRATION PHYSIOLOGY LA English DT Article DE CONTROL OF BREATHING; MAMMALS, HUMANS; SYNDROMES, CONGENITAL CENTRAL HYPOVENTILATION, ONDINE CURSE; VENTILATION; WAKEFULNESS ID CHILDREN; VENTILATION; INFANTS; SLEEP AB Congenital central hypoventilation syndrome (CCHS) is associated with hypoventilation during sleep, but breathing can be adequate during wakefulness. It has been assumed that in awake CCHS patients breathing is activated by the forebrain, even voluntarily (i.e. Ondine's Curse). We tested whether or not an abnormal breathing pattern can be provoked by intense mental concentration in CCHS patients as this would be expected to disturb any voluntary control over breathing if present. Breathing (inductance plethysmography), end-tidal P(CO2) (PET(CO2)), arterial oxygen saturation (Sa(O2)) and EEG were measured in 5 children with CCHS (aged 8-17 years) and 5 controls during 5 min periods while resting; reading; performing mental arithmetic and playing a hand-held ''Nintendo'' game. There were no significant differences between controls and CCHS (unpaired t-tests, P>0.05) in mean breath duration, tidal volume, ventilation, Sa(O2) or PET(CO2) during REST or the conditions of mental stimulation. Both groups increased ventilation during mental stimulation. Respiratory variability was not greater in CCHS in any condition. These data provide indirect evidence that CCHS patients do not require voluntary activation of every breath (they do not have Ondine's Curse) and suggest that mental concentration might stimulate the respiratory complex as part of a generalised CNS arousal. C1 MASSACHUSETTS GEN HOSP,PEDIAT PULM UNIT,BOSTON,MA 02114. TUFTS UNIV,ST ELIZABETHS HOSP,SCH MED,DIV NEUROL,BOSTON,MA 02135. RP SHEA, SA (reprint author), HARVARD UNIV,SCH PUBL HLTH,PHYSIOL PROGRAM,665 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL07118, HL19170, HL46690] NR 28 TC 44 Z9 44 U1 1 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0034-5687 J9 RESP PHYSIOL JI Respir. Physiol. PD DEC PY 1993 VL 94 IS 3 BP 251 EP 263 DI 10.1016/0034-5687(93)90022-3 PG 13 WC Physiology; Respiratory System SC Physiology; Respiratory System GA MH867 UT WOS:A1993MH86700002 PM 8108605 ER PT J AU GAZELLE, GS BOLAND, G DAWSON, SL MUELLER, PR AF GAZELLE, GS BOLAND, G DAWSON, SL MUELLER, PR TI ASPIRATION AND DRAINAGE OF EXTRAARTICULAR FLUID COLLECTIONS SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Article RP GAZELLE, GS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0739-9529 J9 SEMIN INTERVENT RAD JI Semin. Interv. Radiol. PD DEC PY 1993 VL 10 IS 4 BP 273 EP 276 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NM907 UT WOS:A1993NM90700005 ER PT J AU MUELLER, PR AF MUELLER, PR TI MUSCULOSKELETAL INTERVENTIONS SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Editorial Material RP MUELLER, PR (reprint author), MASSACHUSETTS GEN HOSP,DIV ABDOMINAL IMAGING & INTERVENT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0739-9529 J9 SEMIN INTERVENT RAD JI Semin. Interv. Radiol. PD DEC PY 1993 VL 10 IS 4 BP U255 EP U255 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NM907 UT WOS:A1993NM90700001 ER PT J AU BROWN, RH AF BROWN, RH TI INHERITED MOTOR-NEURON DISEASES - RECENT PROGRESS SO SEMINARS IN NEUROLOGY LA English DT Article RP BROWN, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,NEUROMUSCULAR RES LAB,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0271-8235 J9 SEMIN NEUROL JI Semin. Neurol. PD DEC PY 1993 VL 13 IS 4 BP 365 EP 368 DI 10.1055/s-2008-1041148 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA MP116 UT WOS:A1993MP11600010 PM 8146487 ER PT J AU SANDERS, MH KERN, NB COSTANTINO, JP STILLER, RA STUDNICKI, K COATES, J ORRIS, S SCHIMERMAN, S AF SANDERS, MH KERN, NB COSTANTINO, JP STILLER, RA STUDNICKI, K COATES, J ORRIS, S SCHIMERMAN, S TI PRESCRIPTION OF POSITIVE AIRWAY PRESSURE FOR SLEEP-APNEA ON THE BASIS OF A PARTIAL-NIGHT TRIAL SO SLEEP LA English DT Article; Proceedings Paper CT 3rd International Conference on Sleep and Breathing CY AUG 31-SEP 03, 1992 CL PALM COVE, AUSTRALIA SP AMER SLEEP DISORDERS ASSOC, SLEEP RES SOC, EUROPEAN SLEEP RES SOC, LATIN AMER SLEEP RES SOC, JAPANESE SLEEP RES SOC C1 US DEPT VET AFFAIRS,DEPT MED,OAKLAND,PA. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT BIOSTAT,PITTSBURGH,PA 15261. RP SANDERS, MH (reprint author), UNIV PITTSBURGH,SCH MED,DEPT MED,DIV PULM ALLERGY & CRIT CARE MED,PITTSBURGH,PA, USA. FU NHLBI NIH HHS [NHLBI 5T32HL07563-07] NR 2 TC 4 Z9 4 U1 0 U2 0 PU AMER SLEEP DISORDERS ASSOC PI ROCHESTER PA 1610 14TH STREET NW SUITE 300, ROCHESTER, MN 55806 SN 0161-8105 J9 SLEEP JI Sleep PD DEC PY 1993 VL 16 IS 8 SU S BP S106 EP S107 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MW457 UT WOS:A1993MW45700038 PM 8177993 ER PT J AU KOROSHETZ, WJ AF KOROSHETZ, WJ TI EVIDENCE SUPPORTING A ROLE FOR PROGRAMMED CELL-DEATH IN FOCAL CEREBRAL-ISCHEMIA IN RATS - EDITORIAL SO STROKE LA English DT Editorial Material RP KOROSHETZ, WJ (reprint author), MASSACHUSETTS GEN HOSP,STROKE SERV,BOSTON,MA 02114, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD DEC PY 1993 VL 24 IS 12 BP 2008 EP 2009 PG 2 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA MK485 UT WOS:A1993MK48500040 ER PT J AU FINKLESTEIN, SP KEMMOU, A CADAY, CG BERLOVE, DJ AF FINKLESTEIN, SP KEMMOU, A CADAY, CG BERLOVE, DJ TI BASIC FIBROBLAST GROWTH-FACTOR PROTECTS CEREBROCORTICAL NEURONS AGAINST EXCITATORY AMINO-ACID TOXICITY IN-VITRO SO STROKE LA English DT Article; Proceedings Paper CT Cerebrovascular Diseases : 18th Princeton Conference CY MAY 29-31, 1992 CL ROCHESTER, MI DE AMINO ACIDS; GROWTH FACTORS; NEUROPROTECTION ID HIPPOCAMPAL; EXCITOTOXICITY; DEGENERATION; GLUTAMATE; DAMAGE; BRAIN AB Background and Purpose: Previous studies have shown that basic fibroblast growth factor protects against excitatory amino acid toxicity in cultured hippocampal, striatal, and cerebellar neurons. In the current study, we examined the neuroprotective effects of this growth factor on cerebrocortical neurons, which are commonly involved in thromboembolic stroke. Methods: Dissociated neuron-glia cultures of embryonic rat cerebral cortex (12 days in vitro) were preincubated with basic fibroblast growth factor (0.1 to 100 ng/mL) for 6 hours before incubation with glutamate (0 to 1000 mu mol/L) for 16 hours. The number of phase-bright neurons was taken as an index of neuronal survival. Results: Basic fibroblast growth factor protected neurons against glutamate toxicity, especially at lower (10, 25, and 50 mu mol/L), but not higher (100 and 1000 mu mol/L), glutamate concentrations. Neuroprotection was seen at growth factor doses as low as 1 ng/mL. Conclusions: Basic fibroblast growth factor protects cultured cerebrocortical neurons against glutamate neurotoxicity. C1 MASSACHUSETTS GEN HOSP,CNS,GROWTH FACTOR RES LAB,DEPT NEUROL,BOSTON,MA 02114. NR 17 TC 3 Z9 3 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD DEC PY 1993 VL 24 IS 12 SU S BP I141 EP I143 PG 3 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA ML144 UT WOS:A1993ML14400046 ER PT J AU HERSHMAN, JM AF HERSHMAN, JM TI UNTITLED SO THYROID LA English DT Editorial Material RP HERSHMAN, JM (reprint author), W LOS ANGELES VA MED CTR, BLDG 114, ROOM 200, WILSHIRE & SAWTELLE BLVDS, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1050-7256 J9 THYROID JI Thyroid PD WIN PY 1993 VL 3 IS 4 BP 267 EP 267 DI 10.1089/thy.1993.3.267 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ061 UT WOS:A1993MQ06100001 ER PT J AU PANG, XP YOSHIMURA, M HERSHMAN, JM AF PANG, XP YOSHIMURA, M HERSHMAN, JM TI SUPPRESSION OF RAT THYROTROPH AND THYROID-CELL FUNCTION BY TUMOR-NECROSIS-FACTOR-ALPHA SO THYROID LA English DT Note ID FACTOR-KAPPA-B; GAMMA-INTERFERON; FRTL5 CELLS; CACHECTIN; ACTIVATION; ILLNESS; HORMONE; GROWTH; INTERLEUKIN-1; RECEPTORS AB We studied the effect of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and interferon-gamma (IFN-gamma) on the function of thyroid cells and pituitary thyrotrophs. In FRTL-5 rat thyroid cells, both human and murine TNF-alpha inhibited basal and TSH-stimulated [I-125]iodide transport. IL-1 shared this action with TNF-alpha, but was less potent. IL-1 and IFN-gamma did not cause a further reduction of TNF-alpha-induced inhibition of [I-125]iodide transport. TNF-alpha, phorbol ester 12-myristate 13-acetate (PMA), and calcium ionophore (CI) A23817 all inhibited [I-125]iodide transport, but high doses of PMA and CI also blocked the inhibitory action of TNF-alpha on [I-125]iodide transport. Inhibition of protein kinase A and protein kinase C by H7 or HA inhibited TSH-stimulated iodide transport, but did not block the TNF-alpha action, suggesting that the mechanism of TNF-alpha action on thyroid cells is independent of protein kinase A and C. In pituitary cells, both human and murine TNF-alpha did not affect basal TSH secretion, but TNF-alpha reduced TRH-stimulated TSH secretion. This study provides further in vitro evidence that TNF-alpha inhibits the function of the hypothalamus-pituitary-thyroid axis acting directly on both the pituitary and thyroid glands. C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. RP PANG, XP (reprint author), W LOS ANGELES DEPT VET AFFAIRS MED CTR, DIV ENDOCRINOL W111D, ENDOCRINE RES LAB, LOS ANGELES, CA 90073 USA. NR 29 TC 34 Z9 36 U1 0 U2 1 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1050-7256 J9 THYROID JI Thyroid PD WIN PY 1993 VL 3 IS 4 BP 325 EP 330 DI 10.1089/thy.1993.3.325 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ061 UT WOS:A1993MQ06100013 PM 8118227 ER PT J AU ABHYANKAR, S GILLILAND, DG FERRARA, JLM AF ABHYANKAR, S GILLILAND, DG FERRARA, JLM TI INTERLEUKIN-1 IS A CRITICAL EFFECTOR MOLECULE DURING CYTOKINE DYSREGULATION IN GRAFT-VERSUS-HOST DISEASE TO MINOR HISTOCOMPATIBILITY ANTIGENS SO TRANSPLANTATION LA English DT Note ID BONE-MARROW TRANSPLANTATION; IL-1 RECEPTOR ANTAGONIST; NITRIC-OXIDE PRODUCTION; TUMOR-NECROSIS-FACTOR; POLYMERASE CHAIN-REACTION; NATURAL-KILLER-CELLS; MESSENGER-RNA; INVIVO; INHIBITION; LYMPHOCYTES AB Cytokines are believed to cause a number of inflammatory diseases. We have investigated the role of 3 inflammatory cytokines, IL-1, IL-2, and TNF alpha, during graft-versus-host disease (GVHD), a paradigm disease of cytokine dysregulation in vivo. Measuring cytokine mRNA transcripts with a quantitative polymerase chain reaction technique, we demonstrate that IL-1 transcript levels are increased several hundred-fold in GVHD target organs, whereas TNF alpha transcripts increase only 4- to 6-fold. Kinetic studies during the first month after transplant unexpectedly show that GVHD never induces IL-2 transcripts in the skin and only induces IL-2 transcripts in the spleen during the first week, whereas levels of IL-1 transcripts continue to increase throughout the entire 4 weeks. Administration of an IL-1 receptor antagonist after the termination of the IL-2 response and after the establishment of GVHD significantly increases long-term survival, confirming the central role of IL-1 as an effector molecule of GVHD and suggesting new therapeutic strategies for this disorder. C1 DANA FABER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU NCI NIH HHS [CA 39542, CA 57261]; NIAID NIH HHS [AI 30018] NR 40 TC 79 Z9 80 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD DEC PY 1993 VL 56 IS 6 BP 1518 EP 1523 DI 10.1097/00007890-199312000-00045 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA MQ056 UT WOS:A1993MQ05600044 PM 8279027 ER PT J AU SEGRE, GV GOLDRING, SR AF SEGRE, GV GOLDRING, SR TI RECEPTORS FOR SECRETIN, CALCITONIN, PARATHYROID-HORMONE (PTH)/PTH-RELATED PEPTIDE, VASOACTIVE-INTESTINAL-PEPTIDE, GLUCAGON-LIKE PEPTIDE-1, GROWTH HORMONE-RELEASING HORMONE, AND GLUCAGON BELONG TO A NEWLY DISCOVERED G-PROTEIN-LINKED RECEPTOR FAMILY SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID EXPRESSION CLONING; SIGNALING PATHWAYS; ADENOSINE-MONOPHOSPHATE; HUMORAL HYPERCALCEMIA; TISSUE DISTRIBUTION; SEQUENCE ALIGNMENT; MOLECULAR-CLONING; ADENYLATE-CYCLASE; GENE-EXPRESSION; PITUITARY-CELLS AB Seven receptors with highly homologous structural features have recently been discovered that belong to a new family of seven membrane-spanning receptors within the G-protein-linked receptor superfamily. These seven all bind small peptide ligands, and many have the unique property to activate the G(s) and at least one other G protein. C1 MASSACHUSETTS GEN HOSP,ARTHRIT UNIT,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02114. RP SEGRE, GV (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 61 TC 283 Z9 285 U1 2 U2 9 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD DEC PY 1993 VL 4 IS 10 BP 309 EP 314 DI 10.1016/1043-2760(93)90071-L PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MN116 UT WOS:A1993MN11600003 PM 18407176 ER PT J AU GRINSPOON, SK BILEZIKIAN, JP AF GRINSPOON, SK BILEZIKIAN, JP TI ENDOCRINE MANIFESTATIONS OF AIDS SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; VIRUS INFECTION; CYTOKINES AB The endocrine manifestations of AIDS are now appreciated to involve virtually any of the endocrine organs. Some of these manifestations are subtle and clinically not apparent. Others, like adrenal involvement, can eventuate, although rarely, into frank glandular insufficiency. This Endocrine Rounds case illustrates a number of endocrine manifestations of AIDS and discusses their involvement from clinical and pathophysiologic aspects. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT MED,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT PHARMACOL,NEW YORK,NY 10032. RP GRINSPOON, SK (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 18 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD DEC PY 1993 VL 4 IS 10 BP 315 EP 317 DI 10.1016/1043-2760(93)90072-M PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MN116 UT WOS:A1993MN11600004 PM 18407177 ER PT J AU LIPTON, SA AF LIPTON, SA TI PROSPECTS FOR CLINICALLY TOLERATED NMDA ANTAGONISTS - OPEN-CHANNEL BLOCKERS AND ALTERNATIVE REDOX STATES OF NITRIC-OXIDE SO TRENDS IN NEUROSCIENCES LA English DT Article ID METHYL-D-ASPARTATE; RECEPTOR-MEDIATED NEUROTOXICITY; EXCITATORY AMINO-ACIDS; H-3 MK-801 BINDING; GLUTAMATE NEUROTOXICITY; MODULATORY SITE; MOLECULAR DIVERSITY; HIPPOCAMPAL-NEURONS; CORTICAL CULTURES; XENOPUS OOCYTES AB Several acute and chronic neurological diseases might be mediated, at least in part, via stimulation of excitatory amino acid receptors, such as the N-methyl-D-aspartate (NMDA) receptor. Antagonists of excitatory amino acid receptors ameliorate neurotoxic damage in several animal models of these disorders. This review focuses on the potential for clinically tolerated NMDA receptor antagonists, with emphasis on agents that have been in clinical use for other conditions and that recently have been shown to inhibit NMDA receptor activity by a mechanism of open-channel block or redox modification. C1 BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RP LIPTON, SA (reprint author), CHILDRENS HOSP MED CTR,DEPT NEUROL,CELLULAR & MOLEC LAB,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY09024, EY05477]; NICHD NIH HHS [HD29587] NR 69 TC 235 Z9 240 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD DEC PY 1993 VL 16 IS 12 BP 527 EP 532 DI 10.1016/0166-2236(93)90198-U PG 6 WC Neurosciences SC Neurosciences & Neurology GA MK097 UT WOS:A1993MK09700009 PM 7509524 ER PT J AU STANEK, KS GUYTON, GP HURFORD, WE PARK, YS AHN, DW QVIST, J FALKE, KJ HONG, SK KOBAYASHI, K KOBAYASHI, H ZAPOL, WM AF STANEK, KS GUYTON, GP HURFORD, WE PARK, YS AHN, DW QVIST, J FALKE, KJ HONG, SK KOBAYASHI, K KOBAYASHI, H ZAPOL, WM TI CONTINUOUS PULSE OXIMETRY IN THE BREATH-HOLD DIVING WOMEN OF KOREA AND JAPAN SO UNDERSEA & HYPERBARIC MEDICINE LA English DT Article DE PULSE OXIMETRY; ARTERIAL OXYGEN SATURATION; DESATURATION; BREATH-HOLD DIVING; DIVING COMPUTER AB Arterial oxygen saturation during breath-hold diving has not previously been measured continuously. We devised a submersible, waterproof, backpack computer to continuously record heart rate, depth, and arterial oxygen saturation (SP(O2)) as determined by earlobe pulse oximetry. Our measurements showed that one assisted (Funado) diver had reduced SP(O2) values immediately after surfacing from 22 dives which lasted 23-76 s, from a mean of 99 +/- 1% SP(O2) to 96 +/- 3% SP(O2). SP(O2) returned to 97 +/- 2% within 15 s after surfacing (P < 0.05 surface value differs from predive base line). Four unassisted (Cachido) divers showed no significant reduction of mean predive SP(O2) below 98 +/- 2% at any time during the dive or recovery period in 92 routine dives lasting from 15 to 44 s. Upon surfacing from diving, mean SP(O2) was 98 +/- 2% and the mean SP(O2)15 s after surfacing was 97 +/- 3% for the unassisted divers. Three Cachido divers were asked to dive and breath hold for as long as possible. Mean SP(O2) at the conclusion of breath holding was 73% after an average dive and breath hold lasting 69 s. C1 KOSIN MED COLL,DEPT PHYSIOL,PUSAN,SOUTH KOREA. KEIO UNIV,DEPT SURG,TOKYO 108,JAPAN. SUNY BUFFALO,DEPT PHYSIOL,BUFFALO,NY 14260. UNIV COPENHAGEN,HERLEV HOSP,DEPT ANESTHESIA,DK-2730 HERLEV,DENMARK. FREE UNIV BERLIN,DEPT ANESTHESIA,W-1000 BERLIN 33,GERMANY. KITASATO UNIV,DEPT MED,SAGAMIHARA,KANAGAWA 228,JAPAN. RP STANEK, KS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114, USA. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 NR 15 TC 7 Z9 7 U1 0 U2 2 PU UNDERSEA & HYPERBARIC MEDICAL SOC INC PI KENSINGTON PA 10531 METROPOLITAN AVE, KENSINGTON, MD 20895 SN 1066-2936 J9 UNDERSEA HYPERBAR M JI Undersea Hyperb. Med. PD DEC PY 1993 VL 20 IS 4 BP 297 EP 307 PG 11 WC Marine & Freshwater Biology; Medicine, Research & Experimental SC Marine & Freshwater Biology; Research & Experimental Medicine GA MJ911 UT WOS:A1993MJ91100003 PM 8286984 ER PT J AU FOWLER, FJ BARRY, MJ LUYAO, G ROMAN, A WASSON, J WENNBERG, JE AF FOWLER, FJ BARRY, MJ LUYAO, G ROMAN, A WASSON, J WENNBERG, JE TI PATIENT-REPORTED COMPLICATIONS AND FOLLOW-UP TREATMENT AFTER RADICAL PROSTATECTOMY - THE NATIONAL MEDICARE EXPERIENCE - 1988-1990 (UPDATED JUNE 1993) SO UROLOGY LA English DT Article ID LOCALIZED PROSTATIC-CANCER; CARCINOMA AB To estimate the probabilities of complications and follow-up treatment, a sample of Medicare patients who underwent radical prostatectomy (1988 through 1990) was surveyed by mail, telephone, and personal interview. Respondents reported their current status with respect to continence and sexual function as well as post-surgical treatments they had had to treat residual or recurrent cancer or surgical complications. Over 30 percent reported currently wearing pads or clamps to deal with wetness; over 40 percent said they drip urine when they cough or when their bladders are full; 23 percent reported daily wetting of more than a few drops. About 60 percent of patients reported having no full or partial erections since their surgery, and only 11 percent had any erections sufficient for intercourse during the month prior to the survey. Six percent had surgery after the radical prostatectomy to treat incontinence; 15 percent had treatments or used devices to help with sexual function; 20 percent report having had post-surgical treatment for urethral strictures. In addition 16 percent, 22 percent, and 28 percent reported follow-up treatment for cancer (radiation or androgen deprivation therapy) at two, three, and four years after radical prostatectomy. These estimates of complication and follow-up treatment rates are generally higher, and almost certainly more representative for older men, than estimates previously published. Patients and physicians may want to weigh heavily the complications and need for follow-up treatments when considering radical prostatectomy for prostate cancer. C1 DARTMOUTH COLL SCH MED,CTR EVALUAT CLIN SCI,HANOVER,NH. MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA. RP FOWLER, FJ (reprint author), UNIV MASSACHUSETTS,CTR SURVEY RES,100 MORRISSEY BLVD,BOSTON,MA 02125, USA. FU AHRQ HHS [HS 05745, HS 06336] NR 29 TC 491 Z9 502 U1 1 U2 7 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD DEC PY 1993 VL 42 IS 6 BP 622 EP 629 DI 10.1016/0090-4295(93)90524-E PG 8 WC Urology & Nephrology SC Urology & Nephrology GA ML927 UT WOS:A1993ML92700003 PM 8256394 ER PT J AU MULLEY, G AF MULLEY, G TI THE ROLE OF INTERNAL-MEDICINE AND ITS SPECIALITIES RESEARCH, EDUCATION AND PATIENT-CARE SO SCHWEIZERISCHE MEDIZINISCHE WOCHENSCHRIFT LA English DT Article RP MULLEY, G (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 11 TC 0 Z9 0 U1 2 U2 2 PU SCHWABE & CO AG VERLAG PI MUTTENZ 1 PA FARNSBURGERSTRASSE 8, CH-4132 MUTTENZ 1, SWITZERLAND SN 0036-7672 J9 SCHWEIZ MED WSCHR JI Schweiz. Med. Wochenschr. PD NOV 27 PY 1993 VL 123 IS 47 BP 2222 EP 2227 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA MK056 UT WOS:A1993MK05600002 ER PT J AU GIMMI, CD GRIBBEN, JG FREEMAN, GJ NADLER, LM AF GIMMI, CD GRIBBEN, JG FREEMAN, GJ NADLER, LM TI MISSING B7-COSTIMULATION PRODUCES PERIPHERAL CLONAL T-CELL ANERGY IN A HUMAN ANTIGEN-SPECIFIC MODEL SO SCHWEIZERISCHE MEDIZINISCHE WOCHENSCHRIFT LA German DT Article C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP GIMMI, CD (reprint author), KANTONSSPITAL,HAMATOL ABT,CH-4031 BASEL,SWITZERLAND. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SCHWABE & CO AG VERLAG PI MUTTENZ 1 PA FARNSBURGERSTRASSE 8, CH-4132 MUTTENZ 1, SWITZERLAND SN 0036-7672 J9 SCHWEIZ MED WSCHR JI Schweiz. Med. Wochenschr. PD NOV 27 PY 1993 VL 123 IS 47 BP 2255 EP 2256 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MK056 UT WOS:A1993MK05600009 PM 7505950 ER PT J AU REYNET, C KAHN, CR AF REYNET, C KAHN, CR TI RAD - A MEMBER OF THE RAS FAMILY OVEREXPRESSED IN MUSCLE OF TYPE-II DIABETIC HUMANS SO SCIENCE LA English DT Article ID INVIVO INSULIN ACTION; PIMA-INDIANS; SIGNAL TRANSDUCTION; XENOPUS-OOCYTES; GENE-EXPRESSION; BETA-CELL; MELLITUS; NIDDM; PROTEINS; P21 AB To identify the gene or genes associated with insulin resistance in Type II (non-insulin-dependent) diabetes mellitus, subtraction libraries were prepared from skeletal muscle of normal and diabetic humans and screened with subtracted probes. Only one clone out of 4000 was selectively overexpressed in Type II diabetic muscle as compared to muscle of non-diabetic or Type I diabetic individuals. This clone encoded a new 29-kilodalton member of the Ras-guanosine triphosphatase superfamily and was termed Rad (Ras associated with diabetes). Messenger ribonucleic acid of Rad was expressed primarily in skeletal and cardiac muscle and was increased an average of 8.6-fold in the muscle of Type II diabetics as compared to normal individuals. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 36836] NR 59 TC 257 Z9 261 U1 2 U2 5 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD NOV 26 PY 1993 VL 262 IS 5138 BP 1441 EP 1444 DI 10.1126/science.8248782 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MJ046 UT WOS:A1993MJ04600039 PM 8248782 ER PT J AU KINANE, TB SHANG, C FINDER, JD ERCOLANI, L AF KINANE, TB SHANG, C FINDER, JD ERCOLANI, L TI CAMP REGULATES G-PROTEIN-ALPHA(I-2) SUBUNIT GENE-TRANSCRIPTION IN POLARIZED LLC-PK(1) CELLS BY INDUCTION OF A CCAAT BOX NUCLEAR-BINDING FACTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMP RESPONSE ELEMENT; G-PROTEIN; ADENYLATE-CYCLASE; DOWN-REGULATION; CYCLIC-AMP; EXPRESSION; SEQUENCE; DESENSITIZATION; IDENTIFICATION; INHIBITION AB Heterotrimeric G-proteins function as signal transducers for a variety of hormone-coupled enzyme systems in eukaryotic cells. In LLC-PK1 renal cells, vasopressin-stimulated adenylylcyclase activity is regulated in part, by the counterbalancing activity of stimulatory G-proteins (G(s)) and inhibitory pertussis toxin-sensitive G-proteins (G(i)). Two G(i) genes encoding the G(i) isoforms Galpha(i-2) and Galpha(i-3) are expressed in LLC-PK1 cells. In polarized cells, these isoforms are topographically segregated to different membranes, which allows for the selective inhibition of adenylylcyclase by Galpha(i-2). The genes encoding these isoforms are similarly regulated in these cells during growth and differentiation but differ in response to steroid hormone signals (Holtzman, E. J., Kinane, T. B., West, K., Soper, B. W., Karga, H., Ausiello, D. A., and Ercolani, L. (1993) J. Biol. Chem. 268, 3964-3975). We now demonstrate after stimulating polarized LLC-PK1 cells with forskolin, which raises intracellular cAMP levels 50-fold, Galpha(i-2) but not Galpha(i-3) protein is increased 3-fold at 12 h and remains elevated above control values by 24 h. In cells stably transfected with Galpha(i-2) or Galpha(i-3) gene 5'-flanking sequences fused to firefly luciferase cDNA reporter gene, forskolin treatment increased Galpha(i-2) transcription 3-fold but inhibited Galpha(i-3) transcription by 50% at 12 h. In vivo footprinting of forskolin-treated cells was performed to examine the molecular basis for activation of the Galpha(i-2) gene. Protected guanosines were identified in a 135-base pair (bp) area previously associated with enhancer activity of this gene in non-polarized cells. This DNA segment did not contain the classical cAMP response element 5'-TGACGTCA-3'. Utilizing the 135-bp DNA segment as a probe in mobility shift assays, which compared nuclear extracts from cells before and after forskolin treatment, an induced nuclear protein complex was identified. Following systematic reduction and mutation of this DNA segment, a ''CCAAT'' box motif was identified that bound the induced nuclear protein complex during forskolin-induced Galpha(i-2) gene transcriptional activation. Induction of this nuclear protein complex was prevented in forskolin-treated cells by cycloheximide. To demonstrate functional activity of the CCAAT box motif, cells were transiently transfected with plasmids encoding either the minimal 135-bp segment or a multimerized CCAAT box segment fused to a Rous sarcoma minimal promoter/firefly luciferase reporter gene. The transcriptional response of these plasmids in polarized forskolin-treated cells was similar in magnitude but retarded temporally to that observed in cells stably transfected with the Galpha(i-2) firefly luciferase gene. These studies demonstrate that chronic cAMP elevation initiates a counter-regulatory response in fully polarized renal cells that includes increased transcription of the Galpha(i-2) gene. In contrast to other cAMP-responsive genes, increased Galpha(i-2) gene transcription appears to be mediated by a cAMP pathway that requires induction of a member of the CCAAT box family of DNA-binding proteins. C1 MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,PEDIAT PULM UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 42543, F32 DK08838, T32 DK07540] NR 28 TC 38 Z9 39 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 25 PY 1993 VL 268 IS 33 BP 24669 EP 24676 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MG673 UT WOS:A1993MG67300027 PM 8227026 ER PT J AU GARCIA, P SHOELSON, SE GEORGE, ST HINDS, DA GOLDBERG, AR MILLER, WT AF GARCIA, P SHOELSON, SE GEORGE, ST HINDS, DA GOLDBERG, AR MILLER, WT TI PHOSPHORYLATION OF SYNTHETIC PEPTIDES CONTAINING TYR-MET-X-MET MOTIFS BY NONRECEPTOR TYROSINE KINASES IN-VITRO SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GROWTH-FACTOR RECEPTORS; MURINE LEUKEMIA-VIRUS; PROTEIN-KINASE; PHOSPHATIDYLINOSITOL 3-KINASE; BACULOVIRUS EXPRESSION; SIGNAL TRANSDUCTION; P85-ALPHA SUBUNIT; TRANSFORMING GENE; ESCHERICHIA-COLI; SH2 DOMAINS AB Several tyrosine phosphorylation sites in the insulin receptor kinase substrate IRS-1 are predicted to be within Tyr-Met-X-Met (YMXM) motifs, and synthetic peptides corresponding to these sequences are excellent substrates for the insulin receptor kinase in vitro (Shoelson, S. E., Chatterjee, S., Chaudhuri, M., and White, M. F. (1992) Proc. Natl. Acad. Sci. U. S. A 89, 2027-2031). In this study, YMXM-containing peptides are shown to act as substrates for two members of the nonreceptor subfamily of tyrosine kinases, v-Src and v-Abl (the transforming gene products of Rous sarcoma virus and Abelson murine leukemia virus, respectively). For v-Src, a baculovirus expression system was used which was capable of producing milligram quantities of pure 60-kDa v-Src in Spodoptera frugiperda (Sf9) cells. The source of v-Abl was an Escherichia coli expression vector that produces a fusion protein of glutathione S-transferase with the abl catalytic domain. The synthetic YMXM-containing peptides had among the highest apparent affinities described to date for either tyrosine kinase, with K(m) values as low as 97 muM for v-Src and v-Abl. Comparisons with the results obtained with the insulin receptor kinase revealed differences in substrate specificity among the enzymes. In particular, v-Src was more tolerant of substitutions at the Met+1 and Met+3 positions in the YMXM motif than either v-Abl or the insulin receptor kinase but was more dependent on the presence of a preceding acidic amino acid. For v-Abl, the presence of threonine at any position in the YMXM motif caused a reduction in catalytic efficiency. Phosphorylated YMXM motifs are recognition elements for binding to the src homology 2 domains of phosphatidylinositol 3'-kinase and additional proteins; hence, differences in specificity of tyrosine kinases toward YMXM-containing proteins may have relevance to downstream signaling events. C1 SUNY STONY BROOK, SCH MED, DEPT PHYSIOL & BIOPHYS, BASIC SCI TOWER T-6, STONY BROOK, NY 11794 USA. BRIGHAM & WOMENS HOSP, DEPT MED, JOSLIN DIABET CTR, DIV RES, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. ROCKEFELLER UNIV, NEW YORK, NY 10021 USA. NR 40 TC 53 Z9 53 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 NOV 25 PY 1993 VL 268 IS 33 BP 25146 EP 25151 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MG673 UT WOS:A1993MG67300090 PM 8227078 ER PT J AU BLUMENTHAL, D AF BLUMENTHAL, D TI ADMINISTRATIVE COSTS AND HEALTH-CARE REFORM - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP BLUMENTHAL, D (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 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 NOV 25 PY 1993 VL 329 IS 22 BP 1656 EP 1657 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MJ546 UT WOS:A1993MJ54600023 ER PT J AU MERKEL, PA AF MERKEL, PA TI INADVERTENT PLACEMENT OF AN ADVERTISEMENT SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP MERKEL, PA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 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 NOV 25 PY 1993 VL 329 IS 22 BP 1661 EP 1661 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MJ546 UT WOS:A1993MJ54600036 PM 8232453 ER PT J AU GIVER, L BARTEL, D ZAPP, M PAWUL, A GREEN, M ELLINGTON, AD AF GIVER, L BARTEL, D ZAPP, M PAWUL, A GREEN, M ELLINGTON, AD TI SELECTIVE OPTIMIZATION OF THE REV-BINDING ELEMENT OF HIV-1 SO NUCLEIC ACIDS RESEARCH LA English DT Article ID VIRUS TYPE-1 REV; VIRAL MESSENGER-RNA; TARGET SEQUENCE; SECONDARY STRUCTURE; VIRION EXPRESSION; RESPONSE ELEMENT; TRANS-ACTIVATOR; GENE-PRODUCT; PROTEIN; REPLICATION AB RNA molecules that can bind to the Rev protein of HIV-1 have been isolated from random sequence nucleic acid pools based on a minimal Rev-binding element (RBE) found within the Rev Responsive Element (RRE). While the selected sequences are related to the wild-type element, they also contain substitutions that allow them to bind Rev up to 10-fold better in vitro. A hypothesized homopurine pairing at G48:G71 is generally replaced by A48:A71; the occasional selection of C48:A71 suggests that R71 may be in a syn conformation. These data support the structural model for the RBE originally proposed by Bartel et al. (1). Additional interactions with the Rev protein are promoted by the sequence CUC ... UYGAG, found in one class of high-affinity aptamers, but absent from the wild-type element. Within each class of aptamers different residues and substructures covary with one another to generate optimal Rev-binding surfaces. The interdependencies of different nucleotide substitutions suggest structural models for both the wild-type RBE and the selected high-affinity aptamers. C1 INDIANA UNIV,DEPT CHEM,BLOOMINGTON,IN 47405. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02118. UNIV MASSACHUSETTS,MED CTR,PROGRAM MOLEC MED,WORCESTER,MA 01605. NR 38 TC 102 Z9 103 U1 1 U2 10 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD NOV 25 PY 1993 VL 21 IS 23 BP 5509 EP 5516 DI 10.1093/nar/21.23.5509 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MK397 UT WOS:A1993MK39700035 PM 7505429 ER PT J AU BROWN, MC AF BROWN, MC TI FIBER PATHWAYS AND BRANCHING PATTERNS OF BIOCYTIN-LABELED OLIVOCOCHLEAR NEURONS IN THE MOUSE BRAIN-STEM SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE EFFERENT NEURON; AXON COLLATERAL; FEEDBACK PATHWAY; HAIR CELLS; SUPERIOR OLIVARY COMPLEX ID SUPERIOR OLIVARY COMPLEX; GUINEA-PIG COCHLEA; CAT; NUCLEUS; PROJECTIONS; RAT; STEM; ORGANIZATION; BUNDLE; SYSTEM AB Olivocochlear neurons have somata in the superior olivary complex in the brainstem and project fibers to the cochlea. The purpose of the present study was to demonstrate the fiber pathways and branching patterns of olivocochlear fibers within the brainstem. Olivocochlear fibers were labeled by extracellular injections of biocytin into the cochlea of mice. The injections labeled two populations of olivocochlear fibers. Thin olivocochlear fibers arose from small somata of the lateral olivocochlear group located ipsilaterally in the lateral superior olive. Thick olivocochlear fibers arose from larger somata of the medial olivocochlear group located bilaterally in the periolivary nuclei. The lateral olivocochlear and medial olivocochlear fibers had similar courses but differed in their branching patterns. Branches from lateral olivocochlear fibers terminated near their somata of origin in the lateral superior olive or in the lateral vestibular nucleus. Branches from medial olivocochlear fibers terminated in the inferior vestibular nucleus or in the cochlear nuclear complex. A few branches from medial olivocochlear fibers projected to the contralateral side. Although they project primarily to the cochlea, olivocochlear neurons also give off branches to a variety of nuclei in the brainstem, thus involving auditory and non-auditory nuclei in the olivocochlear reflex system. (C) 1993 Wiley-Liss, Inc. C1 HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. RP BROWN, MC (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC00119, DC01089] NR 54 TC 73 Z9 73 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 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD NOV 22 PY 1993 VL 337 IS 4 BP 600 EP 613 DI 10.1002/cne.903370406 PG 14 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA ME910 UT WOS:A1993ME91000005 PM 8288773 ER PT J AU TRIGGS, WJ CROS, D MACDONELL, RAL CHIAPPA, KH FANG, JJ DAY, BJ AF TRIGGS, WJ CROS, D MACDONELL, RAL CHIAPPA, KH FANG, JJ DAY, BJ TI CORTICAL AND SPINAL MOTOR EXCITABILITY DURING THE TRANSCRANIAL MAGNETIC STIMULATION SILENT PERIOD IN HUMANS SO BRAIN RESEARCH LA English DT Article DE TRANSCRANIAL MAGNETIC STIMULATION; SILENT PERIOD ID BRAIN-STIMULATION; COIL STIMULATION; F-WAVE; VOLUNTARY CONTRACTION; NEURON EXCITABILITY; EVOKED-POTENTIALS; UNIT RESPONSES; INTACT MAN; H-REFLEX; CORTEX AB We investigated the electromyographic silent period in abductor pollicis brevis (APB) and flexor carpi radialis muscles following transcranial magnetic stimulation of human motor cortex. In APB, we measured cortical stimulation silent period (CSSP) duration as a function of stimulus intensity, motor-evoked potential (MEP) amplitude and muscle twitch force. We used peri-stimulus-time histograms to study the effect of cortical stimulation on single-motor unit firing patterns. We compared F-waves, H-reflexes and magnetic MEPs elicited during the CSSP to control responses elicited at rest and during voluntary contraction. CSSP duration depended on the intensity of cortical stimulation. However, we found no relationship between CSSP duration and MEP amplitude or muscle twitch force, thus the CSSP is not dependent solely on Renshaw cell inhibition or on changes in la and Ib afferent activity following the cortically induced muscle twitch. At low intensities of stimulation, the interval to resumption of motor unit firing following the peak in the peri-stimulus-time histogram corresponding to MEP latency sometimes exceeded that which could be accounted for by the motor unit's firing rate prior to the stimulus, suggesting that synchronization of motor unit firing by cortical stimulation cannot account for the CSSP. We found brief inhibition of F-waves during the CSSP in some subjects, reflecting activation of inhibitory corticospinal projections or segmental effects. In contrast, we observed longer inhibition of H-reflexes during the CSSP in all subjects, perhaps resulting from presynaptic inhibition of la afferents. Magnetic MEPs also were inhibited during the CSSP, suggesting inhibition of cortical elements by transcranial magnetic stimulation. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BIGELOW 12,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LABS,BOSTON,MA 02114. UNIV FLORIDA,DEPT NEUROL,GAINESVILLE,FL 32611. NR 61 TC 75 Z9 75 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD NOV 19 PY 1993 VL 628 IS 1-2 BP 39 EP 48 DI 10.1016/0006-8993(93)90935-G PG 10 WC Neurosciences SC Neurosciences & Neurology GA MG316 UT WOS:A1993MG31600006 PM 8313168 ER PT J AU YUAN, JY SHAHAM, S LEDOUX, S ELLIS, HM HORVITZ, HR AF YUAN, JY SHAHAM, S LEDOUX, S ELLIS, HM HORVITZ, HR TI THE C-ELEGANS CELL-DEATH GENE CED-3 ENCODES A PROTEIN SIMILAR TO MAMMALIAN INTERLEUKIN-1-BETA-CONVERTING ENZYME SO CELL LA English DT Article ID NEMATODE CAENORHABDITIS-ELEGANS; CONVERTING ENZYME; BCL-2; GENOME; IDENTIFICATION; INTERLEUKIN-1; ABNORMALITIES; CHROMOSOME; PREVENTION; EXPRESSION AB We have cloned the C. elegans cell death gene ced-3. A ced-3 transcript is most abundant during embryogenesis, the stage during which most programmed cell deaths occur. The predicted CED-3 protein shows similarity to human and murine interleukin-1beta-converting enzyme and to the product of the mouse nedd-2 gene, which is expressed in the embryonic brain. The sequences of 12 ced-3 mutations as well as the sequences of ced-3 genes from two related nematode species identify sites of potential functional importance. We propose that the CED-3 protein acts as a cysteine protease in the initiation of programmed cell death in C. elegans and that cysteine proteases also function in programmed cell death in mammals. C1 MIT,HOWARD HUGHES MED INST,DEPT BIOL,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. RP YUAN, JY (reprint author), HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM24663] NR 61 TC 2044 Z9 2121 U1 3 U2 40 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD NOV 19 PY 1993 VL 75 IS 4 BP 641 EP 652 DI 10.1016/0092-8674(93)90485-9 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MH749 UT WOS:A1993MH74900010 PM 8242740 ER PT J AU MIURA, M ZHU, H ROTELLO, R HARTWIEG, EA YUAN, JY AF MIURA, M ZHU, H ROTELLO, R HARTWIEG, EA YUAN, JY TI INDUCTION OF APOPTOSIS IN FIBROBLASTS BY IL-1-BETA-CONVERTING ENZYME, A MAMMALIAN HOMOLOG OF THE C-ELEGANS CELL-DEATH GENE CED-3 SO CELL LA English DT Article ID INTERLEUKIN-1-BETA CONVERTING ENZYME; CAENORHABDITIS-ELEGANS; MOLECULAR-CLONING; BCL-2; PREVENTION; MONOCYTES; SELECTION; RECEPTOR; SURVIVAL; PROTEIN AB The mammalian interleukin-1beta-converting enzyme (ICE) has sequence similarity to the C. elegans cell death gene ced-3. We show here that overexpression of the murine ICE (mICE) gene or of the C. elegans ced-3 gene causes Rat-1 cells to undergo programmed cell death. Point mutations in a region homologous between mICE and CED-3 eliminate the ability of mICE and ced-3 to cause cell death. The cell death caused by mICE can be suppressed by overexpression of the crmA gene, a specific inhibitor of ICE, as well as by bcl-2, a mammalian oncogene that can act to prevent programmed cell death. Our results suggest that ICE may function during mammalian development to cause programmed cell death. C1 MIT,HOWARD HUGHES MED INST,DEPT BIOL,CAMBRIDGE,MA 02139. RP MIURA, M (reprint author), MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129, USA. NR 43 TC 1337 Z9 1362 U1 1 U2 17 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD NOV 19 PY 1993 VL 75 IS 4 BP 653 EP 660 DI 10.1016/0092-8674(93)90486-A PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MH749 UT WOS:A1993MH74900011 PM 8242741 ER PT J AU GYURIS, J GOLEMIS, E CHERTKOV, H BRENT, R AF GYURIS, J GOLEMIS, E CHERTKOV, H BRENT, R TI CDI1, A HUMAN G1-PHASE AND S-PHASE PROTEIN PHOSPHATASE THAT ASSOCIATES WITH CDK2 SO CELL LA English DT Article ID YEAST TRANSCRIPTIONAL ACTIVATORS; HOMEODOMAIN RECOGNITION HELIX; AMINO-ACID SEQUENCE; CELL-CYCLE; TYROSINE-PHOSPHATASE; FISSION-YEAST; SACCHAROMYCES-CEREVISIAE; DNA SPECIFICITY; HUMAN HOMOLOG; G1 CYCLIN AB We used the interaction trap, a yeast genetic selection for interacting proteins, to isolate human cyclin-dependent kinase interactor 1 (Cdi1). In yeast, Cdi1 interacts with cyclin-dependent kinases, including human Cdc2, Cdk2, and Cdk3, but not with Ckd4. In HeLa cells, Cdi1 is expressed at the G1 to S transition, and the protein forms stable complexes with Cdk2. Cdi1 bears weak sequence similarity to known tyrosine and dual specificity phosphatases. In vitro, Cdi1 removes phosphate from tyrosine residues in model substrates, but a mutant protein that bears a lesion in the putative active site cysteine does not. Overexpression of wild-type Cdi1 delays progression through the cell cycle in yeast and HeLa cells; delay is dependent on Cdi1 phosphatase activity. These experiments identify Cdi1 as a novel type of protein phosphatase that forms complexes with cyclin-dependent kinases. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RI Tang, Amy/L-3226-2016 OI Tang, Amy/0000-0002-5772-2878 NR 90 TC 1270 Z9 1282 U1 3 U2 16 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD NOV 19 PY 1993 VL 75 IS 4 BP 791 EP 803 DI 10.1016/0092-8674(93)90498-F PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MH749 UT WOS:A1993MH74900023 PM 8242750 ER PT J AU HARPER, JW ADAMI, GR WEI, N KEYOMARSI, K ELLEDGE, SJ AF HARPER, JW ADAMI, GR WEI, N KEYOMARSI, K ELLEDGE, SJ TI THE P21 CDK-INTERACTING PROTEIN CIP1 IS A POTENT INHIBITOR OF G1 CYCLIN-DEPENDENT KINASES SO CELL LA English DT Article ID CELL-CYCLE; TYROSINE PHOSPHORYLATION; YEAST; PHASE; CDC2; IDENTIFICATION; EXPRESSION; ACTIVATION; P34CDC2; SYSTEM AB The cyclin-dependent kinase Cdk2 associates with cyclins A, D, and E and has been implicated in the control of the G1 to S phase transition in mammals. To identify potential Cdk2 regulators, we have employed an improved two-hybrid system to isolate human genes encoding Cdk-interacting proteins (Cips). CIP1 encodes a novel 21 kd protein that is found in cyclin A, cyclin D1, cyclin E, and Cdk2 immunoprecipitates. p21CIP1 is a potent, tight-binding inhibitor of Cdks and can inhibit the phosphorylation of Rb by cyclin A-Cdk2, cyclin E-Cdk2, cyclin D1-Cdk4, and cyclin D2-Cdk4 complexes. Cotransfection experiments indicate that CIP1 and SV40 T antigen function in a mutually antagonistic manner to control cell cycle progression. C1 BAYLOR COLL MED, HOWARD HUGHES MED INST, HOUSTON, TX 77030 USA. BAYLOR COLL MED, DIV MOLEC VIROL, HOUSTON, TX 77030 USA. BAYLOR COLL MED, INST MOLEC GENET, HOUSTON, TX 77030 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV CELL GROWTH & REGULAT, BOSTON, MA 02115 USA. RP BAYLOR COLL MED, VERNA & MARRS MCLEAN DEPT BIOCHEM, HOUSTON, TX 77030 USA. FU NIA NIH HHS [R01-AG 11066, AG-11085] NR 49 TC 4974 Z9 5094 U1 19 U2 142 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0092-8674 EI 1097-4172 J9 CELL JI Cell PD NOV 19 PY 1993 VL 75 IS 4 BP 805 EP 816 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MH749 UT WOS:A1993MH74900024 PM 8242751 ER PT J AU CANNISTRA, SA AF CANNISTRA, SA TI MEDICAL PROGRESS - CANCER OF THE OVARY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID GYNECOLOGIC-ONCOLOGY-GROUP; COLONY-STIMULATING FACTOR; PHASE-II TRIAL; CISPLATIN-BASED CHEMOTHERAPY; WHOLE-ABDOMINAL IRRADIATION; BONE-MARROW TRANSPLANTATION; HIGH-DOSE CARBOPLATIN; BLOOD PROGENITOR CELLS; NON-HODGKINS LYMPHOMA; 2ND-LOOK LAPAROTOMY C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CANNISTRA, SA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 113 TC 338 Z9 344 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 18 PY 1993 VL 329 IS 21 BP 1550 EP 1559 DI 10.1056/NEJM199311183292108 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA MG188 UT WOS:A1993MG18800008 PM 8155119 ER PT J AU MACCOLLIN, M MOHNEY, T TROFATTER, J WERTELECKI, W RAMESH, V GUSELLA, J AF MACCOLLIN, M MOHNEY, T TROFATTER, J WERTELECKI, W RAMESH, V GUSELLA, J TI DNA DIAGNOSIS OF NEUROFIBROMATOSIS-2 - ALTERED CODING SEQUENCE OF THE MERLIN TUMOR-SUPPRESSOR IN AN EXTENDED PEDIGREE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID BILATERAL ACOUSTIC NEUROFIBROMATOSIS; TYPE-2 NEUROFIBROMATOSIS; UNITED-KINGDOM; CHROMOSOME-22; DISEASE; SCHWANNOMAS; DELETIONS; MUTATIONS; MARKERS; LINKAGE AB Objective.-To define the DNA mutation causing neurofibromatosis 2 (NF2), a severe genetic disorder involving the development of multiple nervous system tumors in adulthood, in a large, well-studied NF2 pedigree previously used to chromosomally map and to isolate the disease gene. Design.-Single-strand conformational polymorphism (SSCP) and DNA sequence analysis of the NF2 gene amplified from affected and unaffected family members. Participants.-Affected, unaffected, and at-risk members of a large pedigree segregating NF2, an autosomal dominant disorder caused by inactivation of the merlin tumor suppressor encoded in chromosome band 22q12. Results.-A DNA alteration in the merlin coding sequence caused a shift on SSCP gels that was characteristic of the disease chromosome in this NF2 pedigree, being transmitted with the disorder, present only in affected members of the pedigree, absent in unaffected members of the family, and absent from 158 unrelated individuals. The alteration caused substitution of a tyrosine for an asparagine at position 220 of the merlin protein, in a region highly conserved in closely related members of the family of cytoskeletal-associated proteins. The DNA change could also be detected by restriction enzyme digestion with Rsa I. Conclusion.-Current practice dictates screening of all those ''at risk'' for NF2 with magnetic resonance imaging, but the frequency and duration of screening are problematic because of the variable course of the disease. The identification of a DNA alteration in the NF2 gene will permit predictive molecular testing of individuals at risk in this specific family, sparing the expense and emotional burden of protracted screening programs. This information, by providing diagnostic certainty, should also reduce psychological and financial burdens and improve medical care for affected family members. A similar approach to defining the underlying lesion and developing a predictive test is applicable in any documented NF2 family. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. UNIV SO ALABAMA,DEPT MED GENET,MOBILE,AL 36688. FU NINDS NIH HHS [NS24279] NR 28 TC 56 Z9 57 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD NOV 17 PY 1993 VL 270 IS 19 BP 2316 EP 2320 DI 10.1001/jama.270.19.2316 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MF993 UT WOS:A1993MF99300025 PM 8230593 ER PT J AU PAYTON, M HU, H SPARROW, D YOUNG, JB LANDSBERG, L WEISS, ST AF PAYTON, M HU, H SPARROW, D YOUNG, JB LANDSBERG, L WEISS, ST TI RELATION BETWEEN BLOOD LEAD AND URINARY BIOGENIC-AMINES IN COMMUNITY-EXPOSED MEN SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE AGE FACTORS; BIOGENIC AMINES; BODY WEIGHT; CREATININE; LEAD; SMOKING ID CATECHOLAMINE METABOLITES; BRAIN CATECHOLAMINES; RENAL-FUNCTION; DOPAMINE; RAT; SEROTONIN; EXCRETION; PRESSURE; SYSTEM; AGE AB The cross-sectional relation between levels of urinary biogenic amines (dopamine, epinephrine, norepinephrine, and serotonin) and levels of blood lead was examined in a study of 645 male participants from a longitudinal study of aging. This stable population of men had initially been recruited from communities in and around Boston, Massachusetts, and had not been selected with regard to lead exposure. Blood lead samples and 24-hour and 2-hour urine specimens were collected during regularly scheduled clinic visits. In multivariate linear regression step-forward models, 24-hour epinephrine excretion was significantly and positively associated with blood lead (beta = 0.101 mu g(mu g/dl)(-1) blood lead, SE (standard error) (beta) = 0.045, p = 0.026). Twenty-four-hour norepinephrine excretion was positively associated with blood lead (beta = 0.023 mu g(mu g/dl)(-1) blood lead, SE(beta) = 0.029, p = 0.425), and both 24-hour dopamine (beta = -4.35 mu g(mu g/dl)(-1) blood lead, SE(beta) = 6.90, p = 0.529) and 2-hour serotonin (beta = -0.348 mu g(mu g/dl)(-1) blood lead, SE(beta) = 0.277, p = 0.210) excretion were negatively associated with blood lead; however, these relations did not achieve statistical significance. An increase of 10 mu g/dl in blood lead was associated with an increase in epinephrine excretion of 11 mu g/24 hours. These results support the hypothesis that epinephrine metabolism is influenced by low levels of lead exposure. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,OCCUPAT HLTH PROGRAM,BOSTON,MA. US DEPT VET AFFAIRS,OUTPATIENT CLIN,NORMAT AGING STUDY,BOSTON,MA. NORTHWESTERN UNIV,MEM HOSP,DEPT MED,CHICAGO,IL. RP PAYTON, M (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,180 LONGWOOD AVE,BOSTON,MA 02115, USA. OI Hu, Howard/0000-0002-3676-2707 FU NHLBI NIH HHS [HL37871]; NIEHS NIH HHS [NIEHS 2 P30 ES 00002, NIEHS ES05257-01A1] NR 63 TC 5 Z9 6 U1 1 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD NOV 15 PY 1993 VL 138 IS 10 BP 815 EP 825 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA ML239 UT WOS:A1993ML23900005 PM 8237970 ER PT J AU TALAMO, JH LARKIN, DS AF TALAMO, JH LARKIN, DS TI BILATERAL ACANTHAMOEBA-KERATITIS AND GAS-PERMEABLE CONTACT-LENSES SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Letter RP TALAMO, JH (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,CORNEA SERV,BOSTON,MA 02114, USA. NR 2 TC 4 Z9 4 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD NOV 15 PY 1993 VL 116 IS 5 BP 651 EP 652 PG 2 WC Ophthalmology SC Ophthalmology GA MF624 UT WOS:A1993MF62400023 PM 8238234 ER PT J AU BARNETT, GO JENDERS, RA CHUEH, HC AF BARNETT, GO JENDERS, RA CHUEH, HC TI THE COMPUTER-BASED CLINICAL RECORD - WHERE DO WE STAND SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material RP BARNETT, GO (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,COMP SCI LAB,50 STANIFORD ST,5TH FLOOR,BOSTON,MA 02114, USA. FU AHRQ HHS [R18 HS06575]; NLM NIH HHS [R01 LM05200, LM-1-3538] NR 17 TC 30 Z9 30 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD NOV 15 PY 1993 VL 119 IS 10 BP 1046 EP 1048 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA MG672 UT WOS:A1993MG67200014 PM 8214984 ER PT J AU BHAVANI, K BROWN, NV CARLSON, RI RHOADS, D WANDS, JR AF BHAVANI, K BROWN, NV CARLSON, RI RHOADS, D WANDS, JR TI THE EFFECT OF ETHANOL AND EXTRACELLULAR-MATRIX ON INDUCTION OF P36-PROTEIN KINASE SUBSTRATE EXPRESSION IN RAT HEPATOCYTES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID GENE-EXPRESSION; SARCOMA VIRUS; PROTEIN; REGENERATION; INHIBITION; CARCINOMA; CALPACTIN; P36 C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,SCH MED,MOLEC HEPATOL LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,SCH MED,TUMOR BIOL LAB,BOSTON,MA 02114. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-02666, AA-00048] NR 18 TC 7 Z9 7 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 15 PY 1993 VL 196 IS 3 BP 1454 EP 1458 DI 10.1006/bbrc.1993.2415 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MG310 UT WOS:A1993MG31000063 PM 7504477 ER PT J AU SAVVIDES, P SHALEV, O JOHN, KM LUX, SE AF SAVVIDES, P SHALEV, O JOHN, KM LUX, SE TI COMBINED SPECTRIN AND ANKYRIN DEFICIENCY IS COMMON IN AUTOSOMAL-DOMINANT HEREDITARY SPHEROCYTOSIS SO BLOOD LA English DT Note ID HUMAN-ERYTHROCYTE ANKYRIN; RED BLOOD-CELL; MEMBRANE-SKELETON; CYTOPLASMIC DOMAIN; HEMOLYTIC-ANEMIA; BINDING-SITES; MOLECULAR DEFECT; ANION-EXCHANGER; GENETIC-DEFECT; PROTEIN 4.1 C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NHLBI NIH HHS [HL32262]; NIDDK NIH HHS [1DK34083] NR 63 TC 58 Z9 59 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 BP 2953 EP 2960 PG 8 WC Hematology SC Hematology GA MH010 UT WOS:A1993MH01000004 PM 8219186 ER PT J AU OZER, H GEORGE, SL SCHIFFER, CA RAO, K RAO, PN WURSTERHILL, DH ARTHUR, DD POWELL, B GOTTLIEB, A PETERSON, BA RAI, K TESTA, JR LEBEAU, M TANTRAVAHI, R BLOOMFIELD, CD AF OZER, H GEORGE, SL SCHIFFER, CA RAO, K RAO, PN WURSTERHILL, DH ARTHUR, DD POWELL, B GOTTLIEB, A PETERSON, BA RAI, K TESTA, JR LEBEAU, M TANTRAVAHI, R BLOOMFIELD, CD TI PROLONGED SUBCUTANEOUS ADMINISTRATION OF RECOMBINANT INTERFERON-ALPHA-2B IN PATIENTS WITH PREVIOUSLY UNTREATED PHILADELPHIA-CHROMOSOME-POSITIVE CHRONIC-PHASE CHRONIC MYELOGENOUS LEUKEMIA - EFFECT ON REMISSION DURATION AND SURVIVAL - CANCER AND LEUKEMIA GROUP-B STUDY-8583 SO BLOOD LA English DT Article ID CHRONIC GRANULOCYTIC-LEUKEMIA; CHRONIC MYELOCYTIC-LEUKEMIA; CHRONIC MYELOID-LEUKEMIA; MARROW TRANSPLANTATION; BLAST CRISIS; INTERFERON; CELLS; THERAPY; ORIGIN C1 DARTMOUTH COLL,SCH MED,LEBANON,NH. SUNY HLTH SCI CTR,SYRACUSE,NY. LONG ISL JEWISH MED CTR,NEW HYDE PK,NY. DUKE UNIV,CALGB STAT CTR,DURHAM,NC 27706. UNIV MARYLAND,CTR CANC,BALTIMORE,MD 21201. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC 27103. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV CHICAGO,CHICAGO,IL 60637. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. RP OZER, H (reprint author), UNIV N CAROLINA,DIV MED ONCOL,3019 OLD CLIN BLDG,CB 7305,CHAPEL HILL,NC 27599, USA. FU NCI NIH HHS [CA44691, CA16450, CA37027, CA32291, CA04326, CA31983, CA11028, CA47559, CA33601, CA03927, CA21060] NR 34 TC 183 Z9 183 U1 0 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 BP 2975 EP 2984 PG 10 WC Hematology SC Hematology GA MH010 UT WOS:A1993MH01000007 PM 8219189 ER PT J AU AJCHENBAUMCYMBALISTA, F SOLA, B ANDO, K DELMER, A ROMEO, PH ZITTOUN, R GRIFFIN, JD AF AJCHENBAUMCYMBALISTA, F SOLA, B ANDO, K DELMER, A ROMEO, PH ZITTOUN, R GRIFFIN, JD TI CONSTITUTIVE EXPRESSION OF CYCLIN D2 UNCOUPLES PROLIFERATION AND DIFFERENTIATION OF MOUSE ERYTHROLEUKEMIA-CELLS SO BLOOD LA English DT Meeting Abstract C1 HOP HOTEL DIEU,SERV HEMATOL,F-75181 PARIS 04,FRANCE. HOP COCHIN,INSERM,U363,F-75674 PARIS 14,FRANCE. HOP HENRI MONDOR,INSERM,U91,F-94010 CRETEIL,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A182 EP A182 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200713 ER PT J AU ANDO, K GRIFFIN, JD AF ANDO, K GRIFFIN, JD TI REGULATION OF G1/S TRANSITION BY CYCLIN D2 AND D3 IN IL-3-DEPENDENT MYELOID CELLS SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A182 EP A182 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200712 ER PT J AU BALDWIN, GC CHUNG, GY HUANG, M WANG, J DUBINETT, SM AF BALDWIN, GC CHUNG, GY HUANG, M WANG, J DUBINETT, SM TI RECOMBINANT INTERLEUKIN-7 INDUCES FUNCTIONAL ACTIVATION OF CULTURED HUMAN MACROPHAGES BY DOWN-REGULATING BOTH TGF-BETA EXPRESSION AND TGF-BETA PROTEIN-PRODUCTION SO BLOOD LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,DIV HEMATOL ONCOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DIV PULM MED,LOS ANGELES,CA 90024. W LOS ANGELES VET ADM,LOS ANGELES,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A24 EP A24 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200084 ER PT J AU BERARDI, AC LOPEZ, P LEVINE, JD CAVACINI, L SCADDEN, DT AF BERARDI, AC LOPEZ, P LEVINE, JD CAVACINI, L SCADDEN, DT TI ISOLATION AND CHARACTERIZATION OF HUMAN BONE-MARROW HEMATOPOIETIC PROGENITOR CELLS IN G(0) PHASE SO BLOOD LA English DT Meeting Abstract C1 NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,FLOW CYTOMETRY FACIL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A12 EP A12 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200038 ER PT J AU BOUSSIOTIS, V FREEMAN, G GRIBBEN, J NADLER, L AF BOUSSIOTIS, V FREEMAN, G GRIBBEN, J NADLER, L TI HUMAN ALLOANTIGEN-SPECIFIC CLONAL ANERGY TO LYMPHOBLASTOID-CELLS IS REVERSED FOLLOWING CULTURE WITH IL-2 OR IL-4 SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A304 EP A304 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201201 ER PT J AU BOUSSIOTIS, V FREEMAN, G GRIBBEN, J NADLER, L AF BOUSSIOTIS, V FREEMAN, G GRIBBEN, J NADLER, L TI B7 BUT NOT ICAM-1 COSTIMULATION PREVENTS THE INDUCTION OF ALLOANTIGEN-SPECIFIC TOLERANCE IN UNPRIMED HUMAN T-CELLS SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A304 EP A304 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201200 ER PT J AU BOUSSIOTIS, V GRIBBEN, J FREEMAN, G NADLER, L AF BOUSSIOTIS, V GRIBBEN, J FREEMAN, G NADLER, L TI ACTIVATED HUMAN B-LYMPHOCYTES EXPRESS 3 CTLA4 COUNTER-RECEPTORS WHICH COSTIMULATE T-CELL ACTIVATION SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A188 EP A188 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200736 ER PT J AU BUSQUE, L KOHLER, S DEHART, D SAXENA, R BERNSTEIN, S STONE, R GREENBERG, P GILLILAND, DG AF BUSQUE, L KOHLER, S DEHART, D SAXENA, R BERNSTEIN, S STONE, R GREENBERG, P GILLILAND, DG TI HIGH-INCIDENCE OF POLYCLONAL GRANULOCYTOPOIESIS IN MYELODYSPLASTIC SYNDROMES (MDS) SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. STANFORD UNIV HOSP,STANFORD,CA 94305. NR 0 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A196 EP A196 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200770 ER PT J AU BUSQUE, L WAYNE, A GIUSTI, V DEHART, D WEINSTEIN, H GOLUB, T GILLILAND, DG AF BUSQUE, L WAYNE, A GIUSTI, V DEHART, D WEINSTEIN, H GOLUB, T GILLILAND, DG TI POLYCLONAL DERIVATION OF MONONUCLEAR-CELLS AND PMN IN JUVENILE CHRONIC MYELOGENOUS LEUKEMIA (JCML) SO BLOOD LA English DT Meeting Abstract C1 ALL CHILDRENS HOSP,ST PETERSBURG,FL. ORLANDO CANC CTR,ORLANDO,FL. BRIGHAM & WOMENS HOSP,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A381 EP A381 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201507 ER PT J AU CARLESSO, N GRIFFIN, JD DRUKER, B AF CARLESSO, N GRIFFIN, JD DRUKER, B TI USE OF A TEMPERATURE-SENSITIVE MUTANT TO DEFINE THE BIOLOGICAL PROPERTIES OF THE P210BCR/ABL ONCOGENE SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. OREGON HLTH SCI UNIV,DIV HEMATOL ONCOL,PORTLAND,OR 97201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A326 EP A326 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201286 ER PT J AU CARROLL, M MATHEYPREVOT, B DANDREA, A AF CARROLL, M MATHEYPREVOT, B DANDREA, A TI THE EXTRACYTOPLASMIC REGION OF THE ERYTHROPOIETIN RECEPTOR DRIVES ERYTHROID-SPECIFIC DIFFERENTIATION IN A HEMATOPOIETIC-CELL LINE SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. BETH ISRAEL HOSP,DIV HEMATOL & ONCOL,BOSTON,MA 02215. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A317 EP A317 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201252 ER PT J AU DAHL, G DUNUSSI, K MOGUL, M BROPHY, N LOWE, K GRIER, H SIKIC, B WEINSTEIN, H ARCECI, R AF DAHL, G DUNUSSI, K MOGUL, M BROPHY, N LOWE, K GRIER, H SIKIC, B WEINSTEIN, H ARCECI, R TI A PEDIATRIC-ONCOLOGY-GROUP (POG) PHASE-II TRIAL OF MITOXANTRONE, ETOPOSIDE AND CYCLOSPORINE A (MEC) THERAPY FOR RELAPSED AND REFRACTORY ACUTE MYELOGENOUS LEUKEMIA (AML) SO BLOOD LA English DT Meeting Abstract C1 STANFORD UNIV,STANFORD,CA 94305. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP,POG,CHICAGO,IL. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A195 EP A195 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200766 ER PT J AU DELMER, A AJCHENBAUMCYMBALISTA, F TANG, RP MARIE, JP GRIFFIN, JD ZITTOUN, R AF DELMER, A AJCHENBAUMCYMBALISTA, F TANG, RP MARIE, JP GRIFFIN, JD ZITTOUN, R TI CYCLIN D2 (BUT NOT CYCLIN D1 AND D3) IS EXPRESSED IN LYMPHOCYTES FROM PATIENTS WITH CHRONIC B-CELL LYMPHOID MALIGNANCIES SO BLOOD LA English DT Meeting Abstract C1 HOP HOTEL DIEU,SERV HEMATOL,F-75181 PARIS 04,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A201 EP A201 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200789 ER PT J AU DEMETRI, GD BUKOWSKI, RM SAMUELS, B GORDON, M ANTMAN, K MERICA, EA SAMUEL, S CAMPION, M LEVITT, D ISAACS, R AF DEMETRI, GD BUKOWSKI, RM SAMUELS, B GORDON, M ANTMAN, K MERICA, EA SAMUEL, S CAMPION, M LEVITT, D ISAACS, R TI STIMULATION OF THROMBOPOIESIS BY RECOMBINANT HUMAN INTERLEUKIN-6 (IL-6) PRE-CHEMOTHERAPY AND POSTCHEMOTHERAPY IN PREVIOUSLY UNTREATED SARCOMA PATIENTS WITH NORMAL HEMATOPOIESIS SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CLEVELAND CLIN,CLEVELAND,OH 44106. LUTHERAN GEN HOSP,CHICAGO,IL. INDIANA UNIV,INDIANAPOLIS,IN 46204. SANDOZ INC,CYTOKINE DEV UNIT,E HANOVER,NJ 07936. NR 0 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A367 EP A367 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201450 ER PT J AU DIACOVO, T DEFOUGEROLLES, AR BAINTON, DF SPRINGER, TA AF DIACOVO, T DEFOUGEROLLES, AR BAINTON, DF SPRINGER, TA TI INTRACELLULAR ADHESION MOLECULE 2 (ICAM-2) IS PRESENT ON RESTING AND ACTIVATED PLATELETS AND BINDS TO PURIFIED (LEUKOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 (LFA-1) SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,CTR BLOOD RES,CAMBRIDGE,MA 02138. UNIV CALIF SAN FRANCISCO,SCH MED,DEPT PATHOL,SAN FRANCISCO,CA 94143. NR 1 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A340 EP A340 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201345 ER PT J AU EMERY, DW SACHS, DH LEGUERN, C AF EMERY, DW SACHS, DH LEGUERN, C TI INCREASED RETROVIRUS-MEDIATED TRANSDUCTION OF SWINE BONE-MARROW USING HUMAN AND MURINE RECOMBINANT CYTOKINES SO BLOOD LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A647 EP A647 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68202569 ER PT J AU ENGELAND, K MATHEYPREVOT, B AF ENGELAND, K MATHEYPREVOT, B TI MULTIPLE DNA-BINDING PROTEINS INTERACT WITH THE NIP REPRESSOR SITE OF THE HUMAN INTERLEUKIN-3 PROMOTER SO BLOOD LA English DT Meeting Abstract 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 W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A319 EP A319 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201260 ER PT J AU ERNST, CA HANCOCK, PR CORLESS, CL ROLLINS, BJ AF ERNST, CA HANCOCK, PR CORLESS, CL ROLLINS, BJ TI MURINE MCP-1 - PHYSICAL AND BIOLOGICAL CHARACTERIZATION SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A26 EP A26 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200094 ER PT J AU ERNST, TJ WAMSLEY, S GRIFFIN, JD AF ERNST, TJ WAMSLEY, S GRIFFIN, JD TI C-FES EXPRESSION AUGMENTS THE TRANSFORMING ACTIVITY OF P210BCR/ABL IN NIH 3T3 FIBROBLASTS SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A327 EP A327 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201291 ER PT J AU ESSELTINE, DL BRAMAN, GM PARK, Y LEVINE, AM MCLAUGHLIN, P MURRAY, JL GROSSBARD, M LYNCH, T RITZ, J NADLER, L EPSTEIN, CL AF ESSELTINE, DL BRAMAN, GM PARK, Y LEVINE, AM MCLAUGHLIN, P MURRAY, JL GROSSBARD, M LYNCH, T RITZ, J NADLER, L EPSTEIN, CL TI USE OF ANTI-B4-BLOCKED RICIN AS AN IMMUNOSUPPRESSANT SO BLOOD LA English DT Meeting Abstract C1 IMMUNOGEN INC,CAMBRIDGE,MA. USC,SCH MED,LOS ANGELES,CA. MD ANDERSON,HOUSTON,TX. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A240 EP A240 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200943 ER PT J AU FISHER, MJ PRCHAL, JF PRCHAL, JT DANDREA, AD AF FISHER, MJ PRCHAL, JF PRCHAL, JT DANDREA, AD TI ANTIERYTHROPOIETIN RECEPTOR MONOCLONAL-ANTIBODIES DISTINGUISH EPO-DEPENDENT AND EPO-INDEPENDENT ERYTHROID PROGENITORS IN POLYCYTHEMIA-VERA SO BLOOD 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. MCGILL UNIV,DEPT MED,MONTREAL H3A 2T5,QUEBEC,CANADA. MCGILL UNIV,DEPT ONCOL,MONTREAL H3A 2T5,QUEBEC,CANADA. UNIV ALABAMA,DEPT MED,DIV HEMATOL ONCOL,UNIVERSITY,AL 35486. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A197 EP A197 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200773 ER PT J AU FREEDMAN, A GRIBBEN, J RABINOWE, S NEUBERG, D MAUCH, P SPECTOR, N ANDERSON, K SOIFFER, R PESEK, K ROBERTSON, M WHELAN, M RITZ, J NADLER, L AF FREEDMAN, A GRIBBEN, J RABINOWE, S NEUBERG, D MAUCH, P SPECTOR, N ANDERSON, K SOIFFER, R PESEK, K ROBERTSON, M WHELAN, M RITZ, J NADLER, L TI AUTOLOGOUS BONE-MARROW TRANSPLANTATION IN ADVANCED LOW-GRADE B-CELL NON-HODGKINS-LYMPHOMA IN 1ST REMISSION SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A332 EP A332 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201312 ER PT J AU FREEMAN, G BORRIELLO, F HODES, R GRIBBEN, J GRAY, G NADLER, L SHARPE, A AF FREEMAN, G BORRIELLO, F HODES, R GRIBBEN, J GRAY, G NADLER, L SHARPE, A TI ANTIGEN-PRESENTING CELLS ISOLATED FROM B7-1 DEFICIENT MICE USE AN ALTERNATIVE CTLA4 COUNTER-RECEPTOR, B7-2, TO COSTIMULATE T-CELL ACTIVATION SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. REPLIGEN CORP,CAMBRIDGE,MA. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A323 EP A323 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201277 ER PT J AU FREEMAN, G GRIBBEN, J BOUSSIOTIS, V GRAY, G NADLER, L AF FREEMAN, G GRIBBEN, J BOUSSIOTIS, V GRAY, G NADLER, L TI HUMAN B7-2, A CTLA-4 COUNTER-RECEPTOR THAT COSTIMULATES T-CELL PROLIFERATION SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. REPLIGEN CORP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A188 EP A188 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200738 ER PT J AU FREYTES, CO SALZMAN, DE BACHIER, C BOLDT, DH ROODMAN, GD CRAIG, F CASTRO, J LEMAISTRE, CF AF FREYTES, CO SALZMAN, DE BACHIER, C BOLDT, DH ROODMAN, GD CRAIG, F CASTRO, J LEMAISTRE, CF TI HIGH-DOSE CHEMOTHERAPY WITH STEM-CELL RESCUE IN OLDER PATIENTS SO BLOOD 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 W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A173 EP A173 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200675 ER PT J AU GALLICCHIO, VS TSE, KF HUGHES, NK GUIGON, M AF GALLICCHIO, VS TSE, KF HUGHES, NK GUIGON, M TI REDUCED ZIDOVUDINE (AZT) MURINE HEMATOPOIETIC TOXICITY IN-VIVO WITH THE TETRAPEPTIDE ACSERASPLYSPRO (ACSDKP, SERASPENIDE) SO BLOOD LA English DT Meeting Abstract C1 UNIV KENTUCKY,MED CTR,LEXINGTON,KY 40506. US DEPT VET AFFAIRS,LEXINGTON,KY. UNIV PARIS 06,HEMATOL LAB,F-75571 PARIS 12,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A103 EP A103 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200396 ER PT J AU GEE, B PLATT, OS AF GEE, B PLATT, OS TI SICKLE RETICULOCYTES ADHERE TO VCAM-1 SO BLOOD LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A179 EP A179 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200701 ER PT J AU GRABOWSKI, EF HEAD, C MICHAIL, HA NEMERSON, Y AF GRABOWSKI, EF HEAD, C MICHAIL, HA NEMERSON, Y TI SUBENDOTHELIAL MATRIX FROM ACTIVATED ENDOTHELIAL-CELL MONOLAYERS EXPRESSES TISSUE FACTOR WHICH PROMOTES PLATELET-ADHESION AGGREGATION UNDER FLOW CONDITIONS SO BLOOD LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MT SINAI MED CTR,NEW YORK,NY 10029. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A275 EP A275 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201083 ER PT J AU GRELLIER, P YEE, D GONZALEZ, M ABBOUD, S AF GRELLIER, P YEE, D GONZALEZ, M ABBOUD, S TI CHARACTERIZATION OF INSULIN-LIKE GROWTH-FACTOR (IGF) BINDING-PROTEINS IN BONE-MARROW STROMAL CELLS SO BLOOD 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 W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A498 EP A498 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201975 ER PT J AU GRIBBEN, J BOUSSIOTIS, V FREEMAN, G GRAY, G NADLER, L AF GRIBBEN, J BOUSSIOTIS, V FREEMAN, G GRAY, G NADLER, L TI BLOCKADE OF THE B7 FAMILY OF COSTIMULATORY MOLECULES SIGNIFICANTLY REDUCES ALLOREACTIVE PRECURSOR T-CELLS CAPABLE OF INDUCING GVHD SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. REPLIGEN CORP,CAMBRIDGE,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A456 EP A456 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201806 ER PT J AU GRIBBEN, J LUNDBERG, A SPECTOR, N FREEMAN, G NADLER, L AF GRIBBEN, J LUNDBERG, A SPECTOR, N FREEMAN, G NADLER, L TI ALTHOUGH EXPRESSING B7 FAMILY MOLECULES, HUMAN MONOCYTES DO NOT COSTIMULATE VIA THE B7-CD28/CTLA4 PATHWAY SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A122 EP A122 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200474 ER PT J AU GROSSBARD, ML ODAY, S GRIBBEN, JG FREEDMAN, AS RABINOWE, SN NEUBERG, D ESSELTINE, DL EPSTEIN, CL NADLER, LM AF GROSSBARD, ML ODAY, S GRIBBEN, JG FREEDMAN, AS RABINOWE, SN NEUBERG, D ESSELTINE, DL EPSTEIN, CL NADLER, LM TI ANTI-B4-BLOCKED RICIN (ANTI-B4-BR) THERAPY FOLLOWING AUTOLOGOUS BONE-MARROW TRANSPLANTATION (ABMT) FOR B-CELL NON-HODGKINS-LYMPHOMA (B-NHL) - UPDATE OF PHASE-I/II TRIALS SO BLOOD LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. IMMUNOGEN INC,CAMBRIDGE,MA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A444 EP A444 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201757 ER PT J AU GRUPP, SA MITCHELL, RN ABBAS, AK AF GRUPP, SA MITCHELL, RN ABBAS, AK TI AN INTRACELLULAR RETENTION SIGNAL FOR IMMUNOGLOBULIN-M SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A322 EP A322 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201270 ER PT J AU GUINAN, E PARSONS, S LONGTINE, J RYAN, H BIERER, B FERRARA, J GILLILAND, G RIMM, I BALLEN, K TARBELL, N NEUBERG, D BURAKOFF, S WEINSTEIN, H ANTIN, J AF GUINAN, E PARSONS, S LONGTINE, J RYAN, H BIERER, B FERRARA, J GILLILAND, G RIMM, I BALLEN, K TARBELL, N NEUBERG, D BURAKOFF, S WEINSTEIN, H ANTIN, J TI DIFFERENT TOXICITIES ASSOCIATED WITH 3 GVHD PROPHYLAXIS REGIMENS FOR UNRELATED DONOR BONE-MARROW TRANSPLANTATION (UDBMT) SO BLOOD LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A421 EP A421 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201667 ER PT J AU HALLEK, M NEUMANN, C DRUKER, B GRIFFIN, JD EMMERICH, B AF HALLEK, M NEUMANN, C DRUKER, B GRIFFIN, JD EMMERICH, B TI INTERLEUKIN-6 (IL-6) INDUCES TYROSINE PHOSPHORYLATION AND ACTIVATION OF THE SRC-FAMILY KINASE P56(LYN) SO BLOOD LA English DT Meeting Abstract C1 UNIV MUNICH,KLINIKUM INNENSTADT,MED KLIN,W-8000 MUNICH 2,GERMANY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A368 EP A368 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201454 ER PT J AU INHORN, RC ASTER, JC SLAPAK, CA SOIFFER, RJ STONE, RM AF INHORN, RC ASTER, JC SLAPAK, CA SOIFFER, RJ STONE, RM TI A SYNDROME OF LYMPHOBLASTIC LYMPHOMA, EOSINOPHILIA, AND MYELOID HYPERPLASIA MALIGNANCY ASSOCIATED WITH T(8, 13) (P11, Q11) SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A388 EP A388 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201535 ER PT J AU ISHIMARU, F SHIPP, MA AF ISHIMARU, F SHIPP, MA TI CD10/NEP REGULATION IN LYMPHOID PROGENITORS - MULTIPLE 5' UNTRANSLATED REGIONS AND LABILE TRANSCRIPTS SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A132 EP A132 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200514 ER PT J AU JANOV, A LEONG, T NATHAN, D GUINAN, E AF JANOV, A LEONG, T NATHAN, D GUINAN, E TI NATURAL-HISTORY AND SEQUELAE OF TREATMENT IN PATIENTS (PTS) WITH DIAMOND-BLACKFAN ANEMIA (DBA) SO BLOOD LA English DT Meeting Abstract C1 CHILDRENS HOSP BOSTON,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A311 EP A311 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201226 ER PT J AU LEE, Y LOPEZ, K GARRISON, L NATHAN, D HOFFMAN, R GUINAN, E AF LEE, Y LOPEZ, K GARRISON, L NATHAN, D HOFFMAN, R GUINAN, E TI A PHASE I/II STUDY OF RECOMBINANT HUMAN INTERLEUKIN-3 (IL-3) AND GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR (GM-CSF) FUSION PROTEIN PIXY321 IN PATIENTS (PTS) WITH CONGENITAL AMEGAKARYOCYTIC THROMBOCYTOPENIA (AMT) SO BLOOD LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,BOSTON,MA 02115. INDIANA UNIV,INDIANAPOLIS,IN 46204. IMMUNEX CORP,SEATTLE,WA. NR 1 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A608 EP A608 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68202413 ER PT J AU LEE, YS LIEN, L ORKIN, SH AF LEE, YS LIEN, L ORKIN, SH TI REGULATED EXPRESSION OF THE HUMAN MYELOID-SPECIFIC GP91-PHOX GENE FOLLOWING YEAST ARTIFICIAL CHROMOSOME (YAC) TRANSFER INTO MOUSE EMBRYONIC STEM (ES) CELLS SO BLOOD LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HHMI,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A321 EP A321 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201266 ER PT J AU LUNDBERG, A GRIBBEN, J LAZO, S NADLER, L AF LUNDBERG, A GRIBBEN, J LAZO, S NADLER, L TI EXPRESSION AND INDUCTION OF B7 ON LEUKEMIC-CELLS ISOLATED FROM PATIENTS WITH HEMATOLOGIC MALIGNANCIES SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A123 EP A123 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200475 ER PT J AU MATSUGUCHI, T SALGIA, R HALLEK, M EDER, M DRUKER, B ERNST, T GRIFFIN, JD AF MATSUGUCHI, T SALGIA, R HALLEK, M EDER, M DRUKER, B ERNST, T GRIFFIN, JD TI SHC PHOSPHORYLATION IN MYELOID CELLS IS REGULATED BY GM-CSF, IL-3, STEEL FACTOR AND IS CONSTITUTIVELY INCREASED BY P210(BCR ABL) SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A438 EP A438 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201734 ER PT J AU MATULONIS, U MAUCH, P FREEMAN, G LAMONT, C NADLER, L GRIFFIN, JD AF MATULONIS, U MAUCH, P FREEMAN, G LAMONT, C NADLER, L GRIFFIN, JD TI PREVENTION OF LEUKEMIA IN IMMUNOLOGICALLY INTACT MICE BY INTRODUCTION OF THE B7 COSTIMULATORY MOLECULE INTO A SYNGENEIC MYELOID CELL-LINE TRANSFORMED BY P210BCR/ABL SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A442 EP A442 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201751 ER PT J AU MIZOBUCHI, T HIRANO, M CLINTON, SK KUFE, DW STONE, RM AF MIZOBUCHI, T HIRANO, M CLINTON, SK KUFE, DW STONE, RM TI STABLE TRANSFECTION OF C-FMS CDNA DOWNSTREAM FROM A METALLOTHIONEIN PROMOTER IN THE HUMAN LEUKEMIC U-937 CELL-LINE - INDUCIBLE EXPRESSION OF FUNCTIONAL M-CSF RECEPTOR SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A235 EP A235 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200923 ER PT J AU OCONNOR, R LIU, C TEICHER, BA SHAH, SA BLATTLER, WA AF OCONNOR, R LIU, C TEICHER, BA SHAH, SA BLATTLER, WA TI ANTI-B4 BLOCKED RICIN AS A CANDIDATE TO REVERSE MULTIDRUG-RESISTANCE IN B-CELL TUMORS SO BLOOD LA English DT Meeting Abstract C1 IMMUNOGEN INC,CAMBRIDGE,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A140 EP A140 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200544 ER PT J AU ODAY, S RABINOWE, S NEUBERG, D FREEDMAN, A SOIFFER, R ROBERTSON, M SPECTOR, N GROSSBARD, M ANDERSON, K WHELAN, M PESEK, K RITZ, J NADLER, L AF ODAY, S RABINOWE, S NEUBERG, D FREEDMAN, A SOIFFER, R ROBERTSON, M SPECTOR, N GROSSBARD, M ANDERSON, K WHELAN, M PESEK, K RITZ, J NADLER, L TI A PHASE-II STUDY OF CONTINUOUS-INFUSION RECOMBINANT HUMAN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR (RHGM-CSF) AS AN ADJUNCT TO AUTOLOGOUS BONE-MARROW TRANSPLANTATION (ABMT) FOR NON-HODGKINS-LYMPHOMA (NHL) IN 1ST REMISSION SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A145 EP A145 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200565 ER PT J AU OKUDA, K ERNST, T GRIFFIN, JD AF OKUDA, K ERNST, T GRIFFIN, JD TI ACTIVATION OF P21RAS BY IL-3 IS REQUIRED FOR PROLIFERATION BUT NOT FOR THE MAINTENANCE OF CELL VIABILITY SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A185 EP A185 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200724 ER PT J AU PAI, SY FRUMAN, D LEONG, T ROSANO, T MCGARIGLE, C ANTIN, JH BIERER, BE AF PAI, SY FRUMAN, D LEONG, T ROSANO, T MCGARIGLE, C ANTIN, JH BIERER, BE TI INHIBITION OF CALCINEURIN (CN) PHOSPHATASE-ACTIVITY IN BMT PATIENTS TREATED WITH CYCLOSPORINE-A (CSA) SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. ALBANY MED COLL,ALBANY,NY 12208. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A348 EP A348 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201373 ER PT J AU PAI, SY CALVO, V WOOD, M BIERER, BE AF PAI, SY CALVO, V WOOD, M BIERER, BE TI CROSS-LINKING CD28 LEADS TO ACTIVATION OF 70 KDA S6 KINASE SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A188 EP A188 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200737 ER PT J AU PAIETTA, E ANDERSEN, J RACEVSKIS, J GALLAGHER, R BENNETT, J YUNIS, J WIERNIK, PH AF PAIETTA, E ANDERSEN, J RACEVSKIS, J GALLAGHER, R BENNETT, J YUNIS, J WIERNIK, PH TI ACUTE PROMYELOCYTIC LEUKEMIA (APL) CELLS LACK P-GLYCOPROTEIN EXPRESSION BY IMMUNOLOGICAL, MOLECULAR AND FUNCTIONAL-ANALYSIS SO BLOOD LA English DT Meeting Abstract C1 ALBERT EINSTEIN CANC CTR,BRONX,NY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV ROCHESTER,ROCHESTER,NY 14627. THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107. EASTERN COOPERAT ONCOL GRP,DENVER,CO. MONTEFIORE MED CTR,BRONX,NY 10467. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A252 EP A252 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200991 ER PT J AU PARSONS, SK MARTIN, T LAVITA, L COHEN, SA NEUBERG, DS GUINAN, EC WEINSTEIN, HJ AF PARSONS, SK MARTIN, T LAVITA, L COHEN, SA NEUBERG, DS GUINAN, EC WEINSTEIN, HJ TI OBSTRUCTIVE AIRWAY DISEASE IN CHILDREN AFTER ALLOGENEIC BONE-MARROW TRANSPLANTATION (BMT) SO BLOOD LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A418 EP A418 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201653 ER PT J AU RAN, JY DOU, P WANG, LY YUAN, RX HAO, JM ZHANG, H JIN, SY LI, ZP QIN, Y HERBERT, V AF RAN, JY DOU, P WANG, LY YUAN, RX HAO, JM ZHANG, H JIN, SY LI, ZP QIN, Y HERBERT, V TI IN A HIGH-FREQUENCY ESOPHAGEAL-CARCINOMA (EC) AREA, FOLATE AND B12 DEFICIENT SUBJECTS WITH ESOPHAGEAL DYSPLASIA (ED) IMPROVE WITH ADDED FOLATE AND B12 SO BLOOD LA English DT Meeting Abstract C1 SHANXI MED COLL,TAIYUAN,PEOPLES R CHINA. BRONX VET AFFAIRS MED CTR,BRONX,NY. MT SINAI MED CTR,NEW YORK,NY 10029. NR 1 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A532 EP A532 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68202110 ER PT J AU RAN, JY DOU, P WANG, LY QIN, Y JIN, SY LI, XF HERBERT, V AF RAN, JY DOU, P WANG, LY QIN, Y JIN, SY LI, XF HERBERT, V TI CORRELATION OF LOW SERUM FOLATE AND TOTAL B12 WITH HIGH-INCIDENCE OF ESOPHAGEAL-CARCINOMA (EC) IN SHANXI, CHINA SO BLOOD LA English DT Meeting Abstract C1 SHANXI MED COLL,TAIYUAN,PEOPLES R CHINA. BRONX VET AFFAIRS MED CTR,BRONX,NY. MT SINAI MED CTR,NEW YORK,NY 10029. NR 1 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A532 EP A532 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68202109 ER PT J AU REDDY, JC MORRIS, JC ENGLISH, MA HABER, DA LUO, XN ATWEH, G LICHT, JD AF REDDY, JC MORRIS, JC ENGLISH, MA HABER, DA LUO, XN ATWEH, G LICHT, JD TI THE WILMS-TUMOR (WT1) GENE-PRODUCT BOTH ACTIVATES AND REPRESSES TRANSCRIPTION SO BLOOD LA English DT Meeting Abstract C1 MT SINAI MED CTR,DIV MOLEC MED,NEW YORK,NY 10029. MT SINAI MED CTR,DIV NEOPLAST DIS,NEW YORK,NY 10029. MT SINAI MED CTR,DIV HEMATOL,NEW YORK,NY 10029. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A324 EP A324 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201281 ER PT J AU REDDY, SV ALCANTARA, O ROODMAN, GD BOLDT, DH AF REDDY, SV ALCANTARA, O ROODMAN, GD BOLDT, DH TI TRANSCRIPTIONAL INHIBITION OF THE TARTRATE-RESISTANT ACID-PHOSPHATASE (TRAP) GENE BY HEMIN SO BLOOD LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A43 EP A43 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200160 ER PT J AU ROBERTSON, MJ ROY, DC SOIFFER, R BELANGER, R GYGER, M PERREAULT, C ANDERSON, K FREEDMAN, A NADLER, LM RITZ, J AF ROBERTSON, MJ ROY, DC SOIFFER, R BELANGER, R GYGER, M PERREAULT, C ANDERSON, K FREEDMAN, A NADLER, LM RITZ, J TI MORE RAPID ENGRAFTMENT AFTER INFUSION OF AUTOLOGOUS BONE-MARROW TREATED WITH ANTI-MY9 BLOCKED RICIN COMPARED TO BONE-MARROW TREATED WITH ANTI-MY9 AND COMPLEMENT SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. HOP MAISON NEUVE ROSEMONT, MONTREAL H1T 2M4, QUEBEC, CANADA. RI Perreault, Claude/A-7220-2008 OI Perreault, Claude/0000-0001-9453-7383 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A640 EP A640 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68202544 ER PT J AU ROBERTSON, MJ COCHRAN, KJ RITZ, J AF ROBERTSON, MJ COCHRAN, KJ RITZ, J TI PHENOTYPIC AND FUNCTIONAL-CHARACTERIZATION OF A NEW MALIGNANT HUMAN NATURAL-KILLER-CELL LINE, N K L SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A242 EP A242 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200954 ER PT J AU ROBERTSON, MJ MANLEY, TJ PICHERT, G CAMERON, C COCHRAN, K RITZ, J AF ROBERTSON, MJ MANLEY, TJ PICHERT, G CAMERON, C COCHRAN, K RITZ, J TI FUNCTIONAL CONSEQUENCES OF APO-1/FAS ANTIGEN EXPRESSION BY NORMAL AND NEOPLASTIC HEMATOPOIETIC-CELLS SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A39 EP A39 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200146 ER PT J AU ROY, DC GYGER, M BELANGER, R PERREAULT, C BONNY, Y SOIFFER, R ESSELTINE, D RITZ, J AF ROY, DC GYGER, M BELANGER, R PERREAULT, C BONNY, Y SOIFFER, R ESSELTINE, D RITZ, J TI ENGRAFTMENT FOLLOWING AUTOLOGOUS BONE-MARROW TRANSPLANTATION WITH ANTI-B4-BR DEPLETED MARROW FOR PATIENTS WITH B-CELL MALIGNANCIES SO BLOOD LA English DT Meeting Abstract C1 HOP MAISON NEUVE ROSEMONT, DIV HEMATOL ONCOL, MONTREAL H1T 2M4, QUEBEC, CANADA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV TUMOR IMMUNOL, BOSTON, MA 02115 USA. IMMUNOGEN INC, CAMBRIDGE, MA USA. RI Perreault, Claude/A-7220-2008 OI Perreault, Claude/0000-0001-9453-7383 NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A81 EP A81 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200311 ER PT J AU RUTLEDGE, BJ RAYBURN, H ROSENBERG, RD CORLESS, CL ROLLINS, BJ AF RUTLEDGE, BJ RAYBURN, H ROSENBERG, RD CORLESS, CL ROLLINS, BJ TI TRANSGENIC MICE OVEREXPRESSING MURINE MCP-1 SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A187 EP A187 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200731 ER PT J AU SALLES, G ZAIN, M BOUSSIOTIS, VA SHIPP, MA AF SALLES, G ZAIN, M BOUSSIOTIS, VA SHIPP, MA TI ALTERNATIVELY SPLICED CD44 TRANSCRIPTS IN DIFFUSE LARGE-CELL LYMPHOMAS (LCL), NORMAL ACTIVATED B-CELLS AND EPITHELIAL MALIGNANCIES SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A201 EP A201 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200788 ER PT J AU SHIKAMA, Y LAURIE, AS JUBINSKY, PT SIEFF, CA AF SHIKAMA, Y LAURIE, AS JUBINSKY, PT SIEFF, CA TI THE COMMON BETA-SUBUNIT OF THE HUMAN GM-CSF RECEPTOR INTERACTS WITH A GM-CSF/ERYTHROPOIETIN RECEPTOR SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A184 EP A184 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200722 ER PT J AU SHIPP, MA SHULMAN, LN KAPLAN, WD NEUBERG, D CANELLOS, GP AF SHIPP, MA SHULMAN, LN KAPLAN, WD NEUBERG, D CANELLOS, GP TI INTENSIFIED INDUCTION THERAPY FOR PATIENTS WITH HIGH-RISK AGGRESSIVE NHL - HIGH-DOSE CHOP SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A332 EP A332 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201311 ER PT J AU SLAPAK, CA MIZUNUMA, N KUFE, DW AF SLAPAK, CA MIZUNUMA, N KUFE, DW TI SIMULTANEOUS OVEREXPRESSION OF P-GLYCOPROTEIN AND THE MULTIDRUG-RESISTANCE ASSOCIATED PROTEIN (MRP) IN DOXORUBICIN-SELECTED HUMAN MYELOID-LEUKEMIA CELLS SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A118 EP A118 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200455 ER PT J AU SOIFFER, RJ CANNING, C GONIN, R RITZ, J AF SOIFFER, RJ CANNING, C GONIN, R RITZ, J TI INFLUENCE OF LOW-DOSE INTERLEUKIN-2 ON RELAPSE RATE AFTER T-CELL DEPLETED ALLOGENEIC BMT SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A215 EP A215 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200845 ER PT J AU SPECTOR, NL RYAN, C WRANA, J MASSAGUE, J ELLINGSWORTH, L NADLER, LM AF SPECTOR, NL RYAN, C WRANA, J MASSAGUE, J ELLINGSWORTH, L NADLER, LM TI HSP28 - A NOVEL INTERMEDIARY IN THE TGF-BETA GROWTH-INHIBITORY PATHWAY SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A437 EP A437 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201732 ER PT J AU SPECTOR, NL RYAN, C MEHLEN, P SAMSON, W LEVINE, H ARRIGO, AP NADLER, LM AF SPECTOR, NL RYAN, C MEHLEN, P SAMSON, W LEVINE, H ARRIGO, AP NADLER, LM TI A NOVEL GROWTH-REGULATORY MOLECULE DURING RETINOID-INDUCED DIFFERENTIATION OF HUMAN LEUKEMIC-CELLS SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. UNIV CLAUDE BERNARD LYON 1,VILLEURBANNE,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A255 EP A255 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201004 ER PT J AU SPITZER, TR BRYSON, JC CIRENZA, E FOELBER, R WALLERSTADT, M STOUT, C KUNKA, RL DUBOIS, A AF SPITZER, TR BRYSON, JC CIRENZA, E FOELBER, R WALLERSTADT, M STOUT, C KUNKA, RL DUBOIS, A TI A RANDOMIZED DOUBLE-BLIND, PLACEBO-CONTROLLED TRIAL OF ONDANSETRON (OND) IN THE PREVENTION OF TOTAL-BODY IRRADIATION (TBI) INDUCED EMESIS SO BLOOD LA English DT Meeting Abstract C1 GLAXO INC,RES TRIANGLE PK,NC. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. USUHS,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A419 EP A419 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201659 ER PT J AU STEINMAN, RA ANDERSON, SM MATULONIS, U TWEARDY, DJ AF STEINMAN, RA ANDERSON, SM MATULONIS, U TWEARDY, DJ TI ONCOGENE-MEDIATED SUPPRESSION OF GRANULOCYTE-COLONY-STIMULATING FACTOR-RECEPTOR (G-CSFR) MESSENGER-RNA EXPRESSION SO BLOOD LA English DT Meeting Abstract C1 UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261. PITTSBURGH CANC INST,PITTSBURGH,PA. SUNY STONY BROOK,STONY BROOK,NY 11794. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A234 EP A234 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200920 ER PT J AU STODDART, JH LYNCH, DC AF STODDART, JH LYNCH, DC TI CLEARANCE OF HUMAN VON-WILLEBRAND-FACTOR (VWF) IN THE RAT SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A446 EP A446 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201767 ER PT J AU STONE, R NEUBERG, D SOIFFER, R WHELAN, M LEAVITT, P ASTER, J TAKVORIAN, R RABINOWE, S RITZ, J FREEDMAN, A NADLER, L AF STONE, R NEUBERG, D SOIFFER, R WHELAN, M LEAVITT, P ASTER, J TAKVORIAN, R RABINOWE, S RITZ, J FREEDMAN, A NADLER, L TI MYELODYSPLASTIC SYNDROME (MDS) AS A COMPLICATION AFTER AUTOLOGOUS BONE-MARROW TRANSPLANTATION (ABMT) FOR NON-HODGKINS-LYMPHOMA (NHL) SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A196 EP A196 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200769 ER PT J AU STONE, RM TORIGOE, PS BERG, DT MIZOBUCHI, T MAYER, RJ CANNISTRA, SA AF STONE, RM TORIGOE, PS BERG, DT MIZOBUCHI, T MAYER, RJ CANNISTRA, SA TI INTERLEUKIN-3 (IL-3) BEFORE AND DURING INTERMITTENT CONTINUOUS-INFUSION HIGH-DOSE ARA-C (ICHDAC) THERAPY FOR REFRACTORY OR SECONDARY ACUTE MYELOID-LEUKEMIA (AML) SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A130 EP A130 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200506 ER PT J AU TAKAHASHI, S GOLDRING, S ROODMAN, GD AF TAKAHASHI, S GOLDRING, S ROODMAN, GD TI REGULATION OF CALCITONIN RECEPTOR (CTR) MESSENGER-RNA EXPRESSION IN OSTEOCLASTS (OCL) AND THEIR PRECURSORS SO BLOOD LA English DT Meeting Abstract C1 VET ADM MED CTR,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A492 EP A492 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68201951 ER PT J AU WALTERS, MC ANDREWS, NC MAGIS, W MARTIN, DIK AF WALTERS, MC ANDREWS, NC MAGIS, W MARTIN, DIK TI AP-1/NF-E2 ELEMENTS BIND AP-1, BUT ERYTHROID ACTIVITY IS RELATED TO NF-E2 BINDING SO BLOOD LA English DT Meeting Abstract C1 FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. UNIV WASHINGTON,SEATTLE,WA 98195. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A218 EP A218 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200856 ER PT J AU YAMASHITA, T BARBER, D ZHU, Y DANDREA, AD AF YAMASHITA, T BARBER, D ZHU, Y DANDREA, AD TI THE FANCONI-ANEMIA (FACC) POLYPEPTIDE BINDS AND FORMS A PROTEIN COMPLEX WITH A 50KD ASSOCIATED PROTEIN (FAP-50) SO BLOOD 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 1 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1993 VL 82 IS 10 SU 1 BP A176 EP A176 PG 1 WC Hematology SC Hematology GA MJ682 UT WOS:A1993MJ68200689 ER EF